Bad Times in Vegas

Well as you may see from my few previous blogs, my life in Las Vegas doesn’t seem to be going all that well. I’m trying to keep a positive attitude about life, but it’s hard for me to see when the these hard times will dissipate. I’d love to be able to express in a better way what it has been like for me these past few years, but producing the correct words presently fail me. By chance, I was listening to a radio program last night from NPR, and felt that it was eloquent enough about what it has been like for many of us who live here to share the web link with everyone. As for Vegas, no matter what the show must go on, so let’s put on our happy faces, get out there, and break a leg. I plan to blog a little more about things here, such as City Center, in a few days. Life, as they say, is too short.

Here is the web site:

http://americanradioworks.publicradio.org/features/foreclosure/index.html

You can download the radio program, listen online, or read the transcript.

Here are a few helpful links found with this program, if your having problems:

• Federal Reserve Bank of San Francisco’s Foreclosure Resource Center
  http://www.frbsf.org/community/issues/assets/preservation/index.html
• Nevada Foreclosure Trends
  http://www.frbsf.org/community/issues/assets/preservation/state_resources_nv.html
• U.S. Department of Housing and Urban Development resources
  http://www.hud.gov/offices/hsg/sfh/econ/econ.cfm
• Homeowner Affordability and Stability Plan
  http://www.treasury.gov/press/releases/tg33.htm
• The White House Blog – Help for Homeowners
  http://www.whitehouse.gov/blog/09/02/18/help-for-homeowners/
• “A Crisis is a Terrible Thing to Waste: Transforming America’s Housing Policy” conference
  http://transformingamericashousingpolicy.org/conference/

What’s up with the Trucker?

OK, first of all I wish to dispel anyone’s morbid concern about my lack of writing and inform you of the not so obvious, I’m still alive and somewhat healthy. Mentally, it’s hard for anyone to express failure, but I’m sure that after you’ve read the next few paragraphs you’ll have a better picture as to why I took a short sabbatical from the blogoshere.

Let’s start where I left you last and write a little of my journey to Claremont, CA. The trip itself was about five hours of travel, with a short pit stop in Bakersfield. The hotel was only separated by a Micky D’s from the Greyhound Station, and orientation what held right there at the hotel.

I was very nervous, excited, and a little too anxious about getting through the whole ordeal that it cause me an unforeseen issue on the very first morning of orientation. Covenant requires all new drivers to take what they refer to as an agility test. It, like the ones give to firemen, is meant to test the new employee’s ability to perform the physically requirement of the job. The way this was done was to give the recruited driver a few physical tasks and check their heart rate at each. If the rate was over a predetermined limit, the driver was failed and sent home.

Well as you can imagine, I was not in the proper state of mind and got a little too zealous towards getting through this test and failed to take enough time to fully understand what I should be doing. I actually did quite well, until I was given this push pull test. It required me to pull against a spring scale and then turn around and push against it. When I pull the required amount was 90lbs and my max. heart rate had to be less than 153. I pull at about 110 and passed. I then turned around and push at almost 120, when I only needed 70lbs, and this pushed my heart to just a little over the limit, and it failed me. Heck, if they would have told me to walk a straight line, I probably would have tried to do it on my hands.

I thought I was fine, but I was coldly give the boot from this lady named, Mike C., just after lunch and was told I had to check out right then. I had no second chance, but I was informed that I could try again in six months. This, as you can imagine, put me in a bad place, but I knew that AIT would help to place with another company, so I gave them a call right away and let them know that I was heading back home.

I filled out quite a few applications the next day at the Lone Mountain location, but I was unwittingly complicating the issue, by disclosing too much unnecessary information on these applications and did not catch this error until it was far too late. I was however soon contacted by Swift and it look very much as if I would be given a second chance with them, but this proved to be a futile experience after an intensive three week effort.

Swift was the last Class A company I worked for over 5 years ago, and it’s obviously that it takes them forever to get over a couple of minor accidents which never showed up on my DAC. They really had me thinking that I might be re-hired, but I do know that if there is anything derogatory here, it should disappear after 7 year period, and I refuse to believe that I am being rejected wholly on just this issue.

I’ve worked very hard these last few weeks to find a place were I can use my class A driving skills, and have currently scaled back my job search effort significantly due to the present situation with the economy. Not that I’m really looking forward to it, but I plan now to go full bore again in February. Fortunately, I was able to go back to A Cab and was back on the job that very Friday with no loss in seniority. In fact, the boss was happy to see me back, and had not as yet terminated me.

So here I am again in Vegas, doing the same old awful low paying job, but with the additional nightmarishly facts that I’m sleeping on the floor in my own house, taking the bus to work, and dealing with having all my belongings in storage at an add expense to my limited dwindling budget. The bum that I spoke of in a previous blog is about to get the boot, and this should give me a room to sleep in about a month from now, if not sooner. That’s all for now, and to be honest, it’s not all been bad, so you should expect me to blog more positively the next time I write. I don’t know about you, but I really do prefer giving out, as well as getting, the bad news first.

Have Fun and Be Safe.

Why drink Vitamin Water?

Ok to begin with, I like drinking the vitamin water. I don’t do this not just because I need the vitamins, but also because it makes the water a little easier to take and it’s much better for me than one of those toxic caffeinated sodas.

First thing to understand, the body only needs a minute amount of nutrients to function. If there is an excess, it is generally expelled down the never land receptical, I affectionately call the crapper. You may think differently about this, but since may of us feel that vitamins and water are important for us, our need to stay healthy can drive us to a wasteful obsession. Please before you go off the deep end and buy allot of expensive supplements destined for the crapper, do a little research on what you about to take. It’s a fact that your body can also be irreversibility harmed by too much of what we are perceiving to be a good thing. So please, think healthy first and be very cautious about what you ingest.

Vitamin B12, like the other B vitamins, is important for metabolism. It helps in the formation of red blood cells and in the maintenance of the central nervous system.

True, there are some vitiamins that you can take in excess like B12, but you should question whether is it actually being used or just pissed away. The B vitamins are vital to a vigorous and energetic long life. What’s more, you can get serious health problems if you lack them. B vitamins are easily flushed out of the body, and people on weight-loss diets, alcoholics or those who take antibiotics or seizure drugs are even more prone to having vitamin B deficiency.

While it is safe for many people to take three times or more of the RDA (Recommended Daily Allowance) for B-vitamins, each of us has unique requirements based on our own individual physiology and lifestyle. Hence, it is important to check with your doctor before beginning a vitamin regimen in order to determine your proper dosage. Because deficiencies usually include more than one B-vitamin, and because the B-vitamins work best as a team, you should take a B-complex supplement along with any single B-vitamin in order to achieve their synergistic effects.

Since there are both fat-soluble and water-soluble vitamins, you most likely drinking only the water-soluble ones in a vitamin water. A word of caution, through the research which I’ve done thus far, it seem that the vitamins which have the highest potential to do harm if ingested in excess are the fat-soluble ones. In fact from all that I’ve read so far, the best means of obtaining safe levels of the fat-soluble ones are from eating green salads and vegetables.

Here is a listing of the two types:

FAT-SOLUBLE VITAMINS

• vitamin A (retinol; carotene is an important precursor of vitamin A)
• vitamin D (ergocalciferol and cholecalciferol)
• vitamin E (tocopherol)
• vitamin K (phylloquinone from plants; menaquinone from gut bacteria)

WATER-SOLUBLE VITAMINS

• vitamin B1 (thiamin)
• vitamin B2 (riboflavin)
• vitamin B6 (pyridoxine)
• vitamin B12 (cobalamin)
• niacin (nicotinic acid and nicotinamide)
• pantothenic acid (vitamin B5)
• biotin (vitamin H)
• folic acid (vitamin B9)
• vitamin C (ascorbic acid)

If you take a look at the lable on one of the popular Propel bottles, you will see that they include vitamin E. So how do they get the fat in the water? Does it float at the top? Why do they do this?

The major function of vitamin E is to serve as a chain-breaking antioxidant, protecting cell membranes against free-radical damage. From the material which I’ve read thus far, I see no reason to take more the recommended RDA of this vitamin, and do not see how they get a fat to be in a water drink unless they use an homogenizer or emulsifying agent. When I look more closely at the label, I can see that they are using the Acetate form of this vitamin. Any acetate form (A salt or ester of acetic acid) mixes well in water.

Since, I love oatmeal for all of the positive things that it does for me, I choose not to take a suplemental vitamin E, so I don’t have an adverse effect an the thyroid problem I have. The excessive supplementation of vitamin E without selenium may deplete selenium and therefore contribute to thyroid disease.

Others sources of vitamin E:

• Wheat germ oil (215.4 mg/100 g)
• Sunflower oil (55.8 mg/100 g)
• Hazelnut (26.0 mg/100 g)
• Walnut oil (20.0 mg/100 g)
• Peanut oil (17.2 mg/100 g)
• Olive oil (12.0 mg/100 g)
• Peanut (9.0 mg/100 g)
• Pollard (2.4 mg/100 g)
• Corn (2.0 mg/100 g)
• Asparagus (1.5 mg/100 g)
• Oats (1.5 mg/100 g)
• Chestnut (1.2 mg/100 g)
• Coconut (1.0 mg/100 g)
• Tomatoes (0.9 mg/100 g)
• Carrots (0.6 mg/100 g)

At a buck or more a bottle, for a 22oz shot of fortified water is to me too expensive. I have found however that there is an alturnative to this. I like the “turn to open plastic” bottles of Gatoraid and Propel, so I save a few of the used bottles (a cheaper way than buying those expensive special bottles), and then buying the one shot powdered energy drink packets from the local grocery store. A very good one that I’ve found is the Kroger brand “In an Instance, Fitness” (The levels of vitiamins are low, so the chance of getting a toxic dose while keeping hydrated seems less likely).

Energy and Hydration:

One of the most important thing that I’ve found while living here in Las Vegas is to keep hydrated. Face it, on one of those famous vegas scorcher, (generally around indepenance day,) you can dehydrate enough to suffer a heat stroke. As far as water is concerned, it’s critical for the body to stay hydrated. You can survive a month without food, but you may not last a week without water. You’re going to have to face it, if you don’t hydrate, you’re going to feel tired. An insufficient amount of water in your system causes a reduction in blood volume, which means less oxygen gets to your working muscles. In fact, some experts even contend that staying well-hydrated contributes to long-term high energy by helping to relieve enervating conditions such as arthritis, body aches, constipation, indigestion, ulcers and stress.

Caffeinated sodas, tea and coffee, which actually leach fluid from your body with their diuretic effects. Why heck, even having a beer or glass of wine will drain the body of water, as good number of individuals know when they realize that they must pay a visit to the nearest restroom. So, although you may feel the need to get stimulated now, going down the the local Starbucks may not be best choice. Not that I’m asking you to swear off any sort of predictable habit, but sometimes the best thing to do is just following your thirst. That is if you feel that your throat is going dry, then maybe this is a signal that it’s time to take a drink of water. If you’re feeling a bit hungry, then perhaps it’s time to take a small protien snack and a large amount of water to get it digested and absorbed easier. And remember a little exercise can do wonders to your energy level (all you just need to do is about 10 to 20 minutes a day of the necessary heart pumping activity for you to break a sweat and begin to feel the energizing effects).

It looks like I’ll leave this here as it is, and call it a day. Again, I’m not really qualified to be giving any real advice, but I’m free to blog on what I’ve found and hope that it’s possibly helpful to someone else. But don’t take my word for it, please do your own research. In my opinion, the vitamin waters do far more good for you than harm, but is it worth the cost to you? I buy the little pouches and add them as I think I need to. Until the next blog.

Have fun and take care.

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More reading at:

http://www.answers.com/vitamins?cat=health

http://www.vitaminmaniac.com/vitamin-absorption-experiment

http://ezinearticles.com/?Vitamin-Absorption-into-the-Body&id=171910

http://www.vitaminsgroup.com/liquid-vitamins-are-destroyed-by-stomach-acid.html

http://deepfitness.com/3602/-1-Liquid-Vitamin-Myth.aspx

http://dietandbody.com/Are_you_getting_vitamins.html

http://www.calorieking.com/library/articles/Hydration-Guide_YwlkPTc1OA.html

http://en.wikipedia.org/wiki/Weight_cutting

http://www.nlm.nih.gov/medlineplus/ency/article/000982.htm

http://heartburn.about.com/od/understandingheartburn/a/digestivesystem_2.htm

http://recipes.howstuffworks.com/alcohol3.htm

http://www.consumeraffairs.com/news04/2007/10/geezer036.html

http://digestive.niddk.nih.gov/ddiseases/pubs/constipation/

http://www.webmd.com/diet/features/the-truth-about-belly-fat

http://www.ithyroid.com/vitamin_e.htm

http://www.thyroid-info.com/articles/topsupplements.htm

http://www.internethealthlibrary.com/Health-problems/Hypothyroidism%20-%20researchDiet&Lifestyle.htm

http://www.rice.edu/~jenky/sports/dehydration.html

http://www.vitamins-nutrition.org/vitamins/vitamin-b-energy.html

Enzymes are the energy givers

A few days ago, I blogged hundreds of words on Healthy Energy. It is known that what we eat has a directed effect on our metabolic and energy level. Even before a bite of food is eaten, our salivary glands (exocrine glands) can kick into high production, and we begin salivating our food softening enzyme, amylase.

Amylase hydrolyzes starch, glycogen, and dextrin to form in all three instances glucose, maltose, and the limit-dextrins. Amylase is not in the saliva of some animals such as horses, dogs, and cats. Amylase is also known as Ptyalin.

Amylase enzymes are used extensively in bread making to break down complex sugars such as starch (found in flour) into simple sugars. Yeast then feeds on these simple sugars and converts it into the waste products of alcohol and CO2. This imparts flavour and causes the bread to rise. While Amylase enzymes are found naturally in yeast cells, it takes time for the yeast to produce enough of these enzymes to break down significant quantities of starch in the bread. This is the reason for long fermented doughs such as sour dough. Modern bread making techniques have included amylase enzymes into bread improver thereby making the bread making process faster and more practical for commercial use.

Two similar types of amylase are made in your body–one is secreted in saliva, where it starts to break down starch grains as you chew, and the other is secreted by the pancreas, where it finishes its job. Then, these little pieces are broken into individual glucose units by a collection of enzymes that are tethered to the walls of the intestine. It takes starch chains and breaks them into smaller pieces with two or three glucose units. Then, these little pieces are broken into individual glucose units by a collection of enzymes that are tethered to the walls of the intestine.

Your blood’s glucose is a major source of energy in your body. One of the major jobs of digestion is to break these chains into their individual glucose units, which are then delivered by the blood to hungry cells throughout your body. Blood glucose levels are maintained in the blood by the hormone activity of insulin and glucagon. Long term insufficient hormone activity to control blood glucose levels will result in diabetes.

So the amylase enzymes in our saliva are biological catalysts, or chemicals that speed up the rate of reaction between substances without themselves being consumed in the reaction.

Enzymes have extremely interesting properties that make them little chemical-reaction machines. The purpose of an enzyme in a cell is to allow the cell to carry out chemical reactions very quickly. These reactions allow the cell to build things or take things apart as needed. This is how a cell grows and reproduces. At the most basic level, a cell is really a little bag full of chemical reactions that are made possible by enzymes!

So how does the body come up with the saliva enzyme?

A type of protein, enzymes sometimes work in tandem with non-proteins called coenzymes. Among the processes in which enzymes play a vital role is fermentation, which takes place in the production of alcohol or the baking of bread and also plays a part in numerous other natural phenomena, such as the purification of wastewater. The body uses long chains of protiens called amino acids to create the enzymes in our bodies. Amino acids are organic compounds made of carbon, hydrogen, oxygen, nitrogen, and (in some cases) sulfur bonded in characteristic formations and are link together by peptide bonds to form proteins or that function as chemical messengers and as intermediates in metabolism. The amino acid sequence in a particular protein is determined by its gene.

Of the 20 amino acids required by humans for making protein, only 12 can be produced within the body, whereas the other eight—isoleucine, leucine, lysine, methionine, phenylalanine, threonine, tryptophan, and valine—must be obtained from the diet. (In addition, adults are capable of synthesizing arginine and histidine, but these amino acids are believed to be essential to growing children, meaning that children cannot produce them on their own.)

A complete protein is one that contains all of the essential amino acids in quantities sufficient for growth and repair of body tissue. Most proteins from animal sources, gelatin being the only exception, contain all the essential amino acids and are therefore considered complete proteins. On the other hand, many plant proteins do not contain all of the essential amino acids. For example, lysine is absent from corn, rice, and wheat, whereas corn also lacks tryptophan and rice lacks threonine. Soybeans are lacking in methionine. Vegans, or vegetarians who consume no animal proteins in their diets (i.e., no eggs, dairy products, or the like) are at risk of malnutrition, because they may fail to assimilate one or more essential amino acid.

All enzymes belong to the protein family, but many of them are unable to participate in a catalytic reaction until they link with a non protein component called a coenzyme. This can be a medium-size molecule called a prosthetic group, or it can be a metal ion (an atom with a net electric charge), in which case it is known as a cofactor. Quite often, though, coenzymes are composed wholly or partly of vitamins. Although some enzymes are attached very tightly to their coenzymes, others can be parted easily; in either case, the parting almost always deactivates both partners.

Enzymes in the human body fulfill one of three basic functions. The largest of all enzyme types, sometimes called metabolic enzymes, assist in a wide range of basic bodily processes, from breathing to thinking. Some such enzymes are devoted to maintaining the immune system, which protects us against disease, and others are involved in controlling the effects of toxins, such as tobacco smoke, converting them to forms that the body can expel more easily.

A second category of enzyme is in the diet and consists of enzymes in raw foods that aid in the process of digesting those foods. They include proteases, which implement the digestion of protein; lipases, which help in digesting lipids or fats; and amylases, which make it possible to digest carbohydrates. Such enzymes set in motion the digestive process even when food is still in the mouth. As these enzymes move with the food into the upper portion of the stomach, they continue to assist with digestion.

The third group of enzymes also is involved in digestion, but these enzymes are already in the body. The digestive glands secrete juices containing enzymes that break down nutrients chemically into smaller molecules that are more easily absorbed by the body. Amylase in the saliva begins the process of breaking down complex carbohydrates into simple sugars. While food is still in the mouth, the stomach begins producing pepsin, which, like protease, helps digest protein.

Later, when food enters the small intestine, the pancreas secretes pancreatic juice—which contains three enzymes that break down carbohydrates, fats, and proteins—into the duodenum, which is part of the small intestine. Enzymes from food wind up among the nutrients circulated to the body through plasma, a watery liquid in which red blood cells are suspended. These enzymes in the blood assist the body in everything from growth to protection against infection.

One digestive enzyme that should be in the body, but is not always present, is lactase. As we noted earlier, lactase works on lactose, the principal carbohydrate in milk, to implement its digestion. If a person lacks this enzyme, consuming dairy products may cause diarrhea, bloating, and cramping. Such a person is said to be “lactose intolerant,” and if he or she is to consume dairy products at all, they must be in forms that contain lactase. For this reason, Lactaid milk is sold in the specialty dairy section of major supermarkets, while many health-food stores sell lactaid tablets.

Amylase is produced by the exocrine pancreas and the salivary glands (in particular the Parotid gland locate near the ear and Submandibular gland localed by the jaw bone).

Besides the catalyzing enzymes, your body has a thyroid gland that produces a hormone called thyroxine. The thyroid controls how quickly the body burns energy, makes proteins, and how sensitive the body should be to other hormones. The thyronines act on the body to increase the basal metabolic rate, affect protein synthesis and increase the body’s sensitivity to catecholamines (such as adrenaline) by permissiveness. The thyroid hormones are essential to proper development and differentiation of all cells of the human body. These hormones also regulate protein, fat, and carbohydrate metabolism, affecting how human cells use energetic compounds. They also stimulate vitamins metabolism. Numerous physiological and pathological stimuli influence thyroid hormone synthesis.

Thyroid hormone leads to heat generation in human. However, the thyronamines function via some unknown mechanism to inhibit neuronal activity; this plays an important role in the hibernation cycles of mammals and the moulting behaviour of birds. One effect of administering the thyronamines is a severe drop in body temperature.

My educated guess is that if your body has low thyroxine production, it probably means low enzyme production, and that you may encounter a problem with the pancreas as well which may lead to diabetes type 2 symptoms. The ability of Hypothyroidism to mimic a number of medical conditions originates in the vast functions of the thyroid hormones, which are reduced or absent in this case. The functions of thyroid hormones include modulation of carbohydrate, protein and fat metabolism, vitamin utilization, mitochondrial function, digestive process, muscle and nerve activity, blood flow, oxygen utilization, hormone secretion and sexual and reproductive health to mention a few. Thus, when the thyroid hormone content gets out of balance, systems covering the whole body are affected. This is why hypothyroidism can look like other diseases. Conversely, sometimes other conditions can be mistaken for hypothyroidism.

It is possible to obtain an over the counter enzyme supplimental which has pancreatin, (a mixture of several digestive enzymes produced by the exocrine cells of the pancreas,) and this may be helpful in weight maintenance as well as having more energy. You should problably research this area for yourself throughly, as it is possible to have a problem where the digestive enzymes start digesting the pancreas itself (Pancreatitis).

I hope that you now have some idea why you see an enzyme blend was listed on an energy drink label.

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Helpful Links:

http://www.answers.com/salivary+gland

http://www.answers.com/amylase

http://www.rcsb.org/pdb/static.do?p=education_discussion/molecule_of_the_month/pdb74_1.html

http://www.answers.com/enzyme?cat=health

http://www.answers.com/Amino+acids+?cat=health

http://science.howstuffworks.com/cell2.htm

http://en.wikipedia.org/wiki/Enzyme

http://en.wikipedia.org/wiki/Thyroid_hormone

http://en.wikipedia.org/wiki/Hypothyroidism

http://journal.diabetes.org/clinicaldiabetes/v18n12000/Pg38.htm

http://thyroid.about.com/cs/dietweightloss/a/12ways.htm

http://www.nlm.nih.gov/medlineplus/pancreaticdiseases.html

Hypothyroidism and Me

Well the last few blogs have talked about Energy and Vitamin B12, and a little here and there about Diabetes. Now, I’d like to blog on the major factor in all of my energy problems. That is Hypothyroidism.

When it comes to feeling down, Hypothyroidism is the most insidious party pooper of them all. This is because it usually takes a back seat to diabetes, and most everyone can’t recognize its symptoms right off. But, as it was in my case, Hypothyroidism can often be found in conjunction with diabetes.

Usually, if you don’t treat the Hypothyroid, you have a greater difficulty in treating the diabetes. So, just because you’ve found that you have high blood sugar, you shouldn’t think that all you symptoms are just related to an insolin issue. As I have blogged earlier, (and fair warning, I’m sure I’ll blog more on this in the future), your metabolizm is key in feeling healthy and energized. I am in no way recommending anything here, just passing on research to help a reader understand me a little better. And, I can only hope that this information might help you in some small way.

Here are some very good sites for tyroid information:

• American Thyroid Association (a thyroid physician organization with a Patient and Public Education Division called Friends of the ATA) at www.thyroid.org
• National Graves’ Foundation at www.ngdf.org
• The Thyroid Cancer Survivors’ Association at www.thyca.org
• The Light of Life Foundation at www.checkyourneck.com
• The Endocrine Society’s Hormone Foundation at www.hormone.org
• The American Association of Clinical Endocrinologists at www.aace.com

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http://www.endocrineweb.com/hypo1.html

Hypothyroidism is a condition in which the body lacks sufficient thyroid hormone. Since the main purpose of thyroid hormone is to “run the body’s metabolism”, it is understandable that people with this condition will have symptoms associated with a slow metabolism. Over five million Americans have this common medical condition. In fact, as many as ten percent of women may have some degree of thyroid hormone deficiency. Hypothyroidism is more common than you would believe…and, millions of people are currently hypothyroid and don’t know it!

There are two fairly common causes of hypothyroidism.

The first is a result of previous (or currently ongoing) inflammation of the thyroid gland which leaves a large percentage of the cells of the thyroid damaged (or dead) and incapable of producing sufficient hormone. The most common cause of thyroid gland failure is called autoimmune thyroiditis (also called Hashimoto’s thyroiditis), a form of thyroid inflammation caused by the patient’s own immune system.

The second major cause is the broad category of “medical treatments”. The treatment of many thyroid conditions warrants surgical removal of a portion or all of the thyroid gland. If the total mass of thyroid producing cells left within the body are not enough to meet the needs of the body, the patient will develop hypothyroidism. Remember, this is often the goal of the surgery as seen in surgery for thyroid cancer. But at other times, the surgery will be to remove a worrisome nodule, leaving half of the thyroid in the neck undisturbed. Sometimes (often), this remaining thyroid lobe and isthmus will produce enough hormone to meet the demands of the body. For other patients, however, it may become apparent years later that the remaining thyroid just can’t quite keep up with demand. Similarly, goiters and some other thyroid conditions can be treated with radioactive iodine therapy. The aim of the radioactive iodine therapy (for benign conditions) is to kill a portion of the thyroid to prevent goiters from growing larger, or producing too much hormone (hyperthyroidism). Occasionally, (often?) the result of radioactive iodine treatment will be that too many cells are damaged so the patient often becomes hypothyroid a year or two later. This is O.K. and usually greatly preferred over the original problem. There are several other rare causes of hypothyroidism, one of them being a completely “normal” thyroid gland which is not making enough hormone because of a problem in the pituitary gland. If the pituitary does not produce enough Thyroid Stimulating Hormone (TSH) then the thyroid simply does not have the “signal” to make hormone, so it doesn’t.

Symptoms of Hypothyroidism

• Fatigue
• Weakness
• Weight gain or increased difficulty losing weight
• Coarse, dry hair
• Dry, rough pale skin
• Hair loss
• Cold intolerance (can’t tolerate the cold like those around you)
• Muscle cramps and frequent muscle aches
• Constipation
• Depression
• Irritability
• Memory loss
• Abnormal menstrual cycles
• Decreased libido

Each individual patient will have any number of these symptoms which will vary with the severity of the thyroid hormone deficiency and the length of time the body has been deprived of the proper amount of hormone. Some patients will have one of these symptoms as their main complaint, while another will not have that problem at all and will be suffering from a different symptom. Most will have a combination of a number of these symptoms. Occasionally, some patients with hypothyroidism have no symptoms at all, or they are just so subtle that they go unnoticed. Note: Although this may sound obvious, if you have these symptoms, you need to discuss them with your doctor and probably seek the skills of an endocrinologist. If you have already been diagnosed and treated for hypothyroidism and you continue to have any or all of these symptoms, you need to discuss it with your physician. Although treatment of hypothyroidism can be quite easy in some individuals, others will have a difficult time finding the right type and amount of replacement thyroid hormone. (More about this on the next page).

Potential Dangers of Hypothyroidism

Because the body is expecting a certain amount of thyroid hormone the pituitary will make additional thyroid-stimulating-hormone (TSH) in an attempt to entice the thyroid to produce more hormone. This constant bombardment with high levels of TSH may cause the thyroid gland to become enlarged and form a goiter (termed a “compensatory goiter”). Our goiter page goes into this topic in detail, and outlines that a deficiency of thyroid hormone is a common cause of goiter formation. Left untreated, the symptoms of hypothyroidism will usually progress. Rarely, complications can result in severe life-threatening depression, heart failure or coma.

Hypothyroidism can often be diagnosed with a simple blood test. In some persons, however, its not so simple and more detailed tests are needed. Most importantly, a good relationship with a good endocrinologist will almost surely be needed. More about treatment on another page.

Hypothyroidism is completely treatable in many patients simply by taking a small pill once a day! Once again, however, we have made a simplified statement and its not always so easy. There are several types of thyroid hormone preparations and one type of medicine will not be the best therapy for all patients. Many factors will go into the treatment of hypothyroidism and it is different for everybody.

Since hypothyroidism is caused by too little thyroid hormone secreted by the thyroid, the diagnosis of hypothyroidism is based almost exclusively upon measuring the amount of thyroid hormone in the blood. There are normal ranges for all thyroid hormones which have been calculated by computers which measured these hormones in tens of thousands of people. If your thyroid hormone levels fall below the normal range, that is consistent with hypothyroidism These tests are very accurate and reliable and are so routine that they are available to everybody.

The idea is to measure blood levels of T4 and TSH. In the typical person with an under-active thyroid gland, the blood level of T4 (the main thyroid hormone) will be low, while the TSH level will be high. This means that the thyroid is not making enough hormone and the pituitary recognizes it and is responding appropriately by making more Thyroid Stimulating Hormone (TSH) in an attempt to force more hormone production out of the thyroid. In the more rare case of hypothyroidism due to pituitary failure, the thyroid hormone T4 will be low, but the TSH level will also be low. The thyroid is behaving “appropriately” under these conditions because it can only make hormone in response to TSH signals from the pituitary. Since the pituitary is not making enough TSH, then the thyroid will never make enough T4. The real question in this situation is what is wrong with the pituitary? But in the typical and most common form of hypothyroidism, the main thyroid hormone T4 is low, and the TSH level is high.

The next question is: When is low too low, and when is high too high? Blood levels have “normal” ranges, but other factors need to be taken into account as well, such as the presence or absence of symptoms. You should discuss your levels with your doctor so you can interpret how they are helping (or not?) fix your problems.

Oh, if only it were this simple all the time! Although the majority of individuals with hypothyroidism will be easy to diagnose with these simple blood tests, many millions will have this disease in mild to moderate forms which are more difficult to diagnose. The solution for these people is more complex and this is due to several factors. First we must realize that not all patients with hypothyroidism are the same. There are many degrees of this disease from very severe to very mild. Additionally, and very importantly, we cannot always predict just how bad (or good) an individual patient will feel just by examining his/her thyroid hormone levels. In other words, some patients with very “mild” deviations in their thyroid laboratory test results will feel just fine while others will be quite symptomatic. The degree of thyroid hormone abnormalities often, but NOT ALWAYS will correlate with the degree of symptoms. It is important for both you and your physician to keep this in mind since the goal is not necessarily to make the lab tests go into the normal range, but to make you feel better as well! We must also keep in mind that even the “normal” thyroid hormone levels in the blood have a fairly large range, so even if a patient is in the “normal” range, it may not be the normal level for them.

For the majority of patients with hypothyroidism, taking some form of thyroid hormone replacement (synthetic or natural, pill or liquid, etc) will make the “thyroid function tests” return to the normal range, AND, this is accompanied by a general improvement in symptoms making the patient feel better. This does not happen to all individuals, however, and for these patients it is very important to find an endocrinologist who will listen and be sympathetic. (We aim to help you find this type of doctor.) Because most patients will be improved (or made completely better) when sufficient thyroid hormone is provided on a daily basis to make the hormone levels in the blood come into the normal range, physicians will often will rely on test results to determine when a patient is on the appropriate dose and therefore doing well. Remember, these tests have a wide normal range. Find a doctor who helps make you FEEL better, not just make your labs better because once given this diagnosis, you are likely to carry it for a long, long time. There is more than one drug, there is more than one lab test, and there is a “just right” doctor for everybody.

Treatment of Hypothyroidism

Hypothyroidism is usually quite easy to treat (for most people)! The easiest and most effective treatment is simply taking a thyroid hormone pill (Levothyroxine) once a day, preferably in the morning. This medication is a pure synthetic form of T4 which is made in a laboratory to be an exact replacement for the T4 that the human thyroid gland normally secretes. It comes in multiple strengths, which means that an appropriate dosage can almost always be found for each patient. The dosage should be re-evaluated and possibly adjusted monthly until the proper level is established. The dose should then be re-evaluated at least annually. If you are on this medication, make sure your physician knows it so he/she can check the levels at least yearly. Note: Just like we discussed above, however, this simple approach does not hold true for everybody. Occasionally the correct dosage is a bit difficult to pin-point and therefore you may need an exam and blood tests more frequently. Also, some patients just don’t do well on some thyroid medications and will be quite happy on another. For these reasons you should not be shy in discussing with your doctor your blood hormone tests, symptoms, how you feel, and the type of medicine you are taking. The goal is to make you feel better, make your body last longer, slow the risk of heart disease and osteoporosis…in addition to making your blood levels normal! Sometimes that’s easy, when its not, you need a physician who is willing to spend the time with you that you deserve while you explore different dosages other types of medications (or alternative diagnoses).

Some patients will notice a slight reduction in symptoms within 1 to 2 weeks, but the full metabolic response to thyroid hormone therapy is often delayed for a month or two before the patient feels completely normal. It is important that the correct amount of thyroid hormone is used. Not enough and the patient may have continued fatigue or some of the other symptoms of hypothyroidism. Too high a dose could cause symptoms of nervousness, palpitations or insomnia typical of hyperthyroidism. Some recent studies have suggested that too much thyroid hormone may cause increased calcium loss from bone increasing the patient’s risk for osteoporosis. For patients with heart conditions or diseases, an optimal thyroid dose is particularly important. Even a slight excess may increase the patient’s risk for heart attack or worsen angina. Some physicians feel that more frequent dose checks and blood hormone levels are appropriate in these patients.

After about one month of treatment, hormone levels are measured in the blood to establish whether the dose of thyroid hormone which the patient is taking is appropriate. We don’t want too much given or subtle symptoms of hyperthyroidism could ensue, and too little would not alleviate the symptoms completely. Often blood samples are also checked to see if there are antibodies against the thyroid, a sign of autoimmune thyroiditis. Remember, this is the most common cause of hypothyroidism. Once treatment for hypothyroidism has been started, it typically will continue for the patient’s life. Therefore, it is of great importance that the diagnosis be firmly established and you have a good relationship with a physician you like and trust.

Synthetic T4 can be safely taken with most other medications. Patients taking cholestyramine (a compound used to lower blood cholesterol) or certain medications for seizures should check with their physician about potential interactions. Women taking T4 who become pregnant should feel confident that the medication is exactly what their own thyroid gland would otherwise make. However, they should check with their physician since the T4 dose may have to be adjusted during pregnancy (usually more hormone is needed to meet the increased demands of the mother’s new increased metabolism). There are other potential problems with other drugs including iron-containing vitamins. Once again, pregnant women (and all women and men for that matter) taking iron supplements should discuss this with your physician. There are three brand name Levothyroxine tablets now available. You may want to consult with your physician or pharmacist on the most cost effective brand since recent studies suggest that none is better than the other.

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http://www.endocrineweb.com/thyroid.html

The thyroid gland is the biggest gland in the neck. It is situated in the anterior (front) neck below the skin and muscle layers. The thyroid gland takes the shape of a butterfly with the two wings being represented by the left and right thyroid lobes which wrap around the trachea. The sole function of the thyroid is to make thyroid hormone. This hormone has an effect on nearly all tissues of the body where it increases cellular activity. The function of the thyroid therefore is to regulate the body’s metabolism.

Common Thyroid Problems

The thyroid gland is prone to several very distinct problems, some of which are extremely common. These problems can be broken down into [1] those concerning the production of hormone (too much, or too little), [2] those due to increased growth of the thyroid causing compression of important neck structures or simply appearing as a mass in the neck, [3] the formation of nodules or lumps within the thyroid which are worrisome for the presence of thyroid cancer, and [4] those which are cancerous. Each thyroid topic is addressed separately and illustrated with actual patient x-rays and pictures to make them easier to understand. The information on this web site is arranged to give you more detailed and complex information as you read further.

Goiters ~ A thyroid goiter is a dramatic enlargement of the thyroid gland. Goiters are often removed because of cosmetic reasons or, more commonly, because they compress other vital structures of the neck including the trachea and the esophagus making breathing and swallowing difficult. Sometimes goiters will actually grow into the chest where they can cause trouble as well. Several nice x-rays will help explain all types of thyroid goiter problems.

Thyroid Cancer ~ Thyroid cancer is a fairly common malignancy, however, the vast majority have excellent long term survival. We now include a separate page on the characteristics of each type of thyroid cancer and its typical treatment, follow-up, and prognosis. Over 30 pages thyroid cancer.

Solitary Thyroid Nodules ~ There are several characteristics of solitary nodules of the thyroid which make them suspicious for malignancy. Although as many as 50% of the population will have a nodule somewhere in their thyroid, the overwhelming majority of these are benign. Occasionally, thyroid nodules can take on characteristics of malignancy and require either a needle biopsy or surgical excision. Now includes risks of radiation exposure and the role of Needle Biopsy for evaluating a thyroid nodule. Also a new page on the role of ultrasound in diagnosing thyroid nodules and masses.

Hyperthyroidism ~ Hyperthyroidism means too much thyroid hormone. Current methods used for treating a hyperthyroid patient are radioactive iodine, anti-thyroid drugs, or surgery. Each method has advantages and disadvantages and is selected for individual patients. Many times the situation will suggest that all three methods are appropriate, while other circumstances will dictate a single best therapeutic option. Surgery is the least common treatment selected for hyperthyroidism. The different causes of hyperthyroidism are covered in detail.

Hypothyroidism ~ Hypothyroidism means too little thyroid hormone and is a common problem. In fact, hypothyroidism is often present for a number of years before it is recognized and treated. There are several common causes, each of which are covered in detail. Hypothyroidism can even be associated with pregnancy. Treatment for all types of hypothyroidism is usually straightforward.

Thyroiditis ~ Thyroiditis is an inflammatory process ongoing within the thyroid gland. Thyroiditis can present with a number of symptoms such as fever and pain, but it can also present as subtle findings of hypo or hyper-thyroidism. There are a number of causes, some more common than others. Each is covered on this site.

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The term nontoxic goiter refers to enlargement of the thyroid which is not associated with overproduction of thyroid hormone or malignancy. The thyroid can become very large so that it can easily be seen as a mass in the neck. This picture depicts the outline of a normal size thyroid in black and the greatly enlarged goiter in pink. There are a number of factors which may cause the thyroid to become enlarged. A diet deficient in iodine can cause a goiter but this is rarely the cause because of the readily available iodine in our diets. A more common cause of goiter in America is an increase in thyroid stimulating hormone (TSH) in response to a defect in normal hormone synthesis within the thyroid gland. The thyroid stimulating hormone comes from the pituitary and causes the thyroid to enlarge. This enlargement usually takes many years to become manifest.

INDICATIONS FOR TREATMENT

Most small to moderate sized goiters can be treated by providing thyroid hormone in the form of a pill. By supplying thyroid hormone in this fashion, the pituitary will make less TSH which should result in stabilization in size of the gland. This technique often will not cause the size of the goiter to decrease but will usually keep it from growing any larger. Patients who do not respond to thyroid hormone therapy are often referred for surgery if it continues to grow.

A more common indication for surgical removal of an enlarged thyroid [goiter] is to remove those glands which are enlarged enough to cause compression on other structures in the neck such as the trachea and esophagus. These patients will typically complain of a cough, a slight change in voice, or nighttime choking episodes because of the way that the gland compresses the trachea while sleeping. This X-ray shows how an enlarged right lobe of the thyroid has moved the trachea to the patient’s left. The trachea (outlined in light yellow) should be straight from the mouth down to the lungs, but in this patient it is compressed and displaced far to the left. The enlarged gland can even compress the blood vessels of the neck which are also an indication for its removal.

As always, suspicion of malignancy in an enlarged thyroid is an indication for removal of the thyroid. There is often a dominant nodule within a multinodular goiter which can cause concern for cancer. It should be remembered that the incidence of malignancy within a multinodular goiter is usually significantly less than 5%. If the nodule is cold on thyroid scanning, then it may be slightly higher than this. For the vast majority of patients, surgical removal of a goiter for fear of cancer is not warranted.

Another reason (although not a very common one) to remove a goiter is for cosmetic reasons. Often a goiter gets large enough that it can be seen as a mass in the neck. When other people begin to notice the mass, it is usually big enough to begin causing compression of other vital neck structures…but not always. Sometimes the large goiter causes no symptoms other than being a cosmetic problem. Realizing of course, if its big enough to be seen by your neighbors, something needs to be done…medications or surgery or it will most likely continue to get bigger.

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http://www.healthy.net/scr/article.asp?ID=528

The Diagnosis and Treatment of Hypothyroidism

Michael Schachter M.D., F.A.C.A.M.

Hypothyroidism, or an underactive thyroid system, is one of the most underdiagnosed and important conditions in the United States. It has been called the “unsuspected illness” and accounts for a great number of complaints in children, adolescents and adults.

What kinds of complaints characterize an underactive thyroid system? Low energy and fatigue or tiredness, especially in the morning are frequent in these patients. Difficulty losing weight, a sensation of coldness–especially of the hands and feet, depression, slowness of thought processes, headaches, swelling of the face or fluid retention in general, dry coarse skin, brittle nails, chronic constipation, menstrual problems-such as PMS and menstrual irregularities including heavy periods, fertility problems, stiffness of joints, muscular cramps, shortness of breath on exertion and chest pain are some of the symptoms that can be seen in people with underactive thyroid systems. Be aware that a person with a low functioning thyroid doesn’t have to have all of these symptoms, he may have only a few.

Function of the Thyroid Gland

Where is the thyroid located in the body and what does it do? The thyroid gland consists of two small lobes connected together. It is located in the front of the neck, just below the voice box. The thyroid gland is responsible for the speed of metabolic processes in the body and therefore affects every organ and organ system. It is the metabolic stimulator, analogous to the accelerator of a car. Normal growth requires normal thyroid functioning. When the thyroid is not functioning properly, organs become infiltrated with metabolic wastes and all functions become sluggish.

When the thyroid gland is working properly, it uses the amino acid tyrosine and iodine to make the thyroid hormone called thyroxine or T4. Thyroxine is called T4 because it contains four iodine atoms. If a person is deprived of iodine in his diet, he develops an enlarged thyroid gland, called a goiter and symptoms of an underactive thyroid or hypothyroidism.

The other important thyroid hormone is triiodothyronine or T3, which has three iodine atoms. T3 is actually the major active thyroid hormone, being much more active than T4. T4 is produced within the thyroid gland and is later converted to the active T3 outside the thyroid gland in peripheral tissues. Under certain conditions, such as stress, the thyroid gland may produce sufficient amounts of T4 to obtain normal thyroid blood tests, but its conversion to T3 may be inhibited, causing a relative insufficiency of active T3. Under this circumstance, the patient will have hypothyroid symptoms in spite of normal thyroid blood tests. As you will see, this fact results in many missed diagnoses of an underactive thyroid system.

The production and release of T4 from the thyroid gland is controlled by a hormone from the pituitary gland, which is located at the base of the brain. This hormone is called thyroid stimulating hormone or TSH. When the level of T4 in the bloodstream is low, the pituitary increases TSH production and release, which in turn stimulates the thyroid gland to produce and release more T4. The T4 then feeds back to the pituitary, reducing the secretion of TSH in a negative feedback loop. When a person has trouble making T4 due to iodine deficiency or for some other reason, one would expect to find an elevated TSH. The pituitary’s TSH is trying to get the thyroid gland to produce more T4. If both T4 and TSH are low, this may indicate a pituitary problem with a low TSH secretion resulting in the low production and secretion of T4.

Diagnosis of Hypothyroidism

So, how is hypothyroidism diagnosed today by conventional medicine? Unfortunately, the diagnosis by conventional physicians, including thyroid specialists called endocrinologists, is made almost exclusively from blood tests. Generally, T4 and TSH are measured in the bloodstream. Additionally, a protein that binds T4 is also measured. From this protein and T4, the free T4 is calculated. If a patient has a normal TSH and a normal free T4, he is told by the conventional physician that he does not have hypothyroidism, no matter how many symptoms or signs of hypothyroidism he has. This is the fatal error because these tests only pick up the most severe cases of hypothyroidism and miss virtually all of the milder cases that would respond favorably to thyroid hormone treatment.

If most hypothyroid cases cannot be diagnosed by the usual blood tests, how can they be diagnosed? Prior to the extensive use of blood tests, hypothyroid states were diagnosed by astute clinicians, who obtained careful medical histories, including family histories from the patient, and who performed a complete physical examination. Later basal metabolic rates were measured using special equipment. Then came the blood tests–the protein bound iodine or PBI, T4, TSH and even T3 by special radioactive studies. Instead of using the blood tests as adjuncts to diagnosis, they were soon relied upon exclusively. To properly diagnose hypothyroidism, the clinician must go back to the careful medical history, physical examination and measurement of the basal temperature of the body. I’ll discuss important aspects of the medical history and physical examination relevant to the diagnosis of hypothyroidism.

Medical History

What in the medical history suggests the likelihood of hypothyroidism? With regard to infancy and childhood, a high birth weight of over 8 lbs. suggests low thyroid. During childhood, early or late teething, late walking or late talking suggests a low functioning thyroid in the child. Also, frequent ear infections, colds, pneumonia, bronchitis or other infections; problems in school including difficulty concentrating, abnormal fatigue–especially having difficulty getting up in the morning and poor athletic ability all suggest a low thyroid. Keep in mind that a person with low thyroid functioning may have only a few of these characteristics. You don’t have to find all of them to suspect a low thyroid.

During puberty, we see the same types of problems in school and with fatigue, which is worse in the morning and gets a little better later in the day. Often, adolescent girls suffer from menstrual irregularity, premenstrual syndrome and painful periods. Drug and alcohol abuse are common.

Throughout life, disorders associated with hypothyroidism include headaches, migraines, sinus infections, post-nasal drip, visual disturbances, frequent respiratory infections, difficulty swallowing, heart palpitations, indigestion, gas, flatulence, constipation, diarrhea, frequent bladder infections, infertility, reduced libido and sleep disturbances, with the person requiring 12 or more hours of sleep at times. Other conditions include intolerance to cold and/or heat, poor circulation, Raynaud’s Syndrome, which involves the hands and feet turning white in response to cold, allergies, asthma, heart problems, benign and malignant tumors, cystic breasts and ovaries, fibroids, dry skin, acne, fluid retention, loss of memory, depression, mood swings, fears, and joint and muscle pain.

With regard to the family history, all of the above disorders can be checked in family members. Particular emphasis should be placed on hypothyroid conditions in parents or siblings. Also, a family history of Tuberculosis suggests the possibility of low thyroid.

Physical Examination

The physical examination often reveals the hair to be dry, brittle and thinning. The outer third of the eyebrows is often missing. One often finds swelling under the eyes. The tongue is often thick and swollen. The skin may be rough, dry and flaky and show evidence of acne. The skin may also have a yellowish tinge due to high carotene in it. Nails tend to be brittle and break easily. The thyroid gland may be enlarged. The patient is more often overweight, but may also be underweight. Hands and feet are frequently cold to the touch. Reflexes are either slow or absent. The pulse rate is often slow even though the patient is not a well trained athlete.

Measuring Basal Body Temperature

Instructions for taking basal body temperatures are relatively easy. Use an oral glass thermometer. Shake the thermometer down before going to bed, and leave it on the bedside table within easy reach. Immediately upon awakening, and with as little movement as possible, place the thermometer firmly in the armpit next to the skin, and leave it in place for 10 minutes. Record the readings for three consecutive days. Menstruating women must only take the basal temperature test for thyroid function on the 1st, 2nd, 3rd or 4th day of menses(preferably beginning on the 2nd day). Males, pre-pubertal girls, and post-menopausal or non-menstruating women may take basal temperatures any day of the month. Women taking progesterone should not take it the day before and the days that the basal temperatures are taken.

Most of the information on the manifestations of hypothyroidism, its diagnosis, including the technique for measuring and interpreting basal temperatures, and the treatment to be discussed was compiled and described by the late Dr. Broda O. Barnes. He is the author of the book Hypothyroidism: the Unsuspected Illness. His work is disseminated to physicians and the public by the foundation bearing his name, which is located in Trumbull, Connecticut.

How does one interpret the results of the basal body axillary temperature test? If the average temperature is below 97.8 Fahrenheit, then the diagnosis of a low functioning thyroid system is likely. An average temperature between 97.8 and 98.2 is considered normal. An average temperature above 98.2 is considered high and might reflect an infection or a hyperthyroid condition.

Treatment of Hypothyroidism

Once a pattern of hypothyroid symptoms is established and the basal body temperatures are found to be low, the next step is a therapeutic trial of thyroid hormone. Dr. Barnes, his physician followers and many patients have found that the most effective thyroid medication is Armour Desiccated Thyroid Hormone. This medication is derived from the thyroid gland of the pig. It most closely resembles the human thyroid gland. It is dried or desiccated and processed into small tablets. In contrast, most conventional physicians prefer to use the synthetically produced thyroxine or T4. In my experience and the experience of many other physicians using Dr. Barnes’ protocol, the synthetic T4 is not as effective as the desiccated thyroid.

How can we monitor the results of treatment if the blood tests are inadequate to the job? We do this by how the person feels, whether or not the thyroid symptoms and signs have improved or disappeared, whether or not symptoms of an overactive thyroid gland have developed, and by monitoring the basal body temperature.

Generally, the dosage of Armour thyroid is best started at a low dose, with a gradual increase every week or two, until the optimal therapeutic dosage is reached. It may take four to six weeks at the optimal dosage to feel the full therapeutic benefits. In my practice, I generally start the patient on 1/4 grain or 15 milligrams daily. Every week or two, I increase the dosage by 1/4 grain per day until 1 to 2 grains daily are reached. Usually, the optimal dosage is in this range, provided that the patient is doing the other adjunctive necessary things, which I will discuss in a moment. Occasionally, the dosage may need to be 2 and a half grains daily or more. Full therapeutic benefits many not be fully realized for months and the basal temperatures may not come up to normal for a year or more. The dosage for infants is usually 1/8 to 1/4 grain daily and from one to six years old, the dosage is usually 1/4 grain. From 7 years to puberty, 1/2 grain is usually used, but it may need to be increased.

Special Cases: Recent Heart Attacks and Weak Adrenal Function

There are a few special cases that needs to be discussed in the context of this treatment. If a person has recently had a heart attack, treatment should not begin for at least two months following the heart attack. After that, the protocol discussed above can be used.

If a person has evidence of weak adrenal function, the adrenal gland problem must be treated first or simultaneous to the thyroid treatment. The reason for this is that hydrocortisone is necessary for the conversion of T4 to the active T3. If the weak adrenal is not addressed, the patient may actually feel worse and/or develop symptoms of an overactive thyroid gland, such as palpitations, a rapid heart beat and increased sweating. Clues to low adrenal functioning include a low blood pressure (less than 120/80), allergies, asthma, breathing difficulties, skin problems (such as acne, eczema, psoriasis, lupus, dry flaky skin), joint or muscle pains, as in arthritis, and emotional problems, such as mood swings, weeping, fears and phobias. Using low physiologic doses of hydrocortisone along with Armour Thyroid, when the patient shows evidence of both low adrenal and low thyroid function, will help to assure the desired results.

Problems in Converting T4 to the T3 Hormone

The conversion of the relatively inactive T4 to the active T3 thyroid hormone is an important process. As mentioned previously, frequently low thyroid function is not due to the low production of thyroxine, T4, by the thyroid, but due to the failure of conversion of T4 to T3 by peripheral tissues. What nutrients are necessary to help with this conversion? In addition to sufficient quantities of cortisol, iron, zinc, copper and selenium are necessary for this conversion. Deficiencies of any of these minerals can prevent the conversion T4 to T3 and should be corrected if present. Sufficient protein and especially the amino acid, tyrosine, and iodine are necessary to make T4 in the thyroid gland.

Another approach to the problem of conversion failure of T4 to T3 has been proposed by a young physician, Dennis Wilson. He has found that the body often adapts to various stressful situations by switching to a conservative mode in order to preserve energy. For example, when a famine occurs, an excellent adaptive change that the body can make in order to use less energy because food calories are unavailable, is to stop converting T4 to T3. However, this response appears to occur to a wide variety of stressors and sometimes this mode is not reversed, even after the stress is removed. This can lead to all of the symptoms and signs of a low thyroid that I have been discussing.

He has suggested the use of a special long acting T3 preparation to reset the conversion of T4 to T3 process. Dosages of T3 are given exactly every 12 hours in increasing amounts with close monitoring of oral temperatures during the day. High doses of T3 may be given and in order to normalize the oral temperature to 98.6 F. After the optimal temperature is reached and maintained for approximately three weeks or if the patient develops an intolerance to the particular dosage of long-acting T3, the dosage is tapered down to zero.

When the treatment is successful, the temperature will remain optimal with the loss of hypothyroid symptoms, even after the medication is tapered to zero. In other words, the thyroid system is reset at a higher temperature. This process may take several cycles of going up and down on the T3. This treatment requires a lot of discipline from the patient and often leads to symptoms during the treatment. However, it does seem to be useful in some patients. If the patient is stressed significantly and again enters the low thyroid system mode, the entire process can be repeated again. Usually, the treatment is easier at each subsequent episode.

Nevertheless, for most patients, especially if there are adrenal problems or other medical complications, the use of Armour desiccated thyroid on a continuous basis is probably easier and preferable.

Recent studies indicate that patients who have been treated with excessive doses of thyroid hormone over long periods of time may be at increased risk for developing osteoporosis. This may be due not only to too much thyroid, but also to an imbalance between the anabolic and catabolic endocrine hormones. The catabolic hormones are those that help to break down dead tissues and rid the body of metabolic waste. These would include thyroid hormone and hydrocortisone. The anabolic hormones are those that help to rebuild the body and would include DHEA, estrogens, progesterone and the male hormone, testosterone. A physician who is trying to balance a person’s thyroid system must also look at all of the other hormones and also all aspects of the person’s lifestyle, including diet, nutritional supplements, exercise patterns and stress coping mechanisms. The nutrients that are especially important to a proper functioning thyroid system are iodine and the amino acid tyrosine to make thyroid hormone in the thyroid gland and the minerals iron, selenium, zinc and copper to convert the inactive T4 to the active T3.

How Long Should Patients Take Thyroid Hormone?

When using the desiccated thyroid protocol, patients often remain on the thyroid for life. However, there may be times when the patient can be weaned off the thyroid as all other functions improve, as long as the patient is carefully monitored for the development of low thyroid symptoms and signs and low basal temperatures. When a person’s basal temperatures are low, many of the enzymes of the body function in a suboptimal way, which leads to all of the problems we have discussed.

On the other hand, well treated hypothyroid patients should enjoy a vibrant life with lowered risks of all of the degenerative diseases including arthritis, cancer and heart disease. I personally have seen a number of patients whose arthritis pains have completely cleared when treated with proper doses of thyroid. With regard to cancer, the well known alternative cancer treatment developed by Max Gerson, involves the use of Armour Desiccated Thyroid in virtually all of his cancer patients. High serum cholesterol and the development of atherosclerosis are well known effects of hypothyroidism. Therefore, all patients with coronary artery disease and other atherosclerotic conditions should be checked carefully for evidence of a low functioning thyroid condition and treated cautiously and appropriately if a low thyroid condition is found. Psychiatrists have found that the addition of thyroid hormone to patients suffering from refractory depression often is helpful, even when the blood tests are normal.

The proper appreciation of low thyroid conditions and their subsequent treatment should aid greatly in reducing the morbidity and premature mortality of virtually all degenerative diseases.

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http://www.mayoclinic.com/health/hypothyroidism/DS00353/DSECTION=8

Treatment

Standard treatment for an underactive thyroid involves daily use of the synthetic thyroid hormone levothyroxine (Levothroid, Levoxyl, Synthroid, Unithroid). The oral medication restores adequate hormone levels, shifting your body back into normal gear.

Soon after starting treatment, you’ll notice that you’re feeling less fatigued. The medication also gradually lowers cholesterol levels elevated by the disease and may reverse any weight gain. Treatment with levothyroxine is usually lifelong, but because the dosage you need may change, your doctor is likely to check your TSH level every year or so.

To determine the right dosage of levothyroxine initially, your doctor generally checks your level of TSH after two to three months. Excessive amounts of the hormone can cause side effects, such as increased appetite, insomnia, heart palpitations and shakiness.

If you have coronary artery disease or severe hypothyroidism, your doctor may start treatment with a smaller amount of medication and gradually increase the dosage. Progressive hormone replacement allows your heart to adjust to the increase in metabolism.

Levothyroxine causes virtually no side effects when used in the appropriate dose and is relatively inexpensive. If you change brands, let your doctor know to ensure you’re still receiving the right dosage. Also, don’t skip doses or stop taking the drug because you’re feeling better. If you do, the symptoms of hypothyroidism will gradually return. People with hypothyroidism need to take medication for the rest of their lives.

Proper absorption of levothyroxine

Certain medications, supplements and even some foods may affect your ability to absorb levothyroxine. Talk to your doctor if you eat large amounts of soy products or a high-fiber diet or you take other medications, such as:

• Iron supplements
• Cholestyramine (Questran)
• Aluminum hydroxide, which is found in some antacids

If you have subclinical hypothyroidism, discuss treatment with your doctor. For a relatively low level of TSH, you probably won’t benefit from thyroid hormone therapy, and treatment could even be harmful. On the other hand, for a higher TSH level, thyroid hormones may improve your cholesterol level, the pumping ability of your heart or your energy level.

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http://www.mayoclinic.com/health/hypothyroidism/DS00353/DSECTION=9

Complementary and alternative medicine

Although most doctors recommend synthetic thyroxine, natural extracts containing thyroid hormone derived from the thyroid glands of pigs are available. These products contain both thyroxine and triiodothyronine. Synthetic thyroid medications contain thyroxine only, and the triiodothyronine your body needs is derived from the thyroxine.

Extracts are available by prescription only and shouldn’t be confused with the glandular concentrates sold in natural foods stores. These products aren’t regulated by the Food and Drug Administration, and their potency isn’t guaranteed.

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http://thyroid.about.com/od/alternativeholisticinfo/a/fatigue.htm

Mind-Body Advice from Dr. Jan Nicholson

Jan Nicholson, EdD is an integrative clinical psychologist in Virginia who brings innovative mind-body approaches to her therapeutic work. I had an opportunity to interview her regarding her insightful mind-body recommendations on fatigue, stress and adrenal burnout that some thyroid patients experience, even after treatment.

MARY SHOMON: Q: Fatigue seems to be a very common problem for thyroid patients — even those of us who are receiving what doctors consider effective treatment. Do you have any mind-body suggestions for patients who struggle with daily fatigue that is not resolved by thyroid treatment?

JAN NICHOLSON, EdD: There are actually ways to build up one’s energy reserves. If you have seen on television people in China doing movements together in a park, they are practicing qi gong, an effective way of building energy.

It is getting quite easy for people in most locations to find a qi gong or a tai chi class. If you are too tired to go out to a class, then look for a DVD about these approaches and do it at home. It is possible for acupuncture to enhance one’s energy wherever it is weak; it also is beneficial to have acupuncture at the start of each season, to help adjust to the ways in which seasonal changes affect one’s functioning. There are hands-on and hands-off energy therapy approaches that can help energize people, such as Reiki, Healing Touch, and Reconnective HealingTM. Exercise helps to build energy for most people and it is usually possible for everyone to find some form of exercise they can handle, even if it is just to walk partway around the block initially. Laughter and having fun is energizing, so read humorous authors like Bill Bryson or watch a comedy. Music can be invigorating. If you are feeling down, you can make yourself a CD of four or five pieces of music starting with a slow quiet piece, and gradually building up to a fast joyful piece; this can give you energy.

Of course, it is not recommended we do what so many of us do when we are tired — relying on caffeine for false energy, or overeating trying to get energy. If you find yourself doing this, try to catch yourself in that moment just before you do it and see what healthier alternative you might try instead.

MARY SHOMON: Q: One aspect of an endocrine imbalance that some thyroid patients face is adrenal fatigue, or what we sometimes call “adrenal burnout.” This is not the same as the medical condition Addison’s disease, where the adrenal glands are unable to produce cortisol. Instead, in adrenal burnout, depending on how burned out we are, we sometimes see overly high adrenal levels, or inconsistent spikes throughout the day, or chronically lower levels, plus an inability of the adrenals to ramp up needed hormone production when we are under stress. Of course, at the same time, many of us with chronic illness are under constant physical and emotional stress — stress from low-level infection or inflammation, toxins, allergies, fatigue, and in some cases, anxiety or depression, plus the impact of stressful events in our lives. This ends up compounding the problem further. While there are medical and nutritional treatments to help support the adrenals, what other approaches do you think are especially helpful for patients as part of an overall effort to calm the adrenals and cope with stress more effectively?

JAN NICHOLSON, EdD: It is important to identify your stressors, especially ongoing ones, and to think in terms of what you can change and what you might be better off to accept, and how you might go about creating change or acceptance. Fighting things that will not change or it is not time to change becomes self-destructive. A great quote from Dr. Schulz is: “You have to know when to hold and when to fold, when to be powerful, when to be vulnerable.” In a mindful way, do what it takes to shift self-destructive habits and to resolve problems. Learn and practice stress management techniques on a daily basis, being sure to get enough rest for your body to heal. Think of yourself as being on a healing path. To shift your approach to life and toward yourself to a kinder, gentler approach is essential when you have gotten to this point in terms of burn out.

MARY SHOMON: Q: Some experts say that autoimmune diseases seem to strike Type A personalities more often, as compared to people who are more laid back and less “stressed out.” Do you have any thoughts about that finding, and perhaps any practical advice for hard-charging Type A folks?

JAN NICHOLSON, EdD: There has been a lot of research bearing out health issues associated with being a Type A personality; the hard-charging behavior tends to happen at home as well as at work, in all relationships, with a tendency to have more hostility/competitiveness and less joy. That is not beneficial for mental or physical health. In my practice, it is always an interesting process to find a way that works for Type A folks to be able to relax more and be gentler with themselves and others partly because hard-charging people often do not have much patience for learning and practicing mind-body approaches.

I would urge you, if that is your tendency, to try to suspend the belief that such things are a waste of time and to give it a try. Massage can feel so good that you might be able to let go and relax (start with a 15-minute seated massage if you are uncomfortable allowing more time); a hot tub, steam room, or sauna can have a similar effect. A great avenue to reduce stress is exercise; forms of meditation that involve movement (e.g., yoga, tai chi, qi gong) are usually preferred to sitting meditation. Acupuncture can help to balance the energy to be more calm. Short, focused relaxation techniques that can be completed in five minutes and get quick results can help to open the door to trying more in-depth approaches.

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http://www.thyroidpower.com/

The Amazing Program to Help Millions To Conquer Disease, Fatigue, Overweight, and Depression.

From Richard Shames MD, Karilee Shames PhD RN

Undiagnosed or under treated low thyroid (hypothyroidism) is an energy-sapping illness with many diverse symptoms — you could feel tired and depressed, gain weight, have low stamina, feel chillier than others, suffer unexplained aches and pains, experience low sex drive and infertility, think more slowly, develop allergies, and more.

The thyroid gland controls every chemical reaction of every organ in the body.

Hidden low thyroid is debilitating – and alarmingly on the rise.

YOU can be low thyroid even with normal tests, AND even if YOU are already taking thyroid medicine.

THYROID POWER REVEALS:

Why you may have low thyroid (hypothyroidism), even if your doctor says the blood tests are normal? Who is most likely to suffer from low thyroid? How low thyroid can masquerade as any other illness such as high cholesterol, high blood pressure, low sex drive, recurrent miscarriages, infertility, difficult menopause, migraines and any autoimmune condition (diabetes, fibromyalgia, chronic fatigue syndrome, rheumatoid arthritis, Multiple Sclerosis, colitis, etc.) OR make any other existing illness worse? How modern life contributes to the problem, from environmental toxins to stress?

Our book, THYROID POWER, (briefly summarized below with 10 Steps and cartoons) presents a step-by-step approach to healing low thyroid. Each step is a separate chapter in the book.

• Early steps reveal the scope of the problem and who is most likelyto suffer from low thyroid.
• The middle steps explain what we believe are the best standard and not-so-standard treatments that modern medicine can offer.
• Next, we discuss how the ovaries and adrenal glands are affected by low thyroid, and which tests and medicines are needed to treat these problems.
• Then we detail which alternative treatments are most helpful and exactly what you can do for optimal management of an autoimmune disease.
• Finally, in Step 10, we review the best health ideas we know for livinga thyroid-friendly lifestyle.
• Then we present a plan for using these ten steps to actualize your highest potential.
• Each of the ten steps can be a journey in itself. These simple steps, taken one at a time, will show you how to create a more effective healing program, and become a more empowered health care consumer.
• In addition to improving low thyroid, this overall approach to healing can be useful with just about any other health condition.

We wish you well on your journey!

For your visual enjoyment, we have included cartoons which summarize the approximately thirty pages of text in our book for each chapter. Enjoy!

STEP ONE: Consider Thyroid The Hidden Factor in Your Overall Health

STEP TWO: Learn How Low Thyroid Makes Any Illness Worse

STEP THREE: Use Signs, Symptoms, & Family History to Support A Diagnosis

STEP FOUR: Realize You May Still Be Low Thyroid Despite Normal Tests

STEP FIVE: Discover Your Best Dose, Brand, or Mix of Medicines

STEP SIX: Re-Balance Your Reproductive System

STEP SEVEN: Determine if Low Adrenal Should Also Be Treated

STEP EIGHT: Boost Your Medication with Natural Therapies

STEP NINE: Improve the Underlying Autoimmune Condition

STEP TEN: Reach Optimal Recovery with An Empowered Lifestyle

BEYOND THE TENTH STEP: Boundless Energy

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http://www.drpodell.org/alternative_thyroid_treatments.shtml

Hypothyroid Diets and Alternative Thyroid Treatments

Hypothyroid diets are too often overlooked in both mainstream and alternative thyroid treatments. Poor diet can harm the thyroid’s ability to make T4 thyroid hormone, as well as the cell’s ability to convert T4 (Synthroid) into the active thyroid hormone, T3 (Cytomel and Armour Thyroid).

Dietary deficiency of iodine was once a very common cause of both hypothyroid as well as thyroid enlargement (goiter). However, since iodine began being added to most brands of table salt, a hypothyroid diet due to iodine deficiency is now relatively rare. People who eat little seafood and who take very little salt might want to check their multivitamin to be sure that it contains iodine.

However, too much iodine is also not good on a hypothyroid diet. Too much iodine can actually block the thyroid’s ability to make hormone, so high dose iodine supplements are not recommended.

Hypothyroid diets due to thyroid-blocking actions from cabbage, brussels sprouts, broccoli, cabbage and cauliflower can block thyroid if these otherwise highly nutritious foods are eaten in very high doses. Certain medicines can also block thyroid hormone such as Lithium. L-Carnitine, a powerful and potentially useful energy promoting nutritional product can also block the thyroid if taken in high doses.

Selenium and Hypothyroid diets. Selenium may be the “sleeping giant” of natural thyroid therapies. Selenium is essential for converting T4 thyroid hormone into it’s active form, T3. Selenium may also have the ability to suppress anti-thyroid antibodies for persons who suffer from thyroid inflammation or thyroiditis. Repairing a selenium deficit, could in some people, actually repair thyroid metabolism by increasing the intracellular conversion of T4 to T3.

Effective hypothyroid diets should seek a broad range of natural foods including whole grains, seafoods, nuts, and seeds. Include a broad based multi-vitamin. Vitamin D and Zinc may be important.

Recent Research On hypothyroid diets and Alternative Thyroid Treatments including Cytomel and Armour Thyroid

Mary Shomon is one of the leading advocates of natural thyroid therapies and alternative thyroid treatments. Thyroid.about.com, has an immense amount of information and links to resources on Cytomel and Armour Thyroid, hypothyroid diets, and alternative thyroid treatments.

Thyroid-Info.com, has additional information, including material on alternative thyroid treatments.

Dr. John Lowe’s website is an excellent source of information about health and alternative thyroid treatments,Cytomel and Armour Thyroid, especially as they relate to fibromyalgia.

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http://www.thyroid-info.com/fiber.htm

The Role of Fiber in Weight Loss With Hypothyroidism

Unique High-Fiber Supplement Helps With Fiber Intake

by Mary Shomon

Getting a good amount of fiber is one of the basic tactics that most thyroid need to follow in order to lose weight. Fiber has so many benefits for hypothyroid people trying to lose weight. With slowed digestion, and sometimes even constipation as a result, fiber can help promote regularity. Fiber also slows the digestive process, and can help prevent dramatic swings in blood sugar. Fiber can help lower cholesterol. And, fiber can help you lose weight, because it fills you up, and may reduce your hunger levels.

As I wrote in my book, The Thyroid Diet

One study found that adding 14 grams per day of fiber was associated with a 10% decrease in energy intake and body, and weight loss of 5 pounds over 4 months.

In another study, among a group of 53 women who were moderately overweight, following a 1200 calorie a day diet, over 24 weeks, half were given a fiber supplement, half received placebo. They were given 6 grams of fiber a day to start, down to 4 grams. After treatment, the fiber group lost a mean amount of 17.6 pounds versus 12.76 pounds in the placebo group.

Men up to 50 require 38 grams of fiber a day, and women need 25 grams. Men over 50 should get at least 30 grams and women at least 21 grams. The typical American diet, however, includes 10 grams a day or less of fiber. To get to the targeted level of fiber a day, you will probably have to add a fiber supplement, in addition to emphasizing fiber-rich foods. Start slow, don’t go from “10 to 30” in one day — you need to give your intestinal system time to adjust, and adding too much fiber too quickly can cause discomfort.

Some fiber supplements to consider include:

Psyllium – one study found that women who took 20 grams of psyllium before a meal ate less fat, and felt full more quickly during that meal, helping with weight reduction. Psyllium husk is found in Metamucil products.

Guar gum – i.e., Benefiber, which dissolves with no grit or bulk into drinks

FiberCon tablets, which use polycarbophil, a synthetic fiber (which has the filling and stool-softening effects of fiber, but may not lower cholesterol or blood sugar like other fibers)

One of my favorite fiber products is “Dr. Levine’s Ultimate Weight Loss Formula.” Developed by internist Scott Levine, MD as a weight loss aid for his patients, the powdered formula makes a drink that contains five types of healthful fiber. It tastes fairly good (I’ve tried both the chocolate and raspberry flavors, and they’re fine, especially compared to trying to choke down a couple of spoonfuls of psyllium husks floating around in a glass of water!) Dr. Levine’s formula provides 17 grams of fiber in one serving, so if you use it, as he suggests, with a serving before both lunch and dinner, you will be getting 35 grams of fiber a day as your baseline.

According to Levine, many people who use his product lose 1.5 to 3 pounds per week without doing anything else differently, a result achieved because of reduction of food intake, combined with reduced insulin resistance and blood sugar levels, due to the increased fiber in the diet. Because Levine’s formula includes both soluble and insoluble fibers, it also has the various health benefits – including reduction of cholesterol. Says Levine:

The right kinds of fiber can be particularly helpful for insulin metabolism, especially in people who have even a few extra pounds around the middle. That abdominal weight gain – which drives increasing insulin levels, and is the start of the whole metabolic syndrome – can be helped by high-fiber consumption.

Important Warning: If you switch from a low-fiber to high-fiber diet, be very careful that you are getting your thyroid medicine at least an hour before eating in the morning, so your absorption is not impaired. High-fiber diets can change your dosage requirements, so 6-8 weeks after starting a high-fiber diet, you may wish to have your thyroid function tested to make sure you don’t need a dosage change.

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Thyroid Diet Secrets: Are You Eating Enough Calories to Lose Weight?

From Mary Shomon,

While you’ll run across an occasional expert who recommend extremely low-calorie diets for weight loss with hypothyroidism, the majority of experts believe you may not be eating enough to maintain your metabolism. Dropping calories too low can lower your metabolism and send your body into “hoard” mode — a process which thyroid patients are particularly susceptible to and which can offset weight loss efforts and keep you from success at your diet.

Personally, when I want to lose weight, going on a 1200 calorie or less per day diet is a sure-fire way to ensure that I don’t lose a pound. And if you’re dieting your heart out, and not getting anywhere, the problem may not be that you’re eating too much — you may be eating too little, and not in the right balance.

To calculate how many calories you need:

Dvide your current weight in pounds by 2.2, in order to convert your weight to kilograms.

Multiply you weight in kilograms by 30. (30 is the number of calories you need per pound of body weight.)

So, if you are 160 pounds, you divide 160 by 2.2, which equals 73 kilograms.

Multiply 73 kilograms by 30, which equals 2190, which would be how many calories you theoretically need to maintain your current weight of 160.

Subtract 200 calories for your thyroid condition, an estimate to reflect the reduction in your metabolism and calorie requirements.

1990 calories is now the estimated calorie requirements for you as a thyroid patient to maintain a weight of 160 pounds.

To lose weight, you need to cut your calorie requirements by 5 calories per kilogram, so that means you multiply your current weight in kilograms by 25 instead of 30.

So, in our example above, if you are 160 pounds, you divide 160 by 2.2, which equals 73 kilograms.

Multiply 73 kilograms by 25, which equals 1825, which would be how many calories you theoretically need to lose about a pound every ten days, at 3500 calories per pound).

Again, subtract 200 calories to account for your thyroid condition.

1625 calories is now the estimated calorie requirements for you as a thyroid patient to lose weight at a safe rate.

Also, most of the effective weight loss programs for thyroid patients also focus on breaking up those calories into multiple “mini-meals” per day.

Some experts believe that people with hypothyroidism should eat 40% protein/25% fat/35% low glycemic carbohydrates in smaller, 250-300 meals.

So, let’s look at one more set of calculations.

Current Weight, in Pounds _____

Divide above by 2.2 _____

Multiply result by 25 _____

Subtract 200 for “Thyroid Factor” -200

Calories Per Day for Weight Loss _____

Divide by 300 = # of 300-calorie “mini-meals” Per Day _____

At 300 calories per meal, a 175 pound hypothyroid person could expect to lose weight eating approximately six balanced mini-meals of around 300 calories each, spaced out evenly throughout the day…along with appropriate exercise, of course!

Totie Fields once said, “I’ve been on a diet for two weeks and all I’ve lost is two weeks.” When you’re trying to lose weight, you may feel like Totie was talking about you. You may have tried diet after diet, joined Weight Watchers, tried herbal diet pills, or read dozens of diet books that tell you to eat all protein, or cabbage soup, or ice cream, or eat 1000 or less calories per day, only to discover that you’re not only not losing weight, but perhaps even GAINING weight! That’s what happened to me ten years ago, when I joined Weight Watchers, followed it to the letter, and gained 2 pounds a week, while everyone else was losing weight.

Or, you may be one of those people who never had a weight problem, and then all of a sudden, pounds starting piling on, seemingly defying all the laws of physics. If it takes 3500 excess calories to gain a pound, how could you possibly gain 10 or 20 pounds in one month? And yet you did. This is what happened to me, at age 33, before my 1995 wedding. After going through my 20s as a slender size 8, I quickly started packing on weight — so much so that I bought a size 12 gown, and in the months before my wedding, I had to have my wedding dress let out 2 more sizes (is that a horrifying thing for a bride or what?), and even after I went on a reduced calorie diet with daily exercise, walked down the aisle as a size 16. And after the honeymoon, the weight kept piling on.

Or maybe you were eating the same way as usual, and getting the same level of physical activity as always, but are wondering why this past six months you have managed to put on a pound a week.

In the midst of any one of these situations, you may head in to see your doctor, saying “I know something is really wrong with me.” And I’ll bet that you were sent home with one of the following:

• A. An antidepressant — because after all, depression makes you gain weight, so that must be it
• B. A diet drug — because writing a prescription gives your doctor something useful and doctor-like to do
• C. A shrug of the shoulders, along with one of those vague non-explanations like “Well, you’re getting older, it’s to be expected” or “must be your hormones” or “it’s normal in the 6 months/year/2 years/5 years after having a baby” and so on
• D. A condescending look, along with some serious medical advice along the lines of, “Well, you must be eating too much and not getting enough exercise, so get off the couch, and stop strapping on the feedbag!”

Gee, doctor, thanks.

You know something is not right, and you know that you are not sitting around lazily, stuffing your face with bonbons, but you don’t get the feeling that the doctor believes you.

And the sad fact is, he or she probably doesn’t. One late 2003 study showed that not only general practitioners — but even health professionals who specialize in treating obesity — have negative stereotypes about people who are overweight. These clinicians typically associate the stereotypes “lazy, stupid, and worthless” with people who are overweight. Most doctors — and the people around you, to an even greater extent — have an automatic anti-fat bias.

You know something is wrong, something is not normal, but who believes you?

I believe you.

Because, while your doctor is busy assuming that you’re too lazy to exercise and don’t have enough willpower to stop eating, what he or she isn’t doing is telling you is that you could have a thyroid problem — a dysfunction in the small, butterfly-shaped gland in your neck that is crucial to your metabolism. While some narrow-minded doctors dismiss thyroid disease as just another lame excuse for being overweight, the reality is that for millions of overweight people, thyroid disease is a very real reason behind weight problems. And learning about thyroid disease and its symptoms — beyond weight problems — and how to get diagnosed, can be critical steps that address the underlying cause of your weight gain, help restore your hope and health, and allow healthy diet and exercise to finally work the way they should!

Recent studies have conservatively estimated that as many as 20 million people have a thyroid problem, the majority of them undiagnosed. Some experts believe that the actual number is substantially higher…and rapidly on the rise. At the same time, studies have shown that 97 million Americans are overweight or obese. That’s nearly three in five (59.4 %) men, and more than half (50.7 %) of all women.

This brings up a critical connection: some people struggling with a weight problem are facing even more of an uphill battle than everyone else, because they are dealing with an underlying thyroid condition — one that is both undiagnosed and untreated.

One study found that as many as 40% of overweight people had evidence of a dysfunctional thyroid, various thyroid conditions that could be contributing to your weight gain in the first place, and to your present difficulty losing weight.

In my case, I went in a number of times to complain about a variety of symptoms. I kept returning, complaining about:

• The unexpected weight gain, despite diet and exercise
• Fatigue and exhaustion
• More hair loss than usual
• Moodiness
• Muscle and joint pains and aches
• Loss of sex drive

My doctor took a “wait and see” approach for a few months, but then she put together the above list of symptoms and decided she should test my thyroid. I was surprised when she called to say she’d discovered I was hypothyroid. I didn’t even know what a thyroid was. Sure, I’d heard people laughingly refer to overweight people as having “glandular problems,” and I had an aunt who had a goiter once, but that was the extent to which I knew about what is actually the master gland of our metabolism.

My doctor put me on thyroid hormone replacement therapy. Blissfully ignorant, I assumed that all the symptoms — and in particular, the weight — would just melt off as quickly as it had appeared, now that I was getting my thyroid back in order.

Surprise! Not so…

Sure, as we tweaked my medicine and dosages, I felt better in some ways — less exhausted, not so moody and achy — but except for several pounds, the weight didn’t budge.

In my 20s, before my thyroid apparently started to go awry, losing weight was simple. I just cut out a bag of chips with lunch a few times a week, and switched to a diet soda instead of regular, and within a few weeks, the extra pounds would be gone.

But nothing I was doing in the beginning moved the scale an ounce. This wasn’t going to be so easy…

So I set out on a mission. To discover how best to optimize my thyroid treatment. To learn what — and how much — I can and can’t eat in order to lose weight. To find out whether I needed to exercise, what type of exercise, and how much. To learn how to get back on track when my weight loss efforts get stalled or even derailed.

Along the way, I turned my own struggle to find the answers into a new role as a patient advocate for others with thyroid and autoimmune diseases. In 1997, I started several websites and newsletters that focus on thyroid disease and the issues patients face; and the sites have become the most popular patient-oriented thyroid websites on the Internet. My first book, Living Well With Hypothyroidism, has gone on to 20 printings, and a second edition. And my Thyroid Diet Success Guide, a simple 40-page summary of weight loss tips that was the inspiration for this book, has inspired many thousands of thyroid patients to successfully lose weight. And throughout it all have been the letters, thousands each month, from people all around the world — describing their symptoms, asking if they could have a thyroid problem, describing their symptoms, their inexplicable and frustration weight gain, their misery over not feeling well. Thyroid patients writing to ask why, despite rigorous diets and exercise programs, they were still not losing weight. People who said they crying as they wrote their emails, describing how being overweight made them feel ugly, old, worthless and unattractive, and nothing was working in their attempts to get the weight off.

Along the way, I’ve been on my own journey, and it’s taken me almost ten years to figure out what I needed to know. And now I’m sharing it here with you, in The Thyroid Diet.

You don’t want to be overweight. I know there are a percentage of people who are overweight who feel comfortable with themselves, and don’t have any body image issues, and more power to them. But I’m not one of them, and if you’re reading this book, neither are you.

When I’ve been overweight, I’m not “proud to be fat.” Like doctors, and most of the public, I see being overweight as a failing, as a sign that I’m less. I don’t need to be model-thin, I just want to feel and look normal…healthy…attractive. And most likely, so do you.

And let’s face it, in addition to what’s known as “psychosocial burden” — basically, suffering emotionally or mental health wise because of the self-esteem and depression issues related to being overweight — there is also an increased risk of many serious health conditions, including:

• Insulin resistance
• Diabetes
• High blood pressure
• High cholesterol
• Cardiovascular disease/heart disease
• Stroke
• Asthma
• Arthritis/degenerative joint disease
• Gallbladder disease
• Sleep apnea
• Fatigue
• Complications of pregnancy
• Menstrual irregularities
• Stress incontinence

Being overweight or obese is also a particular risk for various cancers. A 16-year study by the American Cancer Society found that deaths from a wide variety of cancers — including those of the breast, endometrium, colon, rectum, esophagus, pancreas, kidney, gallbladder, ovary, cervix, liver and prostate, as well as multiple myeloma and non-Hodgkin’s lymphoma — are linked to excess weight and obesity. Only a few cancers — lung cancer, bladder cancer, brain cancer and melanoma were found to have no link to excess weight.

There certainly is enough incentive to lose weight.

But we have to get off the weight loss runaround.

If you read the newspaper and women’s magazine articles, watch the middle-of-the-night infomercials, view the television interviews, talk to the staff at the supplement stores — you’ll hear from experts galore, and every one of them has the one true answer to our problem, the one key to weight loss success.

• The key is: detoxing the liver
• The key is: insulin
• The key is: too many carbohydrates
• The key is: the wrong carbohydrates
• The key is: too many calories
• The key is: not enough calories
• The key is: food combining
• The key is: good fats
• The key is: low fat
• The key is: raw foods
• The key is: juicing
• The key is: vegetarian
• The key is: high-protein
• The key is: grazing all day
• The key is: eating Mediterranean style
• The key is: exercise
• The key is: supplements
• The key is: weight loss drugs
• The key is: cabbage soup
• The key is: SlimFast
• The key is: surgery
• The key is: managing your mind and emotions
• The key is: brain chemistry
• The key is: using your Ab-Swing
• The key is: “figgerin’ out why bein’ fat is workin’ fer ya” (That last one is courtesy of Dr. Phil.)
• Blah blah blah!!!

The bottom line: There is no one answer. What works for YOU is the right answer. And that may be any one of the above, or far more likely, a combination of approaches.

The majority of Americans are overweight. And let’s face it, while some have an underlying thyroid problem, some don’t. Yet most overweight people find it very hard to lose weight, because dropping pounds keeping them off are very plain difficult.

Add to that a thyroid condition, undiagnosed or diagnosed/treated, and it becomes even more difficult, if that is even possible!

You’re not lazy, or lacking willpower. Your weight problem is most likely not an emotional issue that can be shouted and bullied out of you by a television personality. You’re probably not downing an entire box of donuts every night when no one else is watching. Your eating habits are probably not very different than your friend or family members, who are at a normal weight. Your body may truly refuse to lose weight on rabbit food, Weight Watchers, or the Atkins Diet.

Your problem is — your body doesn’t work the way it’s supposed to.

And so a challenge that is already hard for most people may be even harder for you.

That is the most difficult point to get past — to accept that fundamentally, your thyroid condition may, especially in the beginning, and perhaps forever, make weight loss an unfair fight. What you suspect about your body is true. You very well may gain weight more easily than others, and you probably won’t lose weight as easily or quickly as others.

In fact, when hypothyroid, for many of us, the metabolism becomes so efficient at storing every calorie that even the most rigorous diet and exercise programs may not work. Your friend or spouse could go on the same diet as you, lose a pound or two — or even more — a week, and you might stay the same, or even gain weight. It’s NOT FAIR!!

CAN WE SHOUT THAT TOGETHER? IT’S NOT FAIR!!!

Ok, we’ve established that it’s not fair. Now it’s time to move on. That’s life — I’ve got a thyroid problem, you’ve got a thyroid problem, and it’s not likely to go away. This is something we’ll both live with, probably for the rest of our lives. The question is, are we going to live WELL with it, or it is going to define us, and make us miserable? Is it going to stop us from feeling good about ourselves, fitting into clothes we like, feeling sexy, exercising or playing sports, having energy for work, family and children?

I can tell you, I made a decision that it wasn’t going to stop me, and I hope you join me in that decision.

That is where The Thyroid Diet comes in. I’m not going to tell you that you’ll find any magic weight loss secrets in this book. No miracle pill that will make the pounds melt away, or food that will allow you to eat all you want and lose weight overnight. I wish I had that to give you. (I wish I had it myself!)

But for those of you whose weight challenges are due to a thyroid condition that you don’t know you have yet, what you will find in The Thyroid Diet are clear guidelines and straightforward information about thyroid disease that will help you find out more, and get that diagnosis!

And, The Thyroid Diet, in a simple, understandable way, offers you the support, encouragement and information you need to pursue the right diagnosis and treatment with your doctor. Let me tell you, that is no easy task in today’s environment of rigid diagnostic criteria and 10-minute managed care visits.

The best news so far? Excitingly, for some of you, just getting treatment for your previously undiagnosed thyroid problem will be all that you need to return to a healthy weight, without a rigorous change in your diet and exercise!

However, for the majority of thyroid patients, treatment alone doesn’t seem to resolve our weight problems. Losing weight then involves optimizing our thyroid treatment program, because you may not be able to lose weight until you are on the right brand, mix and dosage of thyroid medicine. Simply switching brands, or adding an additional drug, or a slight dosage change may be the minor adjustment that restores your metabolism to normal and allows you to lose weight. Again, The Thyroid Diet will help, as we explore the brands, mixtures and dosage options that may be right for you, along with other lifestyle issues and supplements to help optimize your thyroid treatment.

But despite optimal thyroid treatment, some of us are still struggling. At that point, other approaches become central to losing weight, including ensuring that metabolism works as best as it can, resolving underlying nutritional deficiencies, treating depression and correcting brain chemistry imbalances, reducing stress, combating insulin resistance, treating food allergies and sensitivities, exercise, and many other key activities.

Magical Iodine

Many years ago, when I was a young man, running, exercising, and in very good health, I had a few high voltage shocks due to the job of fixing computer monitors. When I when to the company nurse, I was told that my blood pressure was elevated and I should cut back on my salt intake. What I thought was a good idea at the time, turned out to be a harmful issue as I grew older. This is because I didn’t have all the facts about salt and the value it being iodized. It was not until I was diagnosed with hypothyroidism that I knew I was Iodine deficient.

Beware that with iodine, you can definitely have too much of a good thing. Hope this blog will be of some help in understanding the importance of a diet that includes a little iodine.

Here are some very good sites for tyroid information:

• American Thyroid Association (a thyroid physician organization with a Patient and Public Education Division called Friends of the ATA) at www.thyroid.org
• National Graves’ Foundation at www.ngdf.org
• The Thyroid Cancer Survivors’ Association at www.thyca.org
• The Light of Life Foundation at www.checkyourneck.com
• The Endocrine Society’s Hormone Foundation at www.hormone.org
• The American Association of Clinical Endocrinologists at www.aace.com
• The Endocrine Society at www.endo-society.org

=============================================== http://www.medicinenet.com/hypothyroidism/article.htm What are thyroid hormones? Thyroid hormones are produced by the thyroid gland. This gland is located in the lower part of the neck, below the Adam’s apple. The gland wraps around the windpipe (trachea) and has a shape that is similar to a butterfly – formed by two wings (lobes) and attached by a middle part (isthmus). The thyroid gland uses iodine (mostly available from the diet in foods such as seafood, bread, and salt) to produce thyroid hormones. The two most important thyroid hormones are thyroxine (T4) and triiodothyronine (T3), which account for 99.9% and 0.1% of thyroid hormones present in the blood respectively. However, the hormone with the most biological activity is T3. Once released from the thyroid gland into the blood, a large amount of T4 is converted into T3 – the active hormone that affects the metabolism of cells. =============================================== http://www.medicinenet.com/hypothyroidism/article.htm Thyroid, Iodine, & Diet: What You Should Know Medical Author: Ruchi Mathur, MD Medical Editor: William C. Shiel, Jr, MD, FACP, FACR Many of my patients ask questions or make comments about iodine use in thyroid disease. Examples are: ” Should I increase the iodine in my diet if I’m hypothyroid?” “My mother had hyperthyroidism, and they told her it was because of a lack of iodine.” ” My sister has thyroid disease, and to avoid getting it, I’m taking Kelp tablets.” “Can I eat sushi if I take Synthroid?” Although these questions and comments are relevant, this subject is peppered with “old wives tales” and folklore. In the first part of this discussion, I’d like to focus on the role iodine in relation to the thyroid gland and its function…. a bit of physiology for the beginner. Later, I will discuss how an excess or deficiency of iodine can contribute to diseases of the thyroid gland. Why does the body need iodine? The major function of the thyroid gland is to produce thyroid hormone in an amount sufficient to meet the body’s needs. To make thyroid hormone, the thyroid uses iodine. If iodine is not available in the diet, the thyroid may produce an insufficient amount of hormone. How much iodine does the body need? Areas in the United States where iodine deficiency occurs are scarce. In North America, iodine is added to salt and bread. It is also present in additives, water sources, medications, and dietary supplements. The daily iodine intake varies widely throughout the world. A minimum of 60 micrograms of elemental iodine per day is required to make thyroid hormone. The following lists examples of average iodine intake in various countries and the recommended amount of iodine consumption: Typical Iodine Intakes: North America — 200-700 micrograms/day Germany — 20-150 micrograms/day Chile — 50-150 micrograms/day Switzerland — 130-180 micrograms/day Recommended Daily Intake: Adults 150 micrograms/day Children 90-120 micrograms/day Pregnant Women 200 micrograms/day In North America, the higher values are mainly due to an increased intake in salt. In Japan, where foods rich in iodine are consumed regularly, the intake may be as high as over 1000 micrograms/day. Although iodine consumption is generally lower in Europe, the people in these countries do not usually develop thyroid disease. However, when they are exposed to unaccustomed, large amounts of iodine (such as moving to North America and increasing their iodine intake), they can develop thyroid disease. This occurs particularly in people who have an underlying predisposition to developing thyroid disease. How is iodine used by the thyroid? The process by which the thyroid uses iodine is actually quite complicated and certain steps are still unclear. Essentially, iodine is converted to its free elemental form, called iodide. Iodide enters the thyroid gland through a special transport mechanism. Iodide then undergoes a process called oxidation and is incorporated into intermediate hormones called MIT (Monoiodotyrosine, which contains 1 iodide) and DIT (Diiodotyrosine, which contains 2 iodides.) These compounds then combine to form the active hormones, tri-iodothyronine (T3) and thyroxine (T4). T3 is the most biologically active thyroid hormone. It is formed by combining a MIT with a DIT (so the total of iodides in the molecule is 3). T4 is formed in much greater quantity by combining a DIT with another DIT (so that the total of iodides in the molecule is 4). These hormones are then stored in the thyroid gland and released into the blood stream. Based on the above summary, it is evident that thyroid hormone is actually made up of iodide/iodine directly. So you can see the importance of iodine in relation to the function of the thyroid gland. Whew! Glad the physiology stuff is over!! Iodine Deficiency Most animals, including humans, have an ability to conserve the iodine within their bodies if there is a deficiency of iodine consumed in food. If an inadequate intake continues, however, the ability to make thyroid hormone is slowly depleted. Many cellular processes occur to keep the thyroid as efficient as possible and the thyroid gland often enlarges in an attempt to maintain function. Subsequently, a goiter may form as the thyroid is stimulated to try to make more thyroid hormone. Basically, the changes in hormone levels (namely T4, T3, and TSH) are similar to those that occur in patients who develop low thyroid hormone blood levels (hypothyroidism) from an underlying disease, such as Hashimoto’s disease. Iodine Excess In making thyroid hormone, the body responds to increasing doses of iodine intake by first increasing hormone production and then decreasing production by blocking the incorporation of iodine into thyroid hormone. This blockage is protective. The body simply cannot allow all of the iodine received to turn into hormone without regulation. If this happened, there could be too much hormone produced, thereby resulting in toxic levels of thyroid hormone. While this regulation is complicated, a decrease in the utilization of iodide is called the “Wolff-Chaikoff” effect. If a patient has an underlying problem with the thyroid gland, such as Hashimoto’s disease or Graves’ disease, this protective mechanism may actually be detrimental. In these cases, the gland already is diseased, and, on top of that, the Wolff-Chaikoff effect takes place. In such situations, a goiter can develop or hypothyroidism can occur if large amounts of iodide are given for long periods of time. The gland can sometimes overcome this effect by “escaping” or adapting in a successful way. In these cases, the blockage of hormone formation may be partially relieved and the patient can regain some thyroid function. In large quantities, iodine can reduce the release of thyroid hormones from the thyroid gland. If the hormones are not released, their effects won’t be seen. Occasionally, doctors use this mechanism to control very active thyroid glands that produce too much thyroid hormone. This type of therapy is difficult and is not used as commonly today. An excess of iodine also decreases the blood flow and growth of the thyroid gland, which is characteristic of Graves’ disease. As a result, iodine may be used to reduce the thyroid hormone level in conjunction with surgery to remove some or all of the thyroid gland tissue and assure a good outcome. While I’ve just explained how too much iodine exposure can actually shut down thyroid hormone production, in other situations, an excess of iodine may actually cause an over-production of thyroid hormone and hyperthyroidism. If a person has been exposed to relatively little iodine and then consumes a diet rich in iodine, the individual can develop an excess production of thyroid hormone (iodine-induced hyperthyroidism). In general, this occurs in people who have an underlying thyroid disorder that has not yet manifested clinically. Iodine-induced hyperthyroidism is important in areas of the world where iodine intake is high. We actually see this quite commonly in the United States among populations who have emigrated from countries such as Iran and Africa. The name for this response is the ” Jodbasedow” effect, which actually occurs only in a small fraction of people at risk. Even though it is relatively uncommon, it is important since administering iodine-containing dyes for medical procedures (such as CT scans, barium procedures, etc.) can trigger this effect. What you need to know: It is easy to see why thyroid physiology often makes a medical student’s head swim… and it has the same effect on many practicing doctors too! It is difficult to predict how a particular individual will respond to thyroid depletion or excess. The family history, country of origin, and other factors in the individual’s medical history may help determine what effect, if any, will be seen. In general, it is best to take a moderate approach to iodine consumption. There is no specific reason to advocate kelp or iodine supplementation in our society. Likewise, there is no general reason to discourage eating sushi or seaweed-containing products. If you have questions about specific supplements or food products, or if you have known thyroid disease and have questions, you should consult your doctor. I hope this review has answered some of your questions on iodine intake and thyroid disease. A word to the wise…everything in moderation! =============================================== http://www.thyroid.org/patients/patient_brochures/iodine_deficiency.html What is iodine deficiency? Iodine is an element that is needed for the production of thyroid hormone. The body does not make iodine, so it is an essential part of your diet. Iodine is found in various foods. If you do not have enough iodine in your body, you cannot make enough thyroid hormone. Thus, iodine deficiency can lead to enlargement of the thyroid (goiter), hypothyroidism and to mental retardation in infants and children whose mothers were iodine deficient during pregnancy. Before the 1920s, iodine deficiency was common in the Great Lakes, Appalachian, and Northwestern U.S. regions and in most of Canada. Treatment of iodine deficiency by the introduction of iodized salt has virtually eliminated the “goiter belt” in these areas. However, many other parts of the world do not have enough iodine available through their diet and iodine deficiency continues to be an important public health problem globally. Approximately 40% of the world’s population remains at risk for iodine deficiency. 1 SYMPTOMS What are the symptoms of iodine deficiency? All of the symptoms of iodine deficiency are related to its effect on the thyroid: Goiter – Without adequate iodine, the thyroid progressively enlarges (develops a goiter) as it tries to keep up with demand for thyroid hormone production. Worldwide, iodine deficiency is the most common cause of thyroid enlargement and goiter (see Goiter brochure). Within a goiter, nodules can develop. Patients with a large goiter may experience symptoms of choking, especially when lying down, and difficulty swallowing and breathing. Hypothyroidism – As the body’s iodine levels fall, hypothyroidism may develop, since iodine is essential for making thyroid hormone. While this is uncommon in the United States, iodine deficiency is the most common cause of hypothyroidism worldwide (see Hypothyroidism brochure). Pregnancy-related problems – Iodine deficiency is especially important in women who are pregnant or nursing their infants. Severe iodine deficiency in the mother has been associated with miscarriages, stillbirth, preterm delivery, and congenital abnormalities in their babies. Children of mothers with severe iodine deficiency during pregnancy can have mental retardation and problems with growth, hearing, and speech. In the most severe form, an underactive thyroid can result in cretinism (a syndrome characterized by permanent brain damage, mental retardation, deaf mutism, spasticity, and short stature), though this is not seen in the United States. Congenital hypothyroidism due to iodine deficiency is the most common preventable cause of mental retardation in the world. Even mild iodine deficiency during pregnancy, which may be present in some women in the United States, may be associated with low intelligence in children. 2 CAUSES What are the causes of iodine iodine deficiency? Since the body does not make iodine, it relies on the diet to have enough iodine. Thus, iodine deficiency is caused but not having enough iodine in the diet. Iodine is present naturally in soil and seawater. The availability of iodine in foods differs in various regions of the world (see Table 1). Individuals in the United States can maintain adequate iodine in their diet by using iodized table salt (unless they have to restrict the amount of salt in their diet), by eating foods high in iodine, particularly dairy products, seafood, meat, some breads, and eggs, and by taking a multivitamin containing iodine (see below). However, the amount of iodine in foods is not listed on food packaging in the U.S., and it can be difficult to identify sources of iodine in foods. Common Sources of Dietary Iodine: Breads Iodized table salt Cheese Saltwater fish Cow’s milk Seaweed (including kelp, dulce, nori) Eggs Shellfish Frozen yogurt Soy milk Ice cream Soy sauce Iodine-containing multivitamins Yogurt Table 2. Median Population Urinary Iodine Values and Iodine Nutrition MEDIAN URINARY IODINE CONCENTRATION (µg/L) CORRESPONDING IODINE INTAKE (µg/day) IODINE NUTRITION <20 <30 Severe deficiency 20-49 30-74 Moderate deficiency 50-99 175-149 Mild deficiency 100-199 150-299 Optimal 200-299 300-449 More than adequate >299 >449 Possible excess [From WHO, UNICEF and ICCIDD 2001 Assessment of the Iodine Deficiency Disorders and monitoring their elimination. A guide for programme managers. WHO publ., Geneva. WHO/NHD/01.1] 3 DIAGNOSIS How do you diagnose iodine deficiency? Iodine deficiency is diagnosed across populations and not specifically in individuals. Since iodine is released from the body through the urine, the best way to determine iodine deficiency across a large population is to measure the amounts of iodine in urine samples. Iodine deficiency is defined as a median urinary iodine concentration less than 50 µg/L in a population (see Table 2). In the United States, iodine status has remained generally adequate in the last 2 decades although studies have shown that urinary iodine levels dropped by about half between the early 1970s and the early 1990s. However, iodine deficiency is a major issue in other parts of the world, including parts of Europe, Africa and Asia. 4 TREATMENT How is iodine deficiency treated? There are no tests to confirm if you have enough iodine in your body. When iodine deficiency is seen in an entire population, it is best managed by ensuring that common foods that people eat contain sufficient levels of iodine. Since even mild deficiency during pregnancy can have effects on delivery and the developing baby, all pregnant and breastfeeding women should take a multivitamin containing at least 150 µg iodine per day. How is iodine deficiency prevented? As with many diseases, it is better to prevent the problem rather than have to treat it. Over the last 80 years, world-wide efforts have been made to eliminate iodine deficiency. Indeed, elimination of iodine deficiency has been a major goal of the World Health Organization. Iodized salt has been the mainstay of treatment for iodine deficiency worldwide, including in the United States. Injections of iodized oil are occasionally used in regions of the world where widespread iodized salt use is not possible. Iodination of water supplies also has been effective in some places. United States Recommendations – The Institute of Medicine has set the Recommended Dietary Allowance (RDA) for iodine in adult men and women at 150 µg per day. Individuals who add table salt to their food regularly should use iodized salt. One teaspoon of iodized salt contains approximately 400 µg iodine. Most iodine-containing multivitamins have at least 150 µg iodine, but only about half of the types of multivitamins in the U.S. contain iodine. The RDA is 220 µg iodine per day for pregnant women and 290 µg iodine per day for breastfeeding women. Because the effects of iodine deficiency are most severe in pregnant women and their babies, the American Thyroid Association has recommended that all pregnant and breastfeeding women in the U.S. and Canada take a prenatal multivitamin containing 150 µg iodine per day. Are there problems with taking too much iodine? Taking too much iodine can also cause problems. This is especially true in individuals that already have thyroid problems, such as nodules, hyperthyroidism and autoimmune thyroid disease. Administration of large amounts of iodine through medications (ie Amiodarone), radiology procedures (iodinated intravenous dye) and dietary excess (Dulce, kelp) can cause or worsen hyperthyroidism and hypothyroidism. In addition, individuals who move from an iodine-deficient region (for example, parts of Europe) to a region with adequate iodine intake (for example, the United States) may also develop thyroid problems since their thyroids have become very good at taking up and using small amounts of iodine. In particular, these patients may develop iodine-induced hyperthyroidism (see Hyperthyroidism brochure). =============================================== http://www.suite101.com/article.cfm/graves_disease/115556 Excess consumption of refined, iodized salt is one of the major causes of hyperthyroidism and it’s a well-known trigger for Graves’ disease. Iodine, a mineral that is highly toxic in its pure form, is essential to life in trace amounts. Molecules of iodine react with the amino acid tyrosine to form thyroid hormone. Sea salt is the most widely available source of natural iodine. Sea salt, which is typically brown or gray-tinged, contains 98 percent sodium chloride and 2 percent mineral salt. Mineral salt is made of more than 80 different elements, including magnesium, calcium, potassium, manganese, phosphorus and iodine salts. Sea salt is taken up by plants, animals and, since the beginning of time, consumed by humans. Refined salt is a chemical composed of 99.9 percent sodium chloride, and 0.1 percent additives. In the last half century, potassium iodide has been regularly added to refined salt to help prevent iodine deficiency. Aluminum and sugar are also added to help stabilize the product’s composition and prevent caking. The 80 minerals found in sea salt, with proven health benefits, aren’t found in refined salt. Iodine deficiency is rarely seen today. At one time, glacial runoff caused deficiencies of iodine in glacial areas such as the Alps. The use of sea salt is the best way to prevent iodine deficiencies. However, refined salt, a chemical as clean as heroin or white sugar, is inexpensive to manufacture yet profitable for those who produce it. Refined salt is used as a preservative for processed, pre-packaged foods, adding months to the products shelf life. Early on, however, scientists recognized that this unnatural form of iodine present in refined salt had the potential to cause problems. The body cannot handle refined salt in the same manner it handles sea salt. The kidneys have trouble metabolizing it and blood pressure rises. The thyroid gland is confused by its appearance and consequently forms thyroid antibodies. On top of this, the amount of unnatural iodine consumed in the United States far exceeds the minimum daily requirement. The body needs 75-150 mcg iodine daily for optimal thyroid hormone production. The typical American diet provides 300-700 mcg daily, and diets rich in processed and fast foods contain an excess of 1,000 mcg. Writing in The Nature Doctor in the early 1950’s, the Swiss physician Dr. H.C.A. Vogel reported that amounts of iodine greater than 150 mcg caused palpitations and triggered Graves’ disease in people genetically predisposed to autoimmune thyroid disease. This has been confirmed by the German Commission E, the world authority on herbal medicine in its warnings to avoid kelp, because of its high iodine content. Curezone, an organization dedicated to natural health warns that not all products labeled as sea salt are natural. Some products are harvested mechanically from dirt or concrete basins and subjected to harsh chemical degradation. The finished product is robbed of minerals and often contains additives although it originally started out as sea salt. Resources For more information on sea salt, refined salt and hyperthyroidism, the salt cure and online resources for purchasing sea salt, see http://curezone.com/foods/saltpage.asp Other sources for sea salt from the May 2005 issue of O, the Oprah Magazine, include: Maine Sea Salt, www.maineseasalt.com Borsari Seasoned Salt, www.igourmet.com Espirit du Sel Sea Salt, www.igourmet.com Flaky Fleur de Sel, www.brownetrading.com Blessac Salts from France, www.amazon.com Nirmala’s Kitchen Salt Blends, www.nirmalaskitchen.com =============================================== http://www.saltinstitute.org/iodized_salt_q-a.html National Symposium on “HYPOTHYROIDISM” Draft of Questions and Answers prepared by: The All India Institute of Medical Science, New Delhi Chandrakant S. Pandav Ajay Sood K. Anand Institute of Nuclear Medicine and Allied Sciences, New Delhi Dr. R. Sankar Office of the Salt Commissioner, Jaipur Mr. R. Prakash Mr. Sunderesan UNICEF-India, New Delhi Ms. K. Bishnoi Dr. Kamal Islam International Council for the Control of Iodine Deficiency Disorders, South Asia and Pacific Office, New Delhi Dr. M.G. Karmarkar Question 1 : What is iodised salt? Answer 1 : Iodised salt is used to prevent a health problem now called as iodine deficiency disorders (IDD). It is common salt to which very small quantity of an iodine compound is added. Iodised salt looks, tastes and smells exactly like common salt and it is used in the same way. Question 2 : What is iodine? Answer 2 : Iodine is a natural element which is essential to human life. Some of the most vital functions of the human body such as proper development of brain and body and maintenance of body temperature depend upon a steady supply of iodine. Question 3 : Which are the terms used to identify the iodine compound used in supplementation programmes? Answer 3 : The following terms are often used to identify the iodine compound used in fortification programmes a) Iodination: fortification with any iodine compound b) Iodisation/Iodization: fortification with potassium or sodium iodide c) Iodation: fortification with potassium or sodium iodate However, these terms are frequently used interchangeably. Question 4 : What are the other methods of iodine fortification? Answer 4 : In addition to iodised salt, there are other methods of iodine prophylaxis. Some of these are iodised oil (capsule and injections), iodised water, iodised bread, iodised soya sauce, iodoform compounds used in dairy and poultry, and certain food additives. Question 5 : Why is iodine so important? Answer 5 : Iodine is essential for the normal growth, development and functioning of both the brain and body. A lack of iodine can give rise to a goitre and make a person dull, listless and easily tired. Such a person is less active than a normal individual. But more importantly, without enough iodine, a newborn’s brain and body can become permanently retarded and stunted. Iodine is vitally needed during early childhood, puberty, pregnancy and lactation. A woman who is deficient in iodine is likely to produce an abnormal child. If left untreated, the child’s mental and physical condition worsens as he grows older. Question 6 : What is the role of iodine in human body? Answer 6 : Iodine is an essential component of the thyroid hormones, thyroxine (T4 and tri-iodothyronine (T3), contributing 65% and 59% of their respective molecular weights. To meet the demand for adequate hormone, the thyroid has developed an elaborate mechanism for concentrating iodine from the circulation and converting it into hormone, which it then stores and releases into the circulation as needed. The thyroid hormones act though specific receptors to selectively regulate gene expression in target tissues, particularly liver, pituitary, muscle, and developing brain. Inadequate iodine supply leads first to inadequate hormone production and then to inadequate tissue response, i.e hypothyroidism. Thus, at present, the only physiological role known for iodine in human body is for the synthesis of thyroid hormones by the thyroid gland. Therefore, the dietary requirement of iodine is determined by normal thyroxine (T4) production by the thyroid gland without stressing the thyroid iodide trapping mechanism or raising Thyroid Stimulating Hormone (TSH) levels. Question 7 : What is the metabolism of iodine in the body? Answer 7 : The iodine taken in the diet is absorbed throughout the gastro-intestinal (GI) tract. In whatever form, iodine is present in the diet, it is converted in the form of iodide ion before it is absorbed. This is true for all forms except when it is in the form of thyroid hormones for therapeutic purposes. The iodide ion is bio-available and absorbed totally. It enters the circulation as plasma inorganic iodide (PII). The two major organs which clear PII from circulation are thyroid and kidney. The iodide is used by the thyroid gland for synthesis of thyroid hormones. The kidney excretes iodine with urine. The excretion of iodine in the urine is a good measure of iodine intake. For determining the iodine requirements, the important indices are serum T4 and TSH levels and urinary iodine excretion. The physiological actions of thyroid hormones can be categorized into (a) Growth and Development (b) Control of metabolic processes in the body. Thyroid hormones play a major role in the growth and development of brain and central nervous systems in humans from 15th week of gestation to 3 years of life. If iodine deficiency exists during this period, resulting in thyroid hormone deficiency, the consequence is derangement in the development of brain and central nervous system. These derangements are irreversible, the most serious form being that of cretinism. The other physiological role of thyroxine is to control several metabolic processes in the body. These include carbohydrate, fat, protein, vitamin and mineral metabolism. Question 8 : How much iodine does a person normally need? Answer 8 : The average daily requirement of an adult is 150 mg a day, an amount so small that it could fit onto a pinhead (100,000 micrograms – 1 gram). The average requirement of pregnant and lactating woman is 200 micrograms per day. An average lifetime’s requirement of an individual with 70 years life span would add up to less than a teaspoonful. However, it is important that the body gets this iodine regularly every day. This is why it must form part of every person’s daily diet. Question 9 : What is the optimal iodine intake? Answer 9 : The recommended amount is 150 mg / day for adults, 200 mg for pregnant or lactating women, and lower amounts for children. These recommendations stem from consensus statements by several groups, including the International Council for Control of Iodine Deficiency Disorders (ICCIDD), the World Health Organization (WHO), UNICEF, and the Food and Nutrition Board of the U.S. National Academy of Sciences. The amounts are based on the following: the calculated daily thyroid hormone turnover in euthyroidism, the iodine intake producing the lowest values for serum TSH and for serum thyroglobulin, the amount of thyroid hormone replacement necessary to restore euthyroidism to athyreotic subjects, the iodine intake associated with the smallest thyroid volumes in populations, and the lowest incidence of transient hypothyroidism in neonatal screening with blood spot TSH. Question 10 : From where do we normally get iodine? Answer 10 : Iodine is present in its natural state in the soil and in water. So our normal requirement comes from crops grown on iodine – rich soil. But when the soil of any area lacks iodine, the crops too are deficient in this essential nutrient. Consequently, those people who live on iodine – deficient land and eat the food items grown on such soils regularly, do not get their requirement of this essential element. Question 11 : What happens if a person does not get enough iodine? Answer 11 : Goitre is only one of the many consequences of iodine deficiency. A number of physical and mental abnormalities, some serious, some mild, result from iodine deficiency. The most visible and easily recognizable sign of iodine deficiency is goitre. A goitre is an enlarged thyroid gland. It can range in size from an invisible swelling to a monstrous growth. Question 12 : What are the consequences of too little iodine? Answer 12 : The iodine deficiency disorders include goiter, hypothyroidism, mental retardation, reproductive impairment, and decreased child survival, as extensively reviewed elsewhere. All stem from the insufficient thyroid hormone production that results from inadequate iodine supply. Endemic goiter is the first and most visible sign of iodine deficiency. The thyroid enlarges as an adaptation to the threat of inadequate hormone, a reaction mediated by TSH stimulation and perhaps other growth factors. In mild iodine deficiency, this response may be adequate to preserve euthyroidism, but at the cost of an enlarged thyroid and the attendant risks of neck compression and eventual hyper-functioning autonomous nodules with hyperthyroidism. An insufficient adaptation in adults produces hypothyroidism with its usual clinical stigmata. The damage is greater when iodine deficiency provokes hypothyroidism during fetal or early life, because thyroid hormone is necessary for proper development of the central nervous system, particularly its myelination. Individuals who were hypothyroid at this critical period frequently have permanent mental retardation, which cannot be corrected by later administration of thyroid hormone or iodine. Child survival is also threatened by iodine deficiency, and several studies show that neonatal mortality decreases, sometimes by 50% or more, when the deficiency is corrected. Question 13 : What exactly is a Goitre? Answer 13 : A goitre is a swelling of the neck caused by an enlarged thyroid gland. When the body does not get enough iodine, the thyroid increases in size. Not all goitres are visible. Many of them, particularly in the early stages, can be detected only by an experienced doctor. It is only when a goitre grows quite large that it can be seen and recognized by everyone. A person with a goitre may also have other hidden iodine deficiency disorders. Question 14 : What are Iodine Deficiency Disorders (IDD)? Answer 14 : Iodine Deficiency Disorders (IDD) form a spectrum of abnormalities which includes goitre, mental handicap, deaf mutism, squint, difficulties in standing or walking normally, and stunting of the limbs. Table – 1 gives the spectrum of IDD. Iodine – deficient women frequently suffer abortions and stillbirths. Their children may be born deformed, mentally deficient or even cretins. All these problems are caused by a simple lack of iodine in the diet. Goitre is the least tragic of them. Goitre is only the tip of the iceberg. Question 15 : Why does a child become a Cretin? Answer 15 : A baby growing in the mother’s womb needs a steady supply of iodine for the normal growth and development of its brain and body. Only the mother’s body can provide this essential iodine. But if the mother is iodine – deficient, the child too is deprived of this much – needed nutrient. If the woman’s deficiency is severe, the child’s brain and body are seriously and permanently stunted, and he becomes a cretin, unable to walk, talk or think normally. If the mother’s deficiency is minor, the child will still be affected, even though he may look normal. The damage to his brain usually shows up years later in poor school performance and an inability to perform normal, everyday tasks. Millions in our country suffer from this form of iodine deficiency and it affects the social and economic progress of whole regions. Question 16 : Can the daily consumption of iodised salt cure Goitre, Cretinism and other Iodine Deficiency Disorders? Answer 16 : NO. Cretinism is permanent and incurable. Like many other iodine deficiency disorders with the exception of certain types of goitre, it cannot be cured but it can be easily prevented before it occurs. The regular consumption of iodised salt provides protection to present and future generations against the tragic consequences of iodine deficiency disorders. Goitre in the early stages of occurrence can be “cured”. However, like cretinism, regular intake of iodine easily prevents goitre before it occurs. Question 17 : Where do Iodine Deficiency Disorders (IDD) occur in India? Answer 17 : The areas of severest iodine deficiency lie in the great sub-Himalayan belt that extends from Jammu and Kashmir, all along North India, to the North East, covering an area of 2500 square kms. But recently IDD has been reported from Maharashtra, Gujarat, Madhya Pradesh, Andhra Pradesh, Orissa, Karnataka, Kerala, Tamil Nadu and even Delhi. In fact, no state or Union Territory in India is free from IDD as a public health problem. New pockets of iodine deficiency are being discovered every day. Question 18 : Iodine Deficiency is prevalent in hilly regions only. People living in plains and coastal areas are not suffering from iodine deficiency. Answer 18 : NO. Iodine deficiency is widely prevalent not only in hilly regions but also in the plains and even coastal areas. Surveys conducted by the Government of India and many premiere national institutions indicate that no state is free from iodine deficiency. For example, Delhi, Chandigarh, Bombay. The goitre prevalence rate in the coastal state of Goa is as high as 27.5%. Kerala is having the Total Goitre Rate (TGR) ranging from 4.7% to 21.43% (13 out of the 14 districts are considered to be endemic) the TGR in plain areas like Delhi is 8.6%. Thus, everyone is exposed to the risk of iodine deficiency. Question 19 : Are there any special foods which are rich in Iodine? Answer 19 : Except for certain types of seaweed, there are no foods that are inherently rich in iodine. All food derives its iodine from the soil on which it grows. If the soil is poor in iodine, all the food grown on it will also be low in iodine. Therefore, in areas of iodine deficiency, the most common method is to ensure a steady intake of essential iodine is by adding it to the diet in the form of iodised salt. Question 20 : What are the dietary sources of iodine? Answer 20 : The iodine content of food-stuff depends on the iodine content of the soil on which it is grown. The iodine present in the upper crust of earth is leached out due to glaciation and repeated flooding and is carried to the sea. The sea water, is, therefore, rich source of iodine4. The sea-weeds located near coral reef have inherent biological capacity to concentrate iodine from the sea. The reef fish which thrives on sea-weeds is rich in iodine. Thus, population consuming sea-weeds and reef fish have high intake of iodine, as the case in Japan. The amount of iodine intake by the Japanese is to the tune of 2,000 to 3,000 micrograms per day5. However, there are several areas in Asia, Africa, Latin America and parts of Europe, where iodine intake varies from 20 to 80 micrograms per day. In USA and Canada and some parts of Europe, the intake is around 500 micrograms per day. Question 21 : What is the average iodine content of foods on fresh and dry basis? Answer 21 : The average iodine content of foods on fresh and dry basis is given in Table – 2 . Question 22 : Does the iodine content of various food-stuffs vary with geographical locations? Answer 22 : YES. It is important to note that iodine content of various food-stuffs varies with geographical locations, as there is a large variation in the iodine content of inorganic world as shown in the Table 3. Question 23 : Sea salt provides natural iodine in sufficient quantity to meet the daily iodine requirement. Answer 23 : Contrary to the popular belief, sea salt does not contain adequate iodine. It contains only 2 mg of iodine/gm. of salt. Question 24 : Are all sea foods rich in iodine? Answer 24 : It is generally believed that all sea foods are rich in iodine. However, not all food available from sea is rich in iodine. It is important to note that NOT all organisms in sea has the ability to concentrate iodine. Only sea-weeds and that too of a particular variety have the inherent biological ability to concentrate iodine. These sea-weeds are located near the coral reefs. Therefore, reef fish which feed on these sea-weeds are a very rich source of iodine as compared to the deep sea water fish. Further, consumption of fish after chopping the head does not supply enough iodine. The head of fish contains maximum iodine due to the presence of the thyroid gland as compared to the rest of the parts of the fish. Question 25 : Why is iodine added to salt? Can’t it be taken separately, like other medicines? Answer 25 : An important fact about iodine is that although it is needed in tiny amounts, it is needed regularly, everyday. While it could be taken every day like a medicine or a vitamin tablet, this would involve taking a tablet every day for the rest of our life. Salt, however, is something that is used by all every day. On an average, the same amount of salt 10 to 15 grams a day is consumed every day. If this salt is iodised, then the population will automatically get the required amount of iodine. Question 26 : But if a person lives in an area that is not Iodine-deficient won’t the extra Iodine in the salt be harmful? Answer 26 : No, it will not. All of us need only a certain amount of iodine to function normally. If this iodine is already available to the body, it will simply reject any additional quantities and excrete it unused through the urine. On the other hand, if you are deficient in iodine, the thyroid gland will use as much iodine as it needs and reject the rest. This makes iodine safe for everyone. Question 27 : Can iodised salt be used by pregnant women, lactating mothers, very young children, elders or someone who is ill? Answer 27 : YES, iodised salt can be used by everyone. Every person-young, old, sick or healthy-needs iodine every day. Pregnant women, lactating mothers and young children need it even more than others, so it is not only safe but also necessary for them to use iodated salt every day. Question 28 : Can iodised salt be used like ordinary salt? Answer 28 : Yes. Iodised salt can be used in cooking or at the table the way we always used salt. Just make sure that iodised salt is NOT washed before use, as this will removes all the iodine. Question 29 : Is it possible to use iodised salt for livestock? Answer 29 : Yes. Iodised salt improves the health and productivity of animals and reduces the number of stillbirths and miscarriages. Also, cattle who are fed iodised salt produce milk that is rich in iodine. Question 30 : Can iodised salt be stored like normal salt? Answer 30 : Storing iodised salt involves a few precautions. The iodine in the salt can be destroyed by prolonged exposure to direct sunlight and moisture. Therefore, it is important to store the iodised salt in an airtight container made of plastic, wood, glass or clay, with a well-fitting lid. Make sure that iodised salt is consumed within six months of buying it. Question 31 : What should one do if one cannot find iodised salt in the local market? Answer 31 : The Government of India has decided to make iodised salt available in a phased manner all over the country. If the local market does not stock iodised salt, write to the nearest Salt Commissioner’s Office, the address of which is given on the last page of this booklet. Question 32 : How long will we have to keep using iodised salt? Answer 32 : If one lives in an iodine-deficient environment, there is no likelihood of the deficiency being corrected at the source, namely, in the soil. On the contrary, the increased degradation of our environment is making the problem worse. Large – scale deforestation, among other things, has led to increased flooding and erosion of the top soil, which carries away the precious iodine. With the environmental deficiency growing worse day by day, iodine fortification will have to become part of our everyday lives. Most countries in Europe and America have been iodising salt continuously since the 1920s, for this is the only safe, long-term answer to a problem that threatens the physical and mental well-being of millions of unsuspecting people. Using iodised salt every day is the only way to protect ourselves and our children from the tragic and completely preventable effects of iodine deficiency. It is a small investment towards helping our children and their children to get the best chance to grow up with healthy minds in healthy bodies. Iodine deficiency is present in almost all parts of developed and developing world. As mentioned above, environmental iodine deficiency is the main cause of Iodine Deficiency Disorders (IDD) in all these areas. Unlike nutrients like iron, calcium, vitamins, iodine does not occur naturally in specific foods; rather it is present in the soil and is imbibed through foods grown on that soil. As mentioned above, iodine is irregularly distributed over the earths crust, resulting in acute deficiencies in areas like mountainous regions and flooded riverines. The problem is aggravated by accelerated deforestation and soil erosion. Thus, the food grown in iodine deficient regions can never provide enough iodine to the population and livestock living there. The iodine deficiency results from geological rather than social and economic conditions. It can not be eliminated by changing dietary habits or by eating specific kinds of foods. Rather the correction has to be achieved by supplying iodine from external sources. It has, therefore, been a common practice to use common salt as a vehicle for iodine fortification, for the last 75 years. Salt is consumed approximately the same level through out the year in a given region by all the populations. Universal salt iodisation is now widely accepted strategy for prevention and correction of iodine deficiency disorders. Question 33 : Why is there a ban on sale of common salt? Answer 33 : NO. There is no ban either on production of common salt OR on sale of common salt. There is a ban ONLY against the sale of common salt for direct human consumption unless the same is iodised. Question 34 : Why is there a ban on sale of common salt for direct human consumption? Answer 34 : YES, there is a ban on sale of common salt for direct human consumption. This is because: a) Iodine deficiency is widely prevalent in our country. There is not a single state or union territory where it has not been reported as a public health problem. b) Common salt has been identified as a vehicle for carrying iodine, an essential food item. Question 35 : What is the latest notification in the Prevention of Food Adulteration Rules, 1955 with respect to container or package & label and restriction on sale of common salt? Answer 35 : The latest notification is as follows: In the Prevention of Food Adulteration Rules, 1955 – i) in rule 42, – a) for sub-rule (V), the following sub-rule shall be substituted, namely :- “(v) Every container or package of table iodised salt or iron fortified common salt containing permitted anti-caking agents shall bear the following label, namely:- TABLE IODISED SALT / TABLE IRON FORTIFIED COMMON SALT* CONTAINS PERMITTED ANTICAKING AGENT * Strike out whichever is not applicable. b) in sub-rule (zzz), after cause (10), the following clause shall be inserted, namely:- “11) Every container or package of common salt shall bear the following label, namely:- COMMON SALT FOR IODISATION/IRON FORTIFICATION/ANIMAL USE/PRESERVATION/MEDICINE/INDUSTRIAL USE* * Strike out whichever is not applicable.”, ii) after rule 44F, the following rule shall be inserted, namely:- “44G. Registration on sale of common salt – No person shall, sell or offer or expose for sale or have in his premises for the purpose of sale, common salt for direct human consumption unless the same is iodised. Provided that common salt may be sold or exposed for sale or stored for sale for iodisation, iron fortification, animal use, preservation, manufacturing medicines, and industrial use under proper label declarations as specified under clause (11) of sub-rule (zzz) of rule 42.”, iii) in rule 49 of the said rule, in sub-rule (10), for the words “Table salt or iron fortified common salt”, the words “Table iodised salt or table iron fortified common salt” shall be substituted. Question 36 : Why is there a need to add iodine to the common salt? Answer 36 : Iodine is an essential requirement of the body. It is normally available from natural food items that are grown on iodine rich soils. However, in certain areas of the world, as a result of glaciation and due to repeated flooding; rivers changing their course over a period of time, there is leaching of iodine from soil. The food crops grown on such soil are deficient in iodine thereby leading to iodine deficiency. Further, iodine rich foods are not commonly consumed as there are very few such food items. Hence, it is essential that some food item which consumed by one and all and in more or less fixed quantity has to be fortified with iodine. In this regard, in developing countries salt is the most suitable vehicle for iodine fortification. This mode of fortification has been effectively used and continues to be used NOT ONLY in many developing countries but also in many industrialized countries. Question 37 : How is iodisation of salt done? Answer 37 : The iodisation of salt is done by either spraying potassium iodate or potassium iodide, in certain proportions, so as to ensure a minimum of 150 micrograms of iodine per day. Both, these forms of iodine are absorbed as iodide ions and are completely bio-available. Question 38 : Why there is no option for iodised and non-iodised salt in our country? Answer 38 : In many countries specially industrialized ones, there is an option of buying iodised and non-iodised salt. This is possible because in these countries in addition to iodised salt, iodine is used in baking, food processing and dairy industry. Hence iodine is being supplied through bread, milk and processed food items which are widely consumed in these countries. However such a situation does not exist in several developing countries. Therefore, the use of iodised salt is the main method which has been used for providing iodine to the population in such countries. In India, if there is an option for iodised and non-iodised salt, the population is more likely to purchase and use non-iodised salt for the following reasons: 1) Iodised salt and non-iodised salt are perfectly substitutable products. The appearance, taste, colour etc. of both iodised and non-iodised salt are the same. 2) In general, iodised salt is more expensive than non-iodised salt. In India, we are still in the process of an effective information, education communication efforts regarding the benefits of iodised salt. In such a situation, consumers are likely to purchase non-iodised salt, which is cheaper, to which they have been traditionally using it for years. In general, they are also not aware of the benefits of consuming iodised salt. Question 39 : Compulsory iodisation of salt for direct human consumption curtails an individual’s rights. Answer 39 : No. it does not curtail i.e. this was well argued in the Hon’ble High Court of Madras and in their judgement delivered on Oct. 10, 1995. The court viewed that consumption of salt by all is the most suitable, long term and sustainable solution to prevent the wide spectrum of IDDs. Question 40 : It is a crime to sell or buy ordinary salt after the nation wide ban. Answer 40 : In fact all State Government have issued notifications under the provisions of prohibiting the sale of salt other than iodised salt for edible purposes in their entire state or part of their jurisdictions even before the issue of nation wide notification dated November 27, 1997. Even now, non-iodised salt can be freely sold for non-edible purposes such as industrial uses, fish-curing, hide-curing, water softening etc. Question 41 : Salt iodisation is to benefit big companies and multi-national Government is hand in gloves with them. It is a nexus between politicians and big industries. Answer 41 : Far from truth. So far 795 salt iodisation plants with the annual capacity of 112 lakh tons project have been set up in different categories, as indicated below. – By small common salt manufacturers (upto 10 acres) = 256 – By medium common salt manufacturers (1 to 100 acres) = 87 – By other common salt manufacturers (above 100 acres) = 122 – By Traders —————————————– = 306 – By Refineries ————————————– = 24 TOTAL = 795 Out of the above list there is not even a single multi-national Company. However, one multi-national company is providing marketing assistance to some salt refineries. The country is self-sufficient in common salt. Iodisation plants are fabricated indigenously. All iodine is imported. Manufacturing of KIO3 (potassium iodate) is done in India by 18 Indian firms. There is no involvement of multinational or big company among the manufacturers of potassium iodate. Question 42 : Refineries are patronized by big companies to the detriment of small salt producers. Answer 42 : Any one can put up a refinery, which requires high investment. However, all these refineries buy salt from the same small scale producers. Thus, the small producers can continue to produce iodise salt as such there is no danger of loss of income to them. Question 43 : Which are the different varieties of salt present in the market? Answer 43 : Different varieties of iodised salt present in the market are baragara salt, phoda salt, crystal salt, crushed and powered salt and refined variety salt. Question 44 : What is the cost of iodisation? Answer 44 : The cost of iodisation is not more than 10 paise per kg. Crushing costs at 10 paise and powdering 20 paise per kg. One kg polythene pouch costs about 30-50 paise. Question 45 : The nation wide ban on salt of non-iodised salt for edible purposes affects the small producers of salt. Answer 45 : Not correct. There are about 1600 small producers in the organised sector and 6500 in the unorganized sector whose individual holding does not exceed 10 acres. The ban order in no way interferes with their traditional method of manufacture of salt nor with their trading practices. Question 46 : Salt iodisation programme affects their sales. Answer 46 : No. For edible purpose, the salt is required to be iodised. Otherwise, they can sell their salt without iodisation to industries and other non-edible purposes (as they do now) such as chlor alkali industries, soaps and detergents, fish-curing, tanning, water softening etc. Question 47 : The small salt producers can not afford to have an iodisation plant. Answer 47 : An iodisation plant (Drip feed system) costs about Rs. 40,000/- A group of manufacturers can collectively make use of it, if it is costly for an individual. However, it is pertinent to note here that small producers do not normally trade themselves. It is the middlemen traders who purchase their produce and supply to wholesalers/retailers. The middlemen/traders can put up iodisation plants and iodise salt for edible purpose. However, 40 iodisation plants (each of a capacity of 15,000 tons per year) have been donated with the iodizing chemical for one year, free of cost to associations/cooperative societies of small salt producers in various states. Question 48 : It renders thousand of salt labourers jobless. Answer 48 : Far from truth; on the contrary, iodisation has created more employment opportunities towards iodisation, crushing powdering and packing of salt. Question 49 : It causes tremendous hardships to poor consumers. Answer 49 : The ban notifications really helps the consumers to have access to quality iodised salt for their better health. In a number of states the people especially those below poverty line get iodised salt through public distribution system or fair price shops at a reasonable rate. Question 50 : It has resulted in exorbitant price of salt. Non- iodised (ordinary) salt cost at Rs. 1.50 per kg. whereas iodised salt costs Rs. 6/= per kg. Answer 50 : It is important to note here that one must always compare like with like. In terms of price difference, one must compare the price difference between loose common salt and loose iodised salt. Similarly one must compare packed common salt with packed iodised salt. At salt production centres, iodised salt is available in loose and crystal form at about 40 paise per kg. and crushed / powdered about Re. 1/- per one kg. Transportation charges by rail/road and whole-sailors/ retailers margin form a big share of final retail price. The retail price of iodised salt even in far flung areas are as follows:- Crystal loose : Rs. 1.50 – 2.00 Powdered/Crushed loose : Rs. 2.00 – 2.50 Powdered/Crushed packed : Rs. 2.50 – 4.00 Refined (Branded) : Rs. 5.50 & Above. Free trade is prevalent in salt marketing in the country and no body is compelled to purchase at higher prices. As stated above, iodised salt is made available at a reasonable rate through Public Distribution System (PDS) / fair price shops in several states. In any case, looking to small daily requirement of iodised salt viz 10 gm a day a monthly budget will be about Rs. 1.50/-. This is too small a price for the enormous benefit one gets in being free from IDDs. In case, there is a fear the big companies are trying to monopolies the iodised salt production and sale, this should be controlled rather than curtailing the benefits of Universal Salt Iodisation programme. Question 51 : Iodine in potassium iodate is a poison. Answer 51 : NO. Iodine and potassium iodate are totally safe in quantity consumed. Iodine is not added in elemental form for iodisation of salt. A compound of iodine is used. The chemical chosen in our country is potassium iodate (KIO3) due to its high stability in tropical weather. Its melting point is 560 C. The shelf life of packed and stored iodised salt is reported to be one year. It is has been reported that the average salt consumption in India is 10 gms per day per capita. At the salt iodisation level of 30 parts per million of KIO3, the consumption of 10 gms of iodised salt will provide maximum of 600 mg of KIO3. This quantity is 50,000 times less than lethal dose low of KIO3. Question 52 : Excess of iodine intake is harmful. Answer 52 : A safe daily intake of iodine has been estimated to be 1000 micrograms. The daily iodine intake will be in the range of 150 to 300 mg of Iodine. This iodine intake is 3 to 6 times less than the safe upper limit of iodine intake. Thus consumption of iodised salt is NOT harmful. It is totally safe. About 90% of iodine is eventually excreted in the urine. The median urinary iodine concentration in casual samples, expressed as micrograms per liter (mg/L), is currently the most practical biochemical laboratory marker of community iodine nutrition. It is more useful and much simpler than measuring 24-h samples of calculating urinary iodine/creatinine ratios. Recommendations by the International Council for the Control of Iodine Deficiency Disorders, WHO, and UNICEF (4) set 100 mg/L as the minimal urinary iodine concentration for iodine sufficiency; this figure corresponds roughly to a daily intake of 150 mg iodine. The upper limit for safe iodine intake is uncertain and varies widely among individuals and populations, as discussed below. Intakes up to 1 mg iodine per day are safe for most people, and much higher amounts are usually tolerated without problem. Question 53 : Does the consumption of iodine cause allergy? Answer 53 : No. To date, there has been no report of allergy to iodine when it is consumed in food products. In response to general appeal in the Annals of Allergy in 1974 to report cases of allergy to iodine, no such case has ever been reported. However, Intravenous use of iodine in radiographic contrast has been occasionally reported to cause allergic reaction. Question 54 : Can salt supplementation given in salt iodisation programme cause goitre? Answer 54 : No. only a very large dose of iodine (200 mg = 200,000 micrograms) can lead to “Iodise Goitre” and very rarely cause hypothyroidism. This is 1300 times more than the average intake of individual consuming iodised salt. Thus it is impossible to have any problem due to iodine supplementation given in salt iodisation programme. Question 55 : Can salt iodisation programme lead to increase in thyroid disease? What about its role in thyroid cancer? Answer 55 : In some countries where there was severe iodine deficiency, sudden introduction of increased quantity of iodine in daily diet of the population has led to minimal and mild increase in occurrence of thyrotoxicosis. This was observed in old people who had long history of goitre because of prolonged iodine deficiency and are now suddenly exposed to increased amount of iodine. This is called “Iodine Induced Hyperthyroidism”. Usually such a condition is self limiting and not very common. One should also note that when iodine deficiency has been eliminated in the community, then over years this problem will cease to exist. Question 56 : How much iodine can people tolerate? Answer 56 : Tolerance to iodine is highly variable. Most people can be exposed to large amounts without apparent problems. Important exception to this statement are preexisting iodine deficiency, autoimmune thyroid disease, and papillary cancer. In communities where recent iodine deficiency has been rapidly corrected, iodine-induced hyperthyroidism is a predictable event. In occurred in the United States in the early part of this century and is now showing up in many other countries as they become iodine sufficient. The principle victims are older subjects with autonomous nodules because they are unable to regulate the newly available iodine properly, and instead produce excessive thyroid hormone. The frequency and complications of iodine – induced hyperthyroidism are heightened by poor monitoring of salt iodine concentration, which permits high and uneven rations of iodine, and also by inadequate medical attention, which delays diagnosis and treatment. Without trivializing its seriousness, most observers agree that the risk of iodine-induced hyperthyroidism should not obscure the many benefits that iodine sufficiency has for women and children, and should not slow the pace toward proper correction of the deficiency in a community. Question 57 : What is the relationship between iodine deficiency and autoimmune thyroid disease? Answer 57 : Iodine intake appears causally related to autoimmune thyroid disease. Injection of thyroglobulin into experimental animals induces a thyroiditis similar to human autoimmune thyroiditis, and the immunological response is more vigorous with iodine-rich thyroglobulin. Administration of iodine to goitrous humans provoked a reversible thyroiditis and antibody elevation in some. Epidemiological studies have shown that an increased incidence of autoimmune thyroid disease frequently parallels an increased dietary iodine intake. Question 58 : What is the cost benefit ratio of IDD Elimination Programmes? Answer 58 : The cost of salt iodisation is approximately 5 US cents per person per year – less than the price of a cup of tea. Using the most conservative estimates, the cost benefit ratio of IDD elimination programmes is 1:3. If benefits related to education and livestock populations are included, the ratio would be 1:8. Thus, IDD elimination programmes provide a convincing opportunity of a worthwhile investment in improving the health and nutrition of populations. Question 59 : What is the current status of iodine deficiency in the world? Answer 59 : Almost one third of the world’s population lives in areas of iodine deficiency and risks these consequences. Most of these people are in developing countries, but many in the large industrialized countries of Europe are also affected. Correcting this public health problem is the goal of a massive global campaign that is showing remarkable progress so far. Question 60 : What are the important lessons from history of IDD elimination in other countries? Answer 60 : Like all health problems, we can learn from the history of IDD elimination in other countries. In the 1950s, Guatemala had severe iodine deficiency. Then the country developed a model salt iodization program and by 1972 could claim the eradication of endemic goitre. Following that, the program lased, monitoring of iodized salt became lax, and endemic goitre reappeared (19). Similar failures of initially successful programs occurred in Colombia, Thailand and Mexico. In each, the problem could have been avoided by appropriate monitoring. Many previously deficient countries are now reaching iodine sufficiency, certainly a major achievement, but most still have weak or nonexistent plans for long-range monitoring. In others, e.g. the United Kingdom, iodine sufficiency has been achieved by silent prophylaxis, under circumstances somewhat similar to those in the United States but without iodized salt. Both countries lack any regular monitoring system, and thus can fail to recognize sub-optimal iodine nutrition, either too much or too little. Question 61 : What is the relationship between goitrogens and IDD? Answer 61 : There are areas where consumption of goitrogen in staple diet like cassava affects the proper utilization of iodine by the thyroid gland. For example, in Congo, Africa as a result of cassava diets, there is an overload of thiocyanate. To overcome this problem, appropriate increase in the salt iodisation levels are required so as to ensure the recommended dietary intake. Question 62 : How much of iodine is lost from production point to the household level consumption? Answer 62 : Iodine loss occurs due to improper packaging, humid and moist conditions and transport in open trucks and railway wagons exposed to sunlight. In order to compensate for these losses; at the iodised salt production level, higher levels of iodine are used. There are losses of iodine during cooking process varying from 20% to 40%, depending on the type of cooking used39. =============================================== http://www.liebertonline.com/doi/abs/10.1089/105072501300176462 Iodine-Induced Hypothyroidism ——————————————————————————– To cite this paper: K. Markou, N. Georgopoulos, V. Kyriazopoulou, A.G. Vagenakis. Thyroid. May 1, 2001, 11(5): 501-510. doi:10.1089/105072501300176462. ——————————————————————————– K. Markou, N. Georgopoulos, V. Kyriazopoulou, A.G. Vagenakis Iodine is an essential element for thyroid hormone synthesis. The thyroid gland has the capacity and holds the machinery to handle the iodine efficiently when the availability of iodine becomes scarce, as well as when iodine is available in excessive quantities. The latter situation is handled by the thyroid by acutely inhibiting the organification of iodine, the so-called acute Wolff-Chaikoff effect, by a mechanism not well understood 52 years after the original description. It is proposed that iodopeptide(s) are formed that temporarily inhibit thyroid peroxidase (TPO) mRNA and protein synthesis and, therefore, thyroglobulin iodinations. The Wolff-Chaikoff effect is an effective means of rejecting the large quantities of iodide and therefore preventing the thyroid from synthesizing large quantities of thyroid hormones. The acute Wolff-Chaikoff effect lasts for few a days and then, through the so-called “escape” phenomenon, the organification of intrathyroidal iodide resumes and the normal synthesis of thyroxine (T4) and triiodothyronine (T3) returns. This is achieved by decreasing the intrathyroidal inorganic iodine concentration by down regulation of the sodium iodine symporter (NIS) and therefore permits the TPO-H2O2 system to resume normal activity. However, in a few apparently normal individuals, in newborns and fetuses, in some patients with chronic systemic diseases, euthyroid patients with autoimmune thyroiditis, and Graves’ disease patients previously treated with radioimmunoassay (RAI), surgery or antithyroid drugs, the escape from the inhibitory effect of large doses of iodides is not achieved and clinical or subclinical hypothyroidism ensues. Iodide-induced hypothyroidism has also been observed in patients with a history of postpartum thyroiditis, in euthyroid patients after a previous episode of subacute thyroiditis, and in patients treated with recombinant interferon-a who developed transient thyroid dysfunction during interferon-a treatment. The hypothyroidism is transient and thyroid function returns to normal in 2 to 3 weeks after iodide withdrawal, but transient T4 replacement therapy may be required in some patients. The patients who develop transient iodine-induced hypothyroidism must be followed long term thereafter because many will develop permanent primary hypothyroidism. =============================================== http://naturalmedicine.suite101.com/article.cfm/supplements_for_thyroid_support =============================================== http://www.aace.com/pub/thyroidbrochures/pdfs/Hyperthyroidism.pdf EXCESSIVE IODINE INGESTION Various sources of high iodine concentrations, such as kelp tablets, some expectorants, amiodarone (Cordarone, Pacerone – a medication used to treat certain problems with heart rhythms) and x-ray dyes, may occasionally cause hyperthyroidism in certain patients. OVERMEDICATION WITH THYROID HORMONE Patients who receive excessive thyroxine replacement treatment can develop hyperthyroidism. They should have their thyroid hormone dosage evaluated by a physician at least once each year and should NEVER give themselves “extra” doses. =============================================== http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=2137109 Safe Use of Herbal Kelp Supplements Michael McGuffin and Steven Dentali American Herbal Products Association, Silver Spring, Maryland, E-mail: mmcguffin@ahpa.org, E-mail: sdentali@ahpa.org The authors are employees of a trade association that represents the herbal products industry; 100% of their wages are provided by companies in this trade. Some such companies sell products that contain kelp. The manufacturer of Icelandic Kelp is not a member of this trade association. In their report of a 54-year-old woman with a 2-year history of worsening alopecia, memory loss, and fatigue, Amster et al. (2007) attributed later-emerging symptoms to arsenic in a kelp-containing (Laminaria digitata) supplement. However, the authors failed to report that the product was used at two to four times the suggested amount, of potential significance because of the naturally occurring presence of iodine in kelp. Speciation of arsenic into organic and inorganic forms was not addressed, nor was the amount of arsenic consumed calculated from observed concentration levels. Also, there were errors in marketplace and regulatory descriptions. The supplement was identified as Icelandic Kelp. The patient “initially took two tablets,” which was later increased to “at least four pills per day” (Amster et al. 2007). The authors overlooked the product’s label, which states that one tablet contains 225 µg iodine (150% of daily value) and recommends “one (1) tablet per day” (Nature’s Life, Larkspur, CA). This labeling conforms to the federal regulation that limits daily ingestion of kelp to an amount that provides no more than 225 µg iodine [Food and Drug Administration (FDA) 2006]. The product label also includes the following statement: CAUTION: Do not exceed recommended dosage without first consulting your healthcare practitioner, as excess iodine may adversely affect thyroid function. In neglecting to mention the product’s labeling and their patient’s decision to ignore it, Amster et al. (2007) excluded important information. Under federal law, supplement marketers must disclose material facts associated with use of their products. When a consumer ignores a label caution though, he or she takes on responsibility for that decision. Intake of iodine at least four times this product’s recommended dose must be considered a potential factor in evaluating the observed symptoms. Four tablets contain 900 µg iodine, 600% of its daily value. Amster et al. (2007) noted that the patient had a “more severe presentation than would be expected” from the measured arsenic level. In fact, of the several symptoms recorded after the patient initiated use (and overdose) of the product, only four symptoms—weakness, nausea, vomiting, and possibly erythema—are identified in the presented “clinical manifestations of chronic arsenic exposure.” However, these same symptoms, as well as headache and diarrhea—also observed in this patient—are also associated with iodine toxicity (Pease 1996), albeit usually at higher doses. It would have therefore been no more or less speculative to declare that the patient had a “more severe presentation than would be expected” from the consumed iodine. In their analysis Amster et al. (2007) did not differentiate between organic and inorganic arsenic. Arsenic is commonly found in seaweeds used as food (Rose et al. 2007). With the exception of hijiki, most arsenic found in food seaweeds is the organic form, recognized as less toxic than the inorganic form (Rose et al. 2007). The European Pharmacopoeia (European Pharmacopoeia Commission 2007) allows up to 90 ppm arsenic in kelp used in medicinal products, whereas food regulators have advised that consumption of hijiki—but not kelp or other seaweeds—be avoided due to arsenic concentrations in this species (Food Standards Agency 2004). Although Amster et al. (2007) noted that the arsenic concentration found in most of the analyzed supplements exceeded FDA tolerances for residues in meats and eggs, they did not compare consumed arsenic from these separate sources. Daily consumption of 5 oz chicken—about one-half a chicken breast [the amount of food from the meat or beans group needed daily by women > 51 years of age, according to the U.S. Department of Agriculture's (USDA) current food pyramid (USDA 2007)]—at the allowed arsenic concentration of 0.5 ppm would contain 71 µg arsenic. To take in the same amount of arsenic from the tested samples of Icelandic Kelp, the patient would have needed to consume between 2 g (at 34.8 ppm arsenic) and 45 g (at 1.59 ppm) of these tablets daily. Although she may have used an amount at the lower end of this range, her symptoms would be just as likely to be observed in persons eating more than half a chicken breast each day. Financial data that Amster et al. (2007) attributed to Anonymous (2002) was misstated; sales of supplements in 2001 reached only about one-tenth of the reported $178 billion. Additionally, the authors were apparently uninformed about differences between “homeopathic medications,” regulated as drugs since 1938, and dietary supplements, which have been placed in a specific regulatory class only since 1994. The authors’ reports of adulterated products in Singapore (Tay and Seah 1975), England (Mitchell-Heggs et al. 1990), and Brazil (Mattos et al. 2006) are irrelevant to the U.S. marketplace and its regulations, as is the citation from a 1990 reference about labeling of “botanical medicines” in light of the 1994 law (Mitchell-Heggs et al. 1990), which requires supplement labels to disclose more information than conventional food products. In conclusion, we have no disagreement with the authors’ implication that marketers have a responsibility to control the level of potentially harmful contaminants in herbal products. Inaccurate reporting and speculative science, however, have no place in safety evaluations of case reports associated with supplements. REFERENCES Amster E, Tiwary A, Schenker MB. Case report: potential arsenic toxicosis secondary to herbal kelp supplement. Environ Health Perspect. 2007;115:606–608. [PubMed] Anderson, DM. Mosby’s Medical, Nursing, & Allied Health Dictionary. 6. St. Louis: Mosby, Inc; 2002. Iodine poisoning. Nutr Business Journal. May/June. 2002. Annual industry overview VII; pp. 1–11. [Anonymous]. European Pharmacopoeia Commission. European Pharmacopoeia. 5. Strasbourg, France: Council of Europe; 2006. Kelp; pp. 1869–1870. FDA (Food and Drug Administration). Kelp. 21CFR172.365. 2006 [[accessed 7 November 2007]]. Available: http://a257.g.akamaitech.net/7/257/2422/10apr20061500/edocket.access.gpo.gov/cfr_2006/aprqtr/pdf/21cfr172.365.pdf . Food Standards Agency. Arsenic in Seaweed. London:Food Standards Agency. 2004 [[accessed 19 April 2007]]. Available: http://www.food.gov.uk/science/surveillance/fsis2004branch/fsis6104. Mattos JC, Hahn M, Augusti PR, Conterato GM, Frizzo CP, Unfer TC, et al. Lead content of dietary calcium supplements available in Brazil. Food Addit Contam. 2006;23(2):133–139. [PubMed] Mitchell-Heggs CA, Conway M, Cassar J. Herbal medicine as a cause of combined lead and arsenic poisoning. Hum Exp Toxicol. 1990;9(3):195–196. [PubMed] Pease RW Jr. , editor. Merriam-Webster’s Medical Desk Dictionary. Springfield, MA: Merriam-Webster, Inc; 1996. Iodism. Rose M, Lewis J, Langford N, Baxter M, Origgi S, Barber M, et al. Arsenic in seaweeds—forms, concentration, and dietary exposure. Food Chem Toxicol. 2007;45:1263–1267. [PubMed] Tay CH, Seah CS. Arsenic poisoning from anti-asthmatic herbal preparations. Med J Aust. 1975;2(11):424–428. [PubMed] USDA (U.S. Department of Agriculture). Inside the Pyramid. 2007 [[ accessed 19 April 2007]]. Available: http://www.mypyramid.gov/pyramid/meat_amount.aspx# . =============================================== http://www.dietitian.com/salt.html Ask the Dietitian by Joanne Larsen MS RD LD Salt & Sodium Q: I think my husband salts his food too much. So I switched to Lite Salt. He doesn’t have a blood pressure problem yet, but I think he uses too much salt. I don’t put the salt shaker on the table, but he goes and gets it anyway. How can I stop him from using salt? A: Remember the saying, “you can lead a horse to water, but you can’t make him drink”? Well the same is true for changing another person’s eating habits. It has to be up to him to cut down on added salt. Your body can do fine on just the sodium found in uncooked foods as they are found in nature. This amount would be about 1,000 milligrams of sodium if all foods were cooked without salt. Salt as we know it is actually sodium chloride. Sodium contributes about 40% to the weight of the compound. So 2,500 milligrams of salt is actually only 1,000 milligrams of sodium. What you can do is provide a food environment with less salt in it and allow your husband to make his food choices. Use the following buying and cooking guidelines to reduce salt intake. If you want to cut down on your husband’s salt intake, buy and cook foods that are as close to how they grow on the farm as possible. Eliminate all or most salt cured meats (hot dogs, lunchmeats, sausages, ham, bacon and pickled and smoked meats). When you cook or bake, add none or half of the salt called for in the recipe and be sure to use a measuring spoon. For instance, add 1/4 to 1/2 teaspoon of salt per pound of meat cooked. Don’t add canned or dried soups or bouillon cubes to recipes. Make a white sauce from scratch or add your own blend of dried spices and herbs to recipes. Switch to the salt-less version of spices (e.g. onion powder instead of onion salt). Don’t buy salted snack foods or salted crackers. There are many crackers available in grocery stores with salt-free tops or low salt ingredients. There are even reduced sodium dry roasted peanuts. Pickles and olives are high in salt. Yes, leave the salt shaker off the table. Don’t even fill the salt shaker with salt. If your husband chooses to get the salt shaker, let him be. No amount of nagging or angry looks will change his behavior. Since you have switched to Lite Salt, you should know about those type products. Most reduced sodium salts are half salt (sodium chloride) and half salt substitute (potassium chloride). The potassium chloride causes a person to produce saliva and enhances the taste of food much in the same way salt does. If used to excess, potassium chloride can leave a bitter aftertaste. One-half teaspoon of salt substitute equals the potassium found in one large banana, one-half winter squash and one cup of orange juice or 1 large potato. A word of caution about potassium chloride salt substitute. You need normal functioning kidneys so that the excess potassium is excreted. A high potassium level in your body is as dangerous as high sodium. By substituting Lite Salt in your salt shaker, you may achieve a reduced salt intake for your husband, but he has not changed his shaker habit. I would suggest a pamphlet from the American Heart Association called “Shake the Salt Habit”. It is available from your local heart association or public health department. Suggest your husband read it. Food habits are more likely to change with information, not force

Should a Diabetic take Vitamin B12 Supliments?

Why do energy drinks contain so much Vitamin B? Will it harm or hurt me if I have Diabetes? Am I just wasting my money on energy drinks like 5-hour energy?

Some energy drinks have high amounts of Vitamin B. The question is why? Is it really a good thing for me to take this to boost my energy, if I have diabetes? What should I really do for the tiredness I feel?

This blog is intended to answer many of the concerns that you may have about taking a large amount of B12 to boost your energy and the effect it may have on a diabetic. A good amount of research is below, but you can certainly find more on your own.

My educated conclusion is that it shouldn’t hurt. It is well known to help boost a person’s metabolism by ensuring that homocysteine levels are minimized to a safe and healthy level in the hemoglobin. (http://en.wikipedia.org/wiki/Homocysteine) An unhealthy level of homocysteine affects enzymes with cysteine-containing active sites, for example, it inhibits lysyl oxidase a key enzyme in the production of collagen and elastin, two main structural proteins in artery, bone and skin. A problem with enzymes means that metabolism is effected and energy is also effected. All the research I’ve done so far points to the fact that lowering a persons homocysteine level will help prevent diabetes mellitus (http://en.wikipedia.org/wiki/Diabetes_mellitus), and keep a person avoid the prospect of greater diabetic complications and treatments.

All the research that I’ve done on diabetes points to maintaining a healthy weight through exercise and a properly metabolized diet that is customized for glucose control (watch those high glycemic carbs carefully, because they are killers).

An optimized metabolism means a healthier person and I feel a necessary treatment for diabetes.

More about metabolism and weight control at: http://www.webmd.com/content/article/59/66883.htm

More about diabetic diets at:

http://www.diabetes.org/nutrition-and-recipes/nutrition/diabetes-meal-plan.jsp

http://www.diabetes.org/nutrition-and-recipes/nutrition/diabetes-meal-plan.jsp

http://www.diabetesnet.com/diabetes_food_diet/glycemic_index.php

http://www.glycemicedge.com/

http://www.glycemicedge.com/glycemicindextable.html

http://www.southbeach-diet-plan.com/glycemicfoodchart.htm

http://www.quakeroatmeal.com/qo_HealthProfessionals/diabetesManagement/articlesFour.cfm

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http://www.diabetesincontrol.com/herbs/vitamin_b12.htm

Vitamin B12

Also Known As

Cobalamin, cyanocobalamin, hydroxycyanocobalamin

Physiology and Clinical Effects

Vitamin B12 is needed for normal nerve cell activity, DNA replication, and production of the mood-affecting substance called SAMe (S-adenosyl-L-methionine). Vitamin B12 works with folic acid to control homocysteine levels. An excess of homocysteine, which is an amino acid (protein building block), may increase the risk of heart disease, stroke, and perhaps osteoporosis and Alzheimer’s disease.

Vitamin B12 deficiency can cause fatigue, and some research indicates that individuals who are not deficient in this vitamin have increased energy after injections of vitamin B12.(1) In one unblinded trial, 2,500–5,000 mcg of vitamin B12, given by injection every two to three days, led to improvement in 50–80% of a group of people with chronic fatigue syndrome (CFS), with most improvement appearing after several weeks of B12 shots.(2) While the research in this area remains preliminary, people with CFS interested in considering a trial of vitamin B12 injections should consult a doctor. Oral or sublingual B12 supplements are unlikely to obtain the same results as injectable B12, because the body’s ability to absorb large amounts is relatively poor.

Food Sources

Vitamin B12 is found in all foods of animal origin, including dairy, eggs, meat, fish, and poultry. Inconsistent but small amounts occur in seaweed (including spirulina) and tempeh.

Deficiency Risk and Symptoms

Vegans (vegetarians who also avoid dairy and eggs) frequently become deficient, though the process may take many years. People with malabsorption conditions may suffer from vitamin B12 deficiency. Individuals suffering from pernicious anemia require high-dose supplements of vitamin B12. Older people with urinary incontinence(3) and hearing loss(4) have been reported to be at increased risk of B12 deficiency.

Recommended Dosage

Most people do not require vitamin B12 supplements. However, vegans should take at least 2–3 mcg per day. Treatment for pernicious anemia includes supplements of 1,000 mcg of vitamin B12 per day or vitamin B12 injections. Despite the beliefs of many doctors, scientific proof indicates that oral supplementation (1,000 mg per day) provides successful therapy and that vitamin B12 injections are not needed.(5 6 7 8 9) In addition, the elderly may benefit from 10–25 mcg per day of vitamin B12.(10 11 12)

Contraindications

Vitamin B12 supplements are not associated with side effects.

If a person is deficient in vitamin B12 and takes 1,000 mcg of folic acid per day or more, the folic acid can improve anemia caused by the B12 deficiency, but not affect neurological symptoms. This is not a toxicity but rather a partial solution to one of the problems caused by B12 deficiency. The other problems caused by a lack of vitamin B12 (mostly neurological) do not improve with folic acid supplements.

Vitamin B12 deficiencies often occur without anemia (even in people who don’t take folic acid supplements). Some doctors do not know that the absence of anemia does not rule out a B12 deficiency. If this confusion delays diagnosis of a vitamin B12 deficiency, the patient could be injured, sometimes permanently. This problem is rare and should not happen with doctors knowledgeable in this area using correct testing procedures.

Anyone supplementing more than 1,000 mcg per day of folic acid needs to be initially evaluated by a doctor to avoid this potential problem.

References:

1. Ellis FR, Nasser S. A pilot study of vitamin B12 in the treatment of tiredness. Br J Nutr 1973;30:277–83.

2. Lapp CW, Cheney PR. The rationale for using high-dose cobalamin (vitamin B12). CFIDS Chronicle Physicians’ Forum, 1993;Fall:19–20.

3. Rana S, D’Amico F, Merenstein JH. Relationship of vitamin B12 deficiency with incontinence in older people. J Am Geriatr Soc 1998;46:931 [letter].

4. Houston DK, Johnson MA, Nozza RJ, et al. Age-related hearing loss, vitamin B-12, and folate in elderly women. Am J Clin Nutr 1999;69:564–71.

5. Goldberg TH. Oral vitamin B12 supplementation for elderly patients with B12 deficiency. J Am Geriatr Soc 1995;43:SA73 [abstr #P258].

6. Lederle FA. Oral cobalamin for pernicious anemia—medicine’s best kept secret? JAMA 1991;265:94–5 [commentary].

7. Kondo H. Haematological effects of oral cobalamin preparations on patients with megaloblastic anemia. Acta Haematol 1998;99:200–5.

8. Waif SO, Jansen CJ, Crabtree RE, et al. Oral vitamin B12 without intrinsic factor in the treatment of pernicious anemia. Ann Intern Med 1963;58:810–7.

9. Crosby WH. Oral cyanocobalamin without intrinsic factor for pernicious anemia. Arch Intern Med 1980;140:1582.

10. Kaufman W. The use of vitamin therapy to reverse certain concomitants of aging. J Am Geriatr Soc 1955;3:927–36.

11. Lindenbaum J, Rosenberg IH, Wilson PWF, et al. Prevalence of cobalamin deficiency in the Framingham elderly population. Am J Clin Nutr 1994;60:2–11.

12. Verhaeverbeke I, Mets T, Mulkens K, Vandewoulde M. Normalization of low vitamin B12 serum levels in older people by oral treatment. J Am Geriatr Soc 1997;45:124–5 [letter].

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http://www.yourhealthbase.com/vitamin_B12.html

Summaries of the latest research concerning vitamin B12

By Hans R. Larsen MSc ChE

Vitamin B12 (cobalamin) is an important water-soluble vitamin. In contrast to other water-soluble vitamins it is not excreted quickly in the urine, but rather accumulates and is stored in the liver, kidney and other body tissues. As a result, a vitamin B12 deficiency may not manifest itself until after 5 or 6 years of a diet supplying inadequate amounts. Vitamin B12 functions as a methyl donor and works with folic acid in the synthesis of DNA and red blood cells and is vitally important in maintaining the health of the insulation sheath (myelin sheath) that surrounds nerve cells. The classical vitamin B12 deficiency disease is pernicious anaemia, a serious disease characterized by large, immature red blood cells. It is now clear though, that a vitamin B12 deficiency can have serious consequences long before anaemia is evident. The normal blood level of vitamin B12 ranges between 200 and 600 picogram/milliliter (148-443 picomol/liter). Although deficiency is far more common than excess when it comes to vitamin B12 status cases have been reported where blood levels exceeded 3000 picograms/milliliter. Such high levels may be caused by bacterial overgrowth as outlined in the article Vitamin B-12 Overload

A deficiency often manifests itself first in the development of neurological dysfunction that is almost indistinguishable from senile dementia and Alzheimer’s disease. There is little question that many patients exhibiting symptoms of Alzheimer’s actually suffer from a vitamin B12 deficiency. Their symptoms are totally reversible through effective supplementation. A low level of vitamin B12 has also been associated with asthma, depression, AIDS, multiple sclerosis, tinnitus, diabetic neuropathy and low sperm counts. Clearly, it is very important to maintain adequate body stores of this crucial vitamin.

The amount of vitamin B12 actually needed by the body is very small, probably only about 2 micrograms or 2 millionth of a gram/day. Unfortunately, vitamin B12 is not absorbed very well so much larger amounts need to be supplied through the diet or supplementation. The richest dietary sources of vitamin B12 are liver, especially lamb’s liver, and kidneys. Eggs, cheese and some species of fish also supply small amounts, but vegetables and fruits are very poor sources. Several surveys have shown that most strict, long-term vegetarians are vitamin B12 deficient. Many elderly people are also deficient because their production of the intrinsic factor needed to absorb the vitamin from the small intestine decline rapidly with age.

Fortunately, oral supplementation with vitamin B12 is safe, efficient and inexpensive. Most multi-vitamin pills contain 100-200 microgram of the cyanocobalamin form of B-12. This must be converted to methylcobalamin or adenosylcobalamin before it can be used by the body. The actual absorption of B12 is also a problem with supplements. Swallowing 500 micrograms of cyanocobalamin can result in absorption of as little as 1.8 microgram so most multivitamins do not provide an adequate daily intake. The best approach is to dissolve a sublingual tablet of methylcobalamin (1000 micrograms) under the tongue every day. That will be sufficient to maintain adequate body stores. However, if a deficiency is actually present then 2000 microgram/day for one month is recommended followed by 1000 microgram/day. Some physicians still maintain that monthly injections of vitamin B12 is required to maintain adequate levels in the elderly and in patients with a diagnosed deficiency. There is however, no scientific evidence supporting the notion that injections are more effective than sublingual supplementation.

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http://www.yourhealthbase.com/vitamin_B12.html#overload

Elevated Blood Levels of Vitamin B12

by Georges Mouton, MD

Physicians sometimes encounter cases where a patient’s blood level of vitamin B12 (cobalamin) is substantially higher than the normal upper limit. These cases are often assumed to be due to excessive supplementation, consumption of cobalamin-fortified energy drinks or from intramuscular injections or oral supplements prescribed by a health care professional. In most cases, no action is taken upon discovering the anomaly.

However, careful enquiry very frequently demonstrates that no external human intervention explains the finding of high vitamin B12 levels. Thus the answer to the puzzle must be found within the body’s internal metabolic processes. It is clear that the amount of vitamin B12 excreted in human faeces does not only correspond to what was not absorbed in the ileum (the last of the three sections of the small intestine), but also reflects the production of significant amounts of cobalamin by the colonic microflora [1].

Intestinal Vitamin B synthesis

The fact that intestinal micro-organisms produce significant amounts of B vitamins is fully accepted and has been published in peer-reviewed international medical journals [2,3]. Intestinal bacterial B vitamin biosynthesis involves at least vitamin B1 (thiamine) [4], vitamin B2 (riboflavin) [5], vitamin B5 (pantothenic acid) [6], vitamin B8 (biotin) [6, 7], vitamin B9 (folic acid) [8,9],and vitamin B12 (cobalamin) [1]. As a matter of fact, bacteria obtained from dairy and belonging to the genus Propionibacterium (also abundant in the human intestinal microflora) are extensively used for the biological production of cobalamin [10].

Concerning vitamin B8, also called biotin, “it has long been recognized that the normal microflora of the large intestine synthesize considerable amounts of biotin” [6]. In fact, several studies have shown that the colon is capable of absorbing free biotin and HM Said has shown, for the first time in 1998, the functional existence of a specialized carrier-mediated system for biotin uptake in colonic epithelial cells [7]. “In addition, the uptake process is shared by another water-soluble vitamin, pantothenic acid, (…) which is also synthesized by the normal microflora of the large intestine”, as biotin inhibited the uptake of vitamin B5 and vice versa [6].

The specialized vitamin B transporter has been cloned in the rabbit intestine by another team in 1999 [11] and named the sodium-dependent multivitamin transporter (SMVT). This transporter is also highly expressed in human enterocytes (cells found in the internal lining of the intestines) [11,12], where it serves to take up not only pantothenate and biotin, but also lipoate (the ion from lipoic acid) [11].

Half a century ago, vitamin B2 (also called riboflavin) was known to be synthesized by intestinal bacteria and the amount provided by this source appears to become significantly higher when adhering to a vegetarian diet [13]. Interestingly, as he did for other water-soluble vitamins B, HM Said demonstrated in 2000 “for the first time, the existence of a specialized carrier-mediated mechanism for riboflavin uptake in an in vitro cellular model of human colonocytes” (cells found in the lining of the colon) [5]. Once again in 2001, HM Said showed that a model of human-derived colonic epithelial cells possesses a specific carrier-mediated system for thiamine (vitamin B1) uptake [4]. “It is suggested that bacterially synthesized thiamine in the large intestine may contribute to thiamine nutrition of the host, especially towards (…) the local colonocytes” [4].

Certain bacterial species present in the rat colon are also capable of de novo synthesis of vitamin B9, better known as folic acid [8]. As clearly evidenced by the use of tritiated (marked with radioactive hydrogen) para-aminobenzoic acid (3H PABA), the experimental “data provide direct evidence that some of the folate synthesized by the microflora in the rat large intestine is incorporated into the tissue folate of the host” [8].

More recently, the same methodology has been utilized with humans in order to determine whether folate synthesized by bacteria in the small intestine rather than in the colon is assimilated by the human host [9]. Indeed, the perfusion of tritiated PABA, a classic precursor substrate for the bacterial folate synthesis, led to the identification of bacterially synthesized (as marked) folates aspirated from in the small intestine. Subsequently, tritiated 5-methyltetrahydrofolate, a major metabolite of folate, was isolated from the human host urine, demonstrating that the human host did absorb and consequently metabolized these bacterially synthesized folates [9].

Coming back to cobalamin, it has been shown, already in 1980, that “at least two groups of organisms in the small bowel, Pseudomonas and Klebsiella sp., may synthesize significant amounts of the vitamin [B12]” [1]. Obviously, the two accepted dogma of vitamin B metabolism in the digestive tract don’t seem to correspond to reality: several compounds (vitamins B1, B2, B5, B8 and B9) supposedly absorbed by the small intestine may be assimilated by the colonocytes, while several compounds (vitamins B9 and B12) supposedly synthesized by colonic bacteria may actually be generated in the small intestine! Unfortunately, if we wanted to explain the high vitamin B12 blood levels by some colonic absorption, we must underline that absolutely nothing has been published about this and what seems true for other vitamins B would not be so for cobalamin.

Consequently, we should rather focus on the possibility that bacterially-produced vitamin B12 is absorbed in the small intestine, where most of the assimilation process of other B vitamins takes place. Two different specific proteins ensure the uptake of thiamine (vitamin B1) in the enterocytes of the proximal small intestine and are structurally close to a specific folic acid carrier [14]. Indeed, the intestinal folate (vitamin B9) absorption process occurs via a specialized mechanism that involves the reduced folate carrier (RFC) in the jejunum (the middle part of the small intestine) [15, 16]. We have already mentioned earlier the existence, in the proximal small intestinal enterocytes, of a sodium-dependent multivitamin transporter (SMVT) taking care of biotin (vitamin B8) and of pantothenic acid (vitamin B5). The involvement of a specialized carrier-mediated mechanism for pyridoxine (vitamin B6) by the intestinal epithelial cells has been demonstrated for the first time in 2003 [17]. Finally, a specialized carrier for niacin (vitamin B3) has been uncovered very recently, the article only being published in July 2005 [18].

In contrast to all the other B vitamins, cobalamin is not absorbed in the jejunum or in the proximal (first part of) ileum as they are, but only in the terminal ileum from a quite complex absorption process. This makes absorption very sensitive to diseases affecting specifically, or more frequently, this portion of the digestive tract such as Crohn’s disease.

Vitamin B12 Absorption

The term vitamin B12 or cobalamin actually refers to four different forms found in the diet and mostly bound to proteins: methylcobalamin, hydroxocobalamin, cyanocobalamin, and deoxyadenosylcobalamin.

The absorption process involves five steps:

1. The cobalamins are released from their protein complexes through the action of acid or pepsin in the stomach.
2. They bind to R proteins – cobalamin-binding glycoproteins secreted in saliva and in gastric juice.
3. The cobalamin-protein complexes must then be degraded by pancreatic proteases. This important step may be jeopardized in case of pancreatic insufficiency [19].
4. The free cobalamin combines in the duodenum with another glycoprotein called intrinsic factor which is secreted by the stomach parietal (oxyntic) cells; this glycoprotein dimerises and each part of the dimer binds one molecule of cobalamin, making the complex resistant to digestion [20]. The formation of the cobalamin-intrinsic factor complex appears indispensable for the vitamin to be absorbed in the terminal ileum via an active transport system [19].
5. The brush border membrane of the terminal ileum enterocytes contains a specific receptor for the dimeric complex and its importance in the process is shown by a congenital vitamin B12 malabsorption syndrome due to a defect in this receptor. The absorption is hampered by an abnormally low ileum pH, which may occur in some diseases such as the Zollinger-Ellison syndrome.

The problem with vitamin B12 absorption lies in the small safety margin between the dietary requirements for the vitamin and the maximal absorptive capacity of the five-step process outlined above. Cobalamins can also be absorbed passively, but the passive pathway only accounts for 1 or 2 % of the ingested vitamin, explaining the development of anemia when one of the five steps is not functioning properly [20]. The most frequent cause for vitamin B12 malabsorption is represented by the lack of intrinsic factor [19], which may be explained by a genetic defect, an auto-immune condition (auto-antibodies targeting either the parietal cells or the intrinsic factor itself), or a surgical gastrectomy (removal of part or all of the stomach). But further problems can occur at the level of the blood carriers, transcobalamin I and transcobalamin II, which may be impaired [21].

Now, supposing that all these steps leading to an effective absorption of vitamin B12 function adequately, then the presence in significant amounts of bacteria producing cobalamin in the terminal ileum would explain – at least theoretically – a sharp increase in absorption and lead to higher blood levels of this vitamin. If we consider some specific circumstances in the above mentioned study about folate absorption [9], we might discover the mechanism which could lead to an excessive absorption of cobalamin and to an elevation of blood levels.

The Role of Small Intestinal Bacterial Overgrowth

In an exemplary functional medicine study, two groups of patients were involved – healthy volunteers and subjects suffering from gastric arthritis (inflammation of the stomach lining). The participants were evaluated before and after the administration of omeprazole (a proton pump inhibitor that turns off gastric acid production) [9]. As expected, both patients with atrophic gastritis (chronic inflammation of the stomach lining) and those receiving omeprazole showed an increased duodenal pH (which stands for less acidity), but also an overgrowth of the small intestinal microflora [9]. Under normal physiological conditions, bacterial growth in the small intestine is inhibited by the acidic environment caused by the presence of hydrochloric acid. However, with an increase in pH the small intestinal environment, normally hostile to the local microflora, becomes friendlier and enables what is called a “small intestinal bacterial overgrowth” (SIBO) either in case of atrophic gastritis [22] or in case of drug-induced hyperchlorhydria [23], especially among “subjects taking a hydrogen pump blocking agent [such as] omeprazole” [24]. Interestingly, SIBO seems to provide “a unifying framework for understanding irritable bowel syndrome (IBS) and other functional disorders” [25], such as fibromyalgia [25, 26]. We come back once again to the experimentation with labelled folate to review its conclusions as presented in the corresponding abstract: “(1) Mild bacterial overgrowth caused by atrophic gastritis and administration of omeprazole are associated with de novo folate synthesis in the lumen of the small intestine; (2) the human host absorbs and uses some of these folates” [9]. Indeed, the unexplained increase of blood levels that we are describing about vitamin B12 may also occur with folic acid. We present a first case study concerning a four-year old boy who suffered from diarrhoea and abdominal bloating. Celiac disease had been ruled out, but he showed an increase of specific urinary organic metabolites corresponding to a bacterial overgrowth, typically from Clostridium. This child had never been treated with vitamins at the time of his first blood check, though his erythrocytic folate level (folic acid in red blood cells) was measured at 913µg/l whereas 257µg/l – 582µg/l represents the lab’s normal range for the parameter. Besides, the plasma level of cobalamins was raised to 1324ng/l, contrasting with the laboratory’s normal range of 450ng/l to 1200ng/l. He was treated for intestinal dysbiosis and put on a casein-free diet, improved dramatically… and was not blood tested again!

Case Study involving Elevated Vitamin B 12 Levels

We present a second case study concerning a thirty-year old woman (in 1999) whose blood parameters were monitored for unrelated matters but strikingly presented repetitive high vitamin B12 levels without any related supplementation neither from the vitamin itself, nor through vitamin B complexes / multivitamin formulas.

The original data from our records follows [NOTE: All results for vitamin B12 are expressed in pg/ml and the normal range provided by the Belgian laboratory is 200pg/ml to 900pg/ml, even if the lower limit could be considered as too low to be compatible with optimal health].

The five first measurements, from February 1999 to April 2000, were quite consistently fluctuating around 2500pg/ml (respectively 2796pg/ml on 6/2/99, 2355pg/ml on 19/4/99, 2572pg/ml on 30/7/99, 2697pg/ml on 7/3/2000 and 2325pg/ml on 17/4/00), which is much too high! At the time, the patient’s blood had to be monitored in relation to a drug-based anti-epileptic treatment. However, the young woman was not complaining about her digestive system, even if she occasionally mentioned some severe but transitory abdominal cramps.

Her digestive problems started during the summer season in 2000, with IBS like symptoms, bloating, diarrhoea and excruciating pain in the belly. She was examined thoroughly and the gastroenterologist initially suspected Crohn’s disease due to the presence of mucosal ulcerations in the proximal small intestine. During that period of major clinical deterioration, blood vitamin B12 level increased even further as seen from two measurements performed on 25/08/00 (3220pg/ml) and on 28/11/00 (3221pg/ml). Then, she refused to take the corticoids prescribed by the specialist and went on a natural treatment based on diet modifications (exclusion of high IgG foods, in her case: dairy products, beef, bananas and black pepper), supplements (according to her biological results in blood and in 24-hour urine), antimicrobial herbs (such as grapefruit seed extracts) and probiotics.

She didn’t improve dramatically, but slowly started to complain less within a few weeks, then was feeling slightly better in March 2001 and significantly better when she came back five months later, in August 2001. Very interestingly, vitamin B12 blood levels started to decrease to 2740pg/ml on 24/3/01 and then down to 2132pg/ml on 22/08/01. In fact, the last result provided her lowest blood value since the beginning of the study. In September 2001, we then asked the gastroenterologist to perform a new endoscopy, in order to dismiss the diagnosis of Crohn’s disease and make sure that we were not harming her by not giving the prescribed drugs. The digestive exploration was then considered as normal, besides some “non specific mucosal inflammation”.

So the case was much less worrying and it took about seven months before she consulted again, in March 2003. She was symptom-free, finally expressing a much better digestive capacity since she was on this diet, even though she hadn’t renewed her supplements for a while. The cramps had disappeared and her blood reading for the vitamin B12 was 1001pg/ml on 26/3/02, almost back to the normal range. She definitely reached and stayed within the normal range on further checks with 726pg/ml on 31/08/02, 677npg/ml on 21/5/03 and finally 516pg/ml on 15/5/04. The last time, she was still symptom-free, but also dairy-free. She might have to consider taking vitamin B12 supplements one day in the future, but that’s another story…

About the author: Georges Mouton MD is a medical doctor specializing in functional medicine with practices in Brussels, London and Madrid. His website can be found at http://www.gmouton.com

REFERENCES

1. Albert, M.J., V.I. Mathan, and S.J. Baker, Vitamin B12 synthesis by human small intestinal bacteria. Nature, 1980. 283(5749): p. 781-2.
2. Hill, M.J., Intestinal flora and endogenous vitamin synthesis. Eur J Cancer Prev, 1997. 6 Suppl 1: p. S43-5.
3. Cummings, J.H. and G.T. Macfarlane, Role of intestinal bacteria in nutrient metabolism. JPEN J Parenter Enteral Nutr, 1997. 21(6): p. 357-65.
4. Said, H.M., et al., Mechanism of thiamine uptake by human colonocytes: studies with cultured colonic epithelial cell line NCM460. Am J Physiol Gastrointest Liver Physiol, 2001. 281(1): p. G144-50.
5. Said, H.M., et al., Riboflavin uptake by human-derived colonic epithelial NCM460 cells. Am J Physiol Cell Physiol, 2000. 278(2): p. C270-6.
6. Said, H.M., Cellular uptake of biotin: mechanisms and regulation. J Nutr, 1999. 129(2S Suppl): p. 490S-493S.
7. Said, H.M., et al., Biotin uptake by human colonic epithelial NCM460 cells: a carrier-mediated process shared with pantothenic acid. Am J Physiol, 1998. 275(5 Pt 1): p. C1365-71.
8. Rong, N., et al., Bacterially synthesized folate in rat large intestine is incorporated into host tissue folyl polyglutamates. J Nutr, 1991. 121(12): p. 1955-9.
9. Camilo, E., et al., Folate synthesized by bacteria in the human upper small intestine is assimilated by the host. Gastroenterology, 1996. 110(4): p. 991-8.
10. Zarate, G., S. Gonzalez, and A.P. Chaia, Assessing survival of dairy propionibacteria in gastrointestinal conditions and adherence to intestinal epithelia. Methods Mol Biol, 2004. 268: p. 423-32.
11. Prasad, P.D., et al., Molecular and functional characterization of the intestinal Na+-dependent multivitamin transporter. Arch Biochem Biophys, 1999. 366(1): p. 95-106.
12. Balamurugan, K., A. Ortiz, and H.M. Said, Biotin uptake by human intestinal and liver epithelial cells: role of the SMVT system. Am J Physiol Gastrointest Liver Physiol, 2003. 285(1): p. G73-7.
13. Iinuma, S., Synthesis of riboflavin by intestinal bacteria. J Vitaminol (Kyoto), 1955. 1(2): p. 6-13.
14. Subramanian, V.S., J.S. Marchant, and H.M. Said, Targeting and trafficking of the human thiamine transporter-2 (hTHTR2) in epithelial cells. J Biol Chem, 2005.
15. Matherly, L.H., Molecular and cellular biology of the human reduced folate carrier. Prog Nucleic Acid Res Mol Biol, 2001. 67: p. 131-62.
16. Subramanian, V.S., N. Chatterjee, and H.M. Said, Folate uptake in the human intestine: promoter activity and effect of folate deficiency. J Cell Physiol, 2003. 196(2): p. 403-8.
17. Said, H.M., A. Ortiz, and T.Y. Ma, A carrier-mediated mechanism for pyridoxine uptake by human intestinal epithelial Caco-2 cells: regulation by a PKA-mediated pathway. Am J Physiol Cell Physiol, 2003. 285(5): p. C1219-25.
18. Nabokina, S.M., M.L. Kashyap, and H.M. Said, Mechanism and regulation of human intestinal niacin uptake. Am J Physiol Cell Physiol, 2005. 289(1): p. C97-103.
19. Festen, H.P., Intrinsic factor secretion and cobalamin absorption. Physiology and pathophysiology in the gastrointestinal tract. Scand J Gastroenterol Suppl, 1991. 188: p. 1-7.
20. Oh, R. and D.L. Brown, Vitamin B12 deficiency. Am Fam Physician, 2003. 67(5): p. 979-86.
21. Carmel, R., et al., Update on cobalamin, folate, and homocysteine. Hematology (Am Soc Hematol Educ Program), 2003: p. 62-81.
22. Saltzman, J.R. and R.M. Russell, The aging gut. Nutritional issues. Gastroenterol Clin North Am, 1998. 27(2): p. 309-24.
23. Pereira, S.P., N. Gainsborough, and R.H. Dowling, Drug-induced hypochlorhydria causes high duodenal bacterial counts in the elderly. Aliment Pharmacol Ther, 1998. 12(1): p. 99-104.
24. Paiva, S.A., et al., Interaction between vitamin K nutriture and bacterial overgrowth in hypochlorhydria induced by omeprazole. Am J Clin Nutr, 1998. 68(3): p. 699-704.
25. Lin, H.C., Small intestinal bacterial overgrowth: a framework for understanding irritable bowel syndrome. Jama, 2004. 292(7): p. 852-8.
26. Pimentel, M., et al., A link between irritable bowel syndrome and fibromyalgia may be related to findings on lactulose breath testing. Ann Rheum Dis, 2004. 63(4): p. 450-2.

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http://www.gethsmart.com/diabetes.html

Homocysteine & Diabetes

Elevated Homocysteine levels increase the risk of nearly every complication associated with Type 2 diabetes. In fact, Type 2 diabetic patients with elevated homocysteine levels are nearly 200% more likely to die from a heart attack within 5 years than those with normal Homocysteine levels. In addition, Homocysteine is a stronger risk factor for CVD and death in Type 2 diabetics compared to non-diabetics.

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http://www.ncbi.nlm.nih.gov/pubmed/12795447

Department of Food Science and Human Nutrition, Iowa State University, 220 MacKay Hall, Ames, IA 50011, USA.

Plasma homocysteine levels are elevated during diabetes when there is atherosclerosis or insufficient renal function; however, diminished plasma homocysteine concentrations are observed in diabetes without complications. Recent studies have demonstrated that under diabetic conditions, the catabolism of homocysteine was enhanced by transcriptional regulation of hepatic cystathionine beta-synthase and these changes were prevented by treatment with insulin.

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http://www.defeatdiabetes.org/Articles/aminoaccids_cvd060324.htm

Homocysteine Reduction Shows No Cardiovascular Benefit

posted 03/24/2006

Two large-scale trials ,HOPE-2 and NORVIT trials, have failed to find any significant cardiovascular benefit to lowering plasma homocysteine levels by supplementation with folic acid and vitamins B6 and B12.

Lowering plasma homocysteine levels with vitamin supplements does not lower the risk of major cardiovascular events in patients with vascular disease, and might even be harmful, reported investigators.

The vitamins quite effectively lowered homocysteine levels, the researchers reported at the American College of Cardiology meeting. It’s just that lowering the levels did nothing to prevent myocardial infarction, death from cardiovascular causes, or other major outcomes, results showed in the HOPE-2 trial.

The HOPE-2 (Heart Outcomes Project Evaluation) study evaluated a combination of folic acid and vitamins B6 and B12 versus. placebo in more than 5,000 patients and found that there was no difference in the risk of death from cardiovascular causes, reported Eva Lonn, M.D., of Hamilton General Hospital in Hamilton, Ontario, and colleagues.

The results echoed those of a separate study conducted by Norwegian researchers and reported at the 2005 European Society of Cardiology conference in Stockholm.

The Norwegian Vitamin (NORVIT) trial compared various combinations of B vitamins and folic acid with placebo in nearly 3,800 patients, and found that treatment with B vitamins did not lower the risk of recurrent cardiovascular disease after acute myocardial infarction, and that there might even be a harmful effect from combined B vitamin treatment, reported Kaare Harald Bønaa, M.D., Ph.D., of the University of Tromso and NORVIT colleagues.

Results of the HOPE-2 and NORVIT studies were published simultaneously in the online edition of the New England Journal of Medicine.

“We have been often derailed in our efforts to implement secondary prevention adequately, and the focus should instead be on what has been proven to work,” Dr. Lonn said, “namely a healthy lifestyle, including fruits and vegetables, exercise, and for those who already have an event, certain drugs such as aspirin, statins, beta blockers and ACE-inhibitors which have proven benefit.”

In the HOPE-2 study, researchers from Canada, the United States, and Sweden randomly assigned 5,522 patients 55 and older who had vascular disease or diabetes, to daily treatment for an average of five years with either a vitamin combination or placebo. The combination consisted of 2.5 mg of folic acid, 50 mg of vitamin B6, and 1 mg of vitamin B12. The primary study outcome was a composite of death from cardiovascular causes, myocardial infarction, and stroke.

The authors concluded that B vitamins don’t lower the risk of recurrent cardiovascular disease after acute myocardial infarction, and that the combined B vitamins could be harmful.

“What, then, can we conclude from the results of these trials?” asked Joseph Loscalzo, M.D., Ph.D., of Brigham and Women’s Hospital and Harvard Medical School, in an accompanying NEJM editorial.

“Clearly, folic acid, vitamin B12, and vitamin B6 are not the therapeutic solution expected, and they do not provide a preventive benefit in patients with mild hyperhomocysteinemia.

The straightforward but incorrect view that folic acid can decrease homocysteine levels and, thus, reduce the risk of atherosclerosis effectively may be an unintended consequence of oversimplifying a complicated metabolic network,” he wrote.

Source: Diabetes In Control: Online edition of the New England Journal of Medicine, March 2006

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http://www.defeatdiabetes.org/Articles/gestational051128.htm

Homocysteine Levels Predicts Future Diabetes After Gestational Diabetes

posted 11/28/2005

High homocysteine in the early postpartum period is an independent risk factor for the development of diabetes in women with a history of pregnancy-induced diabetes (a.k.a. gestational diabetes). More than 15 percent of these individuals will have to undergo amputation.

Measurement of homocysteine at six week’s postpartum “would be helpful” to identify women with a previous history of pregnancy-induced diabetes at high risk for developing diabetes, study investigators conclude.

Diabetes that develops during pregnancy normally clears up after delivery. Nowadays, however, full-blown diabetes often develops in women who suffered with pregnancy-induced diabetes.

Homocysteine, an amino acid, has been tied to heart disease and stroke but its relationships to and role in the onset of diabetes is unclear.

To investigate, Dr. Nam H. Cho from Ajou University School of Medicine in Suwon, Korea and colleagues studied 170 women with a history of pregnancy-induced diabetes who had normal glucose tolerance or impaired glucose tolerance (a prediabetic condition) at baseline exams conducted at six weeks postpartum.

Over the next 4 years, 18 women (10.6 percent) became diabetic. Of these, nine had normal glucose tolerance and nine had impaired glucose tolerance at baseline.

Cho’s team found that higher postpartum homocysteine levels were associated with the onset of diabetes, regardless of age, body weight, and family history of diabetes.

The results hint that early postpartum “hyperhomocysteinemia” in mother who had pregnancy-induced diabetes ups the risk of diabetes later on, the authors conclude.

Source: Diabetes In Control: Diabetes Care November 2005.

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http://www.diabetesaction.org/site/PageNavigator/Complementary%20Corner/complementary_10_07

B Vitamins in Diabetes: Just “Expensive Urine”?

Part 1

Ryan Bradley, ND

October 2007

B vitamins are essential vitamins in human nutrition. The most commonly referenced B vitamins include:

• thiamine (B1)
• riboflavin (B2)
• niacin (B3)
• pantothenic acid (B5)
• pyridoxine (B6)
• biotin (B8)
• folic acid (rarely referred to as B9)
• cobalamin (B12)

B vitamins are critical to normal cellular function, replication, repair, metabolism and energy production. Some B vitamins, particularly B1, B6 and B12, are especially important to normal nerve function and repair. In people with diabetes, often due to increased urination from the osmotic effects of high blood sugar, the water-soluble B vitamins may be lost more rapidly than in people without diabetes even if intake is technically adequate.

When reading supplement bottles or published descriptions of the functions of B vitamins, it is tempting to believe that we should be taking large quantities of B vitamins to “offset stress”, “improve energy”, “improve metabolism”, “assist in normal adrenal function”, etc. Unfortunately very little clinical trial research supports these claims. Few quality clinical trials have been performed on single B vitamins, let alone “B complex” combinations in diabetes.

Further complicating matters is homocysteine – a byproduct from protein/amino acid metabolism influenced by B vitamin intake – that has been implicated in causing direct damage to the thin endothelial lining of the small arteries particularly vulnerable in diabetes. Does lowering homocysteine actually reduce the risk of having a heart attack or stroke? Should homocysteine still be measured and checked?

In Part 1 of this article I will highlight the role of B vitamins in diabetes, focusing on those for which we have the most clinical research data (thiamine, niacin, biotin and vitamin B12). Next month, in Part 2 of this article I will discuss the state of the science regarding homocysteine, discuss special considerations in diabetes and give my opinion on when extra B vitamins are appropriate.

Thiamine/B1

Functions:

Thiamine is a water-soluble vitamin essential for normal metabolism of fat, glucose and protein as it is involved in key pathways of cellular energy synthesis. Specifically, thiamine is a cofactor in the actions of the enzymes:

pyruvate dehydrogenase and alpha-ketoglutarate decarboxylase in the breakdown of carbohydrates,

branched chain alpha-keto acid dehydrogenase in the metabolism of some amino acids,

and transketolase which acts to breakdown more complex sugars for energy production.

Abnormalities of transketolase activity have been identified in diabetes, and are partially responsible for the accumulation of sorbitol contributing to cataract formation.

In addition, classic thiamine deficiency has been long associated with heavy alcohol consumption and is known to cause Wernicke’s encephalopathy, a condition marked by nervous system symptoms including numbness, tingling and muscle weakness.

Food Sources:

Thiamine can be found in fortified wheat products, lentils, peas, pork, brazil nuts, pecans, spinach, cantaloupe, pork, milk and eggs[1].

Research:

In recent studies, 75% of patients with diabetes were shown to have reduced levels of thiamine and increased urinary excretion of thiamine relative to controls[2]. Low thiamine levels correlated with increased levels of vascular adhesion molecules, known markers of vascular disease and dysfunction. In a clinical trial performed by Arora et al., intravenous administration of thiamine improved functioning of the inner, endothelial lining of small arteries in patients with diabetes during induced hyperglycemia, reinforcing the role of thiamine in normal vascular function [3]. In addition, a randomized, controlled trial of thiamine (25mg/day) combined with pyridoxine (B6) (50 mg/day) in patients with diabetes demonstrated significant improvements in perceived pain, numbness and paraesthesia (extra nerve sensations)[4].

Recently, a fat-soluble, synthetic form of thiamine called benfotiamine has become available as a nutritional supplement. Interesting research exists on benfotiamine, including research that suggest benfotiamine protects the small and large arteries from the damage caused by elevated blood glucose and increased advanced glycosylation endproduct consumption in food [5](See Complementary Corner December 2006). Benfotiamine appears to be better absorbed than standard water-soluble thiamine, however high dose thiamine appears to have a similar effect and may have advantages. The jury is still out of the safety of benfotiamine, however only minimal safety concerns have been reported in the literature to date.

Niacin/B3

Functions:

Niacin, or nicotinic acid, is another ubiquitous cofactor in human cellular energy production. Niacin functions as an intermediate, in the form of nicotinamide adenine dinucleotide (NADH), in reactions in glycolysis and the Kreb’s cycle, two fundamental energy production cycles in human biochemistry.

Niacin is also necessary for fat metabolism and normal DNA synthesis and repair in the form of nicotinamide adenine dinucleotide phosphate (NADPH).

Niacin, like thiamine, is water-soluble. Niacin deficiency, very rare in this country due to food fortification, is called pellagra.

Food Sources:

Include animal foods, fortified wheat products, coffee, lima beans, lentils and peanuts[1].

Research:

Niacin is best known in medicine as a treatment for high blood cholesterol, or hypercholesterolemia. Niacin is available over-the-counter and as a prescription. The doses typically available in a B vitamin supplements range from 5-50 milligrams, whereas the doses used for cholesterol reduction range from 500-2500 milligrams. Most cholesterol lowering treatments impact only one risk factor; niacin has advantages over other cholesterol-lowering because it lowers LDL cholesterol, raises HDL cholesterol, tends to lower triglycerides and improves LDL particle size and lowers lipoprotein a (Lpa), an additional risk factor of cardiovascular disease [6, 7]. (See Complementary Corner 11/06 for more information on cholesterol and the importance of healthy levels).

In other studies, people with diabetes taking niacin had less progression of the artherosclerosis than those taking placebo, despite poor blood glucose control[8]. Niacin accomplishes these excellent effects because it decreases clearance of HDL cholesterol in the liver and therefore more HDL is in circulation, scavenging less healthy LDL particles.

Niacin is considered a safe and effective treatment for hypercholesterolemia in patients with diabetes, especially at lower doses of 1000-1500 mg/day. Flushing is a common side effect of niacin treatment, and it can be quite uncomfortable for some people. However most people get used to the flushing and it typically does lessen in severity. Niacin treatment for high cholesterol (or low HDL cholesterol or high Lp(a)) should only be implemented with the supervision of a physician who can titrate your dose safely and monitor your cholesterol regularly to be sure it is working as expected.

In addition, niacin in higher doses can cause increases in liver enzymes, a sign of liver inflammation; since liver enzymes are commonly elevated in people with diabetes and the metabolic syndrome (due to deposition of fat in the liver), liver enzymes should be monitored periodically for elevations by a physician.

Biotin/B8

Functions:

If you haven’t already figured this out, many of the B vitamins work together as co-factors in the function of many critical metabolic enzymes. Biotin is no exception. Biotin, like thiamine and niacin, is also required for normal function of:

pyruvate decarboxylase (an enzyme involved in carbohydrate and fat metabolism),

propionyl-coA carboxylase (an enzyme involved in fat metabolism),

and acetyl-coA carboxylase (also involved in carbohydrate and fat metabolism).

Biotin is known to bind to specific sites in these enzymes in order to optimize function, and supplementation of biotin is known to increase the activities of these enzymes in people with diabetes as well as those without diabetes[9, 10].

Food Sources:

Food sources of biotin include animal products, avocado, wheat bran, baker’s yeast, raspberries, artichoke and cauliflower[1].

Research:

Most of the research available on biotin in diabetes comes from recent research supported by Nutrition 21, Inc., a company who manufacturers a nutritional supplement that is a combination of chromium picolinate and biotin (Diachrome®). Recent studies have demonstrated in people with diabetes, the combination of chromium picolinate and biotin resulted in an average 0.54% reduction in HbA1c, significant reductions in LDL and VLDL cholesterol and triglycerides [11-13].

Cobalamin/B12

Functions:

Cobalamin, or vitamin B12, is required for normal nervous system functioning and normal cell proliferation. Vitamin B12 requires a special protein called intrinsic factor for its absorption (pernicious anemia, an autoimmune anemia, results when your body produces antibodies against intrinsic factor impeding absorption).

Intrinsic factor is produced by a special cell type in the lining of the stomach; as we age the lining of our stomach can atrophy or weaken. This atrophy can result in abnormal B12 absorption resulting in deficiency, thus older adults are particularly vulnerable to vitamin B12 deficiency.

Additionally another type of anemia, called a macrocytic anemia, results from vitamin B12 deficiency; macrocytic anemias are characterized by very large red blood cells (macrocytes, or large cells).

Vitamin B12 is also required for normal homocysteine metabolism, a topic covered in great detail in Part 2 of this article next month.

Food Sources:

Sources of vitamin B12 include animal foods such as seafood, beef, pork, chicken, dairy products and eggs[1]. Vegan (non-animal) sources of B12 are extremely limited. Some sources speculate spirulina is an adequate source of B12, however this may be due to contamination by small sea animals.

Research:

Vitamin B12 has been mostly studied in diabetes as treatment for neuropathies. In recent systematic review, vitamin B12 was found to be an effective treatment for diabetic peripheral neuropathy, with pain and paraesthestias reduced the most from treatment[14].>/p>

Also relevant to diabetes, metformin, the first-line prescription medication for treating elevated glucose in diabetes, is known to cause vitamin B12 deficiency and elevate homocysteine[15].

Conclusions (for now…)

As you can tell, the clinical research world has a lot of work to do in order to fully assess the benefits and risks of B vitamin intake and supplementation on the health of people with diabetes. Unfortunately, as is the case with many natural substances that are not patentable and therefore do not generate large profits, B vitamins are not of particular interest to most funding agencies.

Fortunately, innovative researchers do have friends like Diabetes Action to ensure vital research gets performed on important questions of optimal health in diabetes!

Read Part 2 where I will discuss the homocysteine debate in detail as well as offer my recommendations on when extra B vitamin supplementation may be worth trying!

References:

LPI, Micronutrient Information Center. 2007.

Thornalley, P.J., et al., High prevalence of low plasma thiamine concentration in diabetes linked to a marker of vascular disease. Diabetologia, 2007. 50(10): p. 2164-70.

Arora, S., et al., Thiamine (vitamin B1) improves endothelium-dependent vasodilatation in the presence of hyperglycemia. Ann Vasc Surg, 2006. 20(5): p. 653-8.

Abbas, Z.G. and A.B. Swai, Evaluation of the efficacy of thiamine and pyridoxine in the treatment of symptomatic diabetic peripheral neuropathy. East Afr Med J, 1997. 74(12): p. 803-8.

Stirban, A., et al., Benfotiamine prevents macro- and microvascular endothelial dysfunction and oxidative stress following a meal rich in advanced glycation end products in individuals with type 2 diabetes. Diabetes Care, 2006. 29(9): p. 2064-71.

Grundy, S.M., et al., Efficacy, safety, and tolerability of once-daily niacin for the treatment of dyslipidemia associated with type 2 diabetes: results of the assessment of diabetes control and evaluation of the efficacy of niaspan trial. Arch Intern Med, 2002. 162(14): p. 1568-76.

Pan, J., et al., Niacin treatment of the atherogenic lipid profile and Lp(a) in diabetes. Diabetes Obes Metab, 2002. 4(4): p. 255-61.

Taylor, A.J., et al., Relationship between glycemic status and progression of carotid intima-media thickness during treatment with combined statin and extended-release niacin in ARBITER 2. Vasc Health Risk Manag, 2007. 3(1): p. 159-64.

Baez-Saldana, A., et al., Effects of biotin on pyruvate carboxylase, acetyl-CoA carboxylase, propionyl-CoA carboxylase, and markers for glucose and lipid homeostasis in type 2 diabetic patients and nondiabetic subjects. Am J Clin Nutr, 2004. 79(2): p. 238-43.

St Maurice, M., et al., Domain architecture of pyruvate carboxylase, a biotin-dependent multifunctional enzyme. Science, 2007. 317(5841): p. 1076-9.

Albarracin, C., et al., Combination of chromium and biotin improves coronary risk factors in hypercholesterolemic type 2 diabetes mellitus: a placebo-controlled, double-blind randomized clinical trial. J Cardiometab Syndr, 2007. 2(2): p. 91-7.

Albarracin, C.A., et al., Chromium picolinate and biotin combination improves glucose metabolism in treated, uncontrolled overweight to obese patients with type 2 diabetes. Diabetes Metab Res Rev, 2007.

Geohas, J., et al., Chromium picolinate and biotin combination reduces atherogenic index of plasma in patients with type 2 diabetes mellitus: a placebo-controlled, double-blinded, randomized clinical trial. Am J Med Sci, 2007. 333(3): p. 145-53.

Sun, Y., M.S. Lai, and C.J. Lu, Effectiveness of vitamin B12 on diabetic neuropathy: systematic review of clinical controlled trials. Acta Neurol Taiwan, 2005. 14(2): p. 48-54.

Sahin, M., et al., Effects of metformin or rosiglitazone on serum concentrations of homocysteine, folate, and vitamin B12 in patients with type 2 diabetes mellitus. J Diabetes Complications, 2007. 21(2): p. 118-23.

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Part 2

Ryan Bradley, ND

November 2007

In Part 1 of this article series, we discussed the topic of B vitamins in diabetes, including some of the relevant clinical research evaluating B vitamins in the treatment of various concerns in diabetes. Yet one of the most controversial, and still unresolved, questions regarding B vitamins in diabetes, and more broadly in cardiovascular disease, is the issue the importance of homocysteine in cardiovascular health. In this article, I will provide some background on homocysteine, including why the medical community thought is was of concern, and then following the progression of our knowledge on homocysteine to the present, where the danger of homocysteine is being challenged. In addition, I will write briefly about special clinical considerations for B vitamins in diabetes.

What the Heck is Homocysteine Anyway?

Homocysteine is a by-product of our metabolism of sulphur-containing amino acids (amino acids strung together in various combinations form proteins- which we eat!). Homocysteine is converted to methionine (another amino acid) and back again; it is also converted to cysteine (yet another amino acid) by a separate process. The conversion of homocysteine to methionine requires vitamins B12 and folic acid, while the conversion of homocysteine to cysteine requires vitamin B6.

This process is important for several reasons; it serves a role in the interconversion between different forms of folic acid, each with specific jobs; it assists in the availability of specific amino acids, namely cysteine and methionine, which have biologic functions of their own; and some methionine gets converted to S-adenosylmethionine (SAMe) which serves as an important intermediate (methyl group donation) in numerous biologic processes including detoxification in the liver.

Is Homocysteine Dangerous?

The short answer is, we don’t really know. As is usually the case in medical research, we are limited by the answers different types of research methodology are able to give us, and by the studies that have been performed. Specifically, many times in medicine “risk factors” are identified based on following large groups of people for long periods of time and waiting for them to get sick. Studying people in large groups like this allows epidemiologists to look for exposures that increase risk. A key limitation of this type of research is that observational studies cannot say a risk factor causes disease, only that the risk factor is associated with the disease. This limitation occurs because although researchers try to control for other possible contributors (or confounders) to any observed change in risk, no one study can control for all confounders. In some cases, these risk factors stick around and in some cases they do not. Although it may sound like a waste of time to do this type of observation study, they spawn hypotheses to be tested in clinical trials. Clinical trials, when properly designed, do not suffer from the same influence of confounding. Confounding is controlled in clinical trials by “placebo-controlling” trials and by randomization. For this reason, only clinical trials can determine causality.

Observational Studies

Now back to homocysteine. Back in the 1990s, several epidemiologists published papers on the risk of heart attack (myocardial infarction) relative to homocysteine levels. Stampfer et al. published a study demonstrating a greater than 3-fold increased risk of heart attacks in males with elevated homocysteine levels[1]. Supporting these findings was a published report by Verhoef et al. in the American Journal of Epidemiology based on research in the Netherlands showing an 11% increase in risk of heart attack from elevated homocysteine, and the risk seemed to increase as the level of homocysteine increased, i.e. there was graded risk[2].

Findings suggesting homocysteine was associated with harm to the heart were further supported in 1998 by a study by researchers Wald et al. studying homocysteine in over 1300 men in the United Kingdon; this study showed men with the highest levels of homocysteine had 3.7 times the risk of developing ischemic heart disease compared to those with lower levels[3]. Wald et al. also reported that the risk seemed to increase by 41% for every 5 umol/L increase of homocysteine in the blood. These researchers went out on a limb in their study and said, because the associations seemed so strong, that elevated homocysteine appeared causal.

The story continues in 1999 (although many other papers were published during 1997-1999 adding further support to the “homocysteine hypothesis”) when research was published evaluating homocysteine and risk of death in 1933 elderly participants in the Framingham cohort (the Framingham cohort study followed – and still follows – thousands of American men and women in order to determine risk factors for cardiovascular disease; Framingham remains important in determining risk factor reduction guidelines)[4]. The study, published by Bostom et al. in the Archives of Internal Medicine, reported over a doubling of risk of cardiovascular death and all-cause death from homocystiene levels greater than 14.26 umol/L.

By the 2000s, enough observational data was accumulating showing that homocysteine was associated with an increased risk of heart disease and death that researchers began pooling this data together, performing meta-analyses. In 2002, the Homocysteine Studies Collaboration published their meta-analysis in the Journal of the American Medical Association showing an 11% reduced risk for ischemic heart disease and a 19% reduced risk for stroke by lowering homocysteine levels 3 umol/L[5].

In addition to these (and many other) observational studies, animal and bench researchers discovered many possible mechanisms for the observed increase in risk. Included in the probable mechanisms were:

increased endothelial dysfunction (the endothelium is the innermost lining of arteries and serves an important role in responding to chemical signals to dilate or constrict to regulate blood flow)

increased smooth muscle cell proliferation (smooth muscle cells are in the middle of our larger arteries and therefore proliferation of these cells contribute to reduced blood flow)

increased pro-clotting factors and reduced anti-clotting factors in the blood

All of this data fueled the fire for the “homocysteine hypothesis”. Everyone loved homocysteine. Cardiologists loved it because it was something else to measure and easy to treat. Complementary medicine providers loved it because there was finally a strong case for extra B vitamins in the diet, typically through supplements. The public loved it because it supported theories of reduced quality in the food supply. Everyone was happy.

Clinical Trials

All of this data also fueled the development of clinical trials – the necessary step to determine causality. In 2004, The Vitamin Intervention for Stroke Prevention (VISP) trial was published in the Journal of the American Medical Association[6]. This trial randomized 3680 adults with history of stroke to receive either high (5 mg of B6, 0.4 mg of B12, and 2.5 mg of folic acid) or low (200 micrograms of B6, 6 micrograms of B12 and 20 micrograms of folic acid) dose B vitamins for 2 years. The outcomes of interest were recurrent stroke and death. The results of the study showed that B vitamins do reduce homocysteine (with the high dose arm ending up with lower levels than the low dose group), however the study did not find any reduction in risk of second stroke or for death. The study did still see a baseline association between high homocysteine levels and risk of recurrent stroke and death. These findings suggested 2 years was not long enough to reduce stroke risk by lowering homocysteine.

Following the VISP trial, was the NORVIT trial which randomized 3749 men and women with history of heart attack to one of four arms: 0.8 mg of folic acid, 0.4 mg of B12, and 40 mg of B6; 0.8 mg of folic acid and 0.4 mg of B12; 40 mg of B6; or placebo[7]. The primary question in this trial was: will lowering homocysteine after first heart attack reduce the risk of having a second heart attack? or reduce the risk of death? Disappointingly, the NORVIT trial also produced negative findings, there seemed to be no beneficial effect of B vitamin supplementation to lower homocysteine on risk of second heart attack or death. Alarmingly, the arm of the NORVIT trial that received folic acid, B12 and B6 seemed to have an increased risk of second heart attack!

The findings of the homocysteine-lowering elements of the HOPE2 study were also published in 2006 in the New England Journal of Medicine[8]. HOPE2 randomly assigned 5522 men and women with known vascular disease to 2.5 mg of folic acid, 50 mg of vitamin B6, and 1 mg of vitamin B12 or with placebo for an average of five years. The primary aim of the study was to determine if lowering homocysteine reduced the risk of heart attack, stroke or risk of death during the study. The findings of the HOPE2 study similarly showed no benefit for death or cardiac event. The study did show a 25% reduced risk for stroke, however it also showed a 24% increase in risk for unstable angina, a significant risk factor for heart attack.

Unanswered Questions

Obviously there is unsettled business surrounding the issue of homocysteine and the risk of vascular disease. The data to date still suggests lowering homocysteine has some benefit on reducing the risk for stroke[9]. However, what is still not clear is whether assessing and treating homocysteine in patients with or without known heart disease does any good in reducing their risk for cardiovascular events (ischemic heart disease, heart attack, heart-related death). There are still unanswered questions regarding homocysteine, including time. Does lowering homocysteine levels for longer periods of time reduce risk, i.e. does preventing homocysteine elevation reduce risk? How long is necessary before benefits are seen? Do extra B vitamins cause cardiovascular harm – or was this finding an anomaly? We’ll have to wait and see.

What do I do about Homocysteine?

I must admit, I have been less aggressive in my approach to homocysteine lowering since the NORVIT and HOPE2 trials were released last year. However I do think homocysteine is still worth checking and treating in patients with diabetes. We know people with diabetes have an increased risk for stroke, and to date the data seem to suggest treating elevated homocysteine is still protective. My rules of thumb are to lower homocysteine down to less than 10-12 umol/L whenever possible, ideally through dietary B vitamins.

When Do I Recommend Extra Supplemental B Vitamins?

Megaloblastic Anemia – Deficiencies of either folic acid or vitamin B12 can cause a characteristic anemia. “Anemia” is a category of conditions that all have a reduced ability to deliver oxygen in the body, often due to changes in red blood cell number or oxygen saturation. The anemia resulting from deficiencies of vitamin B12 and/or folic acid is characterized by larger than normal red blood cells, or megaloblasts. Your physician can check for this type of anemia by checking for simple characteristics in your blood.

Neuropathy – As discussed in Part 1, patients with diabetes who experience reduced sensation or have known nerve complications of their diabetes often benefit from vitamin B12 treatment.

Special Considerations with Metformin – Metformin is one of the first line medications for the treatment of diabetes. However, a small percentage (estimates vary) of patients can end up with deficiencies of vitamin B12 and elevations in homocysteine[10].

Thiamine vs. Benfotiamine (See Part 1) – The safety of benfotiamine is still too unknown in my opinion. If you have reason to suspect thiamine deficiency, discuss testing and trial treatment with your physician care provider.

Conclusions

B vitamins have vital functions in human health that may be disrupted in conditions like diabetes. Although some clinical trials suggest benefit, the consumption of large (much larger than diet) doses of nutrients should always be discussed with your physician. In the meantime, enjoying fresh vegetable foods that are rich in these nutrients is a sure bet to health improvement/risk reduction in cardiovascular disease and diabetes. Until more research steers me otherwise, I will continue checking and discussing homocysteine in an effort to assist in the optimal health of my patients.

References

1. Stampfer, M.J., et al., A prospective study of plasma homocyst(e)ine and risk of myocardial infarction in US physicians. Jama, 1992. 268(7): p. 877-81.

2. Verhoef, P., et al., Homocysteine metabolism and risk of myocardial infarction: relation with vitamins B6, B12, and folate. Am J Epidemiol, 1996. 143(9): p. 845-59.

3. Wald, N.J., et al., Homocysteine and ischemic heart disease: results of a prospective study with implications regarding prevention. Arch Intern Med, 1998. 158(8): p. 862-7.

4. Bostom, A.G., et al., Nonfasting plasma total homocysteine levels and all-cause and cardiovascular disease mortality in elderly Framingham men and women. Arch Intern Med, 1999. 159(10): p. 1077-80.

5. Grundy, S.M., et al., Efficacy, safety, and tolerability of once-daily niacin for the treatment of dyslipidemia associated with type 2 diabetes: results of the assessment of diabetes control and evaluation of the efficacy of niaspan trial. Arch Intern Med, 2002. 162(14): p. 1568-76.

6. Toole, J.F., et al., Lowering homocysteine in patients with ischemic stroke to prevent recurrent stroke, myocardial infarction, and death: the Vitamin Intervention for Stroke Prevention (VISP) randomized controlled trial. Jama, 2004. 291(5): p. 565-75.

7. Lonn, E., et al., Homocysteine lowering with folic acid and B vitamins in vascular disease. N Engl J Med, 2006. 354(15): p. 1567-77.

8. Bonaa, K.H., et al., Homocysteine lowering and cardiovascular events after acute myocardial infarction. N Engl J Med, 2006. 354(15): p. 1578-88.

9. Spence, J.D., Homocysteine-lowering therapy: a role in stroke prevention? Lancet Neurol, 2007. 6(9): p. 830-8.

10. Sahin, M., et al., Effects of metformin or rosiglitazone on serum concentrations of homocysteine, folate, and vitamin B12 in patients with type 2 diabetes mellitus. J Diabetes Complications, 2007. 21(2): p. 118-23.

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http://nccam.nih.gov/health/diabetes/

Treating Type 2 Diabetes with Dietary Supplements

Key Points

There is limited scientific evidence on the effectiveness of dietary supplements as complementary and alternative medicine (CAM)A group of diverse medical and health care systems, practices, and products that are not presently considered to be part of conventional medicine. Complementary medicine is used together with conventional medicine, and alternative medicine is used in place of conventional medicine. for type 2 diabetes. The evidence that is available is not sufficiently strong to prove that any of the six supplements discussed in this report have benefits for type 2 diabetes or its complications. A possible exception may be the use of omega-3 fatty acidsEssential nutrients that the body cannot make on its own but can obtain from foods such as fish and flaxseed, or from dietary supplements. to lower triglyceridea levels.

It is very important not to replace conventional medical therapy for diabetes with an unproven CAM therapy.

To ensure a safe and coordinated course of care, people should inform their health care providers about any CAM therapy that they are currently using or considering.

The six dietary supplements reviewed in this report appear to be generally safe at low-to-moderate doses. However, each can interact with various prescription medications, affecting the action of the medications. People with type 2 diabetes need to know about these risks and discuss them with their health care provider. Prescribed medicines may need to be adjusted if a person is also using a CAM therapy.

aTerms that are underlined are defined in the dictionary at the end of this report.

1. What is diabetes?

Diabetes is a chronic condition in which the body cannot properly convert food into energy. Most food that a person eats is eventually broken down into blood glucose (also called blood sugar), which cells need for energy and growth. Insulin is a hormone that helps glucose enter cells. In people with diabetes, the body does not make enough insulin, or it does not respond to insulin properly. This causes glucose to build up in the blood instead of moving into the cells. The most common type of diabetes is type 2 diabetes (formerly called adult-onset diabetes or noninsulin-dependent diabetes). People can develop type 2 diabetes at any age, even in childhood.

The symptoms of diabetes include fatigue, nausea, a need to urinate frequently, excessive thirst, weight loss, blurred vision, frequent infections, and sores that do not heal. However, some people with diabetes do not have any symptoms. Over time, the high blood glucose levels caused by diabetes can lead to complications in the eyes, blood vessels, nerves, kidneys, feet, teeth, skin, and, especially, the heart. Such complications can be prevented or delayed by keeping blood glucose, blood pressure, cholesterol, and triglycerides in a normal or close-to-normal range.

Some people develop a condition called insulin resistance before they develop type 2 diabetes. When insulin resistance is present, the body does not respond properly to the insulin it has released to lower blood glucose. So, the pancreas releases more insulin to try to keep up with the excess glucose. If the pancreas cannot produce enough insulin, over time this leads to type 2 diabetes. Obesity, aging, and lack of exercise can all play a role in developing insulin resistance and heightening the risk for diabetes.

To find out more about diabetes and related conditions, contact the National Diabetes Information Clearinghouse (see “For More Information”).

2. How is diabetes managed in conventional medicine?

In conventional medicine’sb approach, people with diabetes learn to keep their blood glucose in as healthy a range as possible. They do this by following a healthy food plan, being physically active, controlling their weight, and testing their blood glucose regularly. Some people also need to take medicine, such as insulin injections or prescription diabetes pills. When lifestyle changes and medical treatment are combined to rigorously maintain and control blood sugar in the normal range, this approach to managing type 2 diabetes minimizes the serious complications of the disease. This enables patients to lead productive, full lives.

b Conventional medicine is medicine as practiced by holders of M.D. (medical doctor) or D.O. (doctor of osteopathy) degrees and by their allied health professionals, such as nurses, physical therapists, and dietitians. Complementary and alternative medicine (CAM) is a group of diverse medical and health care systems, practices, and products that are not presently considered to be part of conventional medicine. Complementary medicine is used along with conventional medicine, and alternative medicine is used instead of conventional medicine. Some practitioners of conventional medicine are also practitioners of CAM.

3. What CAM therapies are discussed in this report?

There are many different CAM therapies used for diabetes and its complications, and it is beyond the scope of this report to discuss them all. Scientific information on any CAM therapy for diabetes can be sought in the PubMed database on the Internet and from the National Center for Complementary and Alternative Medicine (NCCAM) Clearinghouse (for both, see “For More Information”). Overall, there have been few rigorous studies published on the use of CAM approaches for type 2 diabetes. Most of the literature has looked at herbal or other dietary supplements, which reflects the tradition in certain whole medical systems of using plant products with claimed effects on blood sugar. This report focuses on six of the dietary supplements that people try for diabetes: alpha-lipoic acid (ALA), chromium, coenzyme Q10, garlic, magnesium, and omega-3 fatty acids. Discussions of the research findings on these supplements begin in Question 5.

4. What should people do if they have diabetes and are considering using any CAM therapy?

People with diabetes need to be under the care of a physician or other health care provider who will help them learn to manage their diabetes and will monitor their efforts to control it. Dietitians and diabetes educators help people learn and use the skills needed for managing diabetes on a daily basis. In addition, many patients need to be under the care of one or more specialists, such as an endocrinologist, an ophthalmologist, and/or a podiatrist.

It is important to not replace scientifically proven treatments for diabetes with CAM treatments that are unproven. The consequences of not following one’s prescribed medical regimen for diabetes can be very serious, even life-threatening.

People with diabetes should tell their health care provider about any dietary supplements or medications (prescription or over-the-counter) that they are using or considering. Prescribed medicines for diabetes and all other major health conditions may need to be adjusted if a person is also using a CAM therapy. Pharmacists can be another helpful source of information about dietary supplements.

If they decide to use supplements, they should know that what they see on the label may not accurately reflect what is in the bottle. Some herbal supplementsA type of dietary supplement that contains herbs, either alone or in mixtures., for example, have been found to be contaminated; some tests of dietary supplements have found that the contents did not match the labeled dose on the bottle. The NCCAM Clearinghouse (see “For More Information”) has publications on this topic.

Women who are pregnant or nursing, or people who are thinking of using supplements to treat a child, should use extra caution and be sure to consult their health care provider.

If people with diabetes decide to use a supplement and notice any unusual effects, they should stop and contact their health care provider.

5. What is known about the safety and effectiveness of these six dietary supplements as CAM treatments for diabetes?

Below is a brief overview of each dietary supplement and what is known from research about its effectiveness and safety in use for diabetes.

Alpha-Lipoic Acid

Alpha-lipoic acid (ALA, also known as lipoic acid or thioctic acid) is a chemical that is similar to a vitamin. It is an antioxidant–a substance that prevents cell damage caused by substances called free radicals in a process called oxidative stress. High levels of blood glucose are one cause of oxidative stress. ALA is found in some foods, such as liver, spinach, broccoli, and potatoes. ALA can also be made in the laboratory. ALA supplements are marketed as tablets or capsules.c It is theorized that ALA may be beneficial because of its antioxidant activity.

c There is some use, reported from outside the United States, of ALA delivered intravenously (IV). These trials are not discussed in this report.

Summary of the research findings

The evidence on ALA for type 2 diabetes and obesity is limited. There are a number of small studies in animals and in people that have shown hints of beneficial effects. In a few of these studies, some possible benefit from ALA was seen in glucose uptake in muscle; sensitivity of the body to insulin; diabetic neuropathy; and/or weight loss. More research is needed to document whether there is any benefit of ALA in diabetes and to better understand how ALA works.

Side effects and possible risks

While ALA appears to be safe for the general adult population, people with diabetes need to know that ALA might lower blood sugar too much, and thus they would need to monitor their blood sugar level especially carefully. ALA may also lower blood levels of minerals, such as iron; interact with some medicines, such as antacids; and decrease the effectiveness of some anti-cancer drugs. Other possible side effects of ALA include headache, skin rash, and stomach upset.

Chromium

Chromium is a metal and an essential trace mineral. Chromium is found in some foods, such as meats, animal fats, fish, brown sugar, coffee, tea, some spices, whole-wheat and rye breads, and brewer’s yeast. It is marketed in supplement form (capsules and tablets) as chromium picolinate, chromium chloride, and chromium nicotinate.

Summary of the research findings

There are scientific controversies about the use or need for chromium supplementation by persons with diabetes. First, it is difficult to determine, including through tests, whether a person has a chromium deficiency. Second, it is not known whether it is beneficial to take chromium supplementation in diabetes, and there is a lack of rigorous basic science studies to explain or support any evidence of benefit. In sum, there is not enough evidence to show that taking chromium supplements is beneficial for diabetes.

Side effects and other risks

At low doses, short-term use of chromium appears to be safe in the general adult population. However, chromium can add to insulin in its effects on blood sugar; this might cause the blood sugar to go too low. Possible side effects at low doses include weight gain, headache, insomnia, skin irritation, sleep problems, and mood changes. High doses can cause serious side effects. The foremost concern for persons with diabetes who use chromium is the development of kidney problems. Other possible effects include vomiting, diarrhea, bleeding into the gastrointestinal tract, and worsening of any behavioral or psychiatric problems.

Coenzyme Q10

Coenzyme Q10, often referred to as CoQ10 (sometimes written as CoQ10; other names include ubiquinone and ubiquinol) is a vitamin-like substance. CoQ10 helps cells make energy and acts as an antioxidant. Meats and seafood contain small amounts of CoQ10. Supplements are marketed as tablets and capsules.

Summary of the research findings

There have been few studies on CoQ10 and type 2 diabetes so far. The evidence is not sufficient to evaluate CoQ10’s effectiveness as a CAM therapy in diabetes. CoQ10 has not been shown to affect blood glucose control. In theory, it might have use against heart disease in people with diabetes, but well-designed studies looking at heart disease outcomes are needed to answer this question.

Side effects and other risks

CoQ10 appears to be safe for most of the adult population. However, it may interact with and affect the action of some medicines, including warfarin (a blood thinner) and medicines used for high blood pressure or cancer chemotherapy. Other possible side effects of CoQ10 include nausea, vomiting, diarrhea, loss of appetite, and heartburn.

Garlic

Garlic (Allium sativum) is an herbA plant or part of a plant used for its flavor, scent, or potential therapeutic properties. Includes flowers, leaves, bark, fruit, seeds, stems, and roots. used to flavor food. Garlic can also be processed and made into dietary supplements. In some cultures, garlic is used for medicinal purposes. The chemical in garlic of most interest for health purposes is allicin, which gives garlic its strong taste and odor. One of the claims for garlic is that the rates of certain diseases are lower in countries where lots of garlic is consumed. However, it has not been proven that garlic (and not some other factor such as lifestyle) is the reason.

Summary of the research findings

Few rigorous studies have been conducted on garlic, allicin, or both, for type 2 diabetes. In the studies that have been done, findings have been mixed. There are some intriguing basic science studies that suggest that garlic has some biological activities that are relevant to the treatment of diabetes. However, the evidence so far does not support that there is any benefit from garlic for type 2 diabetes.

Side effects and other risks

Garlic is safe for most adults. However, garlic appears to interact with various types of drugs. For example, when combined with certain medicines used to treat HIV/AIDS (NNRTIs and saquinavir), garlic may decrease their effectiveness. Garlic may also interact with and affect the action of birth control pills, cyclosporine, medications that are broken down by the liver, and blood thinners (including warfarin). Other possible side effects of garlic include an odor on the breath or skin, an allergic reaction, stomach disorders, diarrhea, and skin rash.

Magnesium

Magnesium is a mineral. Foods high in magnesium include green leafy vegetables, nuts, seeds, and some whole grains. Various supplemental forms of magnesium are marketed as tablets, capsules, or liquids.

Magnesium has many important functions in the body, including in the heart, nerves, muscles, bones, handling glucose, and making proteins. Low levels of magnesium are commonly seen in people with diabetes. Scientists have studied the relationship between magnesium and diabetes for a long time, but it is not yet fully understood.

Summary of the research findings

There have been a handful of studies on magnesium and type 2 diabetes, many of them very small in size and/or short in length and primarily looking at blood glucose control. The results have been mixed, with most finding that magnesium did not affect blood glucose control. Some studies have suggested that low magnesium levels may make glucose control worse in type 2 diabetes (interrupting insulin secretion in the pancreas and increasing insulin resistance) and contribute to diabetes complications. There is evidence that magnesium supplementation may be helpful for insulin resistance. Additional controlled studies are needed to establish firmly whether magnesium supplements have any role or benefit as a CAM therapy for type 2 diabetes.

Side effects and other risks

Magnesium supplements appear to be safe for most adults at low doses. High doses can be unsafe and cause such problems as nausea, diarrhea, loss of appetite, muscle weakness, difficulty breathing, extremely low blood pressure, irregular heart rate, and confusion. Magnesium can interact with and affect the action of certain drugs, including some antibiotics, drugs to prevent osteoporosis, certain high blood pressure medicines (calcium channel blockers), muscle relaxants, and diuretics (“water pills”).

Omega-3 Fatty Acids

Omega-3 fatty acids (omega-3s, for short) are a group of polyunsaturated fatty acids that come from food sources, such as fish, fish oil, some vegetable oils (primarily canola and soybean), walnuts, wheat germ, and certain dietary supplements. As supplements, omega-3s are marketed as capsules or oils, often as fish oil.

Omega-3s are important in a number of bodily functions, including moving calcium and other substances in and out of cells, the relaxation and contraction of muscles, blood clotting, digestion, fertility, cell division, and growth. Omega-3s have been the subject of much media attention in recent years, because of studies finding they may be useful for such purposes as decreasing the rate of heart disease, reducing inflammation, and lowering triglyceride levels. Some countries and organizations have issued formal recommendations on the intake of omega-3s, through meals, oils, and possibly supplementation. Omega-3s have been of interest for diabetes primarily because having diabetes increases a person’s risk for heart disease and stroke.

Summary of the research findings

Randomized clinical trials have found that omega-3 supplementation reduces the incidence of cardiovascular disease and events (such as heart attack and stroke) and slows the progression of atherosclerosis (hardening of the arteries). However, these studies were not done in populations that were at higher risk, such as those with type 2 diabetes.

With regard to studies on omega-3 supplementation for type 2 diabetes, there is somewhat more literature available than for most other CAM therapies for this condition. A 2001 analysis was published by the Cochrane Collaboration, of 18 randomized placebo-controlled trials on fish oil supplementation in type 2 diabetes. The authors found that fish oil lowered triglycerides and raised LDL cholesterol but had no significant effect on fasting blood glucose, HbA1c, total cholesterol, or HDL cholesterol. (The authors did not identify and include studies with cardiovascular outcomes, but noted that this is an area for further research.) Another analysis was published in 2004 by the Agency for Healthcare Research and Quality, of 18 studies on omega-3 fatty acids for a number of measurable outcomes in type 2 diabetes. This study confirmed virtually all the Cochrane authors’ findings, except for finding no significant effect on LDL cholesterol.

Additional studies are needed to determine whether omega-3 supplements are safe and beneficial for heart problems in people with type 2 diabetes. Studies that look specifically at heart disease outcomes in this population are needed.

Side effects and possible risks

Omega-3s appear to be safe for most adults at low-to-moderate doses. There have been some safety questions raised about fish oil supplements, because certain species of fish can be contaminated with substances from the environment, like mercury, pesticides, or PCBs. Fish oil is on the list of food substances that the U.S. Food and Drug Administration considers to be “generally recognized as safe.” How well a product is prepared is another factor for consumers to consider. Women who are pregnant or breastfeeding should not take fish oil supplements. Fish oil in high doses can possibly interact with, and affect the action of, certain medications, including blood-thinning drugs and drugs for high blood pressure. Potential side effects of fish oil include a fishy aftertaste, belching, stomach disturbances, and nausea.

6. What research is being done on CAM therapies for diabetes?

Recent NCCAM-supported research projects are studying the effects of:

Chromium on high blood glucose levels

Yoga on glucose control in people at risk for diabetes

Ginkgo biloba extract on diabetes medicines

Also, researchers in the Diabetes Unit of NCCAM’s Division of Intramural Research are studying many aspects of diabetes, including what happens when the body does not properly react to insulin. Recent clinical trials, for example, have been studying whether vitamin C supplements are beneficial in diabetes, the safety of glucosamineA substance found in the fluid around joints and used by the body to make and repair cartilage. Glucosamine in dietary supplements is made in the laboratory or from the shells of shrimp, lobster, and crabs. with respect to insulin resistance, and whether dark chocolate lowers blood pressure and improves insulin sensitivity. Diabetes Unit staff note that a category of functional foods containing polyphenols (also available as extracts) may be of benefit for further study in diabetes, including green tea (epigallocatechin gallate), dark chocolate (epicatechin), and red wine (resveratrol).

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http://www.holisticonline.com/Remedies/Diabetes/diabetes_vitamins-and-supplements.htm

Nutritional supplements for Diabetes (note here that much of these are also found in energy drinks such as 5-hour energy or Monster)

Vitamin E

People with diabetes have a higher than usual need for vitamin E, which improves insulin activity and acts as an antioxidant and a blood oxygenator. Research has shown that people with low blood levels of vitamin E are more likely to develop Type 2 diabetes. Double-blind studies show that vitamin E improves glucose tolerance in people with Type 2 diabetes (NIDDM). Vitamin E was found to improve glucose tolerance in elderly non-diabetics.

A vitamin E deficiency results in increased free-radical-induced damage, particularly of the lining of the vascular system. Supplemental vitamin E may help prevent diabetic complications through its antioxidant activity, the inhibition of the platelet-releasing reaction and platelet aggregation, increasing HDL-cholesterol levels and its role in fatty acid metabolism. Vitamin E protects animals from diabetic cataracts.

The most impressive study on vitamin E and diabetes used a total of 1,350 international units of d-alpha-tocopheryl acetate daily, divided into three doses. Begin by taking 400 international units each morning. After two weeks, add another dose of 400 international units in the evening. After two more weeks, add another 400 international units in the afternoon.

It may require three months or more of supplementation for benefits to become apparent. The trace mineral selenium functions synergistically with vitamin E.

Note: If you have high blood pressure, limit your intake of supplemental vitamin E to a total of 400 international units daily. If you are taking an anticoagulant (blood thinner), consult your physician before taking supplemental vitamin E.

Vitamin C

People with Type 1 diabetes (IDDM) have low vitamin C levels. Vitamin C lowers sorbitol in diabetics. Sorbitol is a sugar that can accumulate and damage the eyes, nerves, and kidneys of diabetics. Vitamin C may improve glucose tolerance in Type 2 diabetes (NIDDM).

The transport of vitamin C into cells is facilitated by insulin. It has been postulated that, due to impaired transport or dietary insufficiency, a relative vitamin C deficiency exists in the diabetic and that this may be responsible for the increased capillary permeability and other vascular disturbances seen in diabetics.

If you are diabetic, supplement your diet with 1-3 grams per day of vitamin C.

Vitamin B6 (Pyridoxine)

Diabetics with neuropathy have been shown to be deficient in vitamin B6 and benefit from supplementation. Peripheral neuropathy is a known result of pyridoxine deficiency and is indistinguishable from diabetic neuropathy. Vitamin B6 supplements improve glucose tolerance in women with diabetes caused by pregnancy. Vitamin B6 is also effective for glucose intolerance induced by the birth control pill. 1,800 mg per day of a special form of vitamin B6-pyridoxine alpha-ketoglutarate-improves glucose tolerance dramatically.

Pyridoxine is also important in preventing other diabetic complications because it is an important coenzyme in the cross-linking of collagen and inhibits platelet aggregation.

Vitamin B12

Vitamin B12 supplementation has been used with some success in treating diabetic neuropathy. It is not clear if this is due to the correcting of a deficiency state or normalizing vitamin B12 metabolism.

Vitamin B12 is needed for normal functioning of nerve cells. Vitamin B12 taken orally, intravenously, or by injection reduces nerve damage caused by diabetes in most people.

Oral supplementation may be sufficient, but intramuscular vitamin B12 may be necessary in many cases. Take up to 500 mcg of Vitamin B12 three times per day.

Biotin

Biotin is a B vitamin needed to process glucose. It has been shown to work synergistically with insulin and independently in increasing the activity of glucokinase. This enzyme is responsible for the first step in glucose utilization. Glucokinase is present only in the liver, where, in diabetics, its concentration is very low.

Supplementation with large quantities of biotin may significantly enhance glucokinase activity, thereby improving glucose metabolism in diabetics. When people with Type 1 diabetes (IDDM) were given 16 mg of biotin per day for just one week, their fasting glucose levels dropped by 50%. Similar results have been reported using 9 mg per day for two months in people with Type 2 diabetes (NIDDM). Biotin may also reduce pain from diabetic nerve damage.

Take 16 mg of biotin for a few weeks to see if blood sugar levels will fall.

Niacin

High levels-several grams per day-of niacin, a form of vitamin B3, impair glucose tolerance . So, avoid it if you are diabetic. Smaller amounts (500-750 mg per day for one month followed by 250 mg per day) of niacin may help some people with Type 2 diabetes (NIDDM).

Chromium

As a key constituent of the ‘glucose tolerance factor,’ chromium is a critical nutrient in diabetes. Supplementation in the form of chromium chloride (200 micro g daily) or high-chromium-containing brewer’s yeast (9 g a day) has been demonstrated to decrease fasting glucose levels, improve glucose tolerance, lower insulin levels and decrease total cholesterol and triglyceride levels, while increasing HDL-cholesterol levels.

Double-blind research shows that chromium supplements improve glucose tolerance in people with both Type 1 and Type 2 diabetes, apparently by increasing sensitivity to insulin. Chromium improves the processing of glucose in people with pre-diabetic glucose intolerance and in women with diabetes associated with pregnancy.

The typical amount of chromium used in research trials is 200 mcg per day. Some doctors recommend up to 1,000 mcg per day of Chromium for diabetics.

Niacin administered at relatively low levels (100 mg) along with 200 mcg of chromium has been shown to be more effective than chromium alone. Exercise increases tissue chromium concentrations.

Manganese

Manganese is an important cofactor in the key enzymes of glucose metabolism. A deficiency of manganese was found to result in diabetes in guinea pigs. It also resulted in the frequent birth of offspring who develop pancreatic abnormalities or no pancreas at all. Diabetics have been shown to have only one-half the manganese of normal individuals.

Magnesium

Magnesium levels are significantly lowered in diabetics, and lowest in those with severe retinopathy. Studies suggest that a deficiency in magnesium may worsen the blood sugar control in Type 2 diabetes. Scientists believe that a deficiency of magnesium interrupts insulin secretion in the pancreas and increases insulin resistance in the body’s tissues. Studies suggest that a deficiency in magnesium may worsen the blood sugar control in Type 2 diabetes. Scientists believe that a deficiency of magnesium interrupts insulin secretion in the pancreas and increases insulin resistance in the body’s tissues.

Supplementation with magnesium leads to improved insulin production in elderly people with Type 2 diabetes. Elders without diabetes may also produce more insulin as a result of magnesium supplements. Insulin requirements are lower in people with Type 1 diabetes who supplement with magnesium.

Diabetes-induced damage to the eyes is more likely to occur to magnesium-deficient people with Type 1 diabetes (IDDM). In pregnant women with IDDM who are magnesium deficient, the lack of magnesium may even account for the high rate of spontaneous abortion and birth defects associated with IDDM. Low magnesium levels appears to be a significant risk factor in the development of cardiovascular disease, particularly coronary artery spasm.

Many doctors of natural medicine recommend that diabetics with normal kidney function supplement with 300-400 mg of magnesium per day.

Vanadium

Vanadium is a compound found in tiny amounts in plants and animals. Early studies showed that vanadium normalized blood glucose levels in animals with Type 1 and Type 2 diabetes. A recent study found that when people with diabetes were given vanadium, they developed a modest increase in insulin sensitivity and were able to decrease their insulin requirements.

Potassium

Potassium supplementation yields improved insulin sensitivity, responsiveness and secretion in diabetics. Insulin administration often causes a potassium deficiency.

Zinc

Zinc deficiency has been suggested to play a role in the development of diabetes in humans. Zinc is involved in virtually all aspects of insulin metabolism -synthesis, secretion and utilization. Zinc also has a protective effect against beta cell destruction, and has well-known anti-viral effects.

People with Type 1 diabetes (IDDM) tend to be zinc deficient, which may impair immune function. Zinc supplements have lowered blood sugar levels in people with IDDM. People with Type 2 diabetes (NIDDM) also have low zinc levels, caused by excess loss of zinc in their urine.

People with NIDDM are recommended to supplement their diet with moderate amounts of zinc (15-50 mg per day) as a way to correct for the deficit.

Note: Take zinc with food to prevent stomach upset. If you take over 30 milligrams of zinc on a daily basis for more than one or two months, you should also take 1 to 2 milligrams of copper each day to maintain a proper mineral balance.

Coenzyme Q10

People with diabetes cannot adequately process carbohydrates. Coenzyme Q10, or CoQ10, is needed for normal carbohydrate metabolism. Coenzyme Q10 is an antioxidant that fights free-radical damage and is a blood oxygenator.

Animals with diabetes are CoQ10 deficient. In one trial, blood sugar levels fell substantially in 31% of people with diabetes after they supplemented with 120 mg of CoQ10 per day.

Because the eye is so richly supplied with tiny blood vessels, this is another nutrient that can help in cases of retinopathy. Take 50 milligrams of coenzyme Q10 twice daily for up to three months, then reduce the dosage to 30 milligrams daily.

Inositol

Inositol is needed for normal nerve function. Diabetes can cause nerve damage, or diabetic neuropathy. Some of these abnormalities have been reversed by inositol supplementation (500 mg taken twice per day).

ALA and GLA

Alpha-lipoic acid (ALA) is a powerful natural antioxidant. It has been used to improve diabetic neuropathies (at an intake of 600 mg per day) and has reduced pain in several studies.

Gamma-linolenic acid (GLA), found in black currant seed oil, borage oil, and evening primrose oil, has been shown to be helpful for improving damaged nerve function, which is common in diabetes.

Supplementing with 4 grams of evening primrose oil per day for six months has been found to reverse the cause of diabetic nerve damage and improve this painful condition. In double-blind research, 6 grams per day helps reduce nerve damage in people with both Type 1 and Type 2 diabetes (IDDM and NIDDM).

Take 500 to 1,000 milligrams of any of these oils twice daily.

Carnitine

Carnitine is a substance needed for the body to properly use fat for energy. When diabetics are given carnitine (1 mg per 2.2 pounds of body weight), high blood levels of fats-both cholesterol and triglycerides-dropped 25-39% in just ten days. In addition, carnitine improves the breakdown of fatty acids, possibly playing a role in preventing diabetic ketoacidosis.

Taurine

Taurine is an amino acid found in protein-rich food. People with Type 1 diabetes (IDDM) have low taurine levels, that leads to “thickened” blood-a condition which increases the risk of heart disease. Supplementing taurine (1.5 grams per day) restores taurine levels to normal and corrects the problem of blood viscosity within three months.

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http://www.prevention.com/cda/article/extra-help-taming-diabetes/a26c323b0b803110VgnVCM20000012281eac____/health/healthy.living.centers/diabetes

Extra Help Taming Diabetes

Four supplements are worth a look

By Densie Webb, PhD, RD , Densie Webb, PhD, RD is former contributer to Prevention’s Supplement News column.

Check out these nutritional supplements that may help prevent and control diabetes.

Controls Blood Sugar

Chromium For the body to function, each cell must “open its door” and allow sugar to enter. Chromium has been called the key that unlocks that door. Without it, sugar builds up in the blood, and eventually diabetes develops.

It would seem to make perfect sense, then, to take chromium supplements to ward off diabetes. And some studies have suggested that supplementing with chromium helps keep blood sugar under control. But according to the American Diabetes Association (ADA), only very low chromium levels cause problems. For most people, the ADA says, chromium supplements offer no known benefit. A recent animal study also found that one form of chromium, chromium picolinate, can trigger potentially cancer-causing cell mutations.

But not everyone is so quick to dismiss chromium’s tremendous potential for people with diabetes. “There are several lines of evidence suggesting that higher doses of chromium supplements may be beneficial,” says William Cefalu, MD, associate professor of medicine and director of the clinical trials unit at the University of Vermont College of Medicine in Burlington. Diabetes experts say 600 micrograms (mcg) a day have proven effective. (The animal studies suggesting a cancer link used much larger amounts than you would get from nutritional supplements.)

Chromium is available in a variety of forms: as single nutritional supplements, as an ingredient in multivitamins, or combined with any number of vitamins and/or minerals. Chromium picolinate and chromium histidine are believed to be better absorbed than other forms of the mineral.

Foods that contain chromium include: black pepper, broccoli, dried beans, and whole grains.

Magnesium Diabetes is the most common disorder associated with low magnesium. As many as one out of every three people with diabetes is low on this mineral. Even more convincing: Studies show that as magnesium intake goes up, the risk of developing type 2 diabetes goes down.

Although a few studies have shown that nutritional supplements of about 350 mg a day improve insulin resistance and blood sugar control, there’s little agreement among experts as to whether low magnesium levels are the cause or the result of diabetes.

Still, experts say it’s a good practice to make sure you’re getting enough magnesium. (Most people, especially seniors, don’t.) Supplements come in a variety of forms, including magnesium acetate, aspartate, carbonate, chloride, citrate, glycinate, hydroxide, lactate, oxide, or pidolate. And they come in a variety of combinations, from multis to special-formula supplements for diabetes, heart disease, and osteoporosis. One study found magnesium citrate to be well absorbed.

Green leafy vegetables, legumes, nuts, wheat germ, and whole grains provide magnesium.

Quells Complications

Vitamin E Known for its antioxidant powers, vitamin E appears to reduce the free radical damage that causes the complications of diabetes, such as heart disease and nerve damage, which can lead to blindness and amputation. Research shows that daily nutritional supplements of vitamin E can significantly reduce the damage in diabetics that ultimately leads to cardiovascular disease. Seventy percent of deaths from diabetes are related to damaged and clogged arteries.

Recent studies have not found vitamin E effective in preventing cardiovascular disease in the general population, but most experts still believe it is, and there is evidence suggesting a specific benefit in diabetes.

Ishwarlal Jialal, MD, PhD, professor of internal medicine and pathology at the University of Texas Health Science Center at Dallas found that giving 1,200 IU of E a day to people with diabetes greatly reduced the tendency of LDL cholesterol to begin creating a buildup of fat and other debris on artery walls.

Since it’s impossible to get such large amounts of E from your diet, “it’s not unreasonable to take an E supplement,” he says. Diabetes experts recommend 600 IU of E a day.

There are two types of vitamin E, natural (d-alpha tocopherol) and synthetic (dl-alpha tocopherol). Milligram for milligram, natural is more potent, so it takes less to get the same benefit. Vitamin E can be found in single ingredient supplements, multivitamins, and herbal preparations. But large doses are generally found as single-ingredient nutritional supplements. Good sources of Vitamin E include: avocados, nuts, and vegetable oils.

Alpha-Lipoic Acid Researchers have discovered that this potent antioxidant (experts say it’s more potent than vitamins E or C) may be an effective treatment for a common complication of diabetes, known as diabetic neuropathy, which develops when high blood sugar levels damage delicate nerve endings. The result is a stabbing, tingling, and burning pain in the legs, feet, and hands, especially at night. In Germany, alpha-lipoic acid is a prescription drug used to treat diabetic neuropathy.

“I recommend alpha-lipoic to my patients with diabetic neuropathy who haven’t been helped by conventional treatments,” says Aaron Vinik, MD, PhD, director of the Strelitz Diabetes Research Institute at the Eastern Virginia Medical School in Norfolk. “Clinical trials are underway in the U.S.,” he says, “but the results won’t be in for a few years.”

It may also help control blood sugar in diabetics, possibly by lowering insulin levels and increasing the transport of sugar into cells.

Alpha-lipoic acid is found in small amounts in some foods–spinach and meat, for example–but not enough to make a real difference. For that, studies show you need 600 to 1,200 mg a day, amounts that can come only from nutritional supplements.

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http://ezinearticles.com/?Vitamin-B12-and-Weight-Loss&id=333129

Vitamin B12 and Weight Loss

By Shane Woods

Cobalamin or as it is better known, vitamin B12 is one of the vital nutrients our bodies need in order to work properly. It is necessary to perform many of the body’s more important tasks, including the making of DNA during cell division and the healthy formation of red blood cells.

Vitamin B12 is known as the “energy vitamin” because it gives a real energy boost. It is used to remedy fatigue and it speeds up the metabolism. Red blood cells are also responsible for producing hemoglobin, the part of the blood that takes oxygen from the lungs and transports it to all the different parts of the body.

Vitamin B12 has many functions and uses but does it help people lose weight?

What is the link between Vitamin B12 and weight loss?

Vitamin B12 Injections and Weight Loss

Some people might go to a clinic to get vitamin B12 shots. These shots are administered directly into the muscle, allowing for better absorption.

People who get these shots mainly suffer from chronic fatigue syndrome or vitamin B12 deficiency. They might also claim that taking these shots help them to lose weight.

However, Vitamin B12 injections by themselves do not directly induce weight loss, nor are they intended to. So why do people who get them lose weight?

There are many factors to take into consideration.

Vitamin B12 causes the metabolism to speed up, which in turn increases weight loss.

People who go to get injections tend to be more conscious of their health and are already on a vegetarian, or other weight loss diet.

Vitamin B12 shots give a tremendous boost of energy. This generally helps people to maintain their diets, and motivates them to exercise and increase physical activity.

Vitamin B12 also helps to fight stress and depression, symptoms which are sometimes associated with weight gain.

While vitamin B12 shots can be a great benefit to some, particularly those with Vitamin B12 deficiency, there can be some negative side effects when taken excessively or along with certain other substances. There is also a risk for those who have certain pre-existing conditions. It’s important to consult a physician before undergoing vitamin B12 injections.

Vitamin B12 and Dieting

When undergoing any new weight loss program it is important to make sure that the diet is well balanced and contains all of the essential nutrients. This of course includes vitamin B12. Food sources rich in vitamin B12 include:

- Meat

- Poultry

- Milk and other dairy products

- Eggs

- Fish

Since the only reliable source of vitamin B12 are from animals those practicing a vegetarian or vegan diet will have to get their vitamin B12 from supplements. If a person doesn’t get enough vitamin B12 they may develop a deficiency.

Vitamin B12 Deficiency

Vitamin B12 deficiency can become a serious health threat. The body can normally stock up many years supply of vitamin B12, so it more often materializes when the body is unable to properly absorb vitamin B12 because of illness or old age.

Incidentally, Vitamin B12 deficiency can cause weight loss, among other symptoms. Extreme cases can even result in permanent nerve damage if left untreated.

A person diagnosed with Vitamin B12 deficiency will need to take supplements. These are most often taken as capsules or via intramuscular injections.

Although vitamin B12 does not directly cause weight loss, it is still an essential nutrient that is needed by the body. It is important to get a sufficient amount of it and doing so will ensure better health, all around.

Healthy Energy (Part 1 – the basics)

A few days back, I blogged on why I liked the 5 hour energy drink. I would now like to blog a little on what things I’ve found that contribute to your body’s energy and why. I am only passing on the research I’ve done to reach my own concultions on what I should and shouldn’t take to boost my energy. I’m in no way qualified to tell you what is good for you, and it is only hoped that this information maybe handy as part of considering whether you what you should and shouldn’t do to boost your energy. Please remember to treat all things as if they may be harmful to you, and do your own research as well.

“Energy is defined as the ability to do work, and metabolism represents the biochemical reactions that a cell can perform to produce energy.”

The main sources of chemical energy for most organisms are carbohydrates, fats, and protein. Energy content is expressed in calories or joules. The nutritional calorie, or kilocalorie (kcal), in foodstuffs is equivalent to 1000 calories. The energy content per gram of carbohydrate is 4 kcal (16 J); protein, 4 kcal (16 J); and fat, 9 kcal (36 J). The metabolism of foodstuffs yields chemical energy and heat.

Source: http://www.answers.com/topic/energy-metabolism?cat=technology

“Metabolism is the set of chemical reactions that occur in living organisms in order to maintain life.”

Source: http://en.wikipedia.org/wiki/Metabolism

The term metabolism refers to all of the chemical reactions by which complex molecules taken into an organism are broken down to produce energy and by which energy is used to build up complex molecules. All metabolic reactions fall into one of two general categories: catabolic and anabolic reactions, or the processes of breaking down and building up, respectively. The best example of metabolism from daily life occurs in the process of taking in and digesting nutrients, but sometimes these processes become altered, either through a person’s choice or through outside factors, and metabolic disorders follow. Such disorders range from anorexia and bulimia to obesity. These are all examples of an unhealthy, unnatural alteration to the ordinary course of metabolism; on the other hand, hibernation allows animals to slow down their metabolic rates dramatically as a means of conserving energy during times when food is scarce.

Metabolism is like a furnace, in that it burns energy, and that is the aspect most commonly associated with this concept. But metabolism also involves a function that a furnace does not: building new material. All metabolic reactions can be divided into either catabolic or anabolic reactions. Catabolism is the process by which large molecules are broken down into smaller ones with the release of energy, whereas anabolism is the process by which energy is used to build up complex molecules needed by the body to maintain itself and develop new tissue.

Digestion is the process of breaking down food into simpler chemical compounds as a means of making nutrients absorbable by the body. This is a catabolic process, because the molecules of which foods are made are much too large to pass through the lining of the digestive system and directly into the bloodstream. Thanks to the digestive process, smaller molecules are formed and enter the bloodstream, from whence they are carried to individual cells throughout a person’s body.

The smaller molecules into which nutrients are broken down make up the metabolic pool, which consists of simpler substances. The metabolic pool includes simple sugars, made by the breakdown of complex carbohydrates; glycerol and fatty acids, which come from the conversion of lipids, or fats; and amino acids, formed by the breakdown of proteins. Substances in the metabolic pool provide material from which new tissue is constructed—an anabolic process.

For the body to function efficiently, there has to be an effective means of controlling and integrating the metabolic processes occurring in all the cells, tissues, and organs. This integration and control is mainly achieved by circulating hormones, with their release being regulated in turn partly by the nervous system and partly by direct effects of substances in the blood on the endocrine glands. An example of this integrated control of metabolism is the way in which blood glucose concentration is regulated to ensure an adequate supply of glucose to the brain. After meals, the hormone insulin acts to promote storage of glucose in the form of glycogen in the liver. The brain continuously extracts glucose from the blood to use as a fuel for its metabolic processes. In the periods between meals, this continued use of blood glucose causes the concentration to fall, which could impair brain function. However, a fall in blood glucose is detected in the pancreas and leads to the release of the hormone glucagon, which acts on the liver to cause breakdown of glycogen and release of glucose into the blood. In addition, if blood glucose falls sufficiently to affect brain metabolism, the sympathetic nervous system is activated, causing the adrenal gland to release adrenaline, which also stimulates the release of glucose from the liver; also the individual feels hungry and is prompted to eat.

The main way in which the energy contained in the macronutrients is used in metabolism is via the substance adenosine triphosphate (ATP). Cells require energy for their metabolic processes, so they contain the enzymes and organelles needed to produce ATP from the catabolism of fats, carbohydrates, and/or proteins. In most cases, the production of ATP occurs in association with the oxidation, so that the final products are ATP, carbon dioxide, and water, as illustrated below for the oxidation of glucose (C6H12O6):

C6H12O6 + 6O2 = 6CO2 + 6H2O + ATP

This is an example of aerobic metabolism, requiring the supply of oxygen and the removal of carbon dioxide from the cells by the circulating blood. Thus, in order for this predominant type of metabolism to proceed effectively in the whole body, there needs to be integration of the respiration, circulation, and supply of nutrients.

In some situations, anaerobic metabolism can occur, ATP is produced without the use of oxygen, but the energy-releasing capacity of these systems is very small compared with that of aerobic metabolism, and the anaerobic reactions lead to the production of waste products such as lactic acid which impair cell function if they are present in high concentrations.

ATP is the single most important molecule for the metabolism of almost all the cells of the body. It is used to release the energy needed for muscles to contract, for chemical bonds to be made during the synthesis of complex molecules, and for other bonds to be broken during catabolic processes. Cells do not store large quantities of ATP, but rather produce it when it is needed. Thus, most cells of the body need to regulate the concentration of ATP within them. This occurs via the effects of ATP, and its immediate breakdown product ADP (adenosine diphosphate), on the enzymes responsible for synthesizing ATP: when more ATP is used, its concentration falls, and that of ADP rises, leading to the activation of the enzyme which synthesizes more ATP. This in turn requires more oxygen to be used, and nutrients to be broken down.

An example of the complex integration of metabolism is provided by considering the processes involved in muscle contraction during exercise. This involves the brain and other parts of the nervous system in the initiation of voluntary muscle contraction and movement. Contraction can occur only if ATP is available within the muscle cells. As the ATP already present is used, so the concentration of ADP will rise, which stimulates more ATP production. At the same time the contraction of the muscles stimulates the breakdown of the intramuscular glycogen, and may also stimulate the uptake of glucose and fatty acids from the blood. The increased availability of these fuels is accompanied by stimulation of their oxidation, so the ATP concentration is maintained, and muscle contraction continues, supported by an increase in aerobic energy metabolism. For this to be possible, it is also necessary for the supply of blood to the muscles to increase, in order to deliver more oxygen and carry away more carbon dioxide and heat; the action of chemical products of local metabolism, which dilate local blood vessels, effectively links flow to requirement.

The above examples illustrate the complexity of metabolism in the human body, and show that for normal function it is essential that local processes are co-ordinated and integrated throughout the body.

Source: http://www.answers.com/Metabolism

“Enzymes are catalysts for virtually every biological and chemical reaction in the body, and digestive enzymes are crucial for the breakdown of food into nutrients that the body can absorb. Digestive enzymes, of which a variety are herbs, are used to treat a number of digestive problems and other conditions.”

The Digestive enzymes are enzymes in the alimentary tract that break down food so that the organism can absorb it. The main sites of action are the oral cavity, the stomach, the duodenum and the jejunum. They are secreted by different glands: the salivary glands, the glands in the stomach, the pancreas, and the glands in the small intestines.

Oral cavity

In the oral cavity, salivary glands secrete ptyalin. It is a type of a-amylase, which digests starch into small segments of multiple sugars and into individual soluble sugars. Secreted by small and large salivary glands.

Salivary glands also secrete lysozyme, which kills bacteria but is not classified as a digestive enzyme.

Esophagus

There are no digestive enzymes secreted in the esophagus.

Stomach

The enzymes that get secreted in the stomach are called gastric enzymes. These are the following:

· Pepsin is the main gastric enzyme. As it breaks proteins into smaller peptide fragments, it is a peptidase.

· Gelatinase, degrades type I and type V gelatin and type IV and V collagen, which are proteoglycans in meat.

· Gastric amylase degrades starch, but is of minor significance.

· Gastric lipase is a tributyrase by its biochemical activity, as it acts almost exclusively on tributyrin, a butter fat.

Small intestine

Pancreatic enzymes

The pancreas is the main digestive gland in our body. It secretes the enzymes:

· Trypsin, is a peptidase, that breaks down peptides in the small intestine.

· Chymotrypsin, also a peptidase

· Steapsin, degrades triglycerides into fatty acids and glycerol.

· Carboxypeptidase, splits peptide fragments into individual amino acids. It is a protease.

· Several elastases that degrade the protein elastin and some other proteins.

· Several nucleases that degrade nucleic acids, like DNAase and RNAase

· Pancreatic amylase that, besides starch, glycogen and cellulose, degrades most other carbohydrates.

· Bile from the liver, which emulsifies fat, allowing more efficient use of lipases in the duodenum; in converting lipids to their component fatty acid and glycerol molecules

Proper small intestine enzymes

Several peptidases.

The jejunum and ileum secretes a juice called succus entericus which contains the following:

Six types of enzymes degrade disaccharides into monosaccharides:

· Sucrase, which breaks down sucrose into glucose and fructose

· Maltase, which breaks down maltose into glucose.

· Isomaltase, which breaks down maltose and isomaltose

· Lactase, which breaks down lactose into glucose and galactose

· Intestinal lipase, which breaks down fatty acids

· Erepsin, also a protein-digesting enzyme

Source: http://www.answers.com/Digestive+enzymes

“Digestive — Pertaining to digestion.”

• d. enzymes — include salivary (amylase), gastric (pepsin), pancreatic (trypsin, chymotrypsin, amylase, lipase), small intestinal mucosa (carbohydrases including isomaltase, lactase, maltase, sucrase, trehalase).
• d. inoculant — administered mostly to neonates primarily to provide an inoculum of beneficial bacteria and protozoa essential to proper digestion and usually picked up from the environment. In many commercial products the irresistible temptation to include other materials, including dietary essential vitamins and minerals, clouds the effect of the inoculant, and may, as in iron poisoning in foals, cause disaster.
• d. system — the organs that have as their particular function the ingestion, digestion and absorption of food or nutritive elements. They include the mouth, teeth, tongue, pharynx, esophagus, stomach and intestines. The accessory organs of digestion, which contribute secretions important to digestion, include the salivary glands, pancreas, liver and gallbladder. Birds have an unusual system in that there are no teeth and no soft palate in most. There is a pregastric buffer, the crop; the stomach is separated into two organs, one secretory and one muscular, and the large intestine is replaced by a dual cecum. The rectum empties into a cloaca which is shared with the urogenital tract. The ruminant system is complicated by the presence of the forestomachs, the reticulum, rumen and omasum, and there are no upper incisor teeth. The peculiarities of horses are the greatly distended large intestine and the absence of a gallbladder.
• d. tract — the digestive system less the ancillary organs of salivary glands, liver and pancreas; the luminal organs through which food passes. See also alimentary canal.

Source: http://www.answers.com/topic/digestive?nr=1&lsc=true&cat=health

“How can I tell a great digestive enzyme product by its label?”

There are three things to look for on the label. First, you want to make sure the enzymes are plant enzymes… Aspergillus oryzae and niger (these are the most effective digestive enzymes available). Second, look for ionic minerals within the formulation. These minerals help the digestive enzymes become two to three times more active and effective. Third, look closely at the amount of protease, amylase and lipase within the formulation… 75,000 HUT for Protease, 15,000 SKB for Amylase and 5,000 LU for Lipase. These amounts are very important if you really want to help with digestion and cleaning up the blood.

Source: http://breathing.com/articles/enzymes.htm

“Protease – Any of various enzymes, including the endopeptidases and exopeptidases, that catalyze the hydrolytic breakdown of proteins into peptides or amino acids.

Lipase — Any of a group of enzymes that catalyze the hydrolysis of fats into glycerol and fatty acids.

Amylase — Any of a group of enzymes that are present in saliva, pancreatic juice, and parts of plants and catalyze the hydrolysis of starch to sugar to produce carbohydrate derivatives.

Cellulase — Any of several enzymes produced chiefly by fungi, bacteria, and protozoans that catalyze the hydrolysis of cellulose.

Lactase — An enzyme occurring in certain yeasts and in the intestinal juices of mammals and catalyzing the hydrolysis of lactose into glucose and galactose.”

Sources: http://www.answers.com/Protease ; http://www.answers.com/Lipase ; http://www.answers.com/Amylase ; http://www.answers.com/Cellulase ; http://www.answers.com/Lactase?cat=health

“Excess phenylalanine is not stored in the body and has to be broken down by a specific enzyme.”

One of the 22 a-amino acids commonly found in animal proteins. It is one of several essential amino acids needed in the diet; human beings cannot synthesize it from simpler metabolites. Young adults need about 31 mg of this amino acid per day per kg (14 mg per lb) of body weight. Phenylalanine can be degraded into simpler compounds by the enzymes of the body and is readily converted to the amino acid tyrosine. Phenylketonuria (PKU), an inherited disease that, if left untreated, results in retarded mental development in children, has been shown to be associated with the lack of activity of the enzyme that converts phenylalanine to tyrosine. This results in the buildup of phenylalanine in the blood, an event leading to several pathological consequences. The incidence of this disease, about one in every 10,000 births, is high enough to have prompted several states to institute regular screening procedures for the detection of the disease in newborns. If diagnosed early the disease can be controlled to a great extent by administering a diet very low in phenylalanine. Phenylalanine contributes to the structure of proteins into which it has been incorporated by the tendency of its side chain to participate in hydrophobic interactions (see isoleucine). This amino acid was first isolated from a natural source (lupine sprouts) in 1879; it was first chemically synthesized in 1882.

An essential amino acid; in addition to its role in protein synthesis, it is the metabolic precursor of tyrosine (and hence noradrenaline, adrenaline, and the thyroid hormones). Dietary tyrosine spares phenylalanine, so reducing the requirement.

Persons suffering from PKU must monitor their intake of protein to control the buildup of phenylalanine as their bodies convert protein into its component amino acids.

A related issue is the compound present in many sugarless gums and mints, snack foods, sugarless soft drinks (such as diet sodas including CocaCola Zero, Pepsi Max, some forms of Lipton Tea, Clear Splash flavored water), and a number of other low calorie food products. The artificial sweetener aspartame, sold under the names “Equal” and “NutraSweet”, is an ester that is hydrolyzed in the body to give phenylalanine, aspartic acid, and methanol (wood alcohol). The breakdown problems phenylketonurics have with protein and the attendant build up of phenylalanine in the body also occurs with the ingestion of aspartame, although to a lesser degree. Accordingly, all products in the U.S. and Canada that contain aspartame must be labeled: “Phenylketonurics: Contains phenylalanine.” In the UK, foods containing aspartame must carry ingredients panels that refer to the presence of ‘aspartame or E951′, and they must be labeled with a warning “Contains a source of phenylalanine”. These warnings are specifically placed to aid individuals who suffer from PKU so that they can avoid such foods.

Interestingly, the macaque genome was recently sequenced and it was found that macaques naturally have a mutation that is found in humans who have PKU.

DL-Phenylalanine is marketed as a nutritional supplement for its putative analgesic and antidepressant activities. The putative analgesic activity of DL-phenylalanine may be explained by the possible blockage by D-phenylalanine of enkephalin degradation by the enzyme carboxypeptidase A. The mechanism of DL-phenylalanine’s putative antidepressant activity may be accounted for by the precursor role of L-phenylalanine in the synthesis of the neurotransmitters norepinephrine and dopamine. Elevated brain norepinephrine and dopamine levels are thought to be associated with antidepressant effects. D-phenylalanine is absorbed from the small intestine, following ingestion, and transported to the liver via the portal circulation. A fraction of D-phenylalanine appears to be converted to L-phenylalanine. D-phenylalanine is distributed to the various tissues of the body via the systemic circulation. D-phenylalanine appears to cross the blood-brain barrier with less efficiency than L-phenylalanine. A fraction of an ingested dose of D-phenylalanine is excreted in the urine.

Source: http://www.answers.com/Phenylalanine?cat=health

“In addition to its role in proteins, tyrosine is the precursor for the synthesis of melanin (the black and brown pigment of skin and hair), and adrenaline and noradrenaline.”

One of the amino acids, not essential for humans unless they have the hereditary disorder phenylketonuria. It is the biochemical precursor of many important catecholamines. It is found in small amounts in most proteins, especially insulin and papain (found in papaya). It is used in biochemical research and as a dietary supplement.

Tyrosine is a precursor of the adrenal hormones epinephrine and norepinephrine as well as of the thyroid hormones, including thyroxine. Melanin, the skin and hair pigment, is also derived from this amino acid. Tyrosine residues in enzymes have frequently been shown to be associated with active sites. Modification of these residues with various chemicals often results in a change in the specificity of the enzyme toward its substrates or even in total destruction of its activity. In 1846 tyrosine was obtained as a product of the degradation of the protein casein (from cheese). It was synthesized in the laboratory in 1883, and its structure was thus determined.

L-Tyrosine is sometimes recommended by practitioners as helpful for weight loss, clinical depression, Parkinson’s Disease, Attention Deficit Disorder, and phenylketonuria; however, one study found that it had no impact on endurance exercise performance.

Source: http://www.answers.com/Tyrosine?cat=health&nr=1

“One of the problems with some crash diets is that they do not provide enough essential amino acids and, in some extreme cases, have resulted in death.”

An amino acid that must be obtained from the diet so that the body can synthesize vital proteins. Nine amino acids are generally regarded as essential for humans: isoleucine, leucine, lysine, threonine, tryptophan, methionine, histidine, valine and phenylalanine. In addition, the amino acids arginine, cysteine, glycine, glutamine and tyrosine are considered conditionally essential, meaning they are not normally required in the diet, but must be supplied exogenously to specific populations that do not synthesize it in adequate amounts. (Histidine is required by infants, but it has not been fully established that it is essential for adults.) The essential amino acids must be available in the body simultaneously and in the correct proportions for protein synthesis to occur.

Source: http://www.answers.com/topic/essential-amino-acid?cat=health

“Most essential nutrients are substances that are metabolically necessary but cannot be synthesized by the organism.”

An essential nutrient is a nutrient required for normal body functioning that cannot be synthesized by the body and must be obtained from a dietary source. Some categories of essential nutrient include vitamins, dietary minerals, essential fatty acids, and essential amino acids.

All essential nutrients are toxic in large doses (see hypervitaminosis or the nutrient pages themselves below). Some can be taken in amounts larger than required in a typical diet, with no apparent ill effects. Linus Pauling said of vitamin B3, (either niacin or niacinamide), “What astonished me was the very low toxicity of a substance that has such very great physiological power. A little pinch, 5 mg, every day, is enough to keep a person from dying of pellagra, but it is so lacking in toxicity that ten thousand times as much can [sometimes] be taken without harm.” A similar statement can be made about vitamin C and some other vitamins.

List of essential nutrients

· Essential fatty acids:

1. Linolenic acid (the shortest chain omega-3 fatty acid)

2. Linoleic acid (the shortest chain omega-6 fatty acid)

3. Essential amino acids necessary for all humans:

4. Histidine

5. Isoleucine

6. Lysine

7. Leucine

8. Methionine

9. Phenylalanine

10. Threonine

11. Tryptophan

12. Valine

· Essential amino acids necessary for human children and not adults:

1. Arginine

2. Vitamins:

3. Biotin (vitamin B7, vitamin H)

4. Choline (vitamin Bp)

5. Folate (folic acid, vitamin B9, vitamin M)

6. Niacin (vitamin B3, vitamin P, vitamin PP)

7. Pantothenic acid (vitamin B5)

8. Riboflavin (vitamin B2, vitamin G)

9. Thiamine (vitamin B1)

10. Vitamin A (retinol)

11. Vitamin B6 (pyridoxine, pyridoxamine, or pyridoxal)

12. Vitamin B12 (cobalamin)

13. Vitamin C (ascorbic acid)

14. Vitamin D (Cholecalciferol, Ergocalciferol, Calcitriol)

15. Vitamin E (tocopherol)

16. Vitamin K (naphthoquinoids)

· Dietary minerals: Biochemical studies reported in 2006 indicate that the following elements (aside from H, C, N, and O) are required for human health:

1. Calcium (Ca)

2. Chloride (Cl-)

3. Cobalt (Co)

4. Copper (Cu) [3]

5. Iodine (I)

6. Iron (Fe)

7. Magnesium (Mg)

8. Manganese (Mn)

9. Molybdenum (Mo)

10. Phosphorus (P)

11. Potassium (K)

12. Selenium (Se)

13. Sodium (Na)

14. Sulfur (S)

15. Zinc (Zn)

The body’s requirements vary widely. At one extreme a 70 kg human contains 1.0 kg of calcium but only 3 mg of cobalt or 0.5 mg of bismuth.

Source: http://www.answers.com/topic/essential-nutrient?nr=1&lsc=true&cat=health

Healthy Energy (Part 3 – Facts about Fatigue)

“Fatigue may be defined as a subjective state in which one feels tired or exhausted, and in which the capacity for normal work or activity is reduced.”

Everyone experiences fatigue occasionally. It is the body’s way of signaling its need for rest and sleep. But when fatigue becomes a persistent feeling of tiredness or exhaustion that goes beyond normal sleepiness, it is usually a sign that something more serious is amiss.

Physically, fatigue is characterized by a profound lack of energy, feelings of muscle weakness, and slowed movements or central nervous system reactions. Fatigue can also trigger serious mental exhaustion. Persistent fatigue can cause a lack of mental clarity (or feeling of mental “fuzziness”), difficulty concentrating, and in some cases, memory loss.

There is, however, no commonly accepted definition of fatigue when it is considered in the context of health and illness. This lack of definition results from the fact that a person’s experience of fatigue depends on a variety of factors. These factors include culture, personality, the physical environment (light, noise, and vibration), availability of social support through networks of family members and friends, the nature of a particular fatiguing disease or disorder, and the type and duration of work or exercise. The experience of fatigue associated with disease will be different for someone who is clinically depressed, is socially isolated, and is out of shape, as compared to another person who is not depressed, has many friends, and is aerobically fit.

Some researchers regard fatigue as a defense mechanism that promotes the effective regulation of energy expenditures. According to this theory, when people feel tired they take steps to avoid further stress (physical or emotional) by resting or by avoiding the stressor. They are then conserving energy. Since chronic fatigue is not normal, however, it is a common symptom of some mental disorders, a variety of physical diseases with known etiologies (causes), and medical conditions that have no biological markers although they have recognizable syndromes (patterns of symptoms and signs).

Fatigue is sometimes described as being primary or secondary. Primary fatigue is a symptom of a disease or mental disorder, and may be part of a cluster of such symptoms as pain, fever, or nausea. As the disease or disorder progresses, however, the fatigue may be intensified by the patient’s worsening condition, by the other disease symptoms, or by the surgical or medical treatment given to the patient. This subsequent fatigue is called secondary.

Fatigue is a common experience. It is one of the top ten symptoms that people mention when they visit the doctor. Some people, however, are at higher risk for developing fatigue. The risk for women is about 1.5 times the risk for men, and the risk for people who do not exercise is twice that of active people. Some researchers question whether women really are at higher risk, since women are more likely than men to go to the doctor with health problems; also, men are less likely to admit they feel fatigued. Other risk factors include obesity, smoking, use of alcohol, high stress levels, depression, anxiety, and low blood pressure. Having low blood pressure is usually considered desirable in the United States, but is regarded as a treatable condition in other countries. Low blood pressure or postural hypotension (sudden lowering of blood pressure caused by standing up) may cause fatigue, dizziness, or fainting.

The management of fatigue depends in large measure on its causes and the person’s experience of it. For example, if fatigue is acute and normal, the person will recover from feeling tired after exertion by resting. In cases of fatigue associated with influenza or other infectious illnesses, the person will feel energy return as they recover from the illness. When fatigue is chronic and abnormal, however, the doctor will tailor a treatment program to the patient’s needs. There are a variety of approaches that include:

· Aerobic exercise. Physical activity increases fitness and counteracts depression.

· Hydration (adding water). Water improves muscle turgor, or tension, and helps to carry electrolytes.

· Improving sleep patterns. The patient’s sleep may be more restful when its timing and duration are controlled.

· Pharmacotherapy (treatment with medications). The patient may be given various medications to treat physical diseases or mental disorders, to control pain, or to manage sleeping patterns.

· Psychotherapy. There are several different treatment approaches that help patients manage stress, understand the motives that govern their behavior, or change maladaptive ideas and negative thinking patterns.

· Physical therapy. This form of treatment helps patients improve or manage functional impairments or disabilities.

Source: http://www.answers.com/fatigue?cat=health

“A stimulant is any substance that causes an increase in activity in various parts of the nervous system or directly increases muscle activity.”

Cerebral, or psychic, stimulants act on the central nervous system and provide a temporary sense of alertness and well-being as well as relief from fatigue. Drugs such as caffeine and the amphetamines belong in this category, and several groups of drugs chemically similar to antihistamines and phenothiazines also act as mild psychic stimulants (see psychopharmacology). Cocaine, besides its effect as a local anesthetic, also stimulates the central nervous system, producing excitement and erratic behavior. The hallucinogenic drugs are also central nervous system stimulants.

A second class of stimulants that affect the medulla and spinal cord includes derivatives of niacinamide (nicotinic acid amide) and other chemically diverse compounds; they are sometimes used to speed the return to wakefulness after anesthesia or to counteract barbiturate poisoning. Ammonia, in smelling salts, is also a medullary stimulant; the alkaloid strychnine is a spinal-cord stimulant.

Other substances act mainly on the autonomic nervous system. Drugs that stimulate the parasympathetic portion of the autonomic nervous system, such as pilocarpine, physostigmine, and neostigmine, cause contracted pupils, salivation and sweating, slowed heartbeat, and lowered blood pressure. Drugs such as norepinephrine, epinephrine, and other catecholamines and synthetic analogs stimulate the sympathetic portion of the autonomic nervous system, resulting in dilated pupils, rapid heartbeat, and increased blood pressure. Because the sympathetic and parasympathetic systems have opposing physiological effects, stimulation of one system amounts to depression of the other. Some of the alkaloids from the ergot fungus act by direct stimulation of smooth muscle, inducing contractions in uterine and intestinal muscle.

Source: http://www.answers.com/topic/stimulant?nr=1&lsc=true&cat=health

“Adrenaline increases heart rate, the depth and rate of breathing, and metabolic rate.”

Also known as epinephrine. The so-called ‘fight or flight’ hormone secreted by the inner part of the adrenal gland. It prepares the body for action by its stimulatory effects on muscles, circulation, and carbohydrate and fat metabolism. Adrenaline increases heart rate, the depth and rate of breathing, and metabolic rate. It also improves the force of muscular contractions and delays the onset of fatigue. Its actions oppose those of insulin. Adrenaline accelerates fat mobilization and encourages the conversion of glycogen to glucose.

Adrenaline and adrenaline-related drugs are sometimes used in sport as stimulants. Although these drugs can improve performance, they may produce harmful side-effects such as heart beat irregularities. Consequently, they are on the International Olympic Committee’s list of banned substances.

Source: http://www.answers.com/topic/adrenaline?cat=health

“Foods and drinks (and other substances) that stimulate the consumer to enhanced mental alertness, increased or prolonged physical activity, uninhibited conviviality, or fierce fighting are called “stimulants.””

This definition is intentionally a narrow one. It excludes the great majority of nourishing foods, for example, because a nourishing meal in itself produces, alongside a feeling of well-being, somnolence (sleepiness) rather than alertness and activity. It also excludes substances such as cannabis and opium (both occasionally taken as foods) that depress mental and physical activity: these are sedatives, not stimulants.

We must distinguish enhanced mental alertness from hallucination, the tendency to see what isn’t there; hallucinogens are, therefore, also excluded. Other exclusions include appetizers, which stimulate the appetite for food, and aphrodisiacs, which (to the extent that such foods really exist) stimulate sexual appetites and energies.

Using foods that have a stimulant effect provides ways of intentionally adjusting the body’s metabolism, which carries risks. There is a good reason why a nourishing meal produces sleepiness: after such a meal, the body is occupied with digestion. Postponing or interrupting that activity may produce digestive disturbance. In any case, increased alertness and physical activity will eventually be paid for in greater-than-usual exhaustion, and there may be other undesirable aftereffects. For example, it may be necessary to compensate for the aftereffects of stimulants by using them again. If the desired effect lessens after frequent use, increased quantities might be needed. In this way, regular use turns into dependence and addiction.

It is even more true of stimulants than of foods in general that their use is not independent of its social context, but no simple generalization is possible. Some of the foods discussed here are nearly always taken in company, as part of a social ritual. Some are nearly always taken as part of, or immediately before or after, a meal. Some, however, are customarily taken when one is not in company and not eating a meal; such habits may vary from one culture to another. External observers focusing on individual psychology may see the solitary use of stimulant foods as posing a personal, social, or criminal problem, while social use might be perceived as no problem or as a different kind of problem. Furthermore, observers focusing on social groups will find users of these stimulant foods to be unexpectedly protective, even nationalistic, about the preferred means of preparing them, which may vary widely.

Stimulant foods have been identified, like nearly all other foods and like many thousands of medicinal plants, in the course of very long-term unrecorded experiments: each human community explores its environment, notes animals and plants that may be of use, finds ways to use them, sometimes begins to farm them, and to trade in them. The stimulant effects of these foods were discovered empirically, as were their associated side-effects and dangers. In the last two centuries, chemists and nutrition scientists have identified their active constituents, making possible for the first time a scientific explanation of their effects.

In general, stimulant foods and drinks are either taken in a neutral vehicle, such as hot water, or they are slowly extracted by chewing. Nonfood stimulants are often taken as smoke or snuff. These various methods all ensure gradual absorption with relatively little interference from other foods. Alcoholic drinks are unusual because they are frequently taken without admixture and often contain strong flavorings: however, water is the principal constituent of most alcoholic drinks, and more water is often added.

Most traditional cultures had one, or at the most two, familiar stimulants. Globalization has changed this, producing such effects as the worldwide fashion for coffee; the worldwide marketing of chocolate, instant coffee, and the “cola” drinks; and the complex social interplay between alternative stimulants of almost equal status, neatly symbolized by the ritual question at breakfast in a French hotel, “Café? Thé? Chocolat?” (Coffee? Tea? Hot chocolate?)

Caffeine

Caffeine is among the commonest of stimulants worldwide. It is the chief active constituent in coffee and tea, which are familiar in practically every country, and in maté, guaraná, and cola nut, which are popular in South America and West Africa. It is present in smaller quantities in some other stimulant foods, including chocolate.

Coffee. Coffee consists of the roasted, ground beans of Coffea arabica. Native to Ethiopia, its use spread in late medieval times to Yemen; from there it rapidly became popular around the Mediterranean. Both Arabs and Europeans encouraged its further spread. Details of its use vary. Boiling water is added; commonly sugar is used as a flavoring, and sometimes milk or cream. Often coffee is drunk after meals, but it is also often taken between meals, both by groups as a social drink and by workers as a stimulant. Several substances have been used as coffee substitutes. Most of them had the advantages of being cheap and of tasting somewhat like coffee but the disadvantage of containing little or no caffeine. These substitutes have now been overtaken in popularity by instant coffee, a soluble product manufactured from the beans of Coffea robusta, which does contain caffeine.

Tea. Tea is made from the dried leaves of Camellia sinensis, native to southern China. The use of tea was already spreading beyond China in the ninth century; like coffee, it became popular in Europe in the seventeenth century and its use then spread worldwide. Again, like coffee, details of its use vary. Boiling water is usually poured onto the leaves, which are then allowed to steep for a few minutes. The resulting liquid is much lighter in flavor and color than coffee. Some add sugar to it: fewer, notably the British, add milk; some drink it iced. Tea is more often taken between meals than during meals; like coffee, it is used both as a social drink and by workers as a stimulant.

Caffeine beverages in South America. Maté, also called Paraguayan tea, is made by pouring boiling water onto the dried and roasted leaves of yerba maté (Ilex paraguariensis). Most of the leaves that are used come from wild trees gathered from the forests of southern South America. Maté is traditionally a social drink, made in a gourd or a silver pot and sucked through a shared straw or silver tube. It is drunk while still extremely hot, so added pleasure is provided by watching the reactions of unskillful foreigners who burn their lips and mouths while trying to drink it. It is usually taken without sugar, but sometimes orange zest is added as a flavoring. Maté is the national beverage of Argentina and Paraguay but has never spread beyond the region. The plant is a relative of European holly (Ilex aquifolium), whose leaves have occasionally been used to make a narcotic drink; more importantly, it is related to yaupon or Carolina tea (Ilex vomitoria) and other species that have been used to make stimulating and narcotic drinks by North Americans both before and after European settlement.

Guaraná (Paullinia cupana) is a tropical plant native to Brazil. Its seeds are traditionally roasted, pounded, and made into cakes called “Brazilian chocolate.” They have this name not because they can be eaten solid, like modern chocolate bars, but because in pre-Columbian Mexico travelers used to carry similar cakes of powdered cacao for use in making an instant chocolate drink. Like those, cakes of guaraná are traditionally crumbled into water by tired travelers in Brazil, making a stimulating drink particularly rich in caffeine. Guaraná is now also used as a flavoring for soda, candy, and liqueurs.

Caffeine in Africa. The cola nut, a rich source of caffeine, is the usual native stimulant of West and Central Africa. It might rather be called a seed, since eight or ten of them are found in each fruit of the trees Cola nitida and C. acuminata. These seeds are white, pink, or red: the white ones are said to be the best. They are customarily chewed before meals: they have a bitter flavor but, perhaps as a result of this, foods and drinks taken afterwards seem sweet (water, taken after cola, tastes “like white wine and sugar,” according to one observer). Apart from this effect as an appetizer, cola nuts have a high reputation among their traditional users, as stimulant, digestive, and aphrodisiac. Alongside caffeine, they contain theobromine (as does chocolate) and kolanin, a heart stimulant. Cola nuts can also be ground into powder and mixed with water as a drink, and cola extract is used to flavor sodas and candies: the names of Coca-Cola and Pepsi-Cola allude to cola nuts, which may well be an ingredient in these products.

Theobromine

Theobromine is the chief active ingredient in cacao beans, the seeds of the tropical tree Theobroma cacao. These beans, fermented, roasted, and ground, are the raw material for chocolate, the traditional stimulant of Mexico, familiar worldwide. In pre-Columbian civilizations, chocolate was used as a drink: the ground cacao was mixed into hot water, which was then poured from a height into the serving cup to produce the much-desired foam. Flavors (chili, vanilla, or others) and color (notably annatto) might be added. Popularized in Europe by the Spanish, chocolate became successively a sugary drink and a milky drink; many other flavorings were tried, including the cinnamon now favored in Mexico. Eventually (in the nineteenth century) chocolate was made into bars to be eaten solid, and in many countries this is now its most familiar form. In the Maya and Aztec civilizations, chocolate was a social drink, taken after dinner, serving as a stimulant (and, according to some, an aphrodisiac). Whole chocolate contains caffeine as well as theobromine, and it is also rich in cocoa butter, making it an extremely nourishing food and, therefore, unlikely to produce aftereffects such as exhaustion.

Nicotine

Tobacco, the fermented leaf of Nicotiana tabacum, is usually smoked; in that form it cannot be classified as a food. It can be chewed, however. In Western cultures, chewed tobacco has been typical of sailors and other manual workers subjected to extreme weather conditions that make smoking difficult. Tobacco’s active ingredient, nicotine, a deadly poison in the pure state, acts as a stimulant when slowly absorbed.

In Australia, another plant, Duboisia hopwoodii, has leaves and flowers very rich in nicotine. Aborigines dry and grind the leaves, mix them with the ash of certain other plants, and roll them into balls, called “pituri,” for chewing. These are used by solitary workers and travelers as a stimulant to stave off tiredness and hunger; they are also exchanged as a sign of friendship. They are, or were, used by warrior groups in preparation for a battle. There is a definite advantage in chewing ash in pituri (and also with coca and betel nut), because alkalis in the ash detach the active stimulant substance, in this case nicotine, from the plant acids, allowing it to be more rapidly absorbed. The use of ash in this way has developed, apparently independently, in Australia, southeastern Asia, and South America.

Cocaine

Coca is the dried leaf of a plant species native to western South America, Erythroxylum coca, and of a second species, E. novogranatense, which developed under cultivation. Coca leaves were known as a stimulant to the pre-Columbian peoples of the Andean region, and continued to be used by them and their Spanish conquerors. Their use is extremely widespread in South America. As with the nicotine plants, the principal use of coca leaves has been as a stimulant for workers and travelers. The usual way is to take some leaves, mix them with the ash of burnt coca or another wood, roll the mixture into a ball, and chew it. Coca leaves, like chocolate, are really nourishing, a property that tends to reduce the severity of the exhaustion that usually follows the use of stimulants. The active constituent of coca leaves was isolated (and named cocaine) in 1860. When taken in the pure form, cocaine was found to be a useful medicinal drug but also highly addictive. It was among the first stimulants to arouse strong medical and governmental disapproval. In the early twentieth century, many countries made it illegal. The name of Coca-Cola alludes to coca, and the early recipe for the product contained cocaine, like other soft drinks of the period.

Some other species of genus Erythroxylum contain cocaine or similar compounds and are used as stimulants by various South American peoples: E. cataractum by the Cubeo of Colombia; E. fimbriatum and E. macrophyllum by the Bora and Huitoto of Peru.

Other Stimulants

Betel. The commonest traditional stimulant of southern and southeastern Asia is betel. Like pituri and coca, betel is customarily made up as a chewing packet that includes ash. The active ingredient, arecoline, is contained in the areca nut or betel nut (the nut of the palm Areca catechu), which is cut into long narrow pieces and placed inside the packet along with a “lime” made from burnt coral and oyster shells. The packet is formed from a leaf of the betel pepper vine (Piper betle). In traditional households, the betel chews are made up each day from fresh supplies; as with pituri, it is a sign of friendship and hospitality to offer a chew to any visitor. The habitual chewing of betel eventually stains the mouth red and the teeth black. When it is first tried, betel can produce feelings of anxiety, excitement, and vertigo; to those who use it regularly, it is a mild stimulant.

Khat. Coffee, when it was introduced to Yemen from across the Red Sea, was not the country’s first stimulant. That position belongs to khat (or qat), the leaf of Catha edulis. Khat is used in Yemen, Saudi Arabia, and a large area of East Africa from Ethiopia and Somalia to Mozambique and South Africa. It had not spread outside the region until some Americans acquired the taste for it while they were in Somalia with United Nations troops during the early 1990s. Khat is often taken as a tea, made by pouring boiling water onto the dried or fresh leaves. Fresh leaves can also be chewed; in this form its effect is said to be stronger than coffee but not as strong as alcohol. When chewed, khat is often used socially because it enlivens conversation. The principal active constituent in khat is cathinone, now classified as an illegal drug in the United States; however, cathinone is only present in fresh leaves. The second active constituent, cathine, which is still present in the dried leaves, is an appetite suppressant.

A milder stimulant of the same general type is Mormon tea, the leaf of Ephedra nevadensis. These leaves contain the active ingredient pseudoephedrine, and are made into a tea with boiling water.

Kava. The root of the plant kava-kava, Piper methysticum, is the source of kava, a familiar stimulant used in Hawaii and other Pacific islands. The fresh root is chopped or ground and then soaked and squeezed in water to produce a milky, spicy liquid, which is traditionally served in half coconut shells. Kava is a social drink whose effect is to produce a condition physically resembling drunkenness, though with apparent clarity of mind. The principal active constituents are known as kavalactones.

Kratom. Kratom, a stimulant indigenous to Thailand and little known elsewhere, consists of the leaves of Mitragyna speciosa. These leaves can be smoked or made into a tea. The active constituent is mitragynine, which, like cocaine, is a stimulant at low doses but a narcotic at higher doses.

Alcohol

Alcohol is an atypical stimulant because it is not naturally present in any fresh plant. It is produced from the fermentation by yeast of plant sugars. One starting point is a fruit juice. Grape juice makes wine; apple juice makes (hard) cider; pear juice makes perry. Several other fruits are used in various parts of the world. A second starting point is malted cereal: barley is the commonest choice, and the result is beer. Plant saps can be used if they contain sufficient sugar: liquid cane sugar is so used in India, while pulque, a Mexican alcoholic drink, is made from the sap of the maguey (Agave atrovirens). Finally, honey, mixed with water, can be used, and the result is mead (a beverage that figures importantly in the Old English epic Beowulf ). There are two common adjustments to the process: adding cane or beet sugar to the original juice gives the yeast more raw material to work with, producing more alcohol; distilling the final product achieves much greater concentrations of alcohol, resulting in “hard liquor.”

Wine and beer are both ancient inventions, going back to southwestern Asia several thousand years B.C.E. But yeasts are naturally present in the air; therefore, alcoholic drinks might have been invented or discovered many times in human history; certainly, the origin of pulque is independent of those of wine and beer.

Alcoholic drinks have most generally, in traditional societies, been used as social drinks, and they have commonly been used in a ritualistic way as well. Their production is linked with the seasons (in general the required juices are available only when fruit is ripe, and the fermentation process takes time); therefore, by contrast with most other stimulants, the discovery of alcoholic drinks and the annual vintage (especially of wine) tend to be celebrated in major festivals. In many cultures, the ordinary, everyday consumption of alcohol follows precise rules, tending to ensure, for example, that everyone drinks equally. Both in the major festivals and in everyday social drinking, it is commonly the case that drunkenness is aimed at, at least to the extent of the loss of inhibitions, but sometimes going all the way to unconsciousness.

Like kava—and unlike many stimulants—alcohol tends to produce enhanced mental activity accompanied by physical incapacity. In traditional societies, travelers used coca, maté, guaraná, pituri, and other stimulants to keep them going; they would not use alcohol or kava till they had arrived. Likewise, coffee, tea, and some similar stimulants may enhance one’s ability to drive safely, for a certain period, while kava and alcohol impair it.

Source: http://www.answers.com/topic/stimulant?nr=1&lsc=true&cat=health

“Alcohol is no great friend to the athlete, nor is it to those on a weight-loss diet. Each gram of pure alcohol provides 7 Calories (7000 calories) of energy.”

In medicine, it is used as a tincture and antiseptic but its greatest use is in drinks. It is quickly absorbed into the bloodstream from the mouth cavity and stomach. After absorption, it acts as a depressant on the central nervous system. This may have the beneficial effect of reducing feelings of fatigue but it also reduces judgement, self-control, and concentration. Reactions are slowed by alcohol and muscular coordination is impaired. Alcohol also acts as a diuretic, stimulating the kidneys to eliminate more urine which can result in dehydration.

In addition, alcoholic beverages often contain sugar and other nutrients, increasing their calorific value. A single measure of spirits contains about 50 Calories, and one pint of lager contains about 170 Calories. Drinking too much alcohol can lead to obesity because some is converted to fat. Despite its relatively high energy content, alcohol is a poor energy source compared with carbohydrate because it cannot be used directly by muscles, and because of its adverse effects. Before it can be used by heart muscle and skeletal muscle, alcohol has to be broken down in the liver to acetate or acetaldehydes. The breakdown is relatively slow which is why alcohol can remain in the bloodstream for several hours. Alcohol can also inhibit the conversion of glycogen to glucose in the liver. If it is ingested during prolonged exercise it can increase the likelihood of hypoglycaemia (abnormally low blood sugar).

Moderate drinking has not been linked to any significant health problems. On the contrary, several studies have shown that it can be beneficial and may reduce the risk of coronary heart disease by preventing platelets in the blood from sticking together. However, chronic, heavy drinking is a significant health risk: it can shrink the brain; it irritates the stomach and small intestine, resulting in malabsorption and deficiencies of vitamins and minerals; it can damage the liver and cause cirrhosis; and it can adversely affect the cardiovascular system, increasing the risk of heart attacks. Heavy drinking is not compatible with a healthy, active lifestyle.

Alcoholism is a major cause of malnutrition. The reasons are threefold. First, alcohol interferes with central mechanisms that regulate food intake and causes food intake decreases. Second, alcohol is rich in energy (7.1 kcal/g), and like pure sugar most alcoholic beverages are relatively empty of nutrients. Increasing amounts of alcohol ingested lead to the consumption of decreasing amounts of other foods, making the nutrient content of the diet inadequate, even if total energy intake is sufficient. Thus chronic alcohol abuse causes primary malnutrition by displacing other dietary nutrients. Third, gastrointestinal and liver complications associated with alcoholism also interfere with digestion, absorption, metabolism, and activation of nutrients, and thereby cause secondary malnutrition.

It is important to note that although ethanol is rich in energy, its chronic consumption does not produce the expected gain in body weight. This may be attributed, in part, to damaged mitochondria and the resulting poor coupling of oxidation of fat metabolically utilizable with energy production. The microsomal pathways that oxidize ethanol may be partially responsible. These pathways produce heat rather than adenosine triphosphate (ATP) and thereby fail to couple ethanol oxidation to useful energy-rich intermediates such as ATP. Thus, perhaps because of these energy considerations, alcoholics with higher total caloric intake do not experience expected weight gain despite physical activity levels similar to those of the non-alcohol-consuming overweight population.

Source: http://www.answers.com/Alcohol?nr=1&lsc=true&cat=health

“Despite its presence in many energy drinks, taurine has not been shown to be energy-giving, however the results of the studies into taurine usage have shown that taurine might help to reduce muscle fatigue.”

In recent years, taurine has become a common ingredient in energy drinks. Taurine is often used in combination with bodybuilding supplements such as creatine and anabolic steroids, partly due to recent findings in mice that taurine alleviates muscle fatigue in strenuous workouts and raises exercise capacity. Taurine is also used in some contact lens solutions.

Taurine has also been shown in diabetic rats to decrease weight and decrease blood sugar.

Taurine is conjugated via its amino terminal group with the bile acids chenodeoxycholic acid and cholic acid to form the bile salts sodium taurochenodeoxycholate and sodium taurocholate (see bile). The low pKa (1.5) of taurine’s sulfonic acid group ensures that this moiety is negatively charged in the pH ranges normally found in the intestinal tract and thus improves the surfactant properties of the cholic acid conjugate. Taurine is the only known naturally occurring sulfonic acid.

Taurine has also been implicated in a wide array of other physiological phenomena including inhibitory neurotransmission, long-term potentiation in the striatum/hippocampus, membrane stabilization, feedback inhibition of neutrophil/macrophage respiratory bursts, adipose tissue regulation, and calcium homeostasis.

Recent studies show that taurine supplements taken by mice on a high-fat diet prevented them from becoming overweight. Studies have yet to be done on the effect of taurine on obesity in humans. Currently taurine is being tested as an anti-manic treatment for bipolar depression. Recent studies have also shown that taurine can influence (and possibly reverse) defects in nerve blood flow, motor nerve conduction velocity, and nerve sensory thresholds in experimental diabetic neuropathic rats. Taurine levels were found to be significantly lower in vegans than in a control group on a standard American diet. Plasma taurine was 78% of control values, and urinary taurine 29%.

Taurine is named after the Latin taurus, which means bull, as it was first isolated from ox bile in 1827 by Austrian scientists Friedrich Tiedemann and Leopold Gmelin. It is often called an amino acid, even in scientific literature, but as it lacks a carboxyl group it is not strictly an amino acid. It does contain a sulfonate group and may be called an amino sulfonic acid. Small polypeptides have been identified which contain taurine but to date no aminoacyl tRNA synthetase has been identified as specifically recognizing taurine and capable of incorporating it onto a tRNA. Also, while taurine is present in both bull semen and urine, the taurine used in energy drinks such as Red Bull is not taken from these sources.

Source: http://www.answers.com/Taurine

Healthy Energy (Part 2 – Facts about B12)

“Vitamin B-12 is important for the normal functioning of the brain and nervous system and for the formation of blood. It is normally involved in the metabolism of every cell of the body, especially affecting the DNA synthesis and regulation but also fatty acid synthesis and energy production.”

Vitamin B12 has the largest and most complex chemical structure of all the vitamins. It is unique among vitamins in that it contains a metal ion, cobalt. For this reason cobalamin is the term used to refer to compounds having vitamin B12 activity. Methylcobalamin and 5-deoxyadenosyl cobalamin are the forms of vitamin B12 used in the human body. The form of cobalamin used in most supplements, cyanocobalamin, is readily converted to 5-deoxyadenosyl and methylcobalamin in the body. In mammals, cobalamin is a cofactor for only two enzymes, methionine synthase and L-methylmalonyl-CoA mutase.

Function

Cofactor for methionine synthase

Methylcobalamin is required for the function of the folate-dependent enzyme, methionine synthase. This enzyme is required for the synthesis of the amino acid, methionine, from homocysteine. Methionine in turn is required for the synthesis of S-adenosylmethionine, a methyl group donor used in many biological methylation reactions, including the methylation of a number of sites within DNA and RNA. Methylation of DNA may be important in cancer prevention. Inadequate function of methionine synthase can lead to an accumulation of homocysteine, which has been associated with increased risk of cardiovascular diseases (diagram).

Cofactor for L-methylmalonyl-CoA mutase

5-Deoxyadenosylcobalamin is required by the enzyme that catalyzes the conversion of L-methylmalonyl-CoA to succinyl-CoA. This biochemical reaction plays an important role in the production of energy from fats and proteins. Succinyl CoA is also required for the synthesis of hemoglobin, the oxygen carrying pigment in red blood cells.

Pernicious anemia

Pernicious anemia has been estimated to be present in approximately 2% of individuals over 60. Although anemia is often a symptom, the condition is actually the end stage of an autoimmune inflammation of the stomach, resulting in destruction of stomach cells by one’s own antibodies. Progressive destruction of the cells that line the stomach causes decreased secretion of acid and enzymes required to release food-bound vitamin B12. Antibodies to intrinsic factor (IF) bind to IF preventing formation of the IF-B12 complex, further inhibiting vitamin B12 absorption. If the body’s vitamin B12 stores are adequate prior to the onset of pernicious anemia, it may take years for symptoms of deficiency to develop. About 20% of the relatives of pernicious anemia patients also have pernicious anemia, suggesting a genetic predisposition. Treatment of pernicious anemia generally requires injections of vitamin B12 to bypass intestinal absorption. High-dose oral supplementation is another treatment option, because consuming 1,000 mcg (1 mg)/day of vitamin B12 orally should result in the absorption of about 10 mcg/day (1% of dose) by passive diffusion. In fact, high-dose oral therapy is considered to be as effective as intramuscular injection.

Food-bound vitamin B12 malabsorption

Food-bound vitamin B12 malabsorption is defined as an impaired ability to absorb food or protein-bound vitamin B12, although the free form is fully absorbable. In the elderly, food-bound vitamin B12 malabsorption is thought to result mainly from atrophic gastritis, a chronic inflammation of the lining of the stomach that ultimately results in the loss of glands in the stomach (atrophy) and decreased stomach acid production. Because stomach acid is required for the release of vitamin B12 from the proteins in food, vitamin B12 absorption is diminished. Decreased stomach acid production also provides an environment conducive to the overgrowth of anaerobic bacteria in the stomach, which further interferes with vitamin B12 absorption. Because vitamin B12 in supplements is not bound to protein, and because intrinsic factor (IF) is still available, the absorption of supplemental vitamin B12 is not reduced as it is in pernicious anemia. Thus, individuals with food-bound vitamin B12 malabsorption do not have an increased requirement for vitamin B12; they simply need it in the crystalline form found in fortified foods and dietary supplements.

Atrophic gastritis

Atrophic gastritis is thought to affect 10%-30% of people over 60 years of age, and the condition is frequently associated with infection by the bacteria, Heliobacter pylori. H. pylori infection induces chronic inflammation of the stomach, which may progress to peptic ulcer disease, atrophic gastritis, and/or gastric cancer in some individuals. The relationship of H. pylori infection to atrophic gastritis, gastric cancer, and vitamin B12 deficiency is presently an area of active research.

Other causes of vitamin B12 deficiency

Other causes of vitamin B12 deficiency include surgical resection of the stomach or portions of the small intestine where receptors for the IF-B12 complex are located. Conditions affecting the small intestine, such as malabsorption syndromes (celiac disease and tropical sprue), may also result in vitamin B12 deficiency. Because the pancreas provides critical enzymes as well as calcium required for vitamin B12 absorption, pancreatic insufficiency may contribute to B12 deficiency. Since vitamin B12 is found only in foods of animal origin, a strict vegetarian (vegan) diet has resulted in cases of vitamin B12 deficiency. Alcoholics may experience reduced intestinal absorption of vitamin B12. Individuals with acquired immunodeficiency syndrome (AIDS) appear to be at increased risk of deficiency, possibly related to a failure of the IF-B12 receptor to take up the IF-B12 complex. Long-term use of acid-reducing drugs has also been implicated in vitamin B12 deficiency (see Drug interactions).

Symptoms of vitamin B12 deficiency

Vitamin B12 deficiency results in impairment of the activities of B12-requiring enzymes. Impaired activity of methionine synthase may result in elevated homocysteine levels, while impaired activity of L-methylmalonyl-CoA mutase results in increased levels of a metabolite of methylmalonyl-CoA called methylmalonic acid (MMA). Individuals with mild vitamin B12 deficiency may not experience symptoms, although blood levels of homocysteine and/or MMA may be elevated.

Megaloblastic anemia

Diminished activity of methionine synthase in vitamin B12 deficiency inhibits the regeneration of tetrahydrofolate (THF) and traps folate in a form that is not usable by the body, resulting in symptoms of folate deficiency even in the presence of adequate folate levels. Thus, in both folate and vitamin B12 deficiencies, folate is unavailable to participate in DNA synthesis. This impairment of DNA synthesis affects the rapidly dividing cells of the bone marrow earlier than other cells, resulting in the production of large, immature, hemoglobin-poor red blood cells. The resulting anemia is known as megaloblastic anemia and is the symptom for which the disease, pernicious anemia, was named. Supplementation with folic acid will provide enough usable folate to restore normal red blood cell formation. However, if vitamin B12 deficiency is the cause, it will persist despite the resolution of the anemia. Thus, megaloblastic anemia should not be treated with folic acid until the underlying cause has been determined.

Neurologic symptoms

The neurologic symptoms of vitamin B12 deficiency include numbness and tingling of the arms and, more commonly, the legs, difficulty walking, memory loss, disorientation, and dementia with or without mood changes. Although the progression of neurologic complications is generally gradual, such symptoms are not always reversible with treatment of vitamin B12 deficiency, especially if they have been present for a long time. Neurologic complications are not always associated with megaloblastic anemia and are the only clinical symptom of vitamin B12 deficiency in about 25% of cases. Although vitamin B12 deficiency is known to damage the myelin sheath covering cranial, spinal, and peripheral nerves, the biochemical processes leading to neurological damage in B12 deficiency are not well understood.

Gastrointestinal symptoms

Tongue soreness, appetite loss, and constipation have also been associated with vitamin B12 deficiency. The origins of these symptoms are unclear, but they may be related to the stomach inflammation underlying some cases of B12 deficiency, or to the increased vulnerability of rapidly dividing gastrointestinal cells to impaired DNA synthesis.

Homocysteine and cardiovascular disease

The results of more than 80 studies indicate that even moderately elevated levels of homocysteine in the blood increase the risk of cardiovascular diseases, though the mechanism by which homocysteine increases the disease risk remains the subject of a great deal of research. The amount of homocysteine in the blood is regulated by at least three vitamins: folate, vitamin B12, and vitamin B6 (diagram). Analysis of the results of 12 homocysteine-lowering trials showed folic acid supplementation (0.5-5 mg/day) had the greatest lowering effect on blood homocysteine levels (25% decrease); co-supplementation with folic acid and vitamin B12 (mean 0.5 mg/day or 500 mcg/day) provided an additional 7% reduction (32% decrease) in blood homocysteine concentrations. The results of a sequential supplementation trial in 53 men and women indicated that after folic acid supplementation, vitamin B12 became the major determinant of plasma homocysteine levels. Some evidence indicates that vitamin B12 deficiency is a major cause of elevated homocysteine levels in people over the age of 60. Two studies found blood methylmalonic acid (MMA) levels to be elevated in more than 60% of elderly individuals with elevated homocysteine levels. An elevated MMA level in conjunction with elevated homocysteine, in the absence of impaired kidney function, suggests either a vitamin B12 deficiency or a combined B12 and folate deficiency. Thus, it is important to evaluate vitamin B12 status as well as kidney function in older individuals with elevated homocysteine levels prior to initiating homocysteine-lowering therapy. For more information regarding homocysteine and cardiovascular diseases, see the article on folic acid.

Although increased intake of folic acid and vitamin B12 has been found to decrease homocysteine levels, it is not presently known whether increasing intake of these vitamins will translate to reductions in risk for cardiovascular diseases. However, several randomized placebo-controlled trials are presently being conducted to determine whether homocysteine lowering through folic acid and other B vitamin supplementation reduces the incidence of cardiovascular diseases. A meta-analysis of data from four of the ongoing trials shows that B vitamin supplementation had no significant effect on risk of coronary heart disease or stroke, but only about 14,000 participants were included in analysis and thus any conclusions are limited. Nevertheless, the completion of ongoing clinical trials should help to answer whether or not supplemental B vitamins lower risk for cardiovascular diseases.

Cancer

Folate is required for synthesis of DNA, and there is evidence that decreased availability of folate results in strands of DNA that are more susceptible to damage. Deficiency of vitamin B12 traps folate in a form that is unusable by the body for DNA synthesis. Both vitamin B12 and folate deficiencies result in a diminished capacity for methylation reactions (diagram). Thus, vitamin B12 deficiency may lead to an elevated rate of DNA damage and altered methylation of DNA, both of which are important risk factors for cancer. A recent series of studies in young adults and older men indicated that increased levels of homocysteine and decreased levels of vitamin B12 in the blood were associated with a biomarker of chromosome breakage in white blood cells. In a double- blind, placebo-controlled study, the same biomarker of chromosome breakage was minimized in young adults who were supplemented with 700 mcg of folic acid and 7 mcg of vitamin B12 daily in cereal for two months.

Breast cancer

A case-control study compared prediagnostic levels of serum folate, vitamin B6, and vitamin B12 in 195 women later diagnosed with breast cancer and 195 age-matched women who were not diagnosed with breast cancer. Among women who were postmenopausal at the time of blood donation, the association between blood levels of vitamin B12 and breast cancer suggested a threshold effect. The risk of breast cancer was more than doubled in women with serum vitamin B12 levels in the lowest quintile (1/5) compared to women in the four highest quintiles. The investigators found no relationship between breast cancer and serum levels of vitamin B6, folate, or homocysteine. A case-control study in Mexican women (475 cases and 1,391 controls) reported that breast cancer risk for women in the highest quartile (1/4) of vitamin B12 intake was 68% lower than those in the lowest quartile. Stratification of the data revealed that the inverse association between dietary vitamin B12 intake and breast cancer risk was stronger in postmenopausal women compared to premenopausal women, though both associations were statistically significant. Because these studies were observational, it cannot be determined whether decreased serum levels of vitamin B12 or low dietary vitamin B12 intakes were a cause or a result of breast cancer. Previously, there has been little evidence to suggest a relationship between vitamin B12 status and breast cancer risk. However, high dietary folate intakes have been associated with reduced risk for breast cancer in several studies, and some studies have reported that vitamin B12 intake may modify this association.

Neural tube defects

Neural tube defects (NTD) may result in anencephaly or spina bifida, devastating and sometimes fatal birth defects. The defects occur between the 21st and 27th days after conception, a time when many women do not realize they are pregnant. Randomized controlled trials have demonstrated 60% to 100% reductions in NTD cases when women consumed folic acid supplements in addition to a varied diet during the month before and the month after conception. Increasing evidence indicates that the homocysteine-lowering effect of folic acid plays a critical role in lowering the risk of NTD. Homocysteine may accumulate in the blood when there is inadequate folate and/or vitamin B12 for effective functioning of the methionine synthase enzyme. Decreased vitamin B12 levels in the blood and amniotic fluid of pregnant women have been associated with an increased risk of NTD, suggesting that adequate vitamin B12 intake in addition to folic acid may be beneficial in the prevention of NTD.

Alzheimer’s disease and dementia

Individuals with Alzheimer’s disease often have low blood levels of vitamin B12. One study found lower vitamin B12 levels in the cerebrospinal fluid of patients with Alzheimer’s disease than in patients with other types of dementia, though blood levels of vitamin B12 did not differ. The reason for the association of low vitamin B12 status with Alzheimer’s disease is not clear. Vitamin B12 deficiency, like folate deficiency, may lead to decreased synthesis of methionine and S-adenosylmethionine, thereby adversely affecting methylation reactions. Methylation reactions are essential for the metabolism of components of the myelin sheath of nerve cells as well as neurotransmitters. Also, moderately increased homocysteine levels as well as decreased folate and vitamin B12 levels have been associated with Alzheimer’s disease and vascular dementia.

Some but not all studies have associated elevated homocysteine concentrations or decreased serum levels of vitamin B12 with an increased risk of Alzheimer’s disease. A case-control study of 164 patients with dementia of Alzheimer’s type included 76 cases in which the diagnosis of Alzheimer’s disease was confirmed by examination of brain cells after death. Compared to 108 control subjects without evidence of dementia, subjects with dementia of Alzheimer’s type and confirmed Alzheimer’s disease had higher blood homocysteine levels and lower blood levels of folate and vitamin B12. Measures of general nutritional status indicated that the association of increased homocysteine levels and diminished vitamin B12 status with Alzheimer’s disease was not due to dementia-related malnutrition. In another study, low serum vitamin B12 (< 150 pmol/L) or folate (< 10 nmol/L) levels were associated with a doubling of the risk of developing Alzheimer’s disease in 370 elderly men and women followed over three years. In a sample of 1,092 men and women without dementia followed for an average of ten years, those with higher plasma homocysteine levels at baseline had a significantly higher risk of developing Alzheimer’s disease and other types of dementia. Specifically, those with plasma homocysteine levels greater than 14 micromol/L had nearly double the risk of developing Alzheimer’s disease. A study in 650 elderly men and women reported that the risk of elevated plasma homocysteine levels was significantly higher in those with lower cognitive function scores. A prospective study in 816 elderly men and women reported that those with elevated homocysteine levels (> 15 micromol/L) had a significantly higher risk of developing Alzheimer’s disease or dementia, but vitamin B12 status was not related to risk of Alzheimer’s disease or dementia in this study. Similarly, another prospective study in 965 older adults found that vitamin B12 status was not related to the risk of Alzheimer’s disease. Further, a prospective study in 1,041 older adults, followed for a median of 3.9 years, found that vitamin B12 dietary intake was not associated with risk of developing Alzheimer’s disease.

B vitamin supplementation is commonly used to treat hyperhomocysteinemia. A recent randomized, double-blind, placebo-controlled clinical trial in 253 older individuals with plasma homocysteine concentrations equal to or greater than 13 micromol/L found that daily B vitamin supplementation (1 mg folic acid, 0.5 mg vitamin B12, and 10 mg vitamin B6) for two years did not affect measures of cognitive performance despite an average 4.36 micromol/L reduction in plasma homocysteine concentrations (33). Another randomized, double-blind, placebo-controlled study in 195 elderly adults reported that oral vitamin B12 supplementation (1 mg daily) for six months had no effect on measures of cognitive function. Several of the homocysteine-lowering trials primarily focused on assessing cardiovascular disease risk will also assess measures of cognitive function. Thus, the findings of these ongoing trials may provide insight into whether long-term B vitamin supplementation is protective against dementia.

Depression

Observational studies have found as many as 30% of patients hospitalized for depression are deficient in vitamin B12. A cross-sectional study of 700 community-living, physically disabled women over the age of 65 found that vitamin B12 deficient women were twice as likely to be severely depressed as non-deficient women. A population-based study in 3,884 elderly men and women with depressive disorders found that those with vitamin B12 deficiency were almost 70% more likely to experience depression than those with normal vitamin B12 status. The reasons for the relationship between vitamin B12 deficiency and depression are not clear but may involve S-adenosylmethionine (SAMe). Vitamin B12 and folate are required for the synthesis of SAMe, a methyl group donor essential for the metabolism of neurotransmitters whose bioavailability has been related to depression. This hypothesis is supported by several studies that have shown supplementation with SAMe improves depressive symptoms. Because few studies have examined the relationship of vitamin B12 status and the development of depression over time, it cannot yet be determined if vitamin B12 deficiency plays a causal role in depression. However, due to the high prevalence of vitamin B12 deficiency in older individuals, it may be beneficial to screen for vitamin B12 deficiency as part of a medical evaluation for depression.

Sources

Food sources

Only bacteria can synthesize vitamin B12. Vitamin B12 is present in animal products such as meat, poultry, fish (including shellfish), and to a lesser extent milk, but it is not generally present in plant products or yeast. Fresh pasteurized milk contains 0.9 mcg per cup and is an important source of vitamin B12 for some vegetarians. Those vegetarians who eat no animal products need supplemental vitamin B12 to meet their requirements. Also, individuals over the age of 50 should obtain their vitamin B12 in supplements or fortified foods like fortified cereal because of the increased likelihood of food-bound vitamin B12 malabsorption.

Most people do not have a problem obtaining the RDA of 2.4 mcg/day of vitamin B12 in food. In the United States, the average intake of vitamin B12 is about 4.5 mcg/day for young adult men, and 3 mcg/day for young adult women. In a sample of adults over the age of 60, men were found to have an average dietary intake of 3.4 mcg/day and women had an average dietary intake of 2.6 mcg/day. Some foods with substantial amounts of vitamin B12 are listed in the table below along with their vitamin B12 content in micrograms (mcg). For more information on the nutrient content of specific foods, search the USDA food composition database.

Supplements

Cyanocobalamin is the principal form of vitamin B12 used in supplements but methylcobalamin is also available as a supplement. Cyanocobalamin is available by prescription in an injectable form and as a nasal gel for the treatment of pernicious anemia. Over-the-counter preparations containing cyanocobalamin include multivitamin, vitamin B-complex, and vitamin B12 supplements.

Safety

Toxicity

No toxic or adverse effects have been associated with large intakes of vitamin B12 from food or supplements in healthy people. Doses as high as 1 mg (1000 mcg) daily by mouth or 1 mg monthly by intramuscular (IM) injection have been used to treat pernicious anemia without significant side effects. When high doses of vitamin B12 are given orally, only a small percentage can be absorbed, which may explain the low toxicity. Because of the low toxicity of vitamin B12, no tolerable upper intake level (UL) was set by the Food and Nutrition Board in 1998 when the RDA was revised.

Drug interactions

A number of drugs reduce the absorption of vitamin B12. Proton pump inhibitors (e.g., omeprazole and lansoprazole), used for therapy of Zollinger-Ellison syndrome and gastroesophageal reflux disease (GERD), markedly decrease stomach acid secretion required for the release of vitamin B12 from food but not from supplements. Long-term use of proton pump inhibitors has been found to decrease blood vitamin B12 levels. However, vitamin B12 deficiency does not generally develop until after at least three years of continuous therapy. Another class of gastric acid inhibitors known as H2-receptor antagonists (e.g., Tagamet, Pepsid, Zantac), often used to treat peptic ulcer disease, has also been found to decrease the absorption of vitamin B12 from food. Because inhibition of gastric acid secretion is not as prolonged as with proton pump inhibitors H2-receptor antagonists have not been found to cause overt vitamin B12 deficiency even after long-term use. Individuals taking drugs that inhibit gastric acid secretion should consider taking vitamin B12 in the form of a supplement because gastric acid is not required for its absorption. Other drugs found to inhibit vitamin B12 absorption from food include cholestyramine (a bile acid-binding resin used in the treatment of high cholesterol), chloramphenicol and neomycin (antibiotics), and colchicine (anti-gout medicine). Metformin, a medication for individuals with type 2 (non-insulin dependent) diabetes, decreases vitamin B12 absorption by tying up free calcium required for absorption of the IF-B12 complex. This effect is correctable by drinking milk or taking calcium carbonate tablets along with food or supplements. Previous reports that megadoses of vitamin C destroy vitamin B12 have not been supported and may have been an artifact of the assay used to measure vitamin B12 levels.

Nitrous oxide, a commonly used anesthetic, inhibits both of the vitamin B12- dependent enzymes and can produce many of the clinical features of vitamin B12 deficiency, such as megaloblastic anemia or neuropathy. Because nitrous oxide is commonly used for surgery in the elderly, some experts feel vitamin B12 deficiency should be ruled out prior to its use.

Large doses of folic acid given to an individual with an undiagnosed vitamin B12 deficiency could correct megaloblastic anemia without correcting the underlying vitamin B12 deficiency, leaving the individual at risk of developing irreversible neurologic damage. For this reason the Food and Nutrition Board of the Institute of Medicine advises that all adults limit their intake of folic acid (supplements and fortification) to 1000 mcg (1 mg) daily.

Linus Pauling Institute Recommendation

A varied diet should provide enough vitamin B12 to prevent deficiency in most individuals 50 years of age and younger. Individuals over the age of 50, strict vegetarians, and women planning to become pregnant should take a multivitamin supplement daily or eat a fortified breakfast cereal, which would ensure a daily intake of 6 to 30 mcg of vitamin B12 in a form that is easily absorbed. Higher doses of vitamin B12 supplements are recommended for patients taking medications that interfere with its absorption (see Drug interactions).

Older adults (> 50 years)

Because vitamin B12 malabsorption and vitamin B12 deficiency are more common in older adults, some respected nutritionists recommend that adults older than 50 years take 100 to 400 mcg/day of supplemental vitamin B12, an amount provided by a number of vitamin B-complex supplements.

Source: http://lpi.oregonstate.edu/infocenter/vitamins/vitaminB12/

“B-12 is the most chemically complex of all the vitamins.”

Structure

B-12 is the most chemically complex of all the vitamins. The structure of B-12 is based on a corrin ring, which is similar to the porphyrin ring found in heme, chlorophyll, and cytochrome. The central metal ion is Co (cobalt). Four of the six coordination sites are provided by the corrin ring, and a fifth by a dimethylbenzimidazole group. The sixth coordination site, the center of reactivity, is variable, being a cyano group (-CN), a hydroxyl group (-OH), a methyl group (-CH3) or a 5′-deoxyadenosyl group (here the C5′ atom of the deoxyribose forms the covalent bond with Co), respectively, to yield the four B-12 forms mentioned above. The covalent C-Co bond is one of first examples of carbon-metal bonds in biology. The hydrogenases and, by necessity, enzymes associated with cobalt utilization, involve metal-carbon bonds.

Synthesis

Vitamin B-12 cannot be made by plants or animals, as the only type of organism that have the enzymes required for the synthesis of B-12 is bacteria. The total synthesis of B-12 was reported by Robert Burns Woodward and Albert Eschenmoser, and remains one of the classic feats of total synthesis.

Species from the following genera are known to synthesize B-12: Aerobacter, Agrobacterium, Alcaligenes, Azotobacter, Bacillus, Clostridium, Corynebacterium, Flavobacterium, Micromonospora, Mycobacterium, Nocardia, Propionibacterium, Protaminobacter, Proteus, Pseudomonas, Rhizobium, Salmonella, Serratia, Streptomyces, Streptococcus and Xanthomonas. Industrial production of B-12 is through fermentation of selected microorganisms. The most used species are Pseudomonas denitrificans and Propionibacterium shermanii, often genetically engineered and grown under special conditions to enhance yield.

Functions

Coenzyme B-12’s reactive C-Co bond participates in two types of enzyme-catalyzed reactions.

Rearrangements in which a hydrogen atom is directly transferred between two adjacent atoms with concomitant exchange of the second substituent, X, which may be a carbon atom with substituents, an oxygen atom of an alcohol, or an amine.

Methyl (-CH3) group transfers between two molecules.

In humans, only two corresponding coenzyme B-12-dependent enzymes are known:

Methylmalonyl Coenzyme A mutase (MUT) which uses the AdoB-12 form and reaction type 1 to catalyze a carbon skeleton rearrangement (the X group is -COSCoA). MUT’s reaction converts MMl-CoA to Su-CoA, an important step in the extraction of energy from proteins and fats (for more see MUT’s reaction mechanism). This functionality is lost in vitamin B-12 deficiency, and can be measured clinically as an increased methylmalonic acid (MMA) level. Unfortunately, an elevated MMA, though sensitive to B-12 deficiency, is probably overly sensitive, and not all who have it actually have B-12 deficiency. For example, MMA is elevated in 90-98% of patients with B-12 deficiency; however 25-20% of patients over the age of 70 have elevated levels of MMA, yet 25-33% of them do not have B-12 deficiency. For this reason, MMA is not routinely recommended in the elderly. The “gold standard” test for B-12 deficiency continues to be low blood levels of the vitamin.

The MUT function cannot be affected by folate supplementation, and which is necessary for myelin synthesis (see mechanism below) and certain other functions of the central nervous system. Other functions of B-12 related to DNA synthesis related to MTR dysfunction (see below) can often be corrected with supplementation with the vitamin folic acid, but not the elevated levels of homocysteine, which is normally converted to methionine by MTR.

5-methyltetrahydrofolate-homocysteine methyltransferase (MTR), also known as methionine synthase. This is a methyl transfer enzyme, which uses the MeB-12 and reaction type 2 to catalyze the conversion of the amino acid Hcy back into Met (for more see MTR’s reaction mechanism).[13] This functionality is lost in vitamin B-12 deficiency, and can be measured clinically as an increased homocysteine level in vitro. Increased homocysteine can also be caused by a folic acid deficiency, since B-12 helps to regenerate the tetrahydrofolate (THF) active form of folic acid. Without B-12, folate is trapped as 5-methyl-folate, from which THF cannot be recovered unless a MTR process reacts the 5-methyl-folate with homocysteine to produce methionine and THF, thus decreasing the need for fresh sources of THF from the diet. THF may be produced in the conversion of homocysteine to methionine, or may be obtained in the diet. It is converted by a non-B12-dependent process to 5,10-methylene-THF, which is involved in the synthesis of thymine. Reduced availability of 5,10-methylene-THF results in problems with DNA synthesis, and ultimately in ineffective production cells with rapid turnover, in particular blood cells, and also intestinal wall cells which are responsible for absorption. The failure of blood cell production results in the once-dreaded and fatal disease, pernicious anemia. All of the DNA synthetic effects, including the megaloblastic anemia of pernicious anemia, resolve if sufficient folate is present (since levels of 5,10-methylene-THF still remain adequate with enough dietary folate). Thus the best known function of B-12 (that which is indirectly involved with DNA synthesis and restoration of cell-division and anemia) is actually a facultative function which is mediated by B-12 conservation of active folate which can be used for DNA production.

If folate is present in quantity, then of the two absolutely B-12 dependent reactions, the MUT reaction shows the most direct and characteristic secondary effects, focusing on the nervous system. Since the late 1990’s folic acid has begun to be added to fortify flour in many countries, so that folate deficiency is now more rare. At the same time, since DNA synthetic-sensitive tests for anemia and erythrocyte size are routinely done in even simple medical test clinics (so that these folate mediated-biochemical effects are more often directly detected), the MTR dependent effects of B-12 deficiency are becoming apparent not as anemia (as they were classically), but now mainly as an elevation of homocysteine in the blood and urine (homocysteinuria). This condition may result in long term damage to arteries and in clotting (stroke and heart attack), but is difficult to separate from other processes associated with atherosclerosis and aging.

The B-12 dependent MTR reactions may have neurological effects through an indirect mechanism. Adequate methionine (which must otherwise be obtained in the diet) is needed to make S-adenosyl-methionine, which is in turn necessary for methylation of myelin sheath phospholipids. In addition, SAMe is involved in the manufacture of certain neurotransmitters, catecholamines and in brain metabolism. These neurotransmitters are important for maintaining mood, possibly explaining why depression is associated with B-12 deficiency. Methylation of the myelin sheath phospholipids may also depend on adequate folate, which in turn is dependent on MTR recycling, unless ingested in relatively high amounts.

The specific myelin damage resulting from from B-12 deficiency has also been connected to B-12 reactions related to MUT, which is needed to convert methylmalonyl coenzyme A into succinyl coenzyme A. Failure of this second reaction to occur results in elevated levels of methylmalonic acid (MMA), a myelin destabilizer. Excessive MAA will prevent normal fatty acid synthesis, or it will be incorporated into fatty acid itself rather than normal malonic acid. If this abnormal fatty acid subsequently is incorporated into myelin, the resulting myelin will be too fragile, and demyelination will occur. Although the precise methanism(s) are not known with certainty, the result is subacute combinded degeneration of central nervous system and spinal cord. [15] Whatever the cause, it is known that B-12 deficiency causes neuropathies, even if folic acid is present in good supply, and therefore anemia is not present.

Human absorption and distribution

The human physiology of vitamin B-12 is complex, and therefore is prone to mishaps leading to vitamin B-12 deficiency. The vitamin as it occurs in foods enters the digestive tract bound to proteins, known as salivary R-binders. Stomach proteolysis of these proteins requires an acid pH, and also requires proper pancreatic release of proteolytic enzymes. (Even small amounts of B-12 taken in supplements bypasses these steps and thus any need for gastric acid, which may be blocked by antacid drugs).

The free B-12 then attaches to gastric intrinsic factor, which is generated by the gastric parietal cells. If this step fails due to gastric parietal cell atrophy (the problem in pernicious anemia), sufficient B-12 is not absorbed later on, unless administered orally in relatively massive doses (500 to 1000 mcg/day).

The conjugated vitamin B-12-intrinsic factor complex (IF/B-12) is then normally absorbed by the terminal ileum of the small bowel. Absorption of food vitamin B-12 therefore requires an intact and functioning stomach, exocrine pancreas, intrinsic factor, and small bowel. Problems with any one of these organs makes a vitamin B-12 deficiency possible.

Once the IF/B-12 complex is recognized by specialized ileal receptors, it is transported into the portal circulation. The vitamin is then transferred to transcobalamin II (TC-II/B12), which serves as the plasma transporter of the vitamin. Genetic deficiencies of this protein are known, also leading to functional B-12 deficiency.

For the vitamin to serve inside cells, the TC-II/B-12 complex must bind to a cell receptor, and be endocytosed. The transcobalamin-II is degraded within a lysozyme, and the B-12 is finally released into the cytoplasm, where it may be transformed into the proper coenzyme, by certain cellular enzymes (see above).

Hereditary defects in production of the transcobalamins and their receptors may produce functional deficiencies in B-12 and infantile megaloblastic anemia, and abnormal B-12 related biochemistry, even in some cases with normal blood B-12 levels.

The total amount of vitamin B-12 stored in body is about 2,000-5,000 mcg in adults. Around 80% of this is stored in the liver. 0.1 % of this is lost per day by secretions into the gut as not all these secretions are reabsorbed. How fast B-12 levels change depends on the balance between how much B12 is obtained from the diet, how much is secreted and how much is absorbed. B-12 deficiency may arise in a year if initial stores are low and genetic factors unfavourable or may not appear for decades. In infants, B-12 deficiency can appear much more quickly.

History of B-12 as a treatment for pernicious anemia

B-12 deficiency is the cause of pernicious anemia, a usually-fatal disease of unknown etiology when it was first described in medicine. The cure was discovered by accident. George Whipple had been inducing anemia in dogs by bleeding them, and then conducting experiments in which he fed them various foods to observe which diets allowed them fastest recovery from the anemia produced. In the process, he discovered that ingesting large amounts of liver seemed to most-rapidly cure the anemia of blood loss, and hypothesized that therefore liver ingestion be tried for pernicious anemia, an anemic disease of the time with no known cause or cure. He tried this and reported some signs of success in 1920. After a series of careful clinical studies George Minot and William Murphy set out to partly isolate the substance in liver which cured anemia in dogs, and found that it was iron. They found further that the partly isolated water-soluble liver-substance which cured pernicious anemia in humans, was something else entirely different — and which had no effect at all on canines under the conditions used. The specific factor treatment for pernicious anemia, found in liver juice, had been found by this coincidence. These experiments were reported by Minot and Murphy in 1926, marking the date of the first real progress with this disease, though for several years, patients were still required to eat large amounts of raw liver or to drink considerable amounts of liver juice.

In 1928, the chemist Edwin Cohn prepared a liver extract that was 50 to 100 times more potent than the natural liver products. The extract was the first workable treatment for the disease. For their initial work in pointing the way to a working treatment, Whipple, Minot, and Murphy shared the 1934 Nobel Prize in Physiology or Medicine.

The active ingredient in liver was not isolated until 1948 by the chemists Karl A. Folkers of the United States and Alexander R. Todd of Great Britain. The substance was a cobalamin called vitamin B-12. It could also be injected directly into muscle, making it possible to treat pernicious anemia more easily.

The chemical structure of the molecule was determined by Dorothy Crowfoot Hodgkin and her team in 1956, based on crystallographic data. Eventually, methods of producing the vitamin in large quantities from bacteria cultures were developed in the 1950’s, and these led to the modern form of treatment for the disease.

Symptoms and damage from deficiency

Vitamin B-12 deficiency can potentially cause severe and irreversible damage, especially to the brain and nervous system. At levels only slightly lower than normal, a range of symptoms such as fatigue, depression, and poor memory may be experienced. However, these symptoms by themselves are too nonspecific to diagnose deficiency of the vitamin.

Vitamin B-12 deficiency has the following pathomorphology and symptoms:

Pathomorphology includes: A spongiform state of neural tissue along with edema of fibers and deficiency of tissue. The myelin decays, along with axial fiber. In later phases, fibric sclerosis of nervous tissues occurs. Those changes apply to dorsal parts of the spinal cord, and to pyramidal tracts in lateral cords.

In the brain itself, changes are less severe: they occur as small sources of nervous fibers decay and accumulation of Astrocytes, usually subcortically located, an also round hemorrhages with a torus of glial cells. Pathological changes can be noticed as well in the posterior roots of the cord and, to lesser extent, in peripheral nerves.

Clinical symptoms : The main syndrome of vitamin B-12 deficiency is Addison’s and Biermer’s disease. It is characterized by a triad of symptoms:

1) anemia with bone marrow promegaloblastosis (Megaloblastic anemia) 2) gastrointestinal symptoms; 3) neurological symptoms.

Each of those symptoms can occur either alone or along with others. The neurological complex, defined as myelosis funicularis, consists of the following symptoms: 1) impaired perception of deep touch, pressure and vibration, abolishment of sense of touch, very annoying and persistent paresthesias; 2) ataxia of dorsal cord type; 3) decrease or abolishment of deep muscle-tendon reflexes; 4) pathological reflexes – Babinski, Rossolimo and others, also severe paresis.

During the course of disease, mental disorders can occur: irritablity, focus/concentration problems, depressive state with suicidal tendencies, paraphrenia complex. These symptoms may not reverse after correction of hematological abnormalities, and the chance of complete reversal decreases with the length of time the neurological symptoms have been present.

Sources

Vitamin B-12 is naturally found in foods of animal origin including meat (especially liver and shellfish) and milk products. Animals, in turn, must obtain it directly or indirectly from bacteria, and these bacteria may inhabit a section of the gut which is posterior to the section where B-12 is absorbed. Thus, Herbivorous animals must either obtain B-12 from bacteria in their rumens, or (if fermenting plant material in the hindgut) by reingestion of cecotrope feces. Eggs are often mentioned as a good B-12 source, but they also contain a factor that blocks absorption. Certain insects such as termites contain B-12 produced by their gut bacteria, in a manner analogous to ruminant animals. An NIH Fact Sheet lists a variety of food sources of vitamin B-12.

Plants only supply B-12 to humans when the soil containing B-12-producing microorganisms has not been washed from them. Vegan humans who eat only washed vegetables must take special care to supplement their diets accordingly. According to the U.K. Vegan Society, the only reliable vegans sources of B-12 are foods fortified with B-12 (including some plant milks, some soy products and some breakfast cereals), and B-12 supplements. Fortified breakfast cereals are a particularly valuable source of vitamin B-12 for vegetarians and vegans.

While lacto-ovo vegetarians usually get enough B-12 through consuming dairy products, vitamin B-12 may be found to be lacking in those practicing vegan diets who do not use multivitamin supplements or eat B-12 fortified foods, such as fortified breakfast cereals, fortified soy-based products, and fortified energy bars. Claimed sources of B-12 that have been shown through direct studies of vegans to be inadequate or unreliable include, laver (a seaweed), barley grass, and human gut bacteria. People on a vegan raw food diet are also susceptible to B-12 deficiency if no supplementation is used. However, the more alkaline intestines of vegans are better able to metabolize hydroxocobalamin, a more efficient cobalamin than cyanocobalamin.

The Vegan Society, the Vegetarian Resource Group, and the Physicians Committee for Responsible Medicine, among others, recommend that vegans either consistently eat foods fortified with B-12 or take a daily or weekly B-12 supplement.

Cyanocobalamin is converted to its active forms, first hydroxocobalamin and then methylcobalamin and adenosylcobalamin in the liver. The sublingual route, in which B-12 is presumably or supposedly absorbed more directly under the tongue, has not proven to be necessary or helpful. A 2003 study found no significant difference in absorption for serum levels from oral vs. sublingual delivery of 500 micrograms of cobalamin. However, if patient has inborn errors in the methyltransfer pathway (cobalamin C disease, combined methylmalonic aciduria and homocystinuria), treating with intravenous or intramuscular hydroxocobalamin is needed.

Vitamin B-12 can be supplemented in healthy subjects also by liquid, strip, nasal spray, or injection. B-12 is available singly or in combination with other supplements.

Injection is sometimes used in cases where digestive absorption is impaired, but there is some evidence that this course of action may not be necessary with modern high potency oral supplements (such as 500 to 1000 mcg or more). These supplements carry such large doses of the vitamin that the many different components of the B-12 absorption system are not required, and enough of the vitamin (only a few mcg a day) is obtained simply by mass-action transport across the gut. Even pernicious anemia can be treated entirely by the oral route.

For the much lower amounts of B-12 found in food sources, however, oral absorption is complex and requires stomach acid, and also specific intestinal transport proteins (intrinsic factor) produced in the stomach. Lack of function in these systems is the causes of much of the increased risk in many elderly persons who develop B-12 deficiency later in life. However, it can be treated with a simple high dose oral B-12 supplement. Cyanocobalamin is also sometimes added to beverages including Diet Coke Plus and many energy drinks, in some cases with over 80 times the recommended intake.[citation needed] However, 500 mcg would be needed to reverse biochemical signs of vitamin B-12 deficiency in older adults.

Source: http://en.wikipedia.org/wiki/Vitamin_B12

“High doses of mineral supplements can also lead to side effects and toxicity. Mineral-supplement poisoning does occur occasionally due to excessive and unusual intake of iron-containing supplements, including some multivitamins, but is not common.”

Before 1998, several deaths per year were typically associated with pharmaceutical iron-containing supplements, especially brightly-colored, sugar-coated, high-potency iron supplements, and most deaths were children. The effects of toxic doses of vitamin A. Manifestations include bone fragility, xeroderma, nausea, headache, and loss of hair.

A problem with vitamins A, D, B6, and folic acid, at levels of intake from supplements considerably higher than might be obtained from foods, although hypervitaminosis A and D may result from (enriched) foods.

Overdose can occur when taking megadoses of the active form of vitamin A. Amounts above what is being utilized by the body accumulate in the liver and fatty tissues. Symptoms may include dry lips and skin, bone and joint pain, liver and spleen enlargement, diarrhea, vomiting, headaches, blurry or double vision, confusion, irritability, fatigue, and bulging fontanel (soft spot on the head) in infants; these are most often reversible, but a doctor should be contacted if a known overdose occurs. Very high levels of vitamin A may also create deficiencies of vitamins C, E, and K. Symptoms will generally appear within six hours following an acute overdose, and take a few weeks to resolve after ceasing the supplement. Children are more sensitive to high levels of vitamin A than adults are, so instructions on products designed for children should be followed with particular care. Vitamin supplements should always be kept out of reach of children.

As vitamin A is fat-soluble, disposing of any excesses taken in through diet is a lot harder than with water-soluble vitamins B and C. In chronic cases, hair loss, drying of the mucous membranes, fever, insomnia, fatigue, weight loss, bone fractures, anemia, and diarrhea can all be evident on top of the symptoms associated with less serious toxicity.

Hypercalcaemia (or Hypercalcemia) is an elevated calcium level in the blood. (Normal range: 9-10.5 mg/dL or 2.2-2.6 mmol/L). It can be an asymptomatic laboratory finding, but because an elevated calcium level is often indicative of other diseases, a diagnosis should be undertaken if it persists. It can be due to excessive skeletal calcium release, increased intestinal calcium absorption, or decreased renal calcium excretion.

Hypercalcemia per se can result in fatigue, depression, confusion, anorexia, nausea, vomiting, constipation, pancreatitis or increased urination “Bones, stones, groans, and psychic moans” is a saying which will help you remember the signs and symptoms of hypercalcemia; if it is chronic it can result in urinary calculi (renal stones or bladder stones). Abnormal heart rhythms can result, and EKG findings of a short QT interval and a widened T wave suggest hypercalcemia.

Symptoms are more common at high calcium levels (12.0 mg/dL or 3 mmol/l). Severe hypercalcemia (above 15-16 mg/dL or 3.75-4 mmol/l) is considered a medical emergency: at these levels, coma and cardiac arrest can result.

Very high intakes of supplements of vitamin B6, (pyridoxine), in excess of 200 mg/day, far greater than could be obtained from food, lead to nerve damage.

An overdose of pyridoxine can cause a temporary deadening of certain nerves such as the proprioceptory nerves; causing a feeling of disembodiment common with the loss of proprioception. This condition is reversible when supplementation is stopped.[4]

Because adverse effects have only been documented from vitamin B6 supplements and never from food sources, this article only discusses the safety of the supplemental form of vitamin B6 (pyridoxine). Although vitamin B6 is a water-soluble vitamin and is excreted in the urine, very high doses of pyridoxine over long periods of time may result in painful neurological symptoms known as sensory neuropathy. Symptoms include pain and numbness of the extremities, and in severe cases difficulty walking. Sensory neuropathy typically develops at doses of pyridoxine in excess of 1,000 mg per day. However, there have been a few case reports of individuals who developed sensory neuropathies at doses of less than 500 mg daily over a period of months. None of the studies, in which an objective neurological examination was performed, found evidence of sensory nerve damage at intakes of pyridoxine below 200 mg/day. In order to prevent sensory neuropathy in virtually all individuals, the Food and Nutrition Board of the Institute of Medicine set the tolerable upper intake level (UL) for pyridoxine at 100 mg/day for adults. Because placebo-controlled studies have generally failed to show therapeutic benefits of high doses of pyridoxine, there is little reason to exceed the UL of 100 mg/day. Studies have shown, however, that in the case of individuals diagnosed with autism, high doses of vitamin B6 given with magnesium have been found to be extremely beneficial.

Folic acid in general and specifically leucovorin are usually well-tolerated. However, there are some uncommon side effects that include skin rashes, itching, vomiting, nausea, diarrhea, and difficulty breathing. Although extremely rare, seizures have occurred in some patients taking leucovorin. Since leucovorin is taken with chemotherapeutic drugs, some side effects may be due to drug interaction.

“RDI, dietary reference intakes, is a set of nutritional guidelines concerning the intake of vitamins and minerals from food rather than supplements.”

From the Institute of Medicine of the USA National Academy (IOM), it is the system is used by both the United States and Canada. It is intended for the general public and health professionals.

Applications include:

· Food labels in the United States and Canada

· Composition of diets for schools, prisons, hospitals or nursing homes

· Industries developing new food stuffs

· Healthcare policy makers and public health officials

In 1997, at the suggestion of the Institute of Medicine of the National Academy, the RDA became one part of a broader, more detailed set of dietary guidelines, called the Dietary Reference Intake.

The current Dietary Reference Intake recommendation is composed of:

· Estimated Average Requirements (EAR), expected to satisfy the needs of 50% of the people in that age group.

· Reference Daily Intake (RDI), the daily dietary intake level of a nutrient considered sufficient to meet the requirements of nearly all (97–98%) healthy individuals in each life-stage and gender group.

· Adequate Intake (AI), where no RDI has been established, but the amount established is somewhat less firmly believed to be adequate for everyone in the demographic group.

· Tolerable upper intake levels (UL), to caution against excessive intake of nutrients (like vitamin D) that can be harmful in large amounts.

The RDI is used to determine the Recommended Daily Value (RDV) which is printed on food labels in the U.S. and Canada.

Source: http://www.answers.com/topic/dietary-reference-intake?nr=1&lsc=true&cat=health