TMG-15 (N,N,N-trimethylglycine)

PillManJohn A. Mann, author of “Secrets of Life Extension,” the book that spearheaded the current life-extension movement in 1980, and founder of the life-extension research organization Forefront Health Investigations hails the importance of the new life-extension substance (TMG)

TMG detoxifies the powerful pro-oxidant and free-radical generator homocysteine, which is now known to be a leading cause of heart and artery disease. But that’s not all. TMG is almost the same substance as DMG (dimethylglycine), also known as vitamin B-15, except that DMG contains two methyl groups and TMG contains three. Homocysteine is the same structure as the essential amino acid methionine, except that it lacks a methyl group. In the liver, TMG transfers one of its three methyls to homocysteine, converting that dangerous substance to useful methionine. At the same time, by losing that methyl group, TMG becomes DMG, a substance that millions of people now pay a very high price for as a supplement. TMG is less costly than the equivalent amount of DMG that it provides and performs antioxidant functions against homocysteine that DMG does not. So why spend more money for something that gives you less?

The health-products industry’s first trimethylglycine formula has been reintroduced by the supplement company LifeLink’s TMG-15 Complex. The product combines 500 mg of TMG with appropriate amounts of the essential metabolic cofactors required to assist the transfer of methyls that give TMG its many health-promoting and life-protecting benefits.

For many years, millions of people including many top athletes and members of the Pittsburgh Steelers, New York Yankees and Dallas Cowboys, have been taking DMG for its stamina-increasing effects. Mann, who tends to state exciting news more conservatively than other health and nutrition writers, says: “Athletes, triathlon competitors are reporting even better results from TMG-15 Complex than from DMG. This is not surprising, since TMG 15 Complex converts to DMG in the body which reduces lactic acid in the muscles and detoxifies homocysteine at the same time.”

TMG is not a drug. It is a natural amino acid that occurs in food and is produced in the body during the metabolism of choline. A substantial amount of the choline in our bodies, though, is channeled through other important metabolic pathways. Major among these is its conversion to biological lecithin (phosphatidyl choline) and the nerve-impulse-transmitting substance acetylcholine. Experiments in which large doses of lecithin or other choline precursors that can deliver acetylcholine to the brain and nervous system were given to human and animal subjects have resulted in greatly increased brain and nerve functions, including improved memory, reflex and coordination. By taking supplemental TMG we can spare much of the body’s choline reserves for conversion to acetylcholine. This could also explain the improved muscle response that athletes experienced after taking TMG-15 Complex.

There is an important footnote to this wonderful news about TMG. Many life extension practitioners have been taking massive doses of vitamin B-6 (pyridoxine) because it also neutralizes the pro-oxidant homocysteine, converting it to the important antioxidant cystathione. The August 25, 1983 issue of The New England Journal of Medicine documented cases in which severe sensory nerve damage occurred in humans as a result of using very large daily dosages of B-6 for periods of 4-40 months. If one is trying to keep homocysteine levels down, it is better to take lower doses of B-6 supplements and use the TMG-15 Complex to assist in neutralizing homocysteine. LifeLink’s TMG-15 Complex includes safe but more than adequate amounts of the vitamin B-6 precursor factor required for maximum neutralization of homocysteine and the production of antioxidant cystathione.

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Homocysteine and cardiovascular disease

At U.S. and European medical institutions, major clinical trials are underway to answer an intriguing question with big implications: Can B vitamins reverse or slow down deadly vascular disease?

The research has been prompted by more than 200 medical studies establishing elevated homocysteine as a major risk factor for vascular disease, the No. 1 killer disease in the United States.

Homocysteine is an amino acid that triggers arterial plaque and blood clot formation when it reaches toxic levels in the body. This occurs, research suggests, because of a deficiency of two B-complex vitamins, B-6 and folic acid. Homocysteine may not yet be a household word – such as cholesterol – but it appears headed in that direction. According to Kilmer McCully, M.D., it is more important than cholesterol as a risk factor for blood-vessel disorders, including cardiovascular disease, that take the lives of nearly a million Americans each year and affect more than 57 million individuals. McCully, a pathologist at the Veterans Affairs Medical Center in Providence, Rhode Island, is the “father” of the homocysteine theory, a revolutionary explanation of how vascular disease is caused. Years ago, he was forced to leave positions at Harvard and Brown medical schools for promoting his ideas, which collided with the prevailing “cholesterol paradigm.”

Now, nearly three decades later, his theory has gained worldwide scientific attention, and the once-rejected McCully is gaining celebrity status in the medical community. “Because of my ideas, I was thrown out of two medical schools,” he says. “Now, confirmation is coming from all over.”

For decades, we have all heard that the buildup of cholesterol, fat and plaque in the arteries can cause vascular disease and potentially lethal blockages in the body. Blood vessels, primarily those leading to the heart, brain and legs, become hard and stiffen, a process known as arteriosclerosis. Its most common form is atherosclerosis, which occurs when plaques build up on arterial walls to restrict the flow of blood and increase the prospect for clots to block circulation and cause heart attacks, strokes and amputated legs.

The conventional view has incriminated excess dietary consumption of fats and cholesterol as major players in this process. Over the years, the cholesterol menace has spawned massive research, medical technology and the proliferation of low-fat food products. But studies on the impact of dietary cholesterol on disease have been equivocal. Moreover, research has shown that many people die from vascular and cardiovascular disease with normal and even low levels of cholesterol. And studies have also revealed a disturbing risk of illness, including cancer among men, as a result of lowering cholesterol with pharmaceutical drugs.

McCully views the involvement of cholesterol as secondary to that of homocysteine. “In the production of plaques in the artery wall, it is well known that cholesterol becomes damaged by oxidation,” he says. “But homocysteine is a potent catalyst for this oxidation reaction and orchestrates all the things in the arterial wall that produce the plaque.”

In order to understand why homocysteine may be the most critical risk factor for heart disease, it is helpful to understand how it works in the body.

  • Protein is a basic part of all food. One of the major components of protein is methionine, an essential dietary amino acid needed for proper growth and maintenance of all the cells and tissues in the body.
  • Normally, the liver processes methionine and breaks it down into homocysteine, another amino acid. Some of this homocysteine is then reconverted back into methionine again and used to supply the body’s protein needs. The unused homocysteine is passed out in the urine.
  • This process depends on folic acid and vitamin B-6 to run smoothly. The vitamins are necessary raw materials for specific enzymes that convert methionine and homocysteine.
  • If folic acid and vitamin B-6 are deficient in the diet, this enzymatic process suffers. Homocysteine starts building up in the body and is drawn into the endothelium (inner lining) of arteries. There, the evidence shows, it generates the pathogenic sequence of chemical and oxidative reactions and encourages the formation of blood clots.

Research indicates that elevated homocysteine is not just involved in diseases of the blood vessels. It has been implicated in spontaneous abortion, neural-tube defects, low birth weight, kidney failure, rheumatoid arthritis, alcoholism, osteoporosis, neuropsychiatric disorders, non-insulin dependent diabetes and complications of diabetes. High homocysteine levels have also been found in patients with fibromyalgia and chronic fatigue syndrome.

An intriguing part of McCully’s theory is its nutritional implications and the possibility of a simple solution. Many studies have confirmed the association between elevated homocysteine and a deficiency of vitamin B6 and folic acid. The widespread incidence has much to do with modern eating habits and food processing, both of which minimize important nutrients in the diet. “The depletion of vitamin B-6 and folic acid from the diet is, in my opinion, the underlying cause of the disease.” says McCully. “Eating refined, white-flour products, white rice, sugar, fats and oils deprives you of critical nutrients and generates all these diseases of modern civilization.”

Poor eating habits are another problem. According to the Harvard Health Letter, “On any given day, more than 50 percent of adults fail to eat the three servings of vegetables advised in the Dietary Guidelines for Americans, and only 24 percent consume the recommended two servings of fruit. That’s unfortunate because fruits and vegetables are excellent sources of vitamins B-6 and folic acid.”

Medical studies have shown that supplementation with vitamin B-6 and folic acid rapidly normalizes homocysteine levels in the blood. The scientific community doesn’t know yet whether this translates into actual prevention and improved symptoms for people with vascular disease.

Killian Robinson, M.D., a staff cardiologist at the Cleveland Clinic, has conducted research on homocysteine and says that the medical community is interested in the answer. “Some evidence shows improved endothelial function, that is the function of the lining of the blood-vessel wall, by homocysteine lowering treatment, namely with folic acid supplementation,” he says. “The endothelial lining does not appear to function normally in people with higher homocysteine. So if you reduce the level, you may be doing the patient some good. But we need the therapeutic trials to prove that by a simple vitamin treatment you can save a lot of peoples lives,” he adds.

In the search for answers to the homocysteine question, practitioners who have had success with heart disease patients offer some of the strongest clues. John Ellis, M.D., a retired Texas physician known for discovering the healing effect of vitamin B-6 for many people with carpal tunnel syndrome, found that his patients suffered few heart attacks and had very little angina. When Ellis reviewed medical records, he determined that patients who took B-6 for a year or more had nearly 75 percent less risk for developing angina and heart attacks than patients of other doctors in his community who did not take B-6.

Another important clue is the response of individuals with homocysteinuria, a rare and severe genetic disorder associated with high homocysteine levels, premature vascular disease and mild mental retardation. Among these individuals, B-6 alone has been found to reduce the risk of complications, particularly the formation of blood clots, by about 60 percent. In addition, their mental development is enhanced, and they are less likely to become retarded.

With the results of clinical outcome trials still a few years off, McCully’s advice is to eat as many whole foods as possible and use a good vitamin supplement. “If you have a family history of heart disease or stroke, or if you have a relative who had a disease like this before the age of 55 or so, you’d better get your homocysteine level checked,” advises McCully. “And if it is elevated, you better get it down.”

For a more information on homocysteine see the article at: http://www.ilifelink.com/tmg-15_complex_120_tablets.html

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Xobaline for diabetic neuropathy – human and feline

PillManDiabetic neuropathy is a decrease in nerve function typically affecting the lower limbs in people and animals with diabetes. The peripheral nerves become damaged as a result of metabolic changes (including oxidative stress) that accompany persistently elevated blood sugar levels. Many people with diabetes, whether Type I (juvenile) or Type II (adult-onset), will eventually come down with some form of diabetic neuropathy.

In addition to muscle weakness, depressed reflexes, and disturbances in gait or balance, the symptoms of diabetic neuropathy in humans typically include sensations of numbness, tingling, burning, or shooting pains. As the nerves continue to degenerate, sensation can become completely lost; as a result, minor injuries to the feet may go unnoticed, at least initially. At the same time, damage to the autonomic nervous system results in impaired circulation, so that wounds don’t heal properly. Thus, minor injuries can quickly escalate to major ones, greatly increasing the risk of gangrene. Once gangrene has set in, the conventional treatment is amputation – of the toes or even the entire foot.

Fortunately, there exists a number of nutritional therapies for diabetic neuropathy, of which one of the best is methyl B12. Effective treatment of diabetic neuropathy has reportedly been achieved with methyl B12 delivered intrathecally, i.e., injected directly into the spinal cord via lumbar puncture. Don’t try this one at home, folks – obviously, it’s an experimental procedure done only in a hospital setting. However, according to another study, the same beneficial results can also be obtained with oral supplements of methyl B12 in sufficiently large doses. There have been anecdotal reports of people getting relief from 1 to 3 tablets of Xobaline methylcobalamin per day. The use of methyl B12 can halt degeneration of peripheral nerves, improve or eliminate painful sensations, and in some cases even restore sensation to limbs which have previously gone completely numb.

The mechanism for these beneficial effects is not yet completely understood. It is known that serum B12 deficiency is not especially common in diabetic neuropathy, implying that the effectiveness of methyl B12 is not due to repletion of an underlying systemic vitamin B12 deficiency. Nevertheless, a marked tissue deficiency of methyl B12 only (and not of other forms of B12 occurring naturally in the body) has been reported in the sciatic nerves of diabetic patients compared to controls. Thus, a clear rationale exists for supplementing with methyl B12 rather than with other forms of the vitamin, such as cyanocobalamin.

Perhaps even more significant for the treatment of diabetic neuropathy is the discovery that methyl B12 has neuroprotective effects. In certain neurological conditions – such as Alzheimer’s, Parkinson’s, amyotrophic lateral sclerosis, and AIDS-related dementia – nerve cells are thought to be exposed to excessive amounts of the neurotransmitter glutamate, resulting in neurotoxicity. Recently high-dose methyl B12 has been shown to diminish glutamate-related neurotoxicity in animals, thus offering hope that neurodegenerative diseases can be effectively treated with methyl B12. Peripheral neuropathic pain is similarly associated with activation of glutamate receptors in the spinal cord. Hence methyl B12 may be beneficial for all forms of peripheral neuropathy, including diabetic neuropathy, by regulating neural signaling in the spinal cord.

Diabetes afflicts animals as well as humans, so it’s not surprising that cats can also suffer from diabetic neuropathy. As in humans, diabetes in cats is caused either by inadequate production of insulin by the pancreas (Type 1 diabetes) or by impaired response of cells to insulin (Type 2 diabetes). Although diabetes can strike cats of any age, it typically occurs most often in older, fatter animals. Diabetic neuropathy in cats is characterized by symptoms such as progressive weakness in the hind legs and walking on the hocks (the back part of the legs) rather than on the toes. Cats so afflicted become incapable of climbing stairs or trees and lose the ability to jump to higher surfaces. Often they can’t take more than a few steps without the hind legs sliding out from under them. Cats with neuropathy also seem to tire quickly and tend to rest more often after taking short walks.

The staff at LifeLink has recently told me that many cat lovers are treating their diabetic pets with Zobaline, apparently with great success. Zobaline is the new cat-specific version of our popular Xobaline product, made without fructose or any other sugar-based flavors. A single Zobaline tablet administered once per day appears sufficient to reverse most or all of the symptoms of feline diabetic neuropathy within a few weeks. Although we’re not in the veterinary business and cannot promote the use of Zobaline for veterinary purposes, we’re proud that Zobaline has been singled out as a useful supplement for cats.

[Editor’s note: “Xobaline”  and “Zobaline” are LifeLink’s brand name for vitamin B12 (methylcobalamin).]

http://www.ilifelink.com/xobaline_for_humans_3_mg_x_60_sublinguals.html

http://www.ilifelink.com/zobaline-for_diabetic_cats-3_mg_x_60_tablets.html

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Serotonin solution

by Charles Davidson

The chemical serotonin is important for a variety of brain functions. Its deficit is now believed to be central to the development of depression, agitation, sleep disorders, obesity and addiction. Serotonin can be produced in the body from the dietary amino acid tryptophan in only two steps. Serotonin can also be made from 5-hydroxy L-tryptophan (5-HTP), which is simply the modified amino acid obtained from plant sources.

The pharmaceutical control of brain serotonin levels is the mechanism of action of two commonly prescribed classes of drugs used in the treatment of depression and anxiety, a well known example being Prozac. A relative deficiency of serotonin is also believed to be associated with the brain’s perception of starvation and hunger. For these reasons, 5-HTP has been used as an antidepressant, as an appetite suppressant in obese persons and as an inducer of sleep.

5-HTP: A dietary precursor to an important chemical in the brain

Notwithstanding the fact that electrical impulses travel down an individual nerve fiber, nerves communicate with each other chemically and not electrically. Nerves are classified according to their ability to either secrete or respond to various chemical compounds called neurotransmitters. (These molecules are secreted into the gap between two different nerve cells, called either the synapse or the synaptic cleft. A nerve impulse is fired when enough receptor molecules on the “post-synaptic” nerve bind specifically to one or another class of neurotransmitter that was secreted by the “pre-synaptic” nerve.) Different regions of the brain – and different neurotransmitters – mediate disparate processes, ranging from highly aware mental cognition to unconscious manifestations, such as hunger and sleep.

Neurotransmitters are derived from precursor chemicals found in common food substances. For example, acetylcholine is produced by nerves from choline, a chemical that can be obtained commercially from soybean lecithin. Acetylcholine is secreted by the motor nerves into the neuromuscular junction thereby, stimulating muscular contraction. The neurotransmitters GABA and norepinephrine are derived from proteins that contain the amino acids glutamate and tyrosine, respectively. Adrenaline is chemically related to norepinephrine and is used medically to restart hearts that have been arrested following a heart attack. The neurotransmitter, serotonin, is present in high levels in foods such as bananas and is important for a variety of brain functions. Serotonin, however, cannot cross the blood-brain barrier, although 5-HTP – a nutritional supplement – can enter the brain directly from the general circulation (by being transported across the blood-brain barrier).

5-HTP helps alleviate depression and reduces aggressiveness

It is clinically significant that a deficit of serotonin is central to the development of depression, agitation, sleep disorders, obesity and addiction. For this reason, the pharmaceutical control of brain serotonin levels is the mechanism of action of two commonly prescribed classes of drugs used in the treatment of depression. Prozac is an example of a selective serotonin reuptake inhibitor (SSRI), which prevents the “presynaptic” nerve from reabsorbing serotonin that it has previously secreted. By inhibiting this normal process, Prozac causes an increase in brain serotonin levels and a non-narcotic anti-depressant effect. Another class of antidepressant drugs, the monoamine oxidase (MAO) inhibitors, cause an increase in serotonin levels by preventing its degradation. Conversely, the experimental depletion of serotonin in animals – by eliminating tryptophan from the diet – causes an increase in aggressiveness. [Note later section entitled  “5-HTP or Prozac or Both?”]

5-HTP as an appetite suppressant

Decreased brain serotonin levels are also associated with obesity due to overeating. Drugs like fenfluramine (Fen Phen), which increases serotonin production, are used as an appetite suppressant successfully in the treatment of common obesity. A relative deficiency of serotonin is believed to be associated with the brain’s perception of starvation and hunger. Tryptophan is one of the rarest of the essential amino acids – one that the body cannot produce – but one that is needed for the production of vital proteins. Consequently, the dietary depletion of tryptophan, a serotonin precursor, is an ideal homeostatic mechanism in the brain for regulating the desire for food intake.

Hunger sensation in the brain is believed to occur in the region called the hypothalamus. Opposite to the effect of food deprivation, the specific intake of carbohydrates and various sugars cause an increase in brain serotonin levels. This explains why some people are willing to eat an excess of “junk food” that entirely lacks any protein.

5-HTP – which increases serotonin levels – is an appetite suppressant at low doses (50 to 200 milligrams) if taken one-half hour before meals. At high doses, a common side effect of 5-HTP is nausea. During clinical trials in obese subjects, the intake of 5-HTP caused a voluntary decrease in caloric intake of both carbohydrates and fats, but not of protein. A significant loss of weight occurred, due to a voluntary decrease in caloric intake and not because of a restrictive diet. 5-HTP should also help in the adherence to a diet that is both low in calories and fat, but that is high in protein. 5-HTP should always be taken with adequate amounts of protein in the diet – not with a starvation weight loss regimen. [Note the later section entitled “5-HTP or Prozac or Both?” for a short discussion on the cardiac side effects of fenfluramine (Fen Phen) and the brain damage associated with the use of dexfenfluramine (Redux) another drug commonly prescribed to suppress appetite.]

5-HTP, addiction and pain

Serotonin levels are also increased by the intake of addictive substances, such as alcohol, tobacco, certain narcotics and caffeine. Individuals attempting to kick these habits develop a chemical withdrawal syndrome when serotonin levels plummet. These results are observed in both experimental animals and in people. The above findings indicate that overeating is, in part, chemical dependency related – by low serotonin levels – to other chemical addictions and to depression.

Pain sensitivity increases, as well, when brain serotonin levels are low. This has been presented by some researchers as one contributing factor in pre-menstrual syndrome (PMS). Agitation, pain irritability and depression are characteristic aspects of PMS, perhaps each related to a sex hormone-induced decrease in “serotonergic” activity. Conversely, pain sensitivity is markedly impaired during alcohol intoxification, which temporarily increases serotonin levels in the brain.

5-HTP gently induces sleep

Perhaps the most immediate effect of 5-HTP is its ability to induce sleep when taken on an empty stomach about one hour before going to bed. A 100 mg dose is effective in a large adult male. Both 5-HTP and serotonin (5-HT) are precursors to another neurotransmitter – melatonin – that also induces sleep. 5-HTP, like melatonin, can now be obtained in health food stores. Millions of people have safely taken melatonin for sleep and for eliminating jet lag. Melatonin is produced in the pineal gland deep within the brain, especially at night. Melatonin production is indirectly suppressed by light going into the eye and its levels are directly augmented by the availability of precursors, such as 5-HTP.

5-HTP, stress reduction and aging

The thalamus, is the region in the brain responsible for emotions and for controlling hypothalamic – hormone related – activity. Chemical releasing factors from the hypothalamus direct the adjacent pituitary gland to produce a variety of hormones in all mammals, including man. Pituitary hormones then direct  ‘endocrine ‘ glands in the periphery – such as the adrenal glands and the gonads – to produce secondary hormones. Different emotions, situations and behaviors – especially stress – are frequently associated with the bodies production of different hormones.

Over a century ago, the great physiologist Hans Selye observed that stress – in both humans and in experimental animals – resulted in an increased level of the (adrenal) hormone cortisol. Cortisol is responsible for the “fight, flight or fright” response; its elevation produces states ranging from marked wakefulness to panic. Both high cortisol levels and experimental stress reduce levels of brain serotonin. Long-term exposure to cortisol actually damages certain serotonin producing nerves in the brains of animals.

A number of factors are involved in depression in elderly individuals, exposed to a lifetime of various stresses, including an age-related decrease in brain serotonin levels. Elderly persons frequently have difficulty falling to sleep at right as well. Prozac, which raises serotonin levels, is sometimes prescribed for elderly depression for those reasons.

Interestingly, while moderate food restriction in rodents is known to increased lifespan, it also increases levels of the neurotransmitter melatonin – a metabolite of serotonin (and therefore, of 5-HTP). Additionally, melatonin added to the drinking water of middle-aged mice significantly increased their lifespan over that of controls. Furthermore, the transplanting of the melatonin – producing pineal gland from young mice into old mice increased the life span of the older mice. Therefore, the consumption of low-dose 5-HTP – a precursor to melatonin – might be used to mitigate certain aging aspects of long-term stress that begin to accumulate during mid-life.

5-HTP or Prozac or both?

The title of this article, “Listening to 5-HTP”, is a parody of the title of the book “Listening to Prozac”. The author of “Listening to Prozac” generally extols the virtues of selective serotonin reuptake inhibitor drugs, like Prozac, especially underscoring their marked improvement over previously developed types of anti-depressants. Yet ironically, one six week study of 69 subjects that compared another SSRI to 5-HTP found that both compounds have equal antidepressant capabilities. Moreover, 5-HTP had one-half as many moderate-to-severe side effects as the SSRI. (Also in the news recently has been reports of heart valve damage from the use of fenfluramine (Fen Phen) – another type of serotonin elevating drug in women being treated for obesity. Prozac, however, does not have this effect on the heart.)

One article which reviewed the results of 17 clinical trials which used 5-HTP – mostly for depression – concluded that “oral administration of 5-HTP is associated with few adverse effects.” Two other facts surrounding 5-HTP are ironic vis-vis Prozac. For one, the efficacy of Prozac and other SSRI’s are still dependent upon the brain’s availability or serotonin precursors like tryptophan or its derivative, 5-HTP. When patients receiving SSRI’s were fed a special diet devoid of tryptophan, a relapse into depression was experienced, despite the continued presence of the SSRI. Tryptophan supplementation restored the antidepressant effects of the SSRI. On a related note, Prozac was found to be effective for anorexic individuals – who have low serotonin levels – but only once they were stabilized with a more normal weight and diet. Perhaps malnourished anorexic persons have inadequate levels of the dietary serotonin precursor – 5-HTP – so that Prozac cannot be effective.

Finally, 5-HTP is a supplemental nutrient – an amino acid – and is available without the need for a prescription. However, doses of 5-HTP greater than 200 mg per day are not recommended unless the individual is under the care of a physician.

[The studies described in this article are set forth by the author to contribute to the knowledge of the consumer of this product. The thoughts and ideas represented in this article by the author are a compilation of information found in numerous published reports known to the author at the time of writing this article and do not reflect individual studies conducted by this author.]

5-HTP from LifeLink

The 5-hydroxy-L-tryptophan preparation that can be obtained from supplement companies such as LifeLink is extracted from a seed that is also used in the pharmacological preparation of lectins. Lectins are pharmaceutical-grade compounds that are used in blood typing for transfusions and bone marrow transplants.

http://www.ilifelink.com/5-htp_5-hydroxy-l-tryptophan_50_mg_x_120_capsules.html

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Health benefits of another vitamin E

References to antioxidants often use vitamin E and alpha-tocopherol interchangeably. Yet nature makes a host of structurally similar tocopherols and generally packages them together. In these mixtures, gamma-tocopherol usually dominates.

Now, Stephan Christen of the University of California, Berkeley and his colleagues report that gamma-tocopherol provides valuable protection from nitrogen oxides, a broad class of reactive compounds that alpha-tocopherol largely ignores. That’s important, Christen argues, because the vitamin E sold as a supplement contains primarily alpha-tocopherol.

Christen’s team focused on the ability of tocopherols to defuse nitrogen oxides. Outdoors, these compounds play a role in producing acid rain. In the body, many serve as destructive oxidants that can alter DNA and trigger some of the damage caused by inflammation.

Working with simulated cell membranes and low-density lipoproteins from people who had taken different vitamin E supplements, the scientists tested the tocopherols – ability to detoxify peroxynitrite, a nitrogen oxide that appears to be associated with inflammation. Though alpha-tocopherol “eliminates the oxidant character of the molecule,” Christen says, it leaves behind a reactive nitrogen component. “And that’s where gamma-tocopherol comes in.”

During a follow-up reaction, he observes, “It permanently traps what’s left over and still reactive” This tocopherol exhibits a special affinity for reacting with and inactivating nitrogen oxides, he says.

In an as-yet-unpublished study, Christen’s team induced inflammation in animals and then watched what happened to tocopherols in the blood. Concentrations of the gamma form dropped quickly, they found. At the same time, certain nitrogenous compounds increased, suggesting that the gamma-tocopherol was trapping nitrogen oxides.

Because consumption of large amounts of alpha-tocopherol appears to push gamma-tocopherol out of the system, both forms should be consumed together Christen’s team argues In the April 1 Proceedings Of The National Academy Of Sciences.

Anders G. Olsson, a physician who studies lipids and atherosclerosis at University Hospital in Linkoping, Sweden, agrees. In the March 1 British Medical Journal, he and a team of European colleagues described their investigation into risk factors that might explain why Lithuanian men face four times the heart disease mortality of Swedish men the same age.

Neither conventional risk factors – such as blood pressure or cholesterol – nor alpha-tocopherol concentrations differed substantially between the groups. The Lithuanian men, however, did possess significantly lower gamma-tocopherol concentrations in their blood than the Swedes did.

‘The new paper [by Christen’s group] could explain our findings,” Olsson concludes.

Heart disease isn’t the only degenerative condition linked to low gamma-tocopherol. Robert V. Cooney’s team at the Cancer Research Center of Hawaii in Honolulu has shown in test tube studies that “gamma-tocopherol pretty well blocks the formation of tumor cells at high doses. It’s much more effective than alpha-tocopherol.”

On the basis of such findings, Christen’s group now suspects that “gamma-tocopherol may be as important as alpha-tocopherol in the prevention of degenerative diseases.”

Adds Cooney, “The fact that 75 years after its discovery we still don’t understand what vitamin E really does says a lot about the state of this research.” Moreover, it “argues that we need to get our vitamin E from natural sources,” not synthetic supplements.

An unesterified mixed 400 i.u. vitamin E product is available from the supplement company LifeLink. It contains the alpha, beta, gamma and delta tocopherols, stabilized in a base of vegetable oils to provide the most bioavailable form possible.

J. Raloff, SCIENCE NEWS, April 5, 1997 Vol. 151, No. 14

http://www.ilifelink.com/vitamin_e_mixed_400_i_u_x_100_softgels.html

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