More on Methyl Donors

METHYL DONORS
DEFINITIONS AND CLINICAL INDICATIONS OF NEED
by Ronald L. Myers, CNC
Do you want to slow the aging process…
Would you like to increase your mental capabilities…
Or prevent CAD…
Not interested in having cancer…
THEN LET’S TAKE THE MYSTERY OUT OF METHYL DONORS


By definition, a methyl donor is a substance capable of donating a methyl group (CH3), such as
methionine, betaine (bay‘ ta ine) or trimethylglycine ( according to the MERCK INDEX, these
are different names for the same substance), dimethylglycine or choline. Essential to the
transmethylation process are the coenzymatic forms of the vitamins folic acid (FH4) and B12.
Methyl donors are involved in a biochemical process known as methylation, the transfer of a
methyl group from a donor molecule (see above) to an acceptor molecule such as homocysteine.
Because of this, much research has been directed at the use of methyl donors to lower
homocysteine levels and prevent coronary artery disease (CAD). Thanks to the work of
McCully and Stampfer, elevated homocysteine is now recognized as a major risk factor for
CAD. But this is just the tip of the iceberg, enhancing the methylation process can not only
prevent an untimely death from a heart attack or stroke, it can contribute to our increased
creativity, productivity and overall enjoyment of a longer life. As the saying goes, not just more
years of life, but more life in those years!
Increased homocysteine has become an easily definable marker of inhibited or poor methylation.
RISK FACTORS FOR INCREASED HOMOCYSTEINE AND POOR METHYLATION
Persons who exercise less than three times a week?
Homocysteine is reduced during exercise. Why it is reduced during exercise is not known
A significant part of the diet is from a bag, box or can or fast food.
Processed foods contain a fraction of the critical vitamins, B-6, B-12, and folic acid. These
nutrients are required to lower homocysteine and prevent cardiovascular disease. eBytes Issue 14
Ronald L. Myers, CNC Copyright © 2004 All Rights Reserved
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Family history of death from vascular disease.
This could be due to a family genetic weakness in the body's ability to lower homocysteine and
premature vascular disease. If parents, grandparents, aunts, or uncles suffered from strokes, heart
attack, angina, or any vascular disease, an increased risk for vascular disease exists even if all
standard risk factors are normal. The good news is, researchers have discovered that betaine
(TMG), combined with B-6, B12, and folic acid, can prevent much of the damage created by this
defect. (The original work by McCully was based on children with vascular disease. Increased
homocysteine [due to a genetic defect], not cholesterol, was shown to be the cause. McCully,
K.S. Vascular pathology of homocysteinemia: implications for the pathogenesis of
arteriosclerosis. American Journal of Pathology 56:111-128, 1969.)
High protein, few fruits and vegetables in diet
Research has shown that a high percentage of Americans have never heard the government’s
recommendation to eat five servings of fruits and vegetables each day.
Family history of depression, neurological disease or liver problems.
Person smokes or uses birth control pills.
Both smoking and birth controls pills elevate homocysteine levels and therefore inhibit
methylation.
For patients at risk, the good news is, through nutrition, homocysteine can be reduced and
methylation can be increased. Even people with previously diagnosed vascular disease have
survived dependent on their homocysteine levels.
METHYLATION--BEYOND HOMOCYSTEINE
Methylation is a process necessary for many biological functions aside from homocysteine
regulation. Methylation is involved in maintaining DNA integrity, processing fats, improving
neurological function, detoxifying the liver, and is connected to nearly every biochemical
process in the body. Several scientific peer-reviewed articles have demonstrated that this
methylation process degrades with age, and is associated with a large variety of age-related
diseases. Enhancing the methylation process with nutrition holds great promise for the future
with regard to reduction in age-related disease and the overall increased longevity of man.
Research is showing that the most effective method of enhancing methylation is through the use
of food supplements. Diet has not been shown to be an adequate means of providing the
nutrients required for methylation in the amounts needed. (van den Berg, M., et al. Combined
vitamin B6 plus folic acid therapy in young patients with arteriosclerosis and
hyperhomocysteinemia. Journal of Vascular Surgery, 20(6):933-40, 1994. Graham, I.M. et al.
Plasma homocysteine as a risk factor for vascular disease. Journal of the American Medical
Association, 277(22):1775-1781, 1997.) eBytes Issue 14
Ronald L. Myers, CNC Copyright © 2004 All Rights Reserved
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SLOWING THE AGING PROCESS
There is strong evidence for the theory that impaired methylation is one of the key mechanisms
of aging. Just as long-lived animals have strong antioxidant defenses, they maintain methylation
much better than short-lived animals. If we were to envision a curve showing the inexorable rise
in homocysteine with aging it would depict the peripheral blood vessels clogging up first, then
we seem doomed to end up with homocysteine-related damage to the nervous system, bone
density, cataracts, gray hair--the very changes that define aging. The development of cataracts is
related to rising levels of homocysteine, and inadequate methylation. Graying of the hair has
been related to inhibition of the methylation process. As we age, is it possible to reduce
homocysteine levels and enhance methylation? The answer is YES! Elderly people were
supplemented with nutrients involved in methylation (folate, B12, B6, TMG), at the end of the
study they had homocysteine levels lower than usually seen in healthy 35 year olds. (Cooney,
C.A., Growth, Development and Aging, 57(4):261-73, 1993.) Since homocysteine levels are
currently being used as a marker of the efficacy of the methylation process the results of this
study seem significant.
METHYL DONORS AND THE BRAIN
The brain is insatiable in its demand for methyl donors. For the production of neurotransmitters
and maintaining the myelin sheath around nerve fibers, these nutrients are essential. Nutrients
involved in the methylation process have been found to be effective anti-depressants as well.
Interestingly enough, lack of response to Prozac goes hand in hand with reduced folate levels.
Alzheimer's disease has been associated with high homocysteine and low levels of folate and
B12. Improving methylation is probably one crucial way to protect ourselves against devastating
brain diseases and give us years of continued creativity and productivity. Multiple sclerosis
(MS) has symptoms that resemble those of folate or B12 deficiency. Since methylation is
essential for the formation of the myelin sheath that insulates nerve fibers, a combination of
methyl supplements and anti-inflammatory fatty acids could be used for the treatment of this
disease. (Cooney, C.A.)
ENHANCE CARDIOVASCULAR HEALTH
Research has shown that even moderately high levels of plasma homocysteine are associated
with subsequent risk of MI independent of other coronary risk factors. Because high levels can
be easily treated with vitamin supplements, homocysteine may be an independent modifiable risk
factor. Elevated homocysteine levels can often be normalized with modest doses of folate (1 - 5
mg/d). For cases that are resistant to this therapy, the addition betaine (TMG) is often effective.
These supplements at recommended doses have no side effects under most circumstances.
(Stampfer, Meir J., et al. A prospective study of plasma homocysteine and risk of myocardial
infarction in US physicians. Journal of the American Medical Association, 268(7):877-81,
1992.) This is significant because some researchers estimate that as much as 90% of CAD may
be due to increased homocysteine! A valid question at this point might be what is considered
increased when it comes to homocysteine. There seems to be some agreement that levels of 4 -
6 mmol are probably safe. This range may be lower than the "normal" range reported by your
laboratory. It is probably better to be safe than normal with a one out of three death rate from
CAD.