Methyl
Deficiencies and Cognitive Diseases
By Richard H. Gravelly,
D.C.
In the year 2000,
Weir and Molloy of the Department of Clinical Medicine, Trinity College,
St. James’s Hospital, Dublin published an article in the American
Journal of Clinical Nutrition, Vol 71. No. 4. pp. 859-860. In that article
they made several points which should be quoted here at the outset of
this paper to lay the groundwork for other concepts to be introduced.
They said: “The
function of folate in the brain, as elsewhere is…for the maintenance
of methylation reactions of internal metabolism mediated by S-adenosyl-l0methionine
(SAM).” SAM is known as SAMe when this substance is sold as tablets
to the consumer. It has been well established that lack of methylation
of DNA can result in, among other diseases, colon cancer. Weir and Molloy
also point out that “methylaton processes are essential for the
maintenance of normal brain function.” SAM, according to the authors
produeces “methyl groups” and that the “sole”
function of one of these methylgroups is to “remethylate homocysteine”
and that “the rapid removal of homocysteine is accordingly of
paramount importance to the maintenance of normal methylation process”.
The methyl group
upon which the brain relies to remove homocysteine is known as 5-methylenetetrahydrofolylpentaglutamate
and cobalamin (vitamin B12) dependent methionine synthase. “Thus”
they explain, “when either folate or cobalamin is deficient, homocysteine
accumulates.” The evidence indicates that the vitamin B6 is “at
best…an inefficient means of disposing of homocysteine in the
human brain.”
The conclusion,
it would seem, is that we should all take vitamin B-12 and folinic acid
to prevent brain diseases such as Alzheimer’s and Parkinson’s
disease, as many researchers believe that “hyperhomocysteinemia
is the fundamental link between the observed associations of reduced
folate or vitamin B-12 status and the severity of cognitive dysfunction.
The authors point out however that there is no conclusive evidence although
the damage to vascular and neuronal tissues is consistently associated
with low cobalamin and folate levels. The conclude the article by saying
that “There seems little doubt now that there is an association
between the evolution of certain braindiseases associated with cognitive
decline in the elderly and vitamin deficiencies associated with hyperhomocysteinemia.”
Three years later
the language of Miller writing in Alernative Medicine Reviews 2003 Feb;8(1):7-19
is more confident. “Hyperhomocysteinemia (elevated levels of homocysteine
in the blood) hs been shown to be an independent risk factor for cognitive
dysfunction. Indirect and direct vascular damage can be caused by homocysteine,
which has been implicated in vascular dementia, with an increased risk
of multiple brain infarcts and dementia as homocysteine levels rise.
A significant correlation has been found between risk of Alzheimer’s
disease and high plasma levels of homocysteine, as well as low levels
of folic acid, and vitamins B6 and B12.”
It is somewhat interesting
to note that the RDA (recommended daily allowance) was lowered in 1989
from 400mcg to 200mcg except for women who intend to become pregnant;
and for whom the RDA is 400mcg. This reduction is maintained in the
face of the well researched and accepted finding that elevated homocysteine
levels put one at risk for cardiovascular disease. As Mason, writing
In J. Nutr. 2003 Mar: 133 Suppl 3:941S-947-S put it: “There has
been renewed interest in one-carbon metabolism during the past several
years, engendered by recent insights that indicate that modest dietary
inadequacies of (folate, B12, B6 and B2, choline and methionine), of
a degree insufficient to cause classical deficiency syndromes, can still
contribute to important diseases such as neural tube defects, cardiovascular
disease and cancer.” To the list should be added cognitive diseases.
Good Health!
Related
Products:
