Writer makes an interesting association between milk carbohydrates (and
sugar) and CVD.
Diet-induced Folate Deficiency 23 November 2002
Bill D. Misner,
Director R & D
E-CAPS Inc. Spokane, Wa. USA 99205
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It would appear that an the association between the C677T polymorphism of
methylenetetrahydrofolate reductase (MTHFR) and deep vein thrombosis may
present a predisposition to Homocysteine-related cardiovascular disease.
Grant emphasized dietary links to ischemic heart disease (IHD) and coronary
heart disease (CHD) mortality from a correlation from for various age groups
aged 35+. His paper presented a multi-country statistical approach involving
32 countries suggesting dietary links to IHD and CHD. For IHD, milk
carbohydrates were found to have the highest statistical association for
males aged 35+ and females aged 65+, while for females aged 35-64, sugar was
found to have the highest association. In the case of CHD, non-fat milk was
found to have the highest association for males aged 45+ and females aged
75+, while for females 65-74, milk carbohydrates and sugar had the highest
associations, and for females aged 45-64, sugar had the highest association.
A number of mechanisms proposed in the literature to explain the milk
carbohydrate or non-fat milk association. One of the most prominent theories
is that animal proteins contribute to homocysteine (Hcy) production; however,
milk more than meat lacks adequate B vitamins to convert Hcy to useful
products. Lactose and calcium in conjunction with Hcy from consumption of
non-fat milk may also contribute to calcification of the arteries [1].
Homocysteine Hcy plays an important role in the etiology of heart disease
through its role in the development of atherosclerosis. Hcy is derived from
the amino acid methionine, more common in animal proteins than in vegetable
proteins, and can be converted back to methionine with the help of folic acid
and vitamin B12. It can also be eliminated from the body through the action
of vitamin B6. Those who have elevated levels of Hcy are generally found to
be deficient in the B vitamins [2, 3, 4], which can be overcome by vitamin
supplementation [5, 6, 7, 8]. When dietary vitamin deficiency is factored
along side of genetic predisposition, the significance may hypothetically far
exceed the presented of "highly significant [9]" value. Preventative medicine
supports folate supplementation for reducing the dietary and genetic
influences on cardiovascular disease.
References
[1]-Milk and Other Dietary Influences on Coronary Heart Disease, W. B.
Grant, Ph.D. In Altern Med Rev 1998;3(4):281-294.
[2] Ubbink JB, Vermaak WJH, van der Merwe A, Becker PJ. Vitamin B-12,
vitamin B-6, and folate nutritional status in men with hyperhomocysteinemia.
Am J Clin Nutr 1993;57:47-53.
[3] McCully KS. Homocysteine, folate, vitamin B6, and cardiovascular
disease. JAMA 1998;279:392-393.
[4] Rimm EB, Willett WC, Hu FB, et al. Folate and vitamin B6 from diet and
supplements in relation to risk of coronary heart disease among women. JAMA
1998;279:359-364.
[5] Barber GW, Spaeth GL. The successful treatment of homocystinuria with
pyridoxine. J Pediatrics 1969;463:463-478.
[6] Selhub J, Jacques PF, Wilson PWF, et al. Vitamin status and intake as
primary determinants of homocysteinemia in an elderly population. JAMA
1993;270:2693-2698.
[7] Ubbink JB, Vermaak WJH, van der Merwe A, et al. Vitamin requirements for
the treatment of hyperhomocysteinemia in humans. J Nutr 1994;124:1927-1933.
[8] Ubbink JB, Becker PJ, Vermaak WJH, Delport R. Results of B- vitamin
supplementation study used in a prediction model to define a reference range
for plasma homocysteine. Clin Chem 1995;41:1033-1037.
[9] Wald DS, Law M, Morris JK. Homocysteine and cardiovascular disease:
evidence on causality from a meta-analysis. BMJ 2002; 325: 1202- 6.
Bill Misner Ph.D. C.S.M.T. Director R & D E-CAPS Inc.
Competing interests: The author declares competing interests in exogenous
supplements industry.
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