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WHAT DO HOMOCYSTEINE BLOOD LEVELS HAVE TO DO WITH ALZHEIMER’S?
MAYBE A LOT.

(December 2002)

A very good study from Boston University and Tufts University in Boston strongly suggests that a high blood level of the amino acid homocysteine in persons age 65 and older is a very significant risk factor for Alzheimer's and other dementias. They enrolled 1,092 men and women average age 76 years (range 65 to 94), did blood homocysteine levels, and then followed the subjects for eight years, during which period, 111 of the subjects developed dementia, 80 percent of which was diagnosed as Alzheimer's disease.

As people grow older, homocysteine levels increase, so the investigators divided the group into five-year age categories. They then, in each age group, divided the participants into quartiles from lowest to highest blood homocysteine levels. Those in the highest 25 percent (highest quartile) of homocysteine levels had a doubled risk of developing Alzheimer’s compared to those with homocysteine levels in the lowest 25 percent (lowest quartile). Anyone with a blood homocysteine level considered elevated also had a doubled risk of developing Alzheimer’s.

The authors concluded, "An increased homocysteine level is a strong, independent risk factor for the development of dementia and Alzheimer’s disease".

Commentary: Two prior studies, neither with a study design as good as this one, found generally similar results. The finding is intriguing. A high homocysteine level is a risk factor for arteriosclerosis of arteries in the neck and extremities, and is probably a risk factor for arteriosclerosis of coronary blood vessels and, therefore, a risk factor for coronary heart disease and heart attacks. Why it should be a risk factor for Alzheimer’s and other dementias is not at all clear; so, we need additional confirmatory studies. Furthermore, it is also possible that those with high homocysteine levels had both Alzheimer’s disease and arteriosclerosis of the blood vessels of the brain, and that the elevated homocysteine levels related to the latter, not the Alzheimer’s.

We do have a way of lowering homocysteine levels in many people with high levels and keeping homocysteine levels reasonably low in others, and that is, by getting plenty of folic acid in the diet or in supplements. Everybody should get at least 400 micrograms of folic acid, and preferably 800 micrograms, in the diet daily (CLICK HERE for foods containing good amounts of folic acid). Additionally, all women who plan to or might get pregnant should take a 400 microgram folic acid supplement each day (to prevent certain brain and spinal cord abnormalities in their newborns), as should everyone over age 60 (older people do not absorb dietary folic acid as well).

Very interesting indeed, but we do need additional studies before we can come to any conclusions.

A still not fully-answered question is what should be considered the desirable amount of folic acid intake each day. Some people may need 800 to 1,000 micrograms to lower their homocysteine levels. Folic acid also appears to reduce risk of heart attack by mechanisms other than lowering homocysteine levels. The standard recommendation (including prior recommendations of Healthful Life) is to get 400 micrograms in the diet and, if there is any question about whether you are getting it, take a 400 microgram folic acid supplement (as indicated, women who might get pregnant and those over age 60 should be taking a supplement anyway).

Another, and a perfectly reasonable, recommendation would be for everyone to get at least 400 micrograms in the diet and take a 400 micrograms supplement. Older persons who absorb folates less well could get their dietary folate from folate-fortified foods, particularly some cereals (read the labels). The folic acid in folate-fortified foods is absorbed about as well as supplements. Healthful Life now urges that every adult aim for a daily intake (by diet or by diet plus supplement) of 800 micrograms).

Seshadri, S., et al. Plasma homocysteine as a risk factor for dementia and Alzheimer’s disease. The New England Journal of Medicine. Vol 346 (February 14) Pgs 476-483. 2002.

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