Nov 18, 2009 5 min read

In the April 2, 1994, issue of the Lancet, a study was published that found Alzheimer’s disease to be correlated with pathological changes in the brain that had not been known about before. Using a CT scan, the researchers discovered loss of neurons (nerve cells) in a part of the brain called the medial temporal lobe. They found that the average rate of atrophy or deterioration of the medial temporal lobe was 15% per year in patients with Alzheimer’s disease. Because the medial temporal lobe in normal control subjects of the same age shrank at only one-tenth this rate, it was concluded that Alzheimer’s disease cannot be the result of an acceleration of normal aging, but must be the consequence of a disease process.

In a study in the April 2, 2002, Proceedings of the National Academy of Sciences, Rachael I. Scahill and colleagues confirmed and extended this study. Using magnetic resonance imaging, they found increasing brain atrophy to be occurring with advancing Alzheimer’s disease, and they found this atrophy to be occurring before the onset of symptoms of the disease.

Two questions naturally arise from these findings: First, what causes this deterioration of the brain to begin? Second, what can be done to prevent it?

The Homocysteine Connection

By the age of 85 virtually everyone will have some neurofibrillary tangles (the hallmark of Alzheimer’s disease) in their brain, but not everyone will develop Alzheimer’s disease. What is different about those who do and those who don’t? Well, many things, but one of them is that people with Alzheimer’s disease have higher levels of homocysteine in their blood than people without Alzheimer’s disease. Homocysteine is an amino acid that is a normal by-product of protein metabolism. It is toxic, and the body disposes of it quickly through three different pathways if everything is working right. When it is not, homocysteine can accumulate in the body and initiate disease. It has been implicated as a risk factor in cardiovascular disease, stroke, osteoporosis and, since the mid-nineties, Alzheimer’s disease. Evidence that homocysteine can cause the brain atrophy seen in Alzheimer’s disease can be found in three studies.

In the November 1998 issue of the Archives of Neurology, a study published by Robert Clark and colleagues found that Alzheimer’s patients with elevated homocysteine levels had more rapid atrophy of the medial temporal lobe during 3 years of follow-up than those with lower homocysteine levels. The medial temporal lobe contains the center for smell, some areas for memory and learning, and a region where choice is made of thoughts to express. A study in the January 2002 issue of the journal, Brain, found that in people without Alzheimer’s, those with higher plasma homocysteine had more atrophy of the cortex and the hippocampus, both areas of the brain important for memory, than those with lower levels of homocysteine. And finally, in a study published in the journal, Age Ageing, in November 2002, lead author J. H. Williams and colleagues found that the width of the hippocampus shrank as the level of homocysteine rose in healthy older people. They concluded that reducing homocysteine levels in healthy older people may help prevent Alzheimer’s disease.

Epidemiological Studies

These neurological studies confirm epidemiological studies that show high homocysteine levels to be correlated with Alzheimer’s and cognitive impairment. Among these is a study by Sudha Seshadri and colleagues in the February 14, 2002, New England Journal of Medicine which found that a plasma homocysteine level greater than 14 micromoles per liter caused the risk of Alzheimer’s disease to double. (Homocysteine levels should be less than 10 and ideally less than 7.)

Another study by Pierluigi Quadri together with other researchers found high homocysteine levels in subjects with mild cognitive impairment, often a precursor to Alzheimer’s disease. The average homocysteine level in these subjects was 14.6. The study also found that those subjects with the lowest levels of folate (the vitamin folic acid) had a greater risk of Alzheimer’s disease compared to those with the highest levels of folate.

Two of the most recent studies on homocysteine and Alzheimer’s disease have come to similar conclusions. Giovanni Ravaglia and associates published a study in the September 2005 issue of the American Journal of Clinical Nutrition that found elevated plasma homocysteine and low serum folate concentrations to be independent predictors of the development of dementia and Alzheimer’s disease. In the same issue of this journal, Katherine L. Tucker and her colleagues found that high homocysteine levels and low B vitamin concentrations (specifically, folate and vitamins B-6 and B-12) predicted cognitive decline.

How To Lower Your Risk of Alzheimer’s

The take home message of these studies is to lower homocysteine and increase B vitamins. Fortunately, this is not difficult to do. By increasing B vitamins, we also decrease homocysteine. Homocysteine is controlled by three B vitamins – folic acid, B-6 and B-12. These can be optimized by diet and, if necessary, by supplementation. A diet of fresh, whole, unprocessed food is rich in all three of these vitamins. Folic acid is found in green leafy vegetables like spinach, dark greens, asparagus and many other vegetables and fruits. B-6 is also found in fresh vegetables and fruit as well as fish, poultry and meat. B-12 is found only in food of animal origin, but these foods must be fresh as opposed to processed foods such as bacon, hot dogs, and cold cuts. If diet alone does not lower homocysteine levels, then supplementation may be necessary, but supplementation can never substitute for a healthful diet. As its name implies, supplementation is in addition to, not in place of.

Mary Lou Williams, M. Ed., is a lecturer and writer in the field of nutrition. She welcomes inquiries. She can be reached at (239) 267-6480.