Elevated homocysteine levels may play a role in dementia
Elevated levels of the amino acid homocysteine in the blood have been linked to increased risk of cerebrovascular disease, and stroke in particular. Cerebrovascular disease can lead to cognitive impairment, but elevated homocysteine levels have also been implicated in the development of cognitive impairment independent of cerebrovascular disease. A study recently published in the journal
suggests that elevated homocysteine levels may in fact lead to atrophy of brain tissues, which is a factor in the development of Alzheimer’s disease and other forms of dementia.
Australian researchers studied 36 healthy men and women (average age 71) who volunteered for this study. Participants had no history of neurologic or psychiatric disorders and no history of cerebrovascular disease. Some participants did have conditions known to be risk factors for cerebrovascular disease—high blood pressure, coronary artery disease, and diabetes. In addition, participants were not taking any of the vitamins that are involved in regulating homocysteine levels in the blood—folic acid and vitamins B6 and B12.
Participants underwent the following tests:
- Blood test – fasting blood sample to test for levels of homocysteine, vitamin B12, folate and creatinine (a substance involved in kidney function)
- MRI scans – to look for brain atrophy and white matter hyperintensities (problems in the brain’s white matter tissues that may be involved in the development of dementia)
- Neuropsychological tests – to test cognitive function
Researchers looked at the homocysteine levels of participants, their MRI scans, and their cognitive test scores to see whether people with elevated homocysteine levels had signs of brain atrophy or cognitive decline.
People with elevated blood levels of homocysteine were about 2 times more likely to have brain atrophy visible on their MRI scans than people with normal homocysteine levels. However, elevated homocysteine was not correlated with any signs of cognitive decline or with white matter hyperintensities.
Although these results are interesting, there are limitations to this study. The number of people studied was quite small. Because they all volunteered for the study, they may not be representative of the general population. And because homocysteine levels, MRI scans, and cognitive function tests were all performed at the same point in time, there is no way to know which came first—the elevated homocysteine levels or the brain atrophy. Finally, this study was not designed to compare homocysteine and brain atrophy between groups of people with and without the two conditions. Such a comparison design is necessary to draw conclusions about cause and effect.
This study lends some more evidence to the idea that elevated homocysteine levels may be involved in the development of dementias, such as Alzheimer’s disease. However, another study published in the same issue of
supports the theory that elevated homocysteine affects the risk of Alzheimer’s disease only as a result of its role in the development of cerebrovascular disease.
Either way, keeping your homocysteine levels in the normal range is a good idea to try to ward off cerebrovascular disease or Alzheimer’s disease. How can you manage your homocysteine levels? By eating a diet that contains adequate amounts of folic acid—up to 1 mg per day.
What foods contain folic acid? Plenty! Because research has shown that folic acid intake in the early days of pregnancy helps prevent birth defects, the federal government has mandated that a number of grain products be fortified with folic acid, including:
- Breakfast cereals
- Most enriched breads
Foods that naturally contain folic acid include:
- Leafy dark green vegetables
- Legumes (dried beans and peas)
- Citrus fruits and juices
- Most berries
Sachdev PS, et al. Relationship between plasma homocysteine levels and brain atrophy in healthy elderly individuals.
. May 28, 2002;58:1539-1541.
Toole JF and Jack CR. Food (and vitamins) for thought.
. May 28, 2002;58:1449-1450.
Last reviewed May 31, 2002
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