Last week’s widely reported news about research linking Alzheimer’s disease and elevated levels of homocysteine a blood amino acid might tempt you to start popping folic acid and B vitamin supplements, which are known to lower those levels.

Don’t do it, say experts, before checking with your doctor. Self-treating with these supplements carries a small but serious risk of injury.

Daily doses above 1 milligram of folic acid the vitamin with the best record for lowering homocysteine levels can cover up vitamin B12 deficiency, which in turn can trigger irreversible nerve damage, according to the Institute of Medicine, an arm of the National Academy of Sciences. Choosing a lower-dose folic acid supplement won’t necessarily be the answer. When the folic acid from pills is combined with dietary sources including grain products, which have been fortified with folic acid since 1998 your intake may be high.

“If you take a supplement, you’re sure to be over that (1 mg level),” said Irwin Rosenberg, dean of the Friedman School of Nutrition, Science and Policy at Tufts University and a co-author of the new study. “We don’t know that to be safe unless you’re doing it with some kind of medical supervision.”

Self-medication with vitamins B6 and B12, the other vitamins shown to lower homocysteine, likewise poses problems. These include ineffectiveness at low doses (scientists don’t yet know what doses work) and toxicity at high doses. For example, vitamin B6, also known as pyridoxine, can cause painful nerve damage in daily supplement doses of 50 mg or more, according to experts.

You won’t know if your homocysteine could benefit from adjustment unless you have it tested; in the study, levels above 14 micromoles per liter were considered high. But no quality control for testing exists, so measurements may vary from one lab to another. There’s also the matter that the research does not prove a cause-and-effect relationship between high homocysteine levels and Alzheimer’s, just an association.

Paul Aisen, a professor in the departments of neurology and medicine at Georgetown University, is working on that. But even his research will not speak to the key question of whether supplementation can forestall or prevent the disease in at-risk but symptom-free people.