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Release: Immediate
October 19, 1999
UI study adds evidence linking homocysteine, high-protein diet to heart attack and stroke risk
IOWA CITY, Iowa -- Studies have shown homocysteine plays a role in blood clots and hardening of the arteries, conditions that can lead to heart attack or stroke. A recent University of Iowa Health Care study indicates that elevated homocysteine can rapidly affect small blood vessels, which likely contributes to high blood pressure. In addition, the UI study adds evidence that vitamin C may prevent homocysteine from damaging both small and large blood vessels.
British researchers previously showed that homocysteine damages large blood vessels, thus contributing to atherosclerosis, and that a week-long vitamin C treatment reverses the effect. The UI study suggests that homocysteine also damages the small blood vessels that control blood pressure, and that vitamin C can reverse the impact within hours, said William G. Haynes, M.D, UI assistant professor of internal medicine and lead investigator of the study.
Methionine, an amino acid derived from animal protein, performs essential functions that produce a homocysteine byproduct. If not removed, the homocysteine damages blood vessel linings by increasing the number of oxygen free radicals. High cholesterol can cause risk factors for heart attacks through the same mechanism. Antioxidants such as vitamin C seem to "quench" or neutralize the free radicals.
"An additional implication of our research is that the methionine found in diets high in animal protein needs more consideration as a contributing factor to elevated homocysteine levels," Haynes said. "Most previous research has focused on how genetics and vitamin B deficiencies cause high homocysteine levels."
A genetic deficiency in a small number of people prevents them from producing enough of the enzyme that normally disposes of homocysteine. Vitamin B supplements (folic acid, B6 and B12) usually help lower homocysteine, but not in some individuals.
The UI team studied how methionine and vitamin C affected homocysteine levels in 40 healthy adults (31 males and 9 females) without risk factors or clinical evidence of atherosclerosis. Some participants drank cranberry juice containing about 8 grams of dissolved methionine -- two to three times the amount many people consume daily through protein-rich foods. Other participants drank a plain juice placebo.
Homocysteine levels in people who consumed the methionine rose to about 25 micromoles per liter of plasma within a few hours. The participants' homocysteine levels returned to normal later that day; however, people who regularly eat protein-rich food may repeatedly raise their homocysteine above the healthy norm of 10 micromoles per liter. An 8-oz lean chicken breast contains about 2 grams of methionine. Other methionine-rich foods include beef, tuna, shrimp and cheese. A homocysteine level above 10 micromoles per liter is increasingly considered a risk factor for coronary artery disease.
"We need to further investigate whether high dietary protein can increase homocysteine levels and cause harm, but the findings suggest that a lot of protein in the diet over time is not a good idea," Haynes said.
Haynes said his team's study also builds on a previous UI study using animal models that showed a high methionine and low folic acid diet lasting one month elevates homocysteine to a level that causes blood vessel dysfunction. That investigation was led by Donald D. Heistad, M.D., UI professor of internal medicine and pharmacology, and head of the cardiovascular disease division; and Steven R. Lentz, M.D., Ph.D., UI associate professor of internal medicine.
When individuals in the study led by Haynes ingested methionine and then took a megadose (2 grams) of vitamin C, their large and small blood vessel function rapidly improved. Haynes emphasized that clinically applying the findings to manage a patient's care or prescribe vitamin C treatments is down the road.
"At this time we do not suggest using megadoses of vitamin C to reverse the risk of high homocysteine levels," he said. "However, the findings indicate that if vitamin B treatments do not lower homocysteine levels, then antioxidants might work to help protect blood vessels and prevent heart attack and stroke."
In addition to investigating whether lower levels of homocysteine may cause blood vessel damage, the UI team will study whether the antioxidant vitamin E might also offer protection.
The findings were published in the Sept. 14 issue of Circulation. The lead author was Prapti M. Kanani, M.D., a former UI fellow in pediatric cardiology who is now an assistant professor of pediatric cardiology at the University of Pittsburgh. In addition to Kanani and Haynes, the UI research team included Christine A. Sinkey, assistant nurse manager in internal medicine; Roger L. Browning, ultrasound technician; Margaret Allaman, assistant researcher; and Howard R. Knapp, M.D., Ph.D., UI professor of pharmacology and internal medicine.
The study was supported by grants from the National Institutes of Health, the Iowa Affiliate of the American Heart Association, and the federal Department of Veterans Affairs. In addition, Kanni received a training grant in pediatric cardiology from the National Institutes of Health, and Haynes was supported by a faculty development grant from the Pharamceutical Research Manufacturers of America Foundation.
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10/19/99
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