Public Release: 

High-Fat Meal May Raise Risk Of Blood Clotting -- Increasing Heart Attack And Stroke Risk

American Heart Association

DALLAS, Nov. 25 -- A high-fat meal can spark a dramatic rise in a blood coagulation factor, which may increase the risk of death from heart disease and stroke, researchers report in this month's Arteriosclerosis, Thrombosis and Vascular Biology, a journal of the American Heart Association.

A diet high in saturated fats -- derived mainly from meat and dairy products -- can lead to high cholesterol levels in the blood, which can contribute to fatty buildup, called plaque, in the body's blood vessels. The obstructions can block blood flow and trigger a heart attack or stroke.

The new study indicates that fat from the diet -- even the so-called good "mono" fats -- also may increase heart attack and stroke risk by increasing the activity of Factor VII, a blood clotter, says the report's primary author, Lone Frost Larsen. She is a doctorate student at the research department of human nutrition and centre for advanced food studies, Royal Veterinary and Agricultural University, Frederiksberg, Denmark.

"The consumption of a high-fat meal might contribute to acute clot formation. This, in turn, may cause a heart attack by blocking an artery," says Larsen.

The study involved feeding 18 healthy young men five different fat meals. The young men, studied over a period of nine months, were given six different meal tests, each at least three weeks a part. During each test, the men fasted overnight, then were given one test meal enriched with either rapeseed oil, olive oil, sunflower oil, palm oil or butter in the morning and a low-fat meal consisting of rice, bananas and raisins in mid-morning. The high-fat meals were 42 percent fat mixed with rice, beef, onion, red pepper and corn. Non-fasting blood samples were collected eight times during the day.

All five different high-fat test meals caused significant increases in Factor VII. Plasma FVIIc, the nonactive coagulation factor, rose 7 percent after the high-fat meal. FVIIa, the active factor causing coagulation, was 60 percent higher after consumption of the high-fat meal when compared to blood levels of the men after eating a low-fat meal.

Plasma FVIIa increased from 48.4 units per liter (U/L) to 81.4 U/L after the high-fat meal and FVIIc increased from a mean fasting value of .81 international units (IU) to .84 IU after the high-fat meal but decreased to .72 IU among individuals following consuming the low-fat meal.

"These changes indicate an immediate prothrombotic effect of the high-fat meals," says Larsen.

Normally when Factor VII is activated, there is an increase in fibrin, the main component of a blood clot, explains Larsen. "It starts a cascade and eventually a clot is formed. This could later block a vessel and cause heart attack (or stroke)."

The researchers are unsure how fat promotes the sudden activation of the coagulation factors in the blood. Previous studies suggested that a relationship exists between Factor VII and an immediate rise in triglycercides after consumption of a high-fat meal. However, the Denmark team found no such association.

The Denmark study also found no difference in the type of fat eaten by the men during the study. It was assumed that olive oil and rapeseed oil would not produce the same effects as the other fats. Both oils are monounsaturated fatty acids (MUFA) and have been considered more heart healthy than saturated fats.

It was thought that MUFA's might not produce high levels of the coagulation factors because the incidence of heart disease is low in the Mediterranean populations where olive oil is the primary dietary fat, Larsen says. "The people of the Mediterranean have lower rates of heart disease. But our study showed no differences among the fats."

The results, however, showed that fats rich in MUFA do not differ from fats rich in polyunsaturated or saturated fatty acids with regard to the acute effects on the coagulation factors. This may be because the study was done on Danish men who regularly eat diets high in saturated fat. "It may be that we need to see what happens in individuals who eat different dietary fats for a longer period to time," she says.

Since the study was undertaken in healthy young men, another element that remains unknown is whether a more dramatic response would be seen in individuals who already have heart disease. "People with heart disease already have higher levels of Factor VII," she says. "When they have a fatty meal, Factor VII may rise even higher than in the young healthy men, which might put them at even higher risk."

Further study is needed to evaluate why high-fat meals lead to Factor VII activation as well as the long-term effects of different edible fats.

"The important finding is there is an increase in Factor VII after the consumption of high-fat meals," she says. "There is no difference in the type of fat you eat. Individuals should eat diets low in fats with lots of vegetables and fruits."

Co-authors are: Peter Marckmann, M.D. and D.Sc., associate professor at the department of human nutrition and centre for advanced food studies; Else-Marie Bladbjerg, Ph.D., research fellow, South Jutland University Center; and Jorgen Jespersen, M.D. and D.Sc., professor at South Jutland, Esbjerg, Denmark.


Media advisory: Larsen can be reached at 011 45-352-82506 or faxed at 011 45-352-82469. (Please do not publish telephone numbers.)

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