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Vitamin E reduces stroke & heart disease

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http://www.pslgroup.com/dg/1d9236.htm

Vitamin E Works As Anti-Inflammatory Agent In Type II Diabetes

DALLAS, TX -- July 10, 2000 -- A high intake of vitamin E can help reduce

heart disease and stroke risk in type II diabetics, UT Southwestern

researchers have found.

In a study published in the July 11 issue of Circulation, Drs. Ishwarlal

Jialal and Sridevi Devaraj found that increased inflammation caused by white

blood cells -- monocytes -- was reduced when diabetics were given 1,200

International Units per day of natural vitamin E (alpha-tocopherol) for

three months.

" This is the first study that shows that vitamin E has anti-inflammatory

effects in diabetic patients, " said Dr. Jialal, professor of pathology and

internal medicine. " It could be a further therapy to prevent vascular

complications in diabetes since inflammation seems to be critical as a

causative factor in diabetic vascular disease.''

The main cause of death and morbidity in type II diabetes, also known as

non-insulin dependent diabetes mellitus, are vascular complications.

Previous studies by Dr. Jialal, the principal investigator in this study and

a senior investigator in the Center for Human Nutrition, have shown that

vitamin E is a potent antioxidant.

Type II diabetics with and without macrovascular disease were compared with

nondiabetics.

Twenty-five participants in each of the three groups were given 1,200 IU of

vitamin E daily for three months followed by two-months without the

supplement. Blood was taken from all the patients at the beginning of the

study, after three months and again after the washout. The effect of the

vitamin E was similar in all three groups.

The study showed that type II diabetic patients have increased inflammation,

as shown by the activity of a pivotal cell (the circulating monocyte) in

plaque formation on artery walls.

The monocyte is a crucial and the most readily accessible cell involved in

atherogenesis.

Study data showed that the diabetic monocyte was more active and promoted

more inflammation and more free radicals and cytokines, or messenger

molecules. The diabetic monocyte also caused more adhesion to the lining

cells of the artery wall.

" It was very important to elucidate the pivotal role for inflammation in

diabetic vascular disease and examine how it could be modulated, " said Dr.

Devaraj, assistant professor in the clinical biochemistry and human

metabolism division in the Department of Pathology.

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