New study finds vitamin E supplements reduce heart attacks and heart disease deaths in diabetics

November 22, 2004 Printer Friendly
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New study finds vitamin E supplements reduce heart attacks and heart disease deaths in diabetics



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New study finds vitamin E supplements reduce heart attacks and heart disease deaths in diabetics
The results of a study published in the November 2004 issue of the American Diabetes Association journal Diabetes Care ( demonstrate that approximately 40 percent of diabetics can lower their risk of experiencing a heart attack and dying from heart disease by taking a vitamin E supplement.

Diabetes greatly increases the risk of cardiovascular disease, as well as other disorders. A team at the Technion-Israel Institute of Technology led by Dr. Andrew Levy of the Faculty of Medicine had discovered that diabetics with the 2-2 form of a blood protein known as haptoglobin experienced up to a 500% increased risk of developing heart disease. Approximately 40 percent of all diabetics have this form of haptoglobin.

The cause of the increased risk is due to haptoglobin 2-2 being a poor antioxidant compared to the other two haptoglobin types. Diabetics create more free radicals that destroy antioxidants, leaving this group with a greater antioxidant deficiency than others with the condition. Free radical damage is one of the factors involved in the development of cardiovascular disease and numerous other disorders experienced by diabetics and other individuals.

In the current study, Dr Levy and colleagues analyzed serum samples from the Heart Outcomes Prevention Evaluation (HOPE) trial, which studied the effect of antioxidants on cardiovascular disease. They found that when diabetics with the 2-2 form of haptoglobin consumed 400 international units of vitamin E per day, their heart attack risk was lowered by 43 percent, and the risk of dying from heart disease was reduced by 55 percent. A five year trial involving 2,000 diabetics with haptoglobin 2-2 is currently being conducted in Israel to confirm these results. Dr Levy commented, "If this larger study confirms our findings, the public health implications will be huge. Vitamin E would represent an inexpensive and safe way to reduce the risk of cardiovascular death and heart attack in a significant proportion of diabetic patients."


Diabetes independently imposes such stress upon the heart and vascular system that the diabetic frequently succumbs from a cardiovascular event rather than the disease itself.

Hyperglycemia and excesses of ineffective insulin cause rampant free-radical activity, lipid peroxidation, glycation (the pathological union of protein and sugar), and increased inflammation (Sears 1999). Impotence, depression, cataracts, glaucoma, atherosclerosis, and dementia often negatively impact a diabetic's quality of life.

Vitamin E's antioxidant properties and its ability to enhance insulin's responsiveness are but a few of the reasons the nutrient should be included in a diabetic protocol. This was clearly evidenced in a 4-month study reported in the American Journal of Clinical Nutrition with subjects receiving (approximately) 900 mg of vitamin E a day. The researchers assessed how well 15 Type II diabetics and 10 healthy controls tolerated glucose before and after vitamin E supplementation. In healthy subjects, glucose removal from the blood increased 17%. In diabetics, total glucose removal increased 47% and nonoxidative glucose metabolism increased 63%. The study established that pharmacologic doses of vitamin E in Type II diabetes improve insulin's action and reduce free-radical activity (Paolisso 1993b).

Vascular endothelial dysfunction (an early marker of atherosclerosis) has been demonstrated in Type II diabetes mellitus. It appears hyperglycemia is particularly destructive to endothelial cells because it increases oxidative stress and impairs the activity of nitric oxide, the endothelial derived relaxing factor (Giugliano et al. 1995). Oxidative injury may be increased in diabetes mellitus because of a weakened defense due to reduced endogenous antioxidants (vitamin E and reduced glutathione). With compromised nitric oxide activity, diabetic-cardiovascular complications (smooth muscle proliferation, platelet activation/aggregation, and leukocyte adherence to the endothelium) are compounded.

Some of the strongest recent evidence of a vitamin E-diabetes benefit comes from researchers at the University of Texas Southwestern Medical Center in Dallas. Scientists found that vitamin E (1200 IU daily) reduced the risk of heart failure in 75 diabetics by curtailing vascular inflammation in the heart. Left unchecked, inflammation can cause cardiac vessels to swell, promoting cardiovascular disease. Dr. Sridevi Devaraj, assistant professor of pathology and lead researcher, termed the end results of the study very encouraging (Devaraj 2001).

Last, elevated levels of CRP, an inflammatory marker, have recently been found to predict the development of Type II diabetes. A newer finding relating to the functions of vitamin E is that high dose vitamin E lowers CRP. Administering 1200 IU of alpha-tocopherol (daily for 3 months) lowered CRP levels by 30%. CRP levels remained reduced 2 months postsupplementation. By preventing vascular inflammation, many of the complications arising from diabetes are overcome (Devaraj et al. 2000).

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The primary purpose of supplementing with vitamin E is to suppress damaging free radicals. Scientific studies have identified the gamma-tocopherol form of vitamin E as being critical to human health.

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When alpha-lipoic acid (which consists of 50 percent “R” lipoic acid and 50 percent “S” lipoic acid) is ingested, it is first converted to its reduced form, R-dihydro-lipoic acid where the main action of lipoic acid is initiated.

R-dihydro-lipoic acid is the reduced (or active) form of R-lipoic acid. R-dihydro-lipoic acid produces the majority of the results attributed to R-lipoic acid and alpha-lipoic acid. When R-dihydro-lipoic acid reacts with a free radical, it is oxidized back to R-lipoic acid, thus making possible the redox cycle of R-lipoic and R-dihydro-lipoic acids at the cellular level. (NADH then reduces R-lipoic back to R-dihydro-lipoic acid.)

By consuming R-dihydro-lipoic acid, you are obtaining the form of R-lipoic acid that is immediately available to cells, without first having to be reduced.

If you have questions or comments, send them to or call 954 766 8433 extension 7716.

For longer life,

Dayna Dye
Editor, Life Extension Update
1100 West Commercial Boulevard
Fort Lauderdale FL 33309
954 766 8433 extension 7716

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