Vitamin E supplements may halve the risk of cardiovascular events among diabetics, if they carry a particular version of a gene, says new research from Israel.
Diabetics with the haptoglobin (Hp) 2-2 gene, associated with an inferior antioxidant protection and a raised risk of cardiovascular events, were afforded protection from vitamin E supplements, according to the research published in the journal Arteriosclerosis, Thrombosis, and Vascular Biology. The Hp 2-2 genotype comprises about 2.5 per cent of the general population. "This version of the gene does not determine whether or not an individual will develop diabetes but rather whether an individual with diabetes is susceptible to developing the devastating complications associated with diabetes such as heart disease, kidney disease or visual loss," explained lead researcher Andrew Levy from the Technion Faculty of Medicine. Haptoglobin is a powerful antioxidant protein playing a role in the stabilisation of haemoglobin, preventing inflammation in the walls of arteries. An estimated 19 million people are affected by diabetes in the EU 25, equal to four per cent of the total population. This figure is projected to increase to 26 million by 2030. In the US, there are over 20 million people with diabetes, equal to seven per cent of the population. The total costs are thought to be as much as $132 billion, with $92 billion being direct costs from medication, according to 2002 American Diabetes Association figures. Levy and co-workers recruited 1434 people with type-2 diabetes with the Hp2-2 genee and randomly assigned them to receive a daily vitamin E supplement (400 U/d) or placebo for 18 months. They report that the individuals receiving the vitamin supplements had 50 per cent fewer heart attacks, strokes, and related deaths than Hp 2-2 patients receiving the placebo (2.2 per cent compared to 4.7 per cent, respectively).
"Vitamin E supplementation appears to reduce cardiovascular events in individuals with DM and the Hp 2-2 genotype," stated the authors. Moreover, the researcher report no adverse effects observed in patients who took vitamin E. Levy sais highlights the potential of genetic testing for the Hp 2-2 gene. "[This] may be useful to identify a large group of diabetes individuals who could potentially derive cardiovascular benefit from a very inexpensive treatment," he said. Recently, researchers in Italy reported that daily vitamin E supplements (500 IU) were found to decrease levels of a protein associated with higher risk of atherosclerosis (hardening of the arteries) and ultimately cardiovascular disease in this study with 37 type-2 diabetics (Nutrition, Metabolism and Cardiovascular Diseases). In terms of vitamin E supplements and heart health for the wider population, a recent study reported that a higher dose - 3200 International Units - of vitamin E is needed to reduce oxidative stress in individuals at risk for cardiovascular disease, and this may be why previous trials using lower doses failed to show any benefits for the vitamin (Free Radical Biology and Medicine, doi: 10.1016/j.freeradbiomed.2007.06.019). A number of epidemiological and animal studies have reported that antioxidants like vitamin E, vitamin C and beta-carotene might offer some protection against heart attack in individuals at risk. There are eight forms of vitamin E: four tocopherols (alpha, beta, gamma, delta) and four tocotrienols (alpha, beta, gamma, delta). Alpha-tocopherol (alpha-Toc) is the main source found in supplements and in the European diet, while gamma-tocopherol (gamma-Toc) is the most common form in the American diet. Source: Arteriosclerosis, Thrombosis, and Vascular Biology Published online ahead of print 21 November 2007; doi: 10.1161/ATVBAHA.107.153965
"Vitamin E Supplementation Reduces Cardiovascular Events in a Subgroup of Middle-Aged Individuals With Both Type 2 Diabetes Mellitus and the Haptoglobin 2-2 Genotype. A Prospective Double-Blinded Clinical Trial"
Authors: U. Milman, S. Blum, C. Shapira, D. Aronson, R. Miller-Lotan, Y. Anbinder, J. Alshiek, L. Bennett, M. Kostenko, M. Landau, S. Keidar, Y. Levy, A. Khemlin, A. Radan, and A.P. Levy