Heart, General | December 1, 2015 | Author: The Super Pharmacist
The antioxidant properties of Vitamin E provide many of its benefits and it has been evidenced to play a role in protecting against the oxidation of LDL cholesterol and slowing down the development of arteriosclerosis. As it is a fat soluble vitamin, it also has a preservative quality and acts as a protective agent for Vitamin A both inside the body and food sources (it is also widely used in food industry as a preservative). Vitamin E has also been evidenced to promote the development of normal blood cell formation and the clotting of blood. Some commentators have suggested that Vitamin E also plays a positive role in reducing the likelihood of developing prostate and other cancers, as well as alleviating the impact of a number of other illnesses including skin and joint problems, endometriosis, impaired memory and circulatory disorders. However, the evidence base is small with no conclusive evidence to support these claims. More recent studies have resulted in suggestions that high dose Vitamin E slows the progression of Alzheimer’s disease, but again there is no strong evidence to support this claim.
Vitamin E is found in a wide range of vegetable and seed oils including safflower and corn, sunflower seeds, whole grains and wheat germ, soybean, nuts and a range of leafy vegetables. Refining grains and heavy processing diminishes Vitamin E content, as does cooking at high temperatures and storage of foods. Because of this, foods such as white bread, white rice, pasta and cooking fats aren’t regarded as a Vitamin E source. The large amount of heavily processed food and modern storage methods make it difficult for a large section of the population to obtain an adequate supply of their diet. Babies and children receive their Vitamin E intake via either human milk or commercial formulas, although some premature neonates may require initial supplementation. The evidence suggests that Vitamin E supplementation for this group may reduce the risk of Vitamin E related complications but that it can also increase the risk of infection (1).
Vitamin E deficiency is much more common in developing countries where there is widespread inadequate intake of Vitamin E due to the limited availability of certain foods. In developed countries, deficiency is most often the result of genetic conditions related to fat malabsorption such as cystic fibrosis, pancreatitis, abetaliproproteinemia (a genetic absence of apolipoprotein B that results in Bassen-Kornzweig syndrome) and chronic cholestatic hepatobiliary disease.
Synthetic Vitamin E does not come from food sources and is mainly derived from petroleum products. Most multi-vitamins contain a form of semi-synthetic Vitamin E that has been extracted from plant oil, although due to its chemical structure it is only approximately 12% as potent as naturally occurring Vitamin E. Evidence also suggests that synthetic Vitamin E is also excreted much faster than natural Vitamin E, giving it less time to enter the system, reduced bioavailability, and decreased overall absorption. The molecular structure of naturally occurring Vitamin E makes it much more effective as both a health improving and health protecting option than its synthetic counterpart.
A number of large scale population-based, observational studies have suggested that Vitamin E has a role to play in reducing the risk of developing coronary heart disease (CHD) – a study of approximately 85,000 healthcare professionals, published in the New England Journal of Medicine, found that heart disease rates were 30-40% lower in individuals taking Vitamin E supplements (2). A study undertaken in Finland with a study group of just over 5000 men and women found heart disease rates to be lower in individuals who had a Vitamin E rich diet (3). Due to the wide range of confounding variables present in individuals who may also take Vitamin E supplements, a number of randomised controlled trials have been undertaken to determine the true value of Vitamin E. The Heart Outcomes Prevention Evaluation (HOPE) study – an RCT looking at the impact of Vitamin E supplementation in a study group of over 10,000 people – found that participations taking a 400 IU/day dose of Vitamin E demonstrated no fewer cardiovascular events or incidents of hospitalisation when compared to the control group who took no Vitamin E or a placebo (4). The HOPE – TOO follow up study, conducted 2.5 years later, found that 2500 of the participants who had continued to take Vitamin E supplements demonstrated no significant additional protection against CHD, heart attacks, strokes, unstable angina (5). Interestingly, the same study also discovered the unexpected finding that the control group who had taken Vitamin E had a 13% increased risk factor of experiencing heart failure and 21% increased chance of hospitalisation. These results are statistically significant due the number of participants involved, although there have been no large scale studies to follow up these findings. A similar large scale randomised controlled trial of 40,000 healthy women who were administered either Vitamin E or placebo supplementation over the course of 10 years found that the supplements provided no cardiovascular benefits. Again significantly, all-cause mortality was actually higher in the group taking Vitamin E over the course of the research programme (6). The majority of available clinical evidence does not support the suggestion that the routine use of Vitamin E supplements reduces the risk of CVD. More research is required, over a longer period of time, to determine if supplementation has a genuinely preventative mechanism in place – however, based on current evidence, Vitamin E supplementation provides little or no additional benefit and is a potential risk factor for adverse cardiovascular events in some sections of the population.