Vitamin E

An extensive review noted that the data in relation to a connection between vitamin E and CVD risk are strong and convincing. in a large cross-cultural European (WHO/MONiCA) observational study, a strong inverse relationship (r2 = 0.60, p < 0.005) was found between plasma concentrations of lipid-standardized vitamin E and mortality from coronary heart disease (CHD) across 16 populations. in a detailed analysis, this relationship was found to be stronger than that between mortality and plasma cholesterol, smoking, and diastolic blood pressure combined (r2 = 0.44, p < 0.02). in a case-control study in Scotland, patients with previously undiagnosed angina pectoris were found to have lower levels of plasma lipid-standardized vitamin E than controls. After adjustment for classical CHD risk factors, men in the highest quintile of lipid-standardized vitamin E level had an almost threefold decrease in risk. Confusingly, some studies have reported a higher CVD risk in individuals with increased plasma total vitamin E, but these results are probably driven by elevated blood lipids. Vitamin E is carried in the lipoproteins, and it is important to lipid standardize plasma concentrations of this, and other, lipophilic antioxidants.

The Nurses' Health Study (women) and the Health Professionals Study (men) were initiated in the USA in 1980 and 1986, respectively, and recruited almost 200 000 subjects. it was found that women at the high end of vitamin E intake from diet alone had a small and non-significant decrease in CVD risk; however, those women in the highest quintile of vitamin E intake (more than 100 iU day"1) had an RR (Ci) for CVD of 0.54 (0.36-0.82). it should be noted that an intake of

100 IU day"1 of vitamin E is achievable only by using supplements: intake from food alone is unlikely be more than 15IUday_1. In this study, protection against CVD was seen only in those women who had taken vitamin E supplements for at least 2 years. In the Health Professionals Follow-up Study the findings were very similar. Supplemental, but not dietary, intake of vitamin E (more than 100IUday_1) in men was associated with a significant decrease in CVD risk, averaging over 30%, but again the effect was seen only if supplements had been taken for at least 2 years. A separate study in the USA of more than 11000 elderly subjects showed that the use of vitamin E supplements was associated with a significant decrease in the risk of heart disease (RR (CI) of 0.53 (0.34-0.84)). The results also showed a significant decrease in all-cause mortality in users of vitamin E supplements and suggested that long-term use was beneficial. A study in Finland of more than 5000 men and women showed an average of 40% lower CVD risk in the highest versus the lowest tertile of vitamin E intake. Interestingly, most (97%) of subjects in this study did not take supplements, indicating that the protective effect was due to higher intake from food. An inverse association between dietary vitamin E intake and heart disease was also seen in The Women's Iowa Health Study, which involved almost 35 000 postmenopausal women. In this study, an RR (CI) of 0.38 (0.18-0.80) for CVD mortality was seen in women in the highest quintile relative to those in the lowest quintile of vitamin E intake from food alone. However, the Medical Research Council Trial of Assessment and Management of Older People in the Community (UK) found no relation between either dietary intake of vitamin E or plasma concentration of lipid-standardized a-tocopherol and all-cause mortality or death from CVD in 1214 elderly participants followed for a median of 4.4 years.

Cancer is caused by mutations in key genes. Anything that protects DNA will, in theory, help to prevent cancer-causing mutations. Lipid peroxide degradation products are reported to be carcinogenic, and vitamin E opposes lipid peroxidation, possibly conferring indirect protection against cancer. Furthermore, by interacting with reactive species elsewhere in the cell, vitamin E may spare other antioxidants, thereby also indirectly protecting DNA. Vitamin E reportedly protects against cancer of the upper digestive tract, skin cancer, including melanoma, and lung cancer. Follow-up analysis of the placebo group of the Finnish ATBC (Alpha Tocopherol Beta Carotene) study (incidentally, a study that showed no protection against lung cancer in a high-risk group supplemented with a-tocopherol and/or ^-carotene) showed that there was a 36% higher incidence of lung cancer in those in the lowest quartile than in those in the highest quartile of diet-derived vitamin E. Vitamin E from dietary sources, but not supplements, has been reported to confer modest protection against breast cancer; however, as with vitamin C, no association was seen between vitamin E intake and the risk of ovarian cancer in the Nurses' Health Study follow-up.

Colorectal cancer is the second and third most common cancer in men and women, respectively. Dietary influences on the risk of colorectal cancer are currently unclear, and, based on recent findings of large prospective trials, it has been suggested that the influence of antioxidant-rich foods has been overstated. Nonetheless, there is evidence that vitamin E may be protective. In a case-control study in the USA of almost 1000 cases of rectal cancer, the risk was reported to be modestly decreased in women with a high vitamin E intake, but not in men. In a meta-analysis of five prospective nested case-control studies, there was a marginal decrease in the incidence of colorectal cancer in those in the highest quartile of plasma a-tocopherol, although no significant inverse association was seen in any of the studies individually. In the Iowa Women's Health Study, women with the highest risk of colon cancer were those with the lowest intake of vitamin E, although the relationship was significant only in women aged 55-59 years.

In addition to its antioxidant properties, vitamin E is reported to have immune-boosting and anti-inflammatory effects and to inhibit cell division, all of which may help explain the reported relationship between low intake or plasma concentrations of vitamin E and increased risk of various cancers. Currently, there is much interest in vitamin E in association with selenium in relation to the prevention of prostate, lung, and colon cancer. Indeed, the combination of vitamin E with other antioxidant micronutrients may be much more important than vitamin E alone. Furthermore, the different members of the vitamin E family may play cooperative or complementary roles in modulating the risk of disease. In terms of cancer prevention, 7-tocopherol is attracting much interest. Dietary intake of this form of vitamin E can be up to three times higher than that of a-tocopherol. Corn, canola, palm, soya bean, and peanut oils contain more 7-tocopherol than a-tocopherol. Despite a higher intake, however, our plasma levels of 7-tocopherol are only around 10% of those of a-tocopherol, owing to preferential placement of the a-form into very low-density lipoproteins. Interestingly, higher tissue levels of a-tocopherol are reportedly found in animals fed both a-tocopherol and 7-tocopherol than in animals fed a-tocopherol alone, suggesting that intake of both forms may enhance the enrichment of tissues. Furthermore, the lower reaches of the gastrointestinal tract may contain high levels of 7-tocopherol, and this may help to destroy fecal mutagens. None of the epidemiological studies to date have estimated the dietary intake of 7-tocopherol, but the few studies that have measured plasma levels of 7-tocopherol show interesting results. In a nested case-control study of 6000 Japanese men, there was a statistically significant inverse relationship between the risk of cancer of the upper digestive tract and plasma levels of 7-tocopherol but not a-tocopherol. In a nested case-control study in the USA, a statistically significant protective effect against prostate cancer was found only when both plasma a-tocopherol and 7-tocopherol levels were high, with a five-fold decrease in prostate cancer in those in the highest quintile relative to those in the lowest quintile. Some of the putative effect of 7-tocopherol may be mediated through its antioxidant properties; however, 7-tocopherol has other properties relevant to cancer prevention, including effects on oncogenes and tumor suppressor genes and on cell cycle events, that the a-form does not have or demonstrates to a lesser extent. It is of interest that most vitamin E supplementation trials to date have used a-tocopherol. It may be that intake of both isomers is needed for optimal tissue uptake and effect. Furthermore, in view of the ability of a-tocopherol to displace bound 7-tocopherol, supplementation with the a-form alone may be counterproductive, in that it may deplete tissues of 7-tocopherol. Further studies are needed in this area.

The brain is rich in unsaturated fatty acids, and there is a reasonable rationale for the protection of lipid-rich neurones by vitamin E. Plasma and cere-brospinal a-tocopherol concentrations were found to be low in patients with Alzheimer's disease in some but not all studies. Cognitive function is reported to be directly correlated with plasma a-tocopherol levels. A high intake of vitamin E is associated with a decreased risk of the subsequent development of Alzheimer's disease, and an 8 month delay in significant worsening of Alzheimer's disease was reported in association with increased intakes of vitamin E. In the NHANES III study, better memory performance in elderly participants was reportedly found in those with higher plasma a-tocopherol levels. Based on data such as these, vitamin E (2000IU day-1) is currently being studied in relation to its possible ability to delay the onset of Alzheimer's disease in people with mild cognitive impairment.

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