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Thyroidal function: Vitamin E facilitates selenium metabolism and is therefore critical for normal thyroid function. Excessive supplementation of vitamin E without selenium may deplete selenium and therefore contribute to thyroid disease (both hypo and hyper).

Rough file:

Long-Evans Cinnamon (LEC) rats are autosomal recessive mutants that develop hepatitis and hepatocellular carcinoma. Because copper accumulates in the livers of these rats, and some of their clinical and pathological features are similar to those of patients with Wilson's disease, LEC rats are proposed as an animal model of Wilson's disease. It has been thought that unbound copper generates free radicals, which act as hemolytic and hepatocytotoxic agents. To examine the effects of vitamin E as an antioxidant on hereditary hepatitis in LEC rats, we fed 3-week-old rats for 25 weeks either vitamin E-deficient, control, or vitamin E-supplemented diets which contained < 0.01 mg of total tocopherols, 2 mg of d,l-alpha-tocopheryl acetate (2 I.U.), and 58.5 mg of d,l-alpha-tocopheryl nicotinate (50 I.U.), respectively, per 100 mg of feed. In males, body weight loss was first observed in the vitamin E-deficient group, and mean ages at which jaundice occurred were in the order: deficient younger than control younger than supplemented groups. The ages when plasma glutamic oxaloacetic transaminase and glutamic pyruvic transaminase activities began to increase sharply and peaked followed the same order. Thus, it is likely that free radicals are involved in jaundice and hepatitis in LEC male rats, and they are a model for studying the relationship of copper, free radicals, and hepatitis. Conversely, in females, no apparent differences in clinical and biochemical changes were observed among the three groups. Causes for the discrepancy between the sexes remain to be clarified. vitamin E decreases hepatitis in LEC male rats. not females.doc

The ratio of serum vitamin E to serum lipids (cholesterol, triglycerides, phospholipids) was highest in healthy controls and in patients in group A with cirrhosis and normal transaminases and bilirubin. Patients in group A with acute or chronic ethanol intoxication and high bilirubin levels had a 37% lower lipid-standardized vitamin E level than controls. Patients in group B with hemochromatosis, showing high serum iron (> 180 micrograms/dl), a low free iron binding capacity (< 8 mumol/l) and high ferritin-levels (< 450 micrograms/l), had a 34% lower vitamin E/lipid ratio than healthy controls. No significant lowering of the vitamin E/lipid ratio was observed in the other patients in group B. A significant decrease (37%) in the vitamin E/lipid ratio was only detectable in patients with Wilson's disease (group C) showing high free serum copper (> 10 micrograms/dl). The data support a role for free radicals in the pathogenesis of active liver diseases. vitamin E low in cirrhosis, hemochromatosis, & Wilson's.doc

OBJECTIVE: Oxygen free radicals (OFR) play a role in the pathogenesis of tissue damage in many pathological conditions via the peroxidation of membrane phospholipids. Experimental studies showed an elevated oxidative stress during hyperthyroidism, which is reduced by treatment. Therapy per se might decrease oxidative stress. DESIGN: Fasting plasma levels of thiobarbituric acid reacting substances (TBARS), vitamin E and coenzyme Q10 were measured in 22 hyperthyroid patients, before treatment for their thyroid disease, after 13.9 [SD 9.2] weeks, when they achieved an euthyroid state on thyrostatic drugs, and again after 47.7 [21.0] weeks, off therapy. No patient presented additional risk factors for increased lipoperoxidation and/or increased OFR levels. Smokers were asked to abstain from smoking overnight. METHODS: All analytes were measured by HPLC. RESULTS: In hyperthyroidism, plasma levels of TBARS were increased, whereas vitamin E and coenzyme Q10 were reduced. Average levels of TBARS and antioxidant agents returned to normal in euthyroid patients, without differences in relation to stop of thyrostatic therapy. CONCLUSIONS: Our data confirm the presence of oxidative stress and decreased anti-oxidant metabolites in hyperthyroid patients, which are corrected in euthyroidism, without any influence of thyrostatic drugs per se. Nutritional support with antioxidant agents, which are defective during hyperthyroidism, is warranted.vitamin E and Co-Q-10 deficient in hyperT.doc

Some Vitamin E Supplements May Increase Prostate Cancer Risk

Men with high blood levels of gamma-tocopherol, a form of vitamin E not usually found in vitamin supplements, have a reduced risk for prostate cancer. However, many vitamin E supplements contain only alpha tocopherol, which can actually lower levels of gamma tocopherol.


  • Researchers looked at blood samples taken from nearly 10,500 men.
  • The 20% with the highest levels of gamma-tocopherol were five times less likely than men with the lowest levels of the vitamin to get prostate cancer over the next seven years.
Vitamin E is found naturally in vegetable and seed oils, nuts, whole grains and leafy greens, but levels of the different forms of vitamin E vary.

Men with high levels of alpha-tocopherol and the mineral selenium, were less likely to develop prostate cancer only when gamma-tocopherol was also high, suggesting gamma-tocopherol boosts the power of the other two antioxidants.

In an editorial accompanying the report, Dr. Edward Giovannucci of Harvard Medical School in Boston, Massachusetts calls the findings "further reason for optimism" that vitamin E and other compounds may fight prostate cancer.

However, he notes that some vitamin E supplements--mainly alpha-tocopherol--can lower blood levels of gamma-tocopherol. According to Dr. Giovannucci, the average American's bloodstream is five times richer in alpha-tocopherol than gamma-tocopherol. And, that difference jumps to 20-fold among people who take vitamin E supplements.

Since vitamin E supplements may displace gamma-tocopherol, the researchers conclude, future studies aimed at prostate cancer prevention should include both forms of vitamin E.

Journal of the National Cancer Institute, December 20, 2000; 92: 44-49