Six-year vitamin E supplementation increased tuberculosis risk by 72% in male smokers who had high dietary vitamin C intake, but vitamin E had no effect on those who had low dietary vitamin C intake, according to a study published in the British Journal of Nutrition.

Previous studies had suggested that vitamin E might improve the immune system. In animal studies vitamin E seemed to protect against various infections.

Harri Hemila and Jaakko Kaprio, of the University of Helsinki, Helsinki, Finland, studied whether vitamin E supplementation might decrease the risk of tuberculosis. They analyzed the data of the randomized trial (Alpha-Tocopherol Beta-Carotene Cancer Prevention Study) which was conducted in Finland between 1985-1993 and included male smokers aged 50-69 years. There were 174 cases of tuberculosis in 29,023 participants during the 6-year supplementation of 50 mg/day vitamin E.

The effect of vitamin E on tuberculosis risk was modified by the intake of vitamin C in diet. Vitamin E had no effect on participants who had dietary vitamin C intake less than 90 mg/day. Unexpectedly, vitamin E supplementation increased tuberculosis risk by 72% in those who had dietary vitamin C intake over 90 mg/day. The most dramatic increase in tuberculosis risk by vitamin E was restricted to a one-year period after the initiation of supplementation.

The US nutritional recommendations, issued by the prestigious Institute of Medicine, consider that vitamin E is safe in amounts up to 1000 mg/day. This new study suggests that in some population groups vitamin E supplementation may be harmful at a substantially lower dose, 50 mg/day.

The researchers concluded that “the consumption of vitamin E supplements by the general population should be discouraged because there is evidence of harm for some people.”

From the Abstract

Vitamin E and β-carotene affect the immune function and might influence the predisposition of man to infections. To examine whether vitamin E or β-carotene supplementation affects tuberculosis risk, we analysed data of the Alpha-Tocopherol Beta-Carotene Cancer Prevention (ATBC) Study, a randomised controlled trial which examined the effects of vitamin E (50 mg/d) and β-carotene (20 mg/d) on lung cancer. The trial was conducted in the general community in Finland in 1985–93; the intervention lasted for 6·1 years (median). The ATBC Study cohort consists of 29 023 males aged 50–69 years, smoking at baseline, with no tuberculosis diagnosis prior to randomisation. Vitamin E supplementation had no overall effect on the incidence of tuberculosis (risk ratio (RR) = 1·18; 95 % CI 0·87, 1·59) nor had β-carotene (RR = 1·07; 95 % CI 0·80, 1·45). Nevertheless, dietary vitamin C intake significantly modified the vitamin E effect. Among participants who obtained 90 mg/d or more of vitamin C in foods (n 13 502), vitamin E supplementation increased tuberculosis risk by 72  (95 % CI 4, 185)%. This effect was restricted to participants who smoked heavily. Finally, in participants not supplemented with vitamin E, dietary vitamin C had a negative association with tuberculosis risk so that the adjusted risk was 60 (95 % CI 16, 81) % lower in the highest intake quartile compared with the lowest. Our finding that vitamin E seemed to transiently increase the risk of tuberculosis in those who smoked heavily and had high dietary vitamin C intake should increase caution towards vitamin E supplementation for improving the immune system.