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How dangerous are dietary supplements?
The alleged risks posed by dietary supplements is a popular topic in the media. More such articles have appeared in October 2011 in reaction to two study publications (1, 2), which deal with the relationship between the quantity of dietary supplements ingested and mortality (1) and the incidence of prostate cancer (2).
In the following text, we would like to comment briefly on the two studies, in order to demonstrate the inaccuracy of the often over-generalized and undifferentiated statements made by the press.
Dietary Supplements and Mortality Rate in Older Women (1)
The many methodological errors in this study lead to a rejection of the contention that "dietary supplements may increase mortality" on the grounds that it is unscientific. One of the key arguments for our conclusion, among other deficiencies not addressed further here, is the lack of causality: The question of whether the participants took the products due to existing illness or the disease developed because of the quantity ingested is one this study simply cannot make a statement on. A mathematical correlation was constructed, but causality could not be determined. It is well known that this is one of the main problems with epidemiological studies (as early as 1988, Sies proved a strong correlation between a declining birth rate and the declining number of storks in a region (3), but no one would argue that there is a causal relationship).
Finally we would like to mention that the association is strongest with supplemental iron and copper, both minerals that are known for their pro-oxidative activity and that are not widely used in common dietary supplements.
What concrete conclusions can be drawn from this study must be left open at this time.
Vitamin E and the Risks of Prostate Cancer (SELECT) (2)
SELECT was discontinued in 2008 because it was already becoming apparent that the thesis of a 25% reduction in the risk level for prostate cancer would not be confirmable (4). The subsequent follow-up now even showed an increased cancer risk in the intervention group with vitamin E.
An important reason for the performance of SELECT was provided by data from other studies, which suggested a risk reduction. Among these was the Finnish ATBC study, which demonstrated a risk reduction of 32% with an ingested quantity of 50 IU of vitamin E.
The main difference in the SELECT study is the dosage of 400 IU of vitamin E, a dose that corresponds to eight times the ATBC dosage and must be characterised as unphysiological. It is well known that anti-oxidants may become pro-oxidants in high doses, with the corresponding negative effects. In addition to this, SELECT used the all-rac form of alpha-tocopherol, a synthetic substance with eight stereoisomeric forms, of which only one is bioactive and the potential effects of the other forms are unknown (5).
In this case as well, an over-generalization must be rejected. However, it is clear that the misconception “more is better” must once again be brought to the attention of consumers as being false.
(4) Lippman SM; Effect of selenium and vitamin E on risk of prostate cancer and other cancers: the Selenium and Vitamin E Cancer Prevention Trial (SELECT). JAMA. 2009 Jan 7;301(1):39-51. Epub 2008 Dec 9.