There is a longstanding debate as to whether taking vitamin E supplements increases or decreases a person's risk of developing cancer. A new study suggests that both outcomes are a possibility and also explains why.
What influences vitamin E's effect on cancer risk? - A new study investigates.
Many people believe that taking supplements can improve their well-being and decrease their risk of developing numerous health problems.
However, some recent research has suggested that supplements may not, in fact, bring any health benefits. Certain studies - including this one that Medical News Today covered - have gone so far as to suggest that particular dietary supplements could even harm health.
Still, vitamin supplements remain popular. According to preliminary 2018 data that the Council for Responsible Nutrition (CRN) in the United States released, approximately 78 percent of people in the U.S. believe that the dietary supplement industry is "trustworthy."
Moreover, as Brian Wommack, senior vice president of communications at CRN, reports, "Three-quarters of Americans take dietary supplements."
A new study by researchers from Brigham and Women's Hospital in Boston, MA has been looking into the effects of vitamin E on cancer risk - both overall, and in relation to specific forms of cancer - and asking what factors might influence that effect.
"Observational studies of people taking vitamin E have reported benefits, and studies in animal models have suggested a protective effect, but when vitamin E supplements were brought into placebo-controlled clinical trials, the results were null," explains study author Kathryn Hall.
"This made it easy to assume that vitamin E just doesn't work. But, what we've found is that it may have been protective in some and not in others, and that genetic variation is linked to these outcomes," she adds.
Hall and team's aim was to understand why vitamin E can be beneficial in some cases, while it may have no effect or even have a negative impact in others. The investigators' findings appear in the Journal of the National Cancer Institute.
Genetic makeup offers an explanation
The researchers analyzed the data from the Women's Health Study (WHS), which looked at the "benefits and risks of low-dose aspirin and vitamin E in the primary prevention of cardiovascular disease and cancer" in thousands of women from the U.S.
Additionally, the researchers took into account the Women's Genome Health Study, which allowed them to access relevant information about WHS participants' genetic makeup.
Finally, the researchers verified their findings through the Alpha-Tocopherol, Beta-Carotene Cancer Prevention Study, which also looked into the effects of vitamin E on cancer risk.
The researchers found that certain variations in a gene called "COMT" were responsible for vitamin E's impact on the risk of cancer - whether it decreased or increased it for an individual.
COMT encodes the production of an enzyme called "catechol-O-methyltransferase" (COMT), which influences the way in which a person's body processes vitamin E.
Specifically, the investigators explain, the COMT variant that researchers know the most about has three different variants comprising different alleles: met/met, val/met, and val/val.
The team notes that individuals who have the val/val variant of COMT tend to have a more active COMT enzyme compared with people with the met/met allele. In fact, the enzyme is three to four times more active.
The researchers looked at the rates of cancer among participants in the WHS trial. They noted that in the 10 years of the study and the 10 years following it, the women with the met/met variant of COMT who took vitamin E supplements had 14 percent lower cancer rates than women with the met/met allele who took a placebo.
At the same time, participants with the val/val variant of COMT who took vitamin E supplements had 15 percent higher cancer rates compared with participants with the same genetic variant who took a placebo.
These rates remained similar in the case of specific types of cancer as well, including breast, lung, uterine, and colorectal cancer.
"Significant gene-drug interactions are hard to find, and this one is particularly striking. Now we need to understand which cancers are affected, why and how, and these results encourage us to pursue this with robust and rigorous curiosity."
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