The genetic predisposition to weight gain protects breast and prostate cancer

Although a recent campaign by Cancer Research UK highlighted obesity as a risk factor for cancer on par with smoking, the scientific literature on the link between weight gain and cancer risk is not as clear. In a new analysis, researchers from Brunel University London found that weight gain causally protects against breast and prostate cancer. Hasnat Amin, BSc, PhD student at Brunel University London, presented the results of the study at the virtual meeting of the American Society of Human Genetics 2020.

Most of the studies on the effects of obesity on cancer risk are observational. To distinguish causality from correlation, Mr. Amin and his colleagues used an epidemiological technique known as Mendelian randomization. Using data from the UK biobank, they compared cancer rates between people who are genetically predisposed to be heavier and people who are genetically predisposed to be lighter. This allowed the researchers to estimate a causal link between increased weight and cancer risk regardless of confusing variables.

The researchers found that while heavier women have an increased risk of breast cancer, women who genetically tend to be heavier are less likely to develop breast cancer. This inequality suggests that the increased incidence of breast cancer in heavier women is likely due to additional differences between the two groups. Mr. Amin and his colleagues plan to investigate what these differences might look like in the future.

Heavier men were less likely to develop prostate cancer than lighter men, both when observed and when using genetically predicted measures.

Interestingly, this effect is significantly stronger in men exposed to cancer-causing substances at work, which supports the hypothesis that fat cells play a role in the absorption and safe storage of harmful chemicals.

Although the results show that genetic predisposition to weight gain protects against breast and prostate cancer, Amin says more research is needed to understand exactly how that protection is afforded, particularly in breast cancer.

“First of all, it has to be found out by which mechanisms obesity can protect against cancer or be a risk factor for it,” says Amin. “The next step would be to use these mechanisms to maximize obesity’s protective effects on breast and prostate cancer risk without the often-reported negative effects of weight gain on cardiometabolic health.”

Mr. Amin points out that he and his colleagues are not saying that maintaining a calorie excess is a cancer prevention strategy. Instead, public health messages should target the negative effects of obesity while taking into account the positive aspects.

“Public health campaigns often describe obesity as a causal risk factor for cancer and therefore present weight loss as an effective strategy for cancer prevention,” he says. “However, our results contradict this idea.

“In addition, the recommendation of fat loss can even be associated with certain risks, for example if fat cells are involved in the absorption of cancer-causing substances.”

Increased risk of breast cancer in obesity associated with fat cell chemicals