Intermittent fasting, the study: increases cancer risk in mice

Intermittent fasting is practiced today by millions of people and followed by many celebrities and politicians, including Italian ones. A study published in ‘Nature’ has highlighted – on mice – its lights and shadows. And among the latter there would also be a greater risk of developing forms of cancer, following the re-feeding phase after the fasting period.

Researchers at the Massachusetts Institute of Technology (MIT) in Boston have analyzed the effects of intermittent fasting on intestinal stem cells and discovered that this diet causes their intense proliferation which has consequences, good such as cell regeneration, but also not positive such as a greater propensity to develop oncological pathology.

The study and the 3 groups

The study involved three groups of rodents: one that fasted for 24 hours, the other for 24 hours and then ate anything during a ‘refeeding’ period, and a control group that ate anything during the experiment. The researchers focused on the regeneration-refeeding link and observed that the ability of intestinal stem cells to multiply was higher during the 24-hour refeeding period in mice that had previously fasted, and with more cancer-causing mutations.

Which, correlated to a greater proliferation, can end up having a negative effect. All this happened precisely in the period in which the mouse returned to eat after 24 hours, precisely. “We have demonstrated that Post-fast refeeding increases intestinal stem cell proliferation and tumor formation” early intestinal, the study says.

The litmus test came when scientists changed a cancer-causing gene in all mice, but the animals that were refed were more likely to develop precancerous polyps than animals that had had the gene ‘switched on’ during the fast.

“In light of our findings, fasting-refeeding cycles should be carefully evaluated and tested when planning strategies based on this type of diet,” the authors conclude, “since post-fasting refeeding leads to an explosion in stem cell-driven regeneration and tumorigenicity.”