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MIT Study Uncovers Potential Risks of Fasting on Cancer Development in Mice Despite Regenerative Benefits (120 notícias)

Publicado em 22 de agosto de 2024

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The recent MIT study has brought to light both the upsides and the potential risks of fasting, particularly when it comes to intestinal stem cell regeneration and the development of cancer in mice. The findings show that while fasting can boost the repair of the intestine following injuries, it might also increase the chance of cancer under certain circumstances.

Reported by the esteemed institute yesterday, researchers discovered that fasting activates pathways for enhanced regeneration once refeeding begins. Although offering a new window into the health benefits of dietary interventions, the researchers stumbled upon a critical concern—after fasting, mice were more likely to develop early-stage intestinal tumors when exposed to cancer-causing mutations during their refeeding period.

Focusing on the intricacies of fasting, scientists found that intestinal stem cells, paramount to the regular replenishment of the intestinal lining, diminished their regenerative capabilities during the fast, only to surge once the fast was broken. In essence, the food-deprived state made these cells more resilient, relying on lipids for survival, whereas the post-fast period triggered an increased proliferative state essential for rebuilding the intestinal tissues.

"Having more stem cell activity is good for regeneration, but too much of a good thing over time can have less favorable consequences," Omer Yilmaz, an MIT associate professor of biology and senior author of the new study, told MIT News. The team's prior work dating back to 2018 had already hinted at this regenerative phenomenon, but the latest research paints a more nuanced picture, connecting fasting, refeeding, and the increased risk of cancer when mutations coincide with the regenerative spike.

The study further indicated that this regenerative boost is due, in part, to the activation of the mTOR cellular signaling pathway, which is known for its role in cell growth and metabolism. But, with this uptick in cell proliferation, there's a heightened vulnerability—if a cancer-causing gene is activated during this period, the likelihood of developing precancerous polyps increases compared to the fasting state.

While the implications for human health are not yet concrete, the findings prod at the potential for fasting as a double-edged sword: a healer in times of intestinal duress or a harm accelerator in the face of carcinogenic threats. Yilmaz cautions, while the regenerative benefits for those suffering from intestinal injuries are clear, there's a shadow to the silver lining when considering cancer risks.

Outside input came from Ophir Klein, a professor of medicine not involved in the study, who recognized the research as a pivotal stepping stone towards understanding how diet impacts stem cell behavior and cancer risk. Klein suggests that polyamines, compounds that the study explored in the context of intestinal repair, might hold promise for future treatments but advises caution when aligning dietary regimens with regenerative goals, given the risk factors illuminated by the MIT research team.

This research was rooted in grants from prominent institutions like the Pew-Stewart Trust and the Koch Institute-Dana Farber/Harvard Cancer Center Bridge Project, highlighting the significance of understanding dietary effects on cell regeneration and cancer development.