Recent research from MIT reveals the dual effects of fasting on intestinal health, highlighting both its regenerative benefits and potential cancer risks. Low-calorie diets and intermittent fasting are known to delay age-related diseases and extend lifespan by enhancing the regenerative abilities of intestinal stem cells. However, the new study published in Nature, has identified a critical pathway activated during "refeeding" after fasting that boosts regeneration but also increases cancer risk.
Led by Omer Yilmaz, the study found that while fasting suppresses stem cell regeneration, refeeding triggers a surge in stem cell activity. This heightened regenerative state, beneficial for healing, also makes cells more susceptible to cancerous mutations. "Having more stem cell activity is good for regeneration, but too much of a good thing over time can have less favorable consequences," Yilmaz explains.
The study involved three groups of mice: one fasted for 24 hours, another fasted and then refed, and a control group with no fasting. Results showed that stem cells proliferated most during the refeeding phase, driven by the activation of the mTOR signaling pathway. This pathway enhances protein synthesis, crucial for cell growth, and leads to the production of polyamines, molecules aiding cell division.
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However, the study also found that cancerous mutations occurring during the refeeding phase led to a higher incidence of precancerous polyps compared to mutations during fasting or in non-fasting mice. This suggests that while fasting has health benefits, it may also pose cancer risks if refeeding coincides with exposure to mutagens.
Yilmaz notes that these findings, though based on mouse models, highlight the complexity of fasting's effects on human health. Further research is needed to explore fasting's implications, particularly for individuals undergoing treatments like radiation that damage intestinal lining. The potential for polyamine supplements to stimulate regeneration without fasting is also being investigated.
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