The study recruited 25 healthy young men who intended to fast for the entire month of Ramadan from dawn to dusk. The researchers measured gene expression levels one week before Ramadan, in the middle of Ramadan, in the last days of Ramadan, and one week after Ramadan.

The study found that intermittent fasting activated autophagy, a cellular process that breaks down components within cells. Autophagy has been linked to longevity, and the researchers observed an increase in ULK1, a gene involved in autophagy, two weeks and one month after starting the fasting period. Another gene, ATG5, involved in autophagy induction, also showed a similar pattern. However, BECN1, a gene essential for autophagy, exhibited a different pattern, with an increase in expression two weeks after the start of fasting and a subsequent reduction in its levels.

The researchers also measured inflammation and senescence markers, including the inflammasome and senescence mediator p16INK4a. They found that NLRP3 and IL-1β expression increased two weeks and one month after the start of fasting, but ASC levels were lower than basal levels one month after the start of fasting, suggesting that the inflammasome was not activated. The senescence marker p16INK4a did not show statistically significant changes until the end of the observation period, but p21 levels decreased during and after fasting.

The study’s limitations include a lack of data on food intake, physical activity, and sleeping patterns, which could impact gene expression patterns. Additionally, only young males were included in the study, making the results questionable for other demographic groups. The authors emphasize the need for further research to confirm or refute their findings and to assess the levels of actual proteins rather than just gene expression levels.

Overall, the study provides valuable insights into the molecular effects of prolonged intermittent fasting on human health and longevity markers. While more research is needed to understand the complex interplay between autophagy, the inflammasome, and senescence, the findings suggest that fasting may contribute to delaying the onset of age-related diseases and promoting overall health and longevity.

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David and Matthew additionally highlight the latest evidence behind hyperbaric oxygen therapy, cold therapy, and heat therapy. As they discuss different adversity mimetics, they also explain how these interventions influence aging at the molecular and physiological levels.

• A single mutation doubles lifespan in worms
• Extending lifespan in yeast with one mutation
• Daily step count and health outcomes
• Reversing vascular aging in mice
• Aerobic exercise is linked to a lower biological age
• A lifestyle and diet intervention decreases biological age
• An epigenetic clock that predicts time-to-death
• Ultra-cheap age prediction
• Exercise decreases biomarkers of cellular senescence
• Telomere length is increased by hyperbaric oxygen therapy
• Hyperbaric oxygen therapy improves cognitive performance
• A cold temperature promotes longevity in worm
• Sauna bathing, mortality, and cardiovascular risk

The post Exercise, Heat, Cold & Other Adversity Mimetics for Longevity appeared first on NOMIX.