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Fasting-mimicking diet causes hepatic and blood marker changes indicating reduced biological age and disease risk.

This summary is intended to provide a snapshot of the original research. It is in no way a substitute for the original research article, nor is it intended to be a complete reflection of the original research. 

Originally published in Nature, 20 February 2024

In mice, periodic cycles of a fasting-mimicking diet (FMD) protect normal cells while killing damaged cells, including cancer and autoimmune cells, reduce inflammation, promote multi-system regeneration, and extend longevity. 

In this study researchers performed secondary and exploratory analysis of blood samples from a randomized clinical trial (NCT02158897) and show that 3 FMD cycles in adult study participants are associated with reduced insulin resistance and other pre-diabetes markers, lower hepatic fat (as determined by magnetic resonance imaging) and increased lymphoid to myeloid ratio: an indicator of immune system age.

Based on a validated measure of biological age predictive of morbidity and mortality, 3 FMD cycles were associated with a decrease of 2.5 years in median biological age, independent of weight loss.

Nearly identical findings resulted from a second clinical study (NCT04150159). Together, these results provide initial support for the beneficial effects of FMD on multiple cardiometabolic risk factors and biomarkers of biological age.

The chronic reduction of calorie intake by 15-20% below normal levels has shown potent effects on diabetes, cancer, and cardiovascular disease risk factors. In monkeys, caloric restriction (CR) has prevented diabetes and cancer, but its sustainability and potential adverse effects raise concerns. 

The FMD (Fasting Mimicking Diet) trial investigated its impact on biological age and health span. In a relatively healthy cohort, FMD reduced biological age by 2.5 years after three cycles, with greater benefits observed in those with poor health at baseline. MRI data revealed reductions in total and visceral fat and hepatic fat fraction.

FMD also improved insulin resistance and HbA1c. Shared mechanisms, such as cellular rejuvenation and systemic inflammation reduction, may underlie these effects. Simulation suggests that prolonged FMD practice could decelerate aging, extend life expectancy, and decrease disease-specific mortality. However, limitations include a small sample size, compliance issues, and potential biases. 

Further comparative studies are needed to validate FMD's efficacy against other dietary interventions, highlighting its potential as a periodic intervention to reduce disease risk factors and biological age.

 

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