Source paper here:
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This is interesting… as it suggests (as other research has suggested) that even moderate periods (e.g. months or years) of rapamycin might have long-term benefits:
The hunger strikes back: an epigenetic memory for autophagy
Historical and demographical human cohorts of populations exposed to famine, as well as animal studies, revealed that exposure to food deprivation is associated to lasting health-related effects for the exposed individuals, as well as transgenerational effects in their offspring that affect their diseases’ risk and overall longevity. Autophagy, an evolutionary conserved catabolic process, serves as cellular response to cope with nutrient starvation, allowing the mobilization of an internal source of stored nutrients and the production of energy. We review the evidence obtained in multiple model organisms that support the idea that autophagy induction, including through dietary regimes based on reduced food intake, is in fact associated to improved health span and extended lifespan. Thereafter, we expose autophagy-induced chromatin remodeling, such as DNA methylation and histone posttranslational modifications that are known heritable epigenetic marks, as a plausible mechanism for transgenerational epigenetic inheritance of hunger.
centenarians are excellent subjects to uncover potential mechanisms involved in a healthy aging and consequently human longevity. Remarkably, the genome wide analysis of the transcriptome by RNA sequencing of centenarians, centenarian-children, as well as their spouses revealed that, among the differentially expressed genes, the autophagy pathway was found to be significantly maintained by Centenarians.
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At the molecular level, an evolutionary conserved serine/threonine protein kinase, the mechanistic target of rapamycin (MTOR), when part of mTOR complex 1 (MTORC1), functions as a primary nutrient sensor, in particular for amino acids, linking the activation versus repression of the cellular processes to the nutritional supply [29]. When nutrients are abundant, active MTORC1 promotes numerous anabolic processes, such as protein, nucleotide and lipid biosynthesis, while catabolic processes, including autophagy, are repressed. Upon amino acids limitation, MTORC1 is rapidly inactivated, and autophagy induced, allowing the cells to cope with the occurring nutrients starvation (Fig. 2) [38]. Hence, MTOR has emerged as a nutrient sensor of a plethora of extracellular and intracellular cues, and one of the central regulators of autophagy induction.
Full Paper (open access)
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