Review of fasting, epigenomic regulation and aging: proposed pathways, not proven lifespan gains
This abstract describes a review of how fasting may reshape epigenomic and transcriptional programs via nutrient-sensing pathways such as AMPK and sirtuins, and how this might relate to healthspan and lifespan. The links to lifespan and disease resistance are presented as possible, not established. [1]
Automatic summary · not editorially reviewed
The key findings
The review aims to synthesize current knowledge on how fasting modulates epigenomic landscapes and the transcriptome to affect aging and healthspan. [1]
Nutrient deprivation is described as activating nutrient-sensing pathways including AMPK and sirtuins, which can modulate chromatin accessibility and transcriptomic programs. [1]
The abstract says these processes may link fasting to lifespan and resistance to age-related diseases such as metabolic disorders, neurodegeneration and cancer. [1]
The source at a glance
- Study type / format
- Review (abstract only)
- Population / context
- Not specified in the abstract; the review concerns fasting and aging biology generally.
- Summary based on
- Study abstract
- Original publication
- September 10, 2026
Review scope: fasting effects on epigenome and transcriptome
The authors state that this review aims to synthesize current knowledge on how fasting modulates epigenomic landscapes and the transcriptome to affect aging and healthspan. They describe fasting as a physiological intervention with metabolic effects that also triggers epigenomic and transcriptional remodeling. The review highlights molecular pathways, cell-type-specific effects and emerging translational opportunities, and it discusses challenges, limitations and open questions.
Supporting source [1]
Proposed mechanism: nutrient sensing, chromatin and cellular maintenance
According to the abstract, nutrient deprivation activates evolutionarily conserved nutrient-sensing pathways including AMPK and sirtuins, which can modulate chromatin accessibility and transcriptomic programs. These changes are said to affect histone modifications, DNA methylation and non-coding RNAs, which underlie adaptive transcriptional programs driving cellular maintenance, autophagy and stem cell function. Recent studies are said to suggest that fasting-mediated epigenomic flexibility may help reduce age-related epigenetic drift and dampen chronic inflammation. These are described as suggested mechanisms, not demonstrated causal effects in humans.
Supporting source [1]
Possible links to lifespan and age-related disease resistance
The abstract states that these processes may link fasting to both lifespan and resistance to age-related diseases, including metabolic disorders, neurodegeneration and cancer. The wording is tentative: these are possible links raised in a review, not results of a controlled trial. The authors also note that challenges, limitations and open questions must be addressed before fasting-inspired approaches could be leveraged for healthspan.
Supporting source [1]
How to interpret this
This is an abstract of a review; the full text was not reviewed. The abstract reports no study design, sample, follow-up or outcome data, and the lifespan and disease-resistance links are presented as possibilities rather than demonstrated effects.
Based on the study abstract; the full paper, tables and supplementary data were not reviewed.
Source & supporting passages
Harrath AH, Jalouli M, Rahman MA, Longo V. · europepmc.org · September 10, 2026