Impact of intermittent fasting on health and disease processes.
Level 5 - mechanism / opinion, no new human data
Narrative review synthesizing preclinical mechanisms, animal disease models, and early human studies without systematic review methodology.
PubMed 27810402 · doi:10.1016/j.arr.2016.10.005
What was done
This narrative review summarizes findings on intermittent fasting (IF, e.g., 16–48 h fasts), periodic fasting (PF, 2–21+ days of fasting or fasting-mimicking diets), and time-restricted feeding (TRF, daily eating window of 8 h or less). It covers laboratory rodent models of age-related disease alongside preliminary studies in normal-weight and overweight humans.
What was found
The abstract reports no numerical values or effect sizes. It qualitatively reports that IF and PF improve functional outcomes in experimental animal models of diabetes, cardiovascular disease, cancers, Alzheimer's disease, Parkinson's disease, and stroke. In human studies, IF, PF, and TRF protocols resulted in weight loss and improvements in insulin resistance and cardiovascular risk factors. Proposed mechanisms include adaptive cellular stress response signaling, enhanced mitochondrial health, DNA repair, autophagy, and stem cell-based regeneration.
Why it matters
The paper synthesizes evolutionary and mechanistic rationales for fasting regimens, highlighting conserved cellular pathways that could be targeted to prevent or manage age-related metabolic and degenerative diseases.
Limits
The paper is a non-systematic narrative review without standardized study selection or pooled quantitative analysis. Much of the evidence for specific disease endpoints relies on laboratory rodent models, and the abstract notes that randomized controlled clinical trials comparing intermittent fasting against continuous energy restriction in humans are still required.
Cited by
- context Intermittent fasting extends human lifespan.