Common and divergent molecular mechanisms of fasting and ketogenic diets.
Level 5 - mechanism / opinion, no new human data
Narrative review of proposed molecular mechanisms without empirical trial data or systematic synthesis.
PubMed 38577754 · doi:10.1016/j.tem.2023.10.001
What was done
This narrative review compares the common and distinct cellular and molecular mechanisms engaged by intermittent short-term fasting (ISTF) versus ketogenic diets (KDs).
What was found
The abstract reports no numerical data. It summarizes qualitative mechanistic pathways: ketogenic diets primarily exert effects via ketone bodies, histone deacetylase (HDAC) inhibition, enhanced mitochondrial efficiency, and decreased inflammation and oxidative stress. Intermittent short-term fasting shares the reduction of oxidative stress and inflammation but uniquely engages broader adaptive responses, including autophagy stimulation, improved insulin and leptin sensitivity, AMPK activation, mTOR inhibition, and enhanced mitochondrial resilience. The authors suggest that cycling between ketogenic and nonketogenic states promotes stress resistance and cellular plasticity.
Why it matters
It outlines the distinct molecular profiles of intermittent fasting and ketogenic diets, highlighting that their physiological effects are not entirely interchangeable despite shared metabolic features.
Limits
The abstract describes purely mechanistic concepts without quantitative metrics, comparative clinical trial data, sample sizes, or details on intervention duration, population, or specific health outcomes.
Cited by
- supports Intermittent fasting alternates the body between positive and negative energy balance, activating and deactivating mTOR and AMPK through metabolic switching.