Research paper
Mattson MP, Moehl K, Ghena N, Schmaedick M, Cheng A. Intermittent metabolic switching, neuroplasticity and brain health. Nature Reviews Neuroscience. 2018 Feb;19(2):63-80. doi:10.1038/nrn.2017.156
Why we cite it
Provides the theoretical framework for how fasting is proposed to affect cognitive function — not through catecholamines (covered by `caf01`/`caf02`) but through the metabolic switch to ketones, BDNF upregulation, and neuroplasticity. The mechanism evidence is animal work, and the full text puts a number on it. Extracted 2026-09-02 as `pdf-fulltext.txt`, the review mentions rat or rats 33 times, mice 52 and mouse 17, against human or humans 14 (word-boundary counts, 2026-09-10) — the mechanistic core is rodent throughout. (This line gave ”rats 158 times and mice 63 against humans 16″. Those are substring counts, which reproduce exactly — 159, 63 and 16 — with rat counted inside words such as rate and generation. The conclusion survives the correction; the rat figure was inflated nearly fivefold.) There is some human material and it is correlational, e.g. that ”cathepsin B levels are positively correlated with aerobic fitness and recall memory in humans”, immediately beside the causal work in cathepsin-B-deficient mice. The behavioural claims are explicitly murine: ”mice maintained on a daily TRF schedule (40% CR; see BOX 1) beginning at weaning age exhibit no age-related learning and memory impairment” — a regime that was daily time-restricted feeding with 40% calorie restriction, not time restriction alone. (Corrected 2026-09-10: this line quoted ”Mice on time-restricted feeding exhibit no age-related learning and memory impairment”, a paraphrase in quotation marks that is in no held file, and it dropped the calorie restriction.) Also supplies the evolutionary rationale: brains that functioned well during fasting enabled successful food acquisition.