A Diet Mimicking Fasting Promotes Regeneration and Reduces Autoimmunity and Multiple Sclerosis Symptoms.
Level 2 - randomized trial
Includes preliminary human data from a registered randomized controlled trial alongside preclinical animal models
PubMed 27239035 · doi:10.1016/j.celrep.2016.05.009
What was done
Researchers evaluated periodic 3-day cycles of a fasting-mimicking diet (FMD) in mouse models of multiple sclerosis, specifically experimental autoimmune encephalomyelitis (EAE) and cuprizone-induced demyelination. They measured clinical disease severity, immune cell subsets (Tregs, TH1, TH17, antigen-presenting cells), corticosterone levels, and oligodendrocyte precursor cell regeneration/remyelination. Additionally, they gathered preliminary safety, feasibility, and efficacy data for an FMD or a chronic ketogenic diet in patients with relapsing-remitting multiple sclerosis (RRMS; NCT01538355).
What was found
In the EAE mouse model, FMD cycles reduced clinical disease severity in all treated mice and completely reversed symptoms in 20% of animals. Mechanistically, FMD increased corticosterone and regulatory T (Treg) cell numbers while reducing pro-inflammatory cytokines, TH1 cells, TH17 cells, and antigen-presenting cells. FMD also stimulated oligodendrocyte precursor cell regeneration and axonal remyelination in both EAE and cuprizone models. In human RRMS patients, preliminary trial data showed that FMD and a chronic ketogenic diet were safe, feasible, and potentially effective, though specific numerical outcomes for the human cohort were not reported in the abstract.
Why it matters
This study provides evidence that periodic fasting-mimicking diets can dual-target autoimmune pathology and remyelination pathways in preclinical neuroinflammation, establishing early feasibility for dietary metabolic interventions in multiple sclerosis.
Limits
The human trial findings are described as preliminary without reporting sample size, baseline characteristics, dropout rates, or numerical effect sizes in the abstract. Most efficacy and mechanistic findings rely on mouse models (EAE and cuprizone), which do not fully replicate human multiple sclerosis pathology.
Cited by
- supports In mice and humans undergoing fasting or fasting-mimicking diets, organs and white blood cell levels temporarily shrink or reduce during fasting cycles and return to normal levels upon refeeding through stem cell activation.
- supports In a multiple sclerosis mouse model, fasting-mimicking diet cycles kill autoimmune immune cells, activate stem cells, and stimulate oligodendrocyte progenitor cells to replace damaged cells.