FoundMyFitness · 2016-10-01 · Rhonda Patrick (host), Valter Longo

Valter Longo, Ph.D. on Fasting-Mimicking Diet & Fasting for Longevity, Cancer & Multiple Sclerosis

35 claims checked against research: 2 contradicted 1 needing context 30 supported 2 unverified

In practice

What this episode leaves you with - built only from claims that held up against published research. Not medical advice.

1

Needs context

0:40:20Valter Longoneeds contextlow

By roughly day two of a fasting-mimicking diet, the body switches to a ketogenic mode burning visceral fat, the brain uses beta-hydroxybutyrate, and organs including the liver, heart, immune system, and oligodendrocytes shrink.

"the fasting-mimicking diet really by day two of the diet—and only by day two or so of the diet—the system starts switching to a ketogenic mode. You start burning visceral fat as your major source of energy, your brain starts moving from burning sugar to burning ketone bodies, you know, beta-hydroxybutyrate. So, as I said, everything starts shrinking: the immune system starts shrinking, the liver, the heart, even the oligodendrocytes, as we've shown in our multiple sclerosis paper." (said at 0:40:20)

The speaker describes physiological and cellular responses to a fasting-mimicking diet (FMD) developed in research by Valter Longo and colleagues. Preclinical and clinical studies confirm that prolonged fasting or multi-day FMD cycles induce a shift to ketogenesis, raising circulating beta-hydroxybutyrate, utilizing fat stores, and reducing circulating white blood cells. In animal models, fasting cycles cause reversible decreases in the mass of various organs (such as liver and spleen) through cell shrinkage and autophagy/apoptosis, followed by stem-cell-mediated regeneration during refeeding. In their multiple sclerosis model (Choi et al., 2016), FMD induced apoptosis of autoimmune T cells and stimulated oligodendrocyte precursor cell regeneration and remyelination. However, translating transient cellular depletion and organ mass fluctuations observed in rodent models into broad statements that human organs and oligodendrocytes 'shrink' requires qualification, as direct evidence for organ shrinkage and oligodendrocyte dynamics derives primarily from preclinical animal models.

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