Fasting and Caloric Restriction in Cancer Prevention and Treatment

ByCrossFitSeptember 25, 2019

This 2016 paper reviews the mechanisms by which fasting may improve cancer prognosis or reduce cancer risk.

Caloric restriction has been shown to increase stress resistance in a variety of organisms. Yeast and E.coli have increased lifespans and improved resistance to stressors under conditions of caloric restriction. The same has been shown in rodent and primate models. Specifically relevant to cancer, rodents have been able to survive otherwise-lethal doses of chemotherapy when the drugs are given alongside caloric restriction. Further research has suggested these benefits are tied to the suppression of IGF-1 and growth hormone (GH) induced by fasting, as mouse models with deficient baseline GH production do not see increased lifespan or stress tolerance with fasting.

Similar studies would be challenging to replicate in humans, but existing research suggests fasting is well tolerated. During fasting the body first relies on stored glycogen for energy and then, once glycogen stores are depleted, on fats. During this latter period, the primary fuel source transitions from carbohydrate to ketone bodies. Weight loss is rapid (~0.9 kg/d) during the first week and decreases to ~0.3 kg/d thereafter — a healthy 70-kg adult could live for two to three months off their fat reserves.

Fasting also results in fewer and less severe side effects than caloric restriction, particularly given the needs of cancer patients. Caloric restriction leads to continuous weight loss, delayed wound healing, and impaired immune function, all of which could discourage its use in cancer patients regardless of its benefits. Fasting, conversely, leads to minimal side effects, such as headaches, light-headedness, and weakness.

Fasting drives metabolic improvements distinct from those seen with caloric restriction. Both glucose suppression and IGF-1 suppression would be expected to slow cancer growth — the former by depriving cancer cells of the building blocks for cellular replication and the latter for downregulating key growth-signaling pathways. In mouse models, caloric restriction suppresses glucose levels by 15% and IGF-1 levels by 25%. Fasting, conversely, decreases glucose by 75% and IGF-1 by 70%.

These results, while promising, are yet to be replicated in humans. They suggest, however, that fasting may improve cancer survivability in ways other dietary interventions cannot, both by increasing the vulnerability of cancer cells to treatment and reducing the vulnerability of healthy cells to the same.