Cancer as a metabolic disease
Seyfried TN, Shelton LM · 2010 · Nutrition & Metabolism
DOI: 10.1186/1743-7075-7-7View source ↗
“The origin of cancer is recast as a metabolic disease arising from defects in mitochondrial respiration that drive the dependence on glycolysis.”
Summary
Seyfried and Shelton restate and develop the metabolic theory of cancer first proposed by Otto Warburg, arguing that the origin and progression of cancer is best understood as a mitochondrial-respiratory dysfunction that drives the cellular dependence on glycolysis — the Warburg effect — observed in the majority of tumors. The review compiles evidence from cancer cell biology, tumor metabolism, and animal models suggesting that interventions which restrict glucose availability (caloric restriction, ketogenic diets, multi-day fasting) or that pressure tumor cells through mitochondrial dysfunction may slow tumor growth or sensitize tumors to conventional therapy. The authors propose specific therapeutic implications and discuss the evidence base for ketogenic and caloric-restriction interventions as adjunctive cancer therapy. The review has been influential among researchers exploring metabolic approaches to cancer and is cited heavily in popular content connecting fasting and ketogenic eating to cancer outcomes — sometimes carefully, often less so.
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References cited by this entry
The Hatfield cancer claim references metabolic-theory-of-cancer reasoning that this Seyfried & Shelton review formalized — though the review does not endorse the Hatfield claim or sardine fasting specifically.
- ExtendsA Periodic Diet that Mimics Fasting Promotes Multi-System Regeneration, Enhanced Cognitive Performance, and HealthspanBrandhorst S et al. · 2015
Brandhorst & Longo's fasting-mimicking-diet work explores adjacent terrain — caloric/protein-restriction effects relevant to the metabolic-theory-of-cancer framework.
Entries that reference this one
The metabolic-theory-of-cancer literature (Seyfried, D'Agostino) is what later made Hatfield's earlier anecdotal account intellectually plausible — though the academic literature has never endorsed the Hatfield claim as causal evidence.
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