Cancer

Noakes, T.D.; Kalamian, M.; Seyfried, T.N.; Mukherjee, P.; D’Agostino, D.P.; Arismendi-Morillo, G.; Chinopoulos, C. [Chinopoulos, Christos (Bioenergetika), szerző] Biokémiai Tanszék (SE / AOK / I / BMBI); Tettenborn, M.; Winters, N.

Angol nyelvű Könyvfejezet (Könyvrészlet) Tudományos
    Azonosítók
    Since the discovery of DNA, the metabolic theory of cancer has been sidelined for genetic research. Yet cancer continues to rise. New research recaptures mitochondria as the driver, while upregulation of oncogenes and tumour suppressor mutations are recognised as downstream of the damage to oxidative phosphorylation (OxPhos). Despite the prevalence of the somatic (genetic) mutation theory, there are numerous inconsistencies. In contrast, it appears that all cancers are characterised by dysfunctional mitochondria. Cancer pre-1960 was a rare disease, all of which has changed as diets have. Press-pulse therapy and ketogenic diets (KD) have proven effective therapies, due to cancers’ selective metabolism of glucose and glutamine (Warburg effect), in combination with the non-fermentability of ketones. Some dietary aspects are individualised to the patient and cancer, but follow this general protocol. Fasting induces additional selective stress to cancers. With cancer genetic research stagnating and metabolic approaches showing promise, this perspective offers a new path forward. © 2023 Elsevier Inc. All rights reserved.
    Hivatkozás stílusok: IEEEACMAPAChicagoHarvardCSLMásolásNyomtatás
    2025-04-02 02:36