We propose excessive fructose metabolism not only explains obesity but the epidemics of diabetes, hypertension, non-alcoholic fatty liver disease, obesity-associated cancers, vascular and Alzheimer’s dementia, and even ageing. Moreover, the hypothesis unites current hypotheses on obesity. Reducing activation and/or blocking this pathway and stimulating mitochondrial regeneration may benefit health-span.
R. J. Johnson et al., “The fructose survival hypothesis for obesity,” Philosophical Transactions of the Royal Society B: Biological Sciences, vol. 378, no. 1885, Sep. 2023.