The biohacker & functional lens

The idea (Simpson & Raubenheimer) that we regulate protein tightly and keep eating protein-poor food until we hit our target — over-consuming calories on the way — has real experimental support (in a controlled trial, diluting protein raised total intake ~12%). It neatly explains why protein-poor ultra-processed diets drive overeating. A well-supported contributing mechanism, appropriately hedged by its own authors. Evidence ●●●●○

The core (associated with Dr Gabrielle Lyon) is legitimate and under-appreciated: muscle is the main site of glucose disposal (~70–80%), resistance training improves insulin sensitivity, and strength and fitness are strong mortality predictors. The caveats: raw muscle mass is a much weaker, non-causal predictor than strength, and some influencer protein targets (~1 g per pound) exceed what the evidence requires. Solid substance, mild over-packaging.

The genuine finding is that glucose responses to the same meal are highly individual — which really does undercut one-size-fits-all glycaemic advice. But the leap to ‘flatten your spikes and you’ll lose weight’ is not supported by any randomised trial in healthy people; spikes in metabolically healthy people are normal, device error (~10–13%) can be larger than the ‘spike’ you’re chasing, and clinicians warn about fostering food anxiety. Interesting self-experiment; not a proven weight tool. Evidence ●●○○○ for weight

Fiber, protein and fermented foods genuinely do raise your own GLP-1 — but the rise is small and brief, on the order of ~1,000× weaker than a GLP-1 drug, which is engineered for week-long, high-level receptor activation. Eating more fiber and protein is good advice; it is not a stand-in for semaglutide. Supplements branded ‘nature’s Ozempic’ or ‘GLP-1 boosters’ are the clearest hype in this list, now drawing consumer-fraud lawsuits. Evidence ●○○○○ as a drug substitute