In the burgeoning field of geroscience, a transformative hypothesis has emerged, unifying the disparate theories of metabolic dysfunction and immune senescence into a singular, actionable framework. The pivotal research, “Crosstalk between metabolic signaling and innate immunity in longevity: The mTOR-AMPK-cGAS-STING axis”, published in Experimental Gerontology, provides the Rosetta Stone for understanding why we age. It posits that the age-related decline in cellular recycling (autophagy), governed by the master metabolic switches mTOR and AMPK, leads to the accumulation of damaged mitochondria. These organelles, once the powerhouses of the cell, become saboteurs, leaking their DNA (mtDNA) into the cytoplasm.
This cytosolic DNA is detected by the cGAS-STING pathway—an ancient antiviral defense system that mistakes self-DNA for a viral invader. The result is a perpetual state of sterile inflammation (“inflammaging”) that drives systemic degeneration. This report offers an exhaustive analysis of this mechanism, translating high-level molecular biology into rigorous biohacking protocols. It explores the pharmacological and lifestyle interventions capable of suppressing this lethal feedback loop, providing the “literate biohacker” with a roadmap to modulate the very engines of mortality.
Full Gemini Research Paper Analysis: https://gemini.google.com/share/2c1ed76e20b9
Source (Open Access) Paper: The Crosstalk Between Metabolism and Inflammation in Aging and Longevity