Biohacking
Longevity science: what the literature actually says.
Longevity research covers the cellular hallmarks of ageing — telomere attrition, mitochondrial dysfunction, senescence, and the metabolic interventions studied to extend healthspan. We document the evidence, including where it stops.
Healthspan vs lifespan — and why the distinction matters
“Longevity” is most usefully split into two distinct concepts: healthspan — the period of life spent in good health — and lifespan — total years lived. The literature increasingly reports these separately, because interventions that extend lifespan without improving healthspan can produce miserable outcomes.
When we cover a longevity intervention, we ask whether the evidence supports a healthspan claim, a lifespan claim, or neither. Most do not yet have evidence for either in humans.
The hallmarks of ageing
The dominant framework in contemporary ageing research — refined by López-Otín, Blasco, Partridge, Serrano, and Kroemer in 2013 and updated in 2023 — lists twelve hallmarks grouped into primary, antagonistic, and integrative:
Primary hallmarks
— telomere attrition, epigenetic alterations, loss of proteostasis, disabled macroautophagy, deregulated nutrient sensing, mitochondrial dysfunction.
Antagonistic hallmarks
— cellular senescence, stem cell exhaustion, altered intercellular communication.
Integrative hallmarks
— disabled macroautophagy, chronic inflammation, dysbiosis, mechanical alterations of the tissue microenvironment.
Compounds studied in longevity research — peptides, NAD+ precursors, mTOR inhibitors, biguanides, and others — are usually proposed to act on one or two of these. Mapping a compound’s mechanism to a specific hallmark is the first check on whether a research claim is coherent.
Telomere biology
Telomerase activation, telomere length as a biomarker, and the compounds studied in telomere-repetitive research.
Mitochondrial function
Mitochondrial-derived peptides (MOTS-c), mitochondria-targeted compounds, and the bioenergetic substrate of ageing.
Cellular senescence
Senolytic and senomorphic compounds, the SASP, and the evidence around clearing senescent cells.
Metabolic interventions
Caloric restriction, intermittent fasting, time-restricted eating, and the literature on metabolic healthspan.
Repurposed drugs
Rapamycin, metformin, acarbose, and other drugs studied for off-target longevity effects.
Reproductive longevity
Ovarian ageing, gonadal endocrine changes, and the cellular mechanisms of reproductive healthspan.
Lab access
Browse the longevity library.
Telomere biology, mitochondrial function, senolytics, and metabolic interventions — graded and source-linked.