Research
Hormonal
Attenuated Insulin/IGF-1 Signaling (IIS) extends lifespan in model organisms, but in humans, low IGF-1 is associated with increased risk of cardiovascular disease, diabetes, and osteoporosis, creating a paradox where the mechanism that extends lifespan in animals may be detrimental in humans.
While reducing IIS extends lifespan in animals, humans with naturally low IGF-1 face higher risks of heart disease, diabetes, and bone loss. Therefore, simply trying to lower insulin/IGF-1 or boost it via GH therapy without medical supervision is not a straightforward longevity strategy for humans.
GoodQualifiesHIGH confidence
Paradoxically, a decrease (by genetic modulation) in the expression of key IIS pathway intermediates in model organisms is associated with life span extension... Paradoxically, low IGF-1 concentrations in humans have been associated with increased risk for CVD, stroke, T2DM, and osteoporosis.
Why this rating
Strong evidence in model organisms; strong observational evidence in humans linking low IGF-1 to disease risk, though causality for lifespan is complex.
Source
The Critical Role of Metabolic Pathways in Aging
Nir Barzilai et al. · Diabetes · 2012
DOI 10.2337/db11-1300
narrative_reviewCited 808×
Read the paper DOI resolved against Crossref · corpus check 2026-06-10
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