Impact of Growth Hormone-Related Mutations on Mammalian Aging.
Level 5 - mechanism / opinion, no new human data
Narrative review of animal models and human genetic data without systematic review methodology.
PubMed 30542372 · doi:10.3389/fgene.2018.00586
What was done
This narrative review synthesized evidence from animal models (primarily mice) and human populations regarding the impact of single-gene mutations causing growth hormone (GH) deficiency or resistance on aging, healthspan, lifespan, and downstream cellular mechanisms.
What was found
The abstract reports no quantitative figures or effect sizes. Qualitatively, mice with genetic GH deficiency or resistance display reduced body size and delayed maturation alongside increased stress resistance, decelerated aging, and extended lifespan compared to wild-type siblings. In humans, homologous mutations protect against age-related disease but show no consistent effect on overall lifespan. Mechanistically, these mutations are linked to improved genome and stem cell maintenance, enhanced glucose homeostasis and thermogenesis, and decreased mTORC1 signaling and chronic low-grade inflammation.
Why it matters
It clarifies the conserved physiological and molecular mechanisms by which down-regulated GH signaling enhances healthspan across species, while distinguishing the divergent lifespan effects between rodents and humans.
Limits
The abstract provides no quantitative data, sample sizes, or formal systematic review methodology. Findings from genetically altered rodent models do not directly translate into human lifespan extension, and human observations remain limited to specific genetic cohorts.
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