Mice with growth hormone deficiency lived substantially longer than normal littermates - founding observation linking reduced growth-signaling to mammalian longevity.
| Evidence tier | C Animal in vivo |
| Study type | 4 - Animal Study |
| Model system | Ames dwarf mice (growth-hormone deficient) |
| Journal | Nature |
| Year | 1996 |
| Peer reviewed | Yes |
| Source | DOI 10.1038/384033a0 · PMID 8900272 |
(Brief communication; no formal abstract in PubMed — editorial summary.) This landmark report shows that Ames dwarf mice, which carry a mutation causing combined deficiency of growth hormone, prolactin and thyroid-stimulating hormone, live substantially longer than their normal littermates (both sexes). It was among the first demonstrations that genetically reduced growth hormone / IGF-1 endocrine signalling extends lifespan in a mammal, linking the somatotropic axis — upstream of PI3K-Akt-mTOR — to the ageing process and providing a foundational genetic model for the biology of ageing and longevity.
| Intervention | Genetic – Ames dwarf mutation (GH/prolactin/TSH deficiency) |
| Target | GH/IGF-1 axis (upstream of PI3K-Akt-mTOR) |
| Model | Mouse (Ames dwarf) |
| Effect | Substantially longer lifespan vs normal littermates (both sexes) – early evidence linking reduced growth signaling to longevity |