Switching off growth hormone at midlife extended mouse lifespan

Blocking growth hormone signalling makes mice live longer. That has been known for decades, but nearly every model proving it disrupts the growth hormone/IGF-1 axis from birth, which leaves the question that matters for people unanswered: does it still work if you start after the body is already built?

A team at the Institute for Molecular Medicine and Aging at Ohio University, with collaborators at the Barshop Institute and the University of Southern California, ablated the growth hormone receptor gene in mice at 12 months of age — roughly midlife — using a tamoxifen-inducible model. The paper appeared in Aging Cell in September 2026, with John Kopchick as corresponding author.

Lifespan was significantly extended in both sexes, with no major effect on somatic growth. The mice showed the expected endocrine signature of growth hormone resistance: circulating IGF-1 down, growth hormone up. Males grew fatter yet had better insulin sensitivity, and were protected against age-related decline in neuromuscular performance and bone microarchitecture. Single-nucleus RNA sequencing of liver found fewer B cells in both sexes and, in males, hepatocytes shifting toward a female pattern of gene expression.

This is one genetic model in one species, not a drug. Kopchick told WOUB he has three compounds with the same action moving through patent filing.