Can reducing growth hormone signalling after development influence lifespan? A study published in Aging Cell on 5 September 2026 tested this by switching off the growth hormone receptor in middle-aged mice. [1]
What the researchers did
Duran-Ortiz and colleagues used an inducible genetic system to delete the receptor at 12 months of age. They followed male and female mice for survival and assessed physical function in separate cohorts. This was a genetic experiment, not a test of a medicine. [1]
What they found
Survival-curve comparisons favoured the intervention in both sexes. Female median lifespan was 1,003 days versus 929 in controls; male medians were 1,011 versus 943 days. The female median difference was statistically significant, while the male comparison was not (p = 0.0643). Selected measures of strength and coordination improved in males; frailty scores did not differ significantly. [1]
Median lifespan marks the point at which half a group has died. A survival-curve test considers how survival differs across follow-up. These measures answer different questions, which explains why their statistical results need not match.
What the findings mean
The experiment adds evidence that this pathway can influence mouse survival when altered after development. It does not establish a human longevity treatment. [1]
There is an existing receptor-blocking medicine: pegvisomant, sold as Somavert. The European Medicines Agency authorises it for acromegaly in a defined clinical setting and requires liver-enzyme monitoring. That approval concerns a hormone disorder, not healthy ageing. [2]
For interpreting the findings, the relevant distinction is between changing a gene in mice and giving a medicine to people. An effect in one setting cannot establish the dose, safety or benefit in the other. The result is therefore a finding about ageing biology, with its clinical relevance still to be determined.
The paper reports public and charitable support and declares no conflicts of interest. [1] Ohio University separately documents co-author John Kopchick’s role in developing the technology commercialised as Somavert. [3]