Richard A. Miller
Showed how far the rapamycin lifespan effect goes — dose, sex and starting age — in the ITP's Michigan arm
MD, PhD, Yale · Professor of Pathology · Director, Paul F. Glenn Center for Biology of Aging Research, University of Michigan
Miller Lab, University of Michigan ↗
Richard Miller has spent his career developing rigorous methods to test whether interventions actually slow aging in mice, rather than merely treating a single disease. He directs one of the three collaborating sites of the NIA's Interventions Testing Program (ITP), which he helped design specifically to guard against the false positives that had plagued earlier longevity research.
Through the ITP, Miller's group made the seminal contribution to the 2009 discovery that rapamycin extends mouse lifespan by more than 20%, even when treatment begins in middle age — a result that reshaped the aging field's view of mTOR as a druggable target for healthy aging. His lab continues to study the genetics and cell biology of long-lived mouse strains.
The timeline below follows Miller's contributions gathered in this Atlas.
Milestones in the Atlas
| Year | Evidence | Study |
|---|---|---|
| 2011 | A | Rapamycin, but not resveratrol or simvastatin, extends life span of genetically heterogeneous mice MIL2011 Shows rapamycin, but not resveratrol or simvastatin, extends lifespan in genetically heterogeneous mice. |
| 2012 | A | Evaluation of resveratrol, green tea extract, curcumin, oxaloacetic acid, and medium-chain triglyceride oil on life span of genetically heterogeneous mice STR2012 None of five popular longevity compounds had a statistically significant effect on lifespan. The paper explicitly states the ITP's mission is to publish all results, positive or negative - the exact registry model this Atlas should emulate. |
| 2012 | A | Rapamycin slows aging in mice WIL2012 Answered a crucial objection: does rapamycin really slow AGING, or just prevent the cancers that kill mice? By showing slower age-related change across many tissues (heart, liver, tendon, activity), it argued for genuine slowing of aging. Honestly reported harms too - more cataracts and testicular degeneration - making it a balanced landmark, not hype. |
| 2014 | A | Acarbose, 17-alpha-estradiol, and nordihydroguaiaretic acid extend mouse lifespan preferentially in males HAR2014 Shows acarbose, 17-alpha-estradiol and NDGA extend mouse lifespan in a sex-preferential manner, broadening the ITP's drug set beyond rapamycin. |
| 2014 | A | Rapamycin-mediated lifespan increase in mice is dose and sex dependent and metabolically distinct from dietary restriction MIL2014 Shows rapamycin's lifespan effect in mice depends on dose and sex and is metabolically distinct from dietary restriction. |
| 2022 | A | Lifespan benefits for the combination of rapamycin plus acarbose and for captopril in genetically heterogeneous mice STR2022 NIA Interventions Testing Program C2017 cohort. In MALE mice, rapamycin plus acarbose started at 9 months produced a longer lifespan than either of the two prior ITP cohorts treated with rapamycin alone, suggesting the combination is more potent than its components used separately. In FEMALES the combination was neither better nor worse than rapamycin alone, which the authors relate to the limited survival benefit acarbose alone had shown in earlier female cohorts. Captopril gave a small but significant lifespan increase in females (4-5%). CAVEAT (important for how this is cited): the rapamycin-only comparison is HISTORICAL, against prior cohorts, not a concurrent rapamycin-only arm in the same experiment, so 'more potent than either component' is the authors' suggestion rather than a within-experiment randomised comparison. |