Dudley W. Lamming
Showed rapamycin's side effects come from hitting mTORC2, not mTORC1
Postdoc, Whitehead Institute/MIT (Sabatini lab) · Professor of Medicine, University of Wisconsin–Madison · Co-director, Wisconsin Nathan Shock Center
Lamming Lab, UW-Madison ↗ Bluesky@lamminglab.bsky.social ↗
Portrait: UW–Madison Dept. of Medicine
During postdoctoral training in David Sabatini's lab, Dudley Lamming discovered that many of rapamycin's unwanted metabolic side effects, such as insulin resistance and elevated blood glucose, come from off-target inhibition of mTORC2 rather than from blocking mTORC1, the complex thought to mediate the drug's lifespan benefit. This distinction reframed how the field thinks about designing safer mTOR-targeted longevity interventions.
Since 2014, Lamming has run his own lab at the University of Wisconsin–Madison, where he studies how nutrient-responsive pathways, especially dietary protein and branched-chain amino acids acting through mTOR, can be tuned to promote healthy lifespan without rapamycin's side effects. He served as president of the American Aging Association in 2023–2024.
The timeline below follows Lamming's contributions gathered in this Atlas.
Milestones in the Atlas
| Year | Evidence | Study |
|---|---|---|
| 2012 | A | Rapamycin-induced insulin resistance is mediated by mTORC2 loss and uncoupled from longevity LAM2012 Shows rapamycin-induced insulin resistance is mediated by mTORC2 loss, uncoupled from the drug's longevity benefit. |
| 2015 | A | Alternative rapamycin treatment regimens mitigate the impact of rapamycin on glucose homeostasis and the immune system ARR2015 Shows alternative rapamycin dosing regimens can reduce its metabolic side effects while preserving benefits. |
| 2016 | R | The Mechanistic Target of Rapamycin: The Grand ConducTOR of Metabolism and Aging KEN2016 A Cell Metabolism review framing mTOR as the 'grand conductor' that coordinates whole-body metabolism, tissue by tissue. Especially valuable for its clear-eyed section on WHY rapamycin causes metabolic side effects (the mTORC2 problem) - which is the main barrier to using it against aging. Pairs perfectly with Lamming's own 2012 mechanism paper. |
| 2026 | R | The hallmarks of protein and amino acid restriction in aging and longevity KNO2026 Defines the "hallmarks" of dietary protein restriction (PR) through the lens of aging: PR and restriction of specific essential amino acids — especially methionine, isoleucine and valine — improve metabolic health, healthspan and lifespan across organisms, with amino-acid composition (not just protein quantity) acting as a key determinant via nutrient-sensing pathways including mTORC1. |
| 2026 | A | Restriction of individual branched-chain amino acids has distinct effects on the development and progression of Alzheimer's disease in 3xTg mice BAB2025 Shows restricting individual branched-chain amino acids has distinct metabolic effects, extending mTOR-nutrient research into diet design. |
On the programme
Meetings in the Atlas calendar where Dudley W. Lamming is listed among the speakers or organisers.
- upcoming CSHL: Mechanisms of Aging 2026 ↗ 22–26 Sep 2026 · Cold Spring Harbor, NY, USA · Tier 2