Dudley W. Lamming
Showed as a postdoc that rapamycin's harm to glucose metabolism comes largely from its effect on mTORC2, while the lifespan benefit tracks mTORC1. His Wisconsin lab studies intermittent rapamycin dosing and how restricting dietary protein or single amino acids affects metabolism and ageing
Professor of Medicine, University of Wisconsin–Madison · Co-director, Wisconsin Nathan Shock Center · Postdoc, Whitehead Institute/MIT (Sabatini lab)
Lamming Lab, UW-Madison (Madison, Wisconsin, USA) ↗ Lab lineagetrained under David M. Sabatini → Bluesky@lamminglab.bsky.social ↗ ORCID0000-0002-0079-4467 ↗
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 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
A selection, not a full bibliography: only papers that meet the Atlas inclusion criteria.
| 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. |
| 2012 | A | TOR signaling and rapamycin influence longevity by regulating SKN-1/Nrf and DAF-16/FoxO ROB2012 In C. elegans, genetic TORC1 inhibition extends lifespan through SKN-1/Nrf and DAF-16/FoxO, whereas rapamycin's lifespan effect requires SKN-1 but not DAF-16, apparently because it also hits TORC2. |
| 2012 | M | mTORC1 in the Paneth cell niche couples intestinal stem-cell function to calorie intake YIL2012 Co-author: shows that calorie restriction boosts mouse intestinal stem cells by lowering mTORC1 in the neighbouring Paneth cells, an effect rapamycin copies. |
| 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 and immune side effects compared with daily dosing. |
| 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. |
| 2016 | A | Intermittent Administration of Rapamycin Extends the Life Span of Female C57BL/6J Mice ARR2016 Shows an intermittent rapamycin schedule started late in life extends lifespan in female mice, the benefit side of the lab's work on separating rapamycin's effects from its side effects. |
| 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 effects on metabolism, Alzheimer's disease pathology and cognition in 3xTg mice, extending mTOR-nutrient research into diet design. |
| 2026 | H | Rapamycin in Frail Older Subjects with Heart Failure with Preserved Ejection Fraction LAN2026 Trial of low-dose rapamycin in frail older adults with heart failure with preserved ejection fraction (HFpEF), from a Mayo Clinic/UW-Madison team including senolytics/mTOR-aging researchers Kirkland and Lamming; abstract not yet available (ahead-of-print). |
Co-authors in the Atlas 20
People with a profile here who share at least one study with Dudley W. Lamming.
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- David M. Sabatini 3 shared studies Identified mTOR (as RAFT1) in 1994. His lab then mapped much of the machinery around it: raptor and rictor at the core of mTORC1 and mTORC2, the Rag–Ragulator system that docks mTORC1 on the lysosome, and the sensors that detect leucine, arginine and SAM
- Bailey A. Knopf 2 shared studies Graduate student in Dudley Lamming's lab at the University of Wisconsin-Madison and first author of a 2026 review that sets out the hallmarks of protein and amino acid restriction in aging
- Cassidy P. Pumper 2 shared studies Member of Dudley Lamming's group at the University of Wisconsin-Madison who contributed to the intermittent rapamycin studies in mice
- Emma L. Baar 2 shared studies Researcher in Dudley Lamming's group at the University of Wisconsin-Madison who mapped how mTOR signalling changes with age in different mouse tissues and helped test gentler rapamycin dosing schedules
- Nicole E. Cummings 2 shared studies Graduate researcher in Dudley Lamming's lab at the University of Wisconsin-Madison and first author of a 2017 study reporting that eating fewer branched-chain amino acids restores metabolic health
- Sebastian I. Arriola Apelo 2 shared studies Showed that giving rapamycin intermittently rather than daily lessens its effects on glucose metabolism and the immune system in mice
- Adam B. Salmon Biologist of aging at UT Health San Antonio whose work in this Atlas spans rapamycin in mice and in common marmosets. He is a co-author on the Interventions Testing Program reports from the San Antonio site and on the marmoset rapamycin studies on blood markers, epigenetic age and the salivary gland
- Arlan Richardson Studies how rapamycin slows ageing in mice, including the broad changes it causes in the liver, and co-authored early studies showing that rapamycin protects memory in Alzheimer's-model mice
- Brian K. Kennedy Showed with Matt Kaeberlein that reducing TOR or Sch9 signalling extends yeast lifespan in the same way as dietary restriction, and has since championed mTOR as a target for slowing human ageing
- Conor M. Lane Cardiologist at Mayo Clinic in Rochester, working in interventional cardiology, and first author of a trial of low-dose rapamycin in frail older adults with heart failure with preserved ejection fraction
- David A. Guertin Built the mouse genetics that defined mTORC2's biological roles
- James L. Kirkland Founder of the field of senolytics, drugs that clear senescent cells, and a leader of clinical trials of ageing-targeted therapies
- Joseph A. Baur Biologist of aging at the University of Pennsylvania whose lab showed that rapamycin's harm to glucose control comes from mTORC2 loss and studies how NAD levels shape health
- Kivanç Birsoy Cancer metabolism researcher who trained with Jeffrey Friedman and David Sabatini and now heads the Laboratory of Metabolic Regulation and Genetics at The Rockefeller University, using genetic screens to find how cancer cells rewire their metabolism
- Mandeep Singh Interventional cardiologist and professor of medicine at Mayo Clinic; corresponding author on a 2026 trial of low-dose rapamycin in frail older adults with heart failure with preserved ejection fraction (HFpEF)
- Ömer H. Yilmaz Pathologist and stem-cell biologist who studies how diet and nutrient sensing control intestinal stem cells; as a postdoc with David Sabatini he showed that calorie restriction acts on the stem-cell niche through mTORC1 in Paneth cells
- Reji Babygirija Researcher in Dudley Lamming's lab at the University of Wisconsin-Madison who studies how restricting single amino acids in the diet affects metabolism, memory and Alzheimer's disease in mice
- Shomit Sengupta Showed that mTORC1 controls whether the liver makes ketone bodies during fasting, and now leads biology for drug discovery at a metabolic-disease biotech
- Stacey Robida-Stubbs Researcher in Keith Blackwell's worm lab at the Joslin Diabetes Center who showed that TOR inhibition and rapamycin extend C. elegans lifespan through the protective factors SKN-1/Nrf and DAF-16/FoxO
- T. Keith Blackwell Geneticist who uses the worm C. elegans to study how the SKN-1/Nrf stress-response factor, insulin signaling and TOR shape stress resistance and lifespan.
Every researcher with a profile →
On the programme
Meetings in the Atlas calendar where Dudley W. Lamming is listed among the speakers or organisers.
- past CSHL: Mechanisms of Aging 2026 ↗ 22–26 Sep 2026 ·
Cold Spring Harbor, NY, USA · ★★
All meetings in the calendar →
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