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Rapamycin extends mouse lifespan 9–14%
NAD+ precursors reverse aging in humans
Blue-light glasses improve sleep quality
Walking 10 min after meals blunts glucose
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A unifying theory of aging (Qualy #19) — Whalespan

Content›Video›A unifying theory of aging (…

A unifying theory of aging (Qualy #19)

Peter Attia11m · 2020-02-13

Claims Made

10

Claims Supported

9

Support Rate

90%

Support rate

9 of 10 claims supported

9 supported1 partial / not

Claims from this content

8

✓Well SupportedThe genome is largely intact even in old age and contains the instructions to be young.✓Well SupportedGenes promoting early-life advantages can have detrimental effects after reproductive age due to antagonistic pleiotropy.✓Well SupportedManipulating the epigenome in cells and mice can alter animal outcomes, supporting the theory that epigenetic changes drive aging.◐Partially SupportedHistorical longevity gains were primarily due to solving infectious diseases and improving sanitation, not chronic disease management.Partially Supported

More from Peter Attia

Peter Attia on Zone 2 Cardio

Peter Attia on Rapamycin (with Matt Kaeberlein)

Attia walks back the clinic protocol: too aggressive for healthy adults

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A. Volkovreader

4h

Bookmarking — the dossier-vs-overview split is the right call. Most of the time I want overview; sometimes I want receipts.

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N. Park

2d

Would love a "what would change this verdict" RSS feed. Sign me up if it exists.

◐

Cellular responses to stressors can lead to proteins disrupting gene programming over time.

◐Partially SupportedDNA double-strand breaks and other genome insults cause proteins like sirtuins to have a dual role in DNA repair and stress response, disrupting chromatin structure.

◐Partially SupportedStep-function changes in human longevity are expected within our lifetime due to new technologies, investment, and increased research personnel.

◐Partially SupportedThe eight or nine central tenets of aging include epigenetic change, cell-to-cell communication, senescence, protein misfolding, loss of proteostasis, genomic instability, and metabolic changes.