Topic
Aging biology
The cellular and molecular hallmarks of aging — and how honestly they map onto the interventions marketed against them.
Aging biology is the substrate under every longevity claim. This hub covers the mechanisms — cellular, mitochondrial, and systemic — and holds them against the interventions that invoke them, noting where the mechanism is established and where the leap to a marketed product is not.
Publications on this topic
What Is Autophagy?
Autophagy is the cell's recycling system: it packages up worn-out and damaged parts, digests them in the lysosome, and returns the raw materials as building blocks and fuel. This explainer covers what it is, its three types, how Ohsumi's yeast work won a Nobel Prize, how nutrient sensors control it, why its failure is a hallmark of aging, and what the fasting, exercise, rapamycin, and spermidine evidence does — and does not — show in humans.
Lifespan vs Healthspan
Lifespan measures how long you live; healthspan measures how long you live in good health. This explainer defines both, quantifies the gap between them with population data, and explains why closing that gap — not simply adding years — is the goal.
Mitochondrial Dysfunction
Mitochondria make most of a cell's ATP, and their function declines with age — one of the recognized hallmarks of aging. This explainer covers what 'mitochondrial dysfunction' means, the mtDNA-mutation and free-radical mechanisms proposed for it (and how the free-radical theory has been substantially revised), mitochondria as signaling hubs linked to senescence and inflammation, the disease associations, and the honest human evidence for exercise, NAD+ precursors, and urolithin A.
What Is mTOR?
mTOR is the enzyme that decides whether a cell should build or maintain itself, and one of the central levers in the biology of ageing. This explainer covers what mTOR is, the two complexes it runs as, how reduced signalling extends lifespan in animals, why rapamycin lengthens the lives of mice, and why a proven human longevity effect does not yet exist.
Why We Age
Why does aging happen at all? This explainer separates the two great families of theory — stochastic damage (wear, mutation, free radicals, failing proteostasis) and evolutionary explanation (why selection permits aging once reproduction is done) — shows how they combine into a proximate 'how' and an ultimate 'why', and reviews the evidence that aging rates are not fixed.
What Is Cellular Senescence?
Cellular senescence is a stable state in which a stressed cell stops dividing, resists death, and secretes an inflammatory signal its neighbours can hear. This explainer covers what triggers it, how it is identified, why it protects early in life yet harms when senescent cells accumulate, and what clearing them with senolytics does — and does not yet — show in humans.
The Hallmarks of Aging
The hallmarks of aging are a proposed framework that organizes the biology of getting old into a small set of recurring processes — nine in the original 2013 paper, twelve after a 2023 update. This explainer covers what the hallmarks are, how they are grouped, what qualifies as a hallmark, the critiques of the framework, and why most of the hard causal evidence still comes from worms, flies, and mice rather than people.
What Is Longevity Science?
Longevity science studies healthspan — years lived in good health — and asks whether aging itself can be slowed. Its evidence is a ladder: strong for unglamorous lifestyle factors, weaker for the drugs that make headlines, and weakest of all for what supplements promise.
Noninvasive Neuromodulation Technologies
An evidence review of noninvasive brain-stimulation technologies — TMS, tDCS, tACS, tRNS, and CES — covering the underlying physics, targeting and dosing, mechanism from field to synapse, and the current evidence and safety landscape.