Glossary
The words of longevity science, one paragraph each.
AGEs (advanced glycation end products)
Products of uncontrolled bonding between sugar and protein; they stiffen collagen (skin, vessels, joints). High blood sugar makes them internally, roasted, fried and grilled food brings them from outside.
Allostatic load
The body's “wear-and-tear cost” of chronic stress: persistently high cortisol, blood pressure, inflammation and glucose together. A measurable score that predicts mortality better than any component alone.
AMPK
An energy-shortage sensor; activating it (exercise, fasting, metformin, berberine) triggers fat burning and mitochondrial biogenesis. The counterpart of mTOR.
ApoB
Apolipoprotein B — the protein common to all atherogenic lipoprotein particles (LDL, VLDL, Lp(a)). One per particle, so it counts particles.
APOE ε4
The strongest common gene variant for Alzheimer's: one copy 2–3× risk, two copies 8–12×; 25% of Europeans carry it. Not destiny: in carriers the effect of exercise, good sleep and ApoB control is LARGER than in others.
Autophagy
The cell's “self-eating” clean-up: breaking down and recycling damaged proteins and organelles. Stimulated by fasting, exercise and spermidine; subject of the 2016 Nobel Prize in Medicine.
BDNF
Brain-derived neurotrophic factor — “fertiliser” for neurons: supports new connections and hippocampal growth. Aerobic exercise is its strongest known booster; chronic stress and sleep loss lower it.
Bioimpedance (BIA)
Smart scales' body-fat estimate from resistance to a weak current. Hydration, meals and exercise skew it by up to ±5%; fine for tracking a trend, not for the absolute value — that needs DEXA.
Biological age
Age estimated from the body's functional state, versus calendar age. Measured by epigenetic clocks, blood-marker panels (PhenoAge) or simple functional tests (VO2max, grip strength, one-leg stand).
Blue Zones
Five regions (Okinawa, Sardinia, Ikaria, Nicoya, Loma Linda) with strikingly many centenarians. Common threads: daily natural movement, plant-leaning diet, strong community, purpose. Critique: some data may rest on birth-record errors (Newman 2024).
Brown adipose tissue
Heat-producing fat that burns calories from glucose and fat; cold activates it. Adults have little (50–100 g), which is why cold exposure burns modest calories — the effect on insulin sensitivity is larger.
Caloric restriction
Sustained 10–30% calorie reduction without malnutrition — the longest-known life-extending intervention in lab animals. In humans, CALERIE showed cardiometabolic and epigenetic benefits.
Cellular senescence
A state in which a cell stops dividing but doesn't die, instead secreting inflammatory factors (SASP). Accumulating “zombie cells” drive tissue ageing.
Centenarians and supercentenarians
People over 100 and over 110. They don't live healthier than average — they postpone disease (compression of morbidity). Genetics (FOXO3, APOE ε2) explain ~25%; their siblings' odds of reaching 100 are 8–17 times higher.
Chronotype
Partly genetic internal timing: “lark” or “owl”. An owl forced onto the social clock accumulates chronic sleep debt (social jetlag); with age everyone drifts larkwards.
Circadian rhythm
The ≈24-hour internal clock, set mainly by light. Governs sleep, hormones and metabolism; disruption (shift work, night light) links to insulin resistance and mortality.
Cognitive reserve
The brain's “buffer”: education, complex work, bilingualism and social life delay symptoms for the same amount of Alzheimer's pathology. It doesn't prevent the disease, but buys years.
Cohort study
Following a large group for years without intervening (e.g. UK Biobank, Nurses' Health Study). Shows association, not causation: coffee drinkers may live longer because they were healthier to begin with (“healthy user bias”).
Compression of morbidity
Fries' (1980) idea: the goal is to squeeze the period of illness into the very end of life — long healthy, briefly sick.
Coronary artery calcium score (CAC)
A low-dose CT quantifying calcified plaque in the coronary arteries (Agatston). 0 = very low 10-year risk; >100 = treat. The one test that shows disease already laid down, not just risk.
Cortisol
The adrenal stress hormone; high in the morning, low at night — that's the normal rhythm. A flattened curve (high at night too) tracks with worse sleep, belly fat and faster epigenetic ageing.
Deep sleep (N3)
The slow-wave sleep stage, mostly in the first half of the night. Growth-hormone release, brain “washing” (glymphatic system) and memory consolidation happen here; alcohol and age reduce it.
Deprescribing
The planned, doctor-led withdrawal of medicines no longer warranted. Targets: years-long proton-pump inhibitors, sleeping pills, anticholinergics (dementia risk), too many blood-pressure drugs in the elderly. Never on your own.
DEXA
Dual-energy X-ray absorptiometry: a low-dose scan measuring bone density, lean mass and fat mass (including visceral fat) by body region.
Dietary fibre
Indigestible plant carbohydrate; gut bacteria turn it into short-chain fatty acids. 25–29 g a day means 15–30% lower mortality (Lancet 2019). The European average is 18 g.
DNA methylation
Attaching a methyl group to cytosines in DNA (CpG sites); a gene-silencing mark. The methylation state of hundreds of thousands of sites together is the most precise known fingerprint of biological age.
Dysbiosis
A disrupted gut ecosystem: fewer beneficial, more inflammatory species. Caused by antibiotics, ultra-processed food, alcohol and stress; feeds inflammation through a leaky gut wall.
Epigenetic clock
Biological age computed from DNA methylation patterns (Horvath, GrimAge, DunedinPACE). GrimAge predicts mortality; DunedinPACE measures the PACE of ageing and responded to calorie restriction in CALERIE.
Epigenetics
The marks (methylation, histone modification) that switch genes on and off without changing the DNA sequence. With age the pattern “blurs”; epigenetic clocks measure this.
FOXO
A family of transcription factors that switch on stress response, DNA repair and autophagy. A FOXO3 variant is the most common shared gene variant among centenarians; low insulin/IGF-1 activates it.
Frailty
A clinical syndrome: at least three of weight loss, exhaustion, weakness, slow walking, low activity. The strongest geriatric predictor of hospitalisation and death; sarcopenia is its engine.
Gait speed
The “sixth vital sign”: usual walking pace in m/s. Below 0.8 m/s signals frailty; above 1.2 life expectancy exceeds average (Studenski 2011, n=34,485). Measurable at home over 4 metres.
Genomic instability
The build-up of DNA damage as repair systems wear out; the first hallmark of ageing. UV, tobacco smoke and alcohol accelerate it; good sleep and folate status protect repair.
Geroprotector
A compound that slows the ageing process rather than treating one disease. Proven in mice: rapamycin, acarbose, 17α-oestradiol, canagliflozin; none proven for human lifespan — hence “experimental”.
Geroscience
The field holding that ageing itself is the shared risk factor for chronic disease — so slowing ageing prevents cancer, heart disease and dementia at once. The ITP and the TAME trial are its programme.
GLP-1
A gut hormone that releases insulin after meals, slows gastric emptying and signals fullness to the brain. Its analogues (semaglutide, tirzepatide) are the first obesity drugs to move hard endpoints.
Glycaemic load
How much and how fast a serving raises blood sugar (glycaemic index × carbohydrate amount). Fibre, protein, vinegar and meal order (vegetables first) lower it.
Glymphatic system
The brain's “sewer”: during deep sleep cerebrospinal fluid flushes the tissue and washes out beta-amyloid. After one sleepless night measurably more amyloid remains.
Hallmarks of ageing
López-Otín's 2013/2023 framework: 12 cellular and molecular processes (genomic instability, telomere attrition, epigenetic alteration, senescence, mitochondrial dysfunction etc.) that drive ageing.
Hazard ratio (HR) and relative risk
HR 0.80 = 20% lower event rate during follow-up. Always ask for the absolute number too: a 20% relative cut from 1% to 0.8% means one prevented event per 500 people (NNT).
HbA1c
Glycated haemoglobin: the share of sugar-bound red cells, mirroring average glucose over the past ~3 months. Above 5.7% prediabetes, above 6.5% diabetes; the longevity target is 5.0–5.4.
Healthspan
The part of life lived free of chronic disease and loss of function. Longevity science aims to extend this, not merely lifespan.
Heart rate variability (HRV)
The variation in time between heartbeats; a marker of parasympathetic (rest) nervous-system strength. Higher = better recovery and stress tolerance. It varies hugely between people — your own trend matters, not the absolute number.
Heat-shock proteins
“Chaperone” proteins produced by heat (sauna, fever) and exercise that refold damaged proteins. One proposed route for the sauna's cognitive and cardiac benefits.
HIIT
High-intensity interval training: short (30 s–4 min) near-maximal bouts with rests. The most efficient way to raise VO2max; the “Norwegian 4×4” (4×4 min at 90%) is the best-studied form.
Hormesis
The principle that a mild stressor (exercise, heat, cold, fasting) triggers an adaptive response that makes you stronger — “what doesn't kill you”, dose-dependently.
hs-CRP
High-sensitivity C-reactive protein: the liver's inflammation signal. Below 1 mg/l low, above 3 high cardiovascular risk. Infection or injury raises it temporarily — only meaningful when measured while well.
IGF-1 / growth-hormone axis
The hormone pathway that drives growth. Low activity extends life in every species studied (dwarf mice, Laron syndrome), high activity builds muscle — the longevity goal is the middle: enough against sarcopenia, no more.
Inflammaging
The low-grade chronic inflammation (hs-CRP, IL-6) accompanying ageing — the common backdrop to heart, brain and muscle disease. Fed by visceral fat, senescent cells and gut-flora shifts.
Insulin resistance
Reduced cellular response to insulin; the pancreas compensates with ever more insulin until it fails (type 2 diabetes). Visceral fat and inactivity are the main causes.
ITP (Interventions Testing Program)
The US NIA's mouse-lifespan programme run in three labs in parallel since 2004 — the field's “gold standard”. What passed: rapamycin, acarbose, 17α-oestradiol, glycine, canagliflozin, astaxanthin. What failed: resveratrol, fisetin, curcumin, NR, metformin.
Ketosis
A metabolic state in which the liver makes ketone bodies from fat as fuel; sets in after 12–16 hours of fasting or very low carbohydrate. It can cover 60–70% of the brain's needs. Not the same as ketoacidosis.
Klotho
A kidney-made “anti-ageing” protein; its lack causes rapid ageing in mice, its excess 20–30% longer life. In humans higher levels track with better cognition; exercise and vitamin D raise it.
Lactate threshold
The intensity above which lactate is produced faster than the body clears it (≈2 mmol/l first, 4 second threshold). Zone 2 sits below the first threshold; fitness pushes it up.
Leucine threshold
The per-meal leucine amount (≈2.5–3 g, i.e. 25–40 g quality protein) that triggers muscle protein synthesis. The threshold rises with age — which is why “little and often” isn't enough.
Lifespan
Time from birth to death. The human maximum is ≈115–122 years; life expectancy in rich countries is 80–84.
Loneliness as a risk factor
Subjective loneliness (not being alone) raises mortality 26%, social isolation 29% (Holt-Lunstad meta-analysis) — comparable to smoking. It raises inflammation and cortisol; regular weekly social contact is protective.
Lp(a) — lipoprotein(a)
A genetically set, LDL-like particle; high in 20% of people and an independent risk for heart attack and aortic stenosis. Lifestyle doesn't move it; measure once in a lifetime, drugs arriving from 2025.
Mendelian randomisation
A method using randomly inherited gene variants as a “natural experiment”: if variants that genetically lower LDL mean fewer heart attacks, LDL is causal. This is how the LDL versus HDL debate was settled.
Menopause and HRT
The loss of oestrogen between 45 and 55 accelerates bone loss, atherosclerosis and visceral fat gain. Hormone therapy started before 60 or within 10 years of menopause (transdermal oestradiol) was re-evaluated after the 2002 WHI panic: benefits mostly exceed risks.
Meta-analysis
The statistical pooling of several studies' results. The top of the evidence pyramid — but only as good as the studies included; bad trials added together are still bad (“garbage in, garbage out”).
Metabolic syndrome
At least three of five: abdominal obesity, high triglycerides, low HDL, high blood pressure, high fasting glucose. A third of adults are affected; it doubles cardiovascular risk.
Metformin
The most common diabetes drug (AMPK activator). Diabetics on it show lower cancer and mortality rates; the TAME trial would test whether it extends healthspan in healthy people — no result yet.
Microbiome
The ~38 trillion bacteria in the gut and their genes. Diversity falls with age; a fibre-rich, varied plant diet (30 plant types a week) raises it. Centenarians' microbiomes look “younger”.
Mitochondria
The cell's energy-producing organelles. Their number and quality fall with age; zone 2 training is the strongest known stimulus for making new ones.
Mitophagy
Autophagy specialised for mitochondria: clearing damaged “power plants”. Boosted by urolithin A and exercise.
mTOR
The cell's “grow or clean up” switch: nutrient abundance drives growth, scarcity drives autophagy. Rapamycin inhibits it; protein and insulin activate it.
NAD+
The central coenzyme in energy production and DNA repair. Falls 30–50% with age in some tissues; precursors (NMN, NR) raise it, clinical benefit still under proof.
Neuroplasticity
The brain's lifelong ability to build new connections and reorganise. Learning new skills (a language, an instrument), exercise and sleep maintain it; routine lets it wither.
NNT (number needed to treat)
How many people must take the treatment for a given time to prevent one event. Statins in primary prevention over 5 years NNT ≈ 100–200; blood-pressure lowering in hypertension ≈ 30–60. A small NNT signals real benefit.
Osteopenia / osteoporosis
Loss of bone density (T-score between −1 and −2.5 osteopenia, below that osteoporosis). Causes fractures in a third of women and a fifth of men over 50; one-year mortality after hip fracture is 20–30%. Strength training, protein, D3+K2 and timely treatment slow it.
Oxidative stress
An excess of free radicals (ROS) over antioxidant defences. In small doses a signal and training stimulus (hormesis), chronically cell damage — which is why high-dose antioxidant pills failed.
Partial reprogramming
Briefly switching on the Yamanaka factors (OSKM), which “rewinds” a cell's epigenetic age without turning it into a stem cell. Vision restored in mice (2020), first human trials from 2025. The biggest promise and the biggest tumour risk.
Polypharmacy
Taking more than five medicines at once; 40% of people over 65. A source of interactions, falls and cognitive decline — “deprescribing” is a longevity tool in its own right.
Polyphenols
Thousands of plant defence compounds (flavonoids, stilbenes, lignans) in berries, cocoa, olive oil, tea, coffee. In the body they act not as antioxidants but as mild stressors (xenohormesis) and via the gut flora.
Protein leverage
Simpson and Raubenheimer's hypothesis: the body keeps eating until its protein need is met. When the diet is protein-dilute (UPF) we overeat calories — a 15–20% protein share satiates.
Proteostasis
The balance of correct protein folding and disposal. Losing it leads to misfolded aggregates (amyloid, tau, alpha-synuclein) — the common root of Alzheimer's and Parkinson's.
Publication bias
Positive results get published more easily than negative ones; supplement literature is therefore too rosy. Funnel plots and pre-registered trials help — a small, industry-funded trial is always suspect.
Purpose in life (ikigai)
The sense that life has direction and meaning. In cohorts (Health and Retirement Study, n=6,985) the highest purpose scores meant 2.4× lower mortality than the lowest, adjusted. The most important protective factor after retirement.
Rapamycin
An mTOR inhibitor isolated from Easter Island soil, originally a transplant immunosuppressant. The only molecule to have extended lifespan in every species tested (yeast, worms, flies, mice).
RCT (randomised controlled trial)
Participants are randomly assigned to treatment or control, ideally blinded. The only design that proves cause and effect. Its limits: short, selected populations, expensive — which is why 10-year longevity RCTs are rare.
REM sleep
The rapid-eye-movement, dream-rich phase, dominant in the second half of the night; emotional processing and memory integration happen here. Alcohol and late sedatives suppress it; early rising cuts it short.
Resting heart rate
Heart rate measured on waking; 50–60 signals good fitness. Every +10 beats/min tracks with 10–20% higher mortality in cohorts. Zone 2 training lowers it most effectively.
Sarcopenia
Age-related loss of muscle mass and strength: 3–8% per decade from age 30, faster after 60. Predicts falls, fractures, diabetes and mortality; reversible with strength training and protein.
SASP
Senescence-associated secretory phenotype: the inflammatory “shout” of senescent cells (IL-6, IL-8, MMPs) that ages their neighbours too. Senolytics remove this source.
Senolytics
Compounds (dasatinib+quercetin, fisetin) that selectively kill senescent cells. Convincing in mice; human trials are ongoing.
Short-chain fatty acids
Butyrate, propionate, acetate — products of bacterial fibre fermentation. Butyrate is the main fuel of gut-wall cells, anti-inflammatory, and improves glucose control.
Sirtuins
A NAD+-dependent enzyme family (SIRT1–7) regulating DNA repair, metabolism and inflammation. “Activating” them (resveratrol) has not delivered in humans.
Sleep apnoea
Repeated breathing pauses in sleep, more than 5 per hour (AHI). Present in 20–30% of adult men, 80% of them unaware. Causes hypertension, atrial fibrillation and dementia; CPAP treatment reverses this.
Sleep pressure (adenosine)
Adenosine accumulating in the brain with hours awake; it creates sleepiness and deep sleep clears it. Caffeine blocks the adenosine receptor — it doesn't reduce the pressure, only hides it.
Stem cell exhaustion
The depletion of tissues' renewal reserve: fewer, poorer-functioning stem cells in marrow, muscle and gut. The main reason regeneration slows; exercise and caloric restriction slow it.
Surrogate endpoint
A measure (NAD level, telomere length, epigenetic age) used instead of the hard endpoint (disease, death) because it's faster. The danger: the marker can improve without the person living longer — most NMN trials are like this.
Telomerase
The enzyme that rebuilds telomeres; switched off in most adult cells, on in cancer cells. Activating it cuts both ways: more divisions but tumour risk — which is why it isn't a “longevity drug”.
Telomeres
Protective caps on chromosomes that shorten with every division. Length correlates with ageing but is a poor individual biomarker (high variance); chronic stress speeds attrition.
Testosterone decline (andropause)
In men testosterone falls ~1% a year after 30; most of it is driven by obesity, sleep loss and inactivity, not age. The TRAVERSE trial (2023) found replacement heart-safe, but it's only warranted for true deficiency.
Time-restricted eating
Confining eating to an 8–10-hour daily window. A simplified form of calorie restriction; on its own it doesn't beat the same calories spread differently.
TMAO
Trimethylamine N-oxide: made by gut bacteria from red meat, eggs and choline, then oxidised by the liver. High levels track with cardiovascular events; fish raises it too yet is protective — the signal's meaning is debated.
Ultra-processed food (UPF)
NOVA group 4: products made from industrial ingredients (modified starch, isolates, emulsifiers, flavourings). They provide 50% of energy in Anglo-Saxon diets; every +10% means 3–4% more mortality (cohorts).
Visceral fat
Fat stored inside the abdomen around the organs — not under the skin. Hormonally active, it fuels inflammation and insulin resistance. Waist-to-height ratio approximates it well; DEXA measures it precisely.
VO2max
The body's maximal oxygen uptake in ml/kg/min; the measure of cardiorespiratory fitness and the strongest known mortality predictor.
Zone 2
The training intensity at which lactate doesn't yet accumulate (≈60–70% of max heart rate, conversational pace). The main builder of mitochondrial capacity and fat metabolism.
Last reviewed: 6 September 2026
This site is educational and does not replace medical advice. Start any supplement or drug only after consulting a doctor or pharmacist.