Longevity glossary

Healthspan

Also known as: health span, healthy life expectancy

Healthspan is the period of life spent in good health, free of chronic disease and disability, as distinct from lifespan, which is the total number of years lived. The gap between the two matters: across populations, people commonly spend roughly the final decade of life managing illness or losing function. Compressing that period, so that decline occurs as close to the end of life as possible, is the central aim of preventive longevity medicine. Healthspan cannot be captured in a single number, but its main determinants are measurable, including cardiorespiratory fitness, muscle mass, metabolic health, inflammation and sleep quality.

Biological age

Also known as: physiological age

Biological age is an estimate of how well the body is functioning relative to the number of years lived. Two people of the same chronological age can have measurably different physiology, and that difference tends to predict future disease and mortality more accurately than a birth date does. Biological age can be estimated from epigenetic clocks, from panels of clinical biomarkers, or from composite measures combining fitness, body composition and metabolic data. No single method is definitive and estimates differ between approaches, so biological age is most useful as a trend tracked consistently over time rather than as a fixed verdict.

Epigenetic age

Also known as: DNA methylation age, epigenetic clock

Epigenetic age is an estimate of biological ageing derived from DNA methylation, the pattern of chemical marks that accumulate on the genome over time. Algorithms known as epigenetic clocks read these patterns and express the result in years. First-generation clocks such as Horvath were trained to predict chronological age; later clocks including PhenoAge and GrimAge were trained on health outcomes and predict disease and mortality risk more usefully. Results vary between different clocks and between laboratories, so a trend measured consistently over time carries considerably more information than any single reading taken in isolation.

DunedinPACE

Also known as: pace of ageing

DunedinPACE is an epigenetic measure that estimates the current rate of biological ageing rather than accumulated biological age. It is expressed as biological years elapsed per calendar year, so a value of 1.0 indicates ageing at approximately the population average, while higher values indicate a faster pace. It was developed from a long-running birth cohort study in which participants were tracked with repeated physiological measurements across decades. Because pace can change in response to intervention, whereas accumulated age cannot be undone, it is often more actionable than a static age estimate, though it remains subject to laboratory variation.

Hallmarks of ageing

Also known as: hallmarks of aging

The hallmarks of ageing are a framework describing the biological processes that drive ageing across species. First published in 2013 and expanded in 2023, they include genomic instability, telomere attrition, epigenetic alteration, loss of proteostasis, disabled macroautophagy, deregulated nutrient sensing, mitochondrial dysfunction, cellular senescence, stem cell exhaustion, altered intercellular communication, chronic inflammation and dysbiosis. The framework is useful because it organises ageing into processes that can in principle be measured and targeted, rather than treating ageing as a single inevitable event. Most are interconnected, so interventions rarely affect one in isolation.

Geroscience

Also known as: geroprotector

Geroscience is the field studying the biology of ageing itself, on the premise that ageing is the largest shared risk factor for most chronic disease. Rather than treating heart disease, diabetes, dementia and cancer as separate problems, geroscience asks whether slowing the underlying ageing processes could delay all of them at once. A geroprotector is any intervention proposed to do this. The field is scientifically serious and well funded, though few interventions have yet demonstrated benefit in large human trials, so the distance between the hypothesis and clinical practice remains considerable.

Telomeres

Also known as: telomere length

Telomeres are the repetitive DNA sequences that cap the ends of chromosomes and protect them from degradation, much as the plastic tip protects the end of a shoelace. They shorten each time a cell divides, and once critically short the cell stops dividing and enters senescence. Telomere length is therefore used as one marker of cellular ageing, and shorter leukocyte telomeres have been associated with cardiovascular disease and mortality in population studies. Measurement varies considerably between methods and laboratories, and length is influenced by inherited factors as well as lifestyle, so it is best interpreted alongside other markers.

Inflammaging

Also known as: chronic low-grade inflammation

Inflammaging describes the chronic, low-grade inflammation that develops with age in the absence of infection. Unlike acute inflammation, which resolves after injury, it persists at a low level for years and is measurable through markers such as high-sensitivity C-reactive protein and interleukin-6. It is thought to arise from accumulated senescent cells, visceral fat tissue, changes in gut permeability and declining immune regulation. Inflammaging is associated with cardiovascular disease, type 2 diabetes, frailty, cognitive decline and several cancers, which is why it is regarded as one of the shared mechanisms linking ageing to multiple chronic conditions rather than a disease in itself.

Cellular senescence

Also known as: senescent cells, zombie cells

Cellular senescence is a state in which a cell permanently stops dividing but does not die, remaining metabolically active within the tissue. Senescence is a protective mechanism that prevents damaged cells from replicating, but senescent cells accumulate with age and secrete inflammatory signals collectively known as the senescence-associated secretory phenotype. This secretion contributes to chronic low-grade inflammation and can impair the function of surrounding healthy tissue. Senescent cell accumulation is one of the recognised hallmarks of ageing. Therapies intended to clear these cells are an active research field but remain investigational rather than established clinical practice.

Autophagy

Also known as: cellular recycling

Autophagy is the cellular process of breaking down and recycling damaged proteins, organelles and other internal components. The term means self-eating, and the mechanism allows cells to clear accumulated debris and reuse the raw materials. Autophagy declines with age, and impaired clearance is thought to contribute to the build-up of dysfunctional cellular material seen in ageing tissues. It is stimulated by fasting, energy restriction and exercise in laboratory studies. Much of the direct evidence comes from animal and cell models, and the extent to which specific human fasting protocols meaningfully alter autophagy in tissue remains under investigation.

Mitochondrial function

Also known as: mitochondria, mitochondrial health

Mitochondria are the cellular structures that generate most of the body's usable energy, converting fuel and oxygen into adenosine triphosphate. Mitochondrial function tends to decline with age, with reduced efficiency, lower density in tissues such as skeletal muscle, and increased production of reactive oxygen species. This decline is one of the recognised hallmarks of ageing and is associated with fatigue, reduced exercise capacity and metabolic dysfunction. Aerobic exercise, particularly sustained cardiorespiratory training, has the strongest evidence for improving mitochondrial density and function, notably in skeletal muscle where the effect can be measured directly.

NAD+

Also known as: nicotinamide adenine dinucleotide

NAD+ is a coenzyme present in every cell, essential for energy production, DNA repair and the activity of enzymes involved in cellular maintenance. Tissue NAD+ levels decline with age, and restoring them improves markers of ageing in animal studies, which is why it has attracted intense interest. Supplements such as nicotinamide riboside and nicotinamide mononucleotide do raise NAD+ measured in blood in human trials. Whether that translates into meaningful health outcomes in people is not yet established, and current human evidence is short-term and largely limited to surrogate markers.

Sirtuins

Also known as: SIRT1

Sirtuins are a family of enzymes that regulate cellular processes including DNA repair, inflammation, metabolism and mitochondrial function. They depend on NAD+ to work, which links them to nutrient availability, and their activity increases during fasting and energy restriction. Sirtuins became prominent through research suggesting they mediate some benefits of caloric restriction, and through interest in compounds proposed to activate them. The animal evidence is substantial; the human evidence that supplementing to influence sirtuin activity changes health outcomes remains limited and considerably less certain than the marketing suggests.

mTOR

Also known as: mechanistic target of rapamycin

mTOR is a cellular sensor that detects nutrient availability, particularly protein and amino acids, and switches the cell between growth and maintenance. When nutrients are plentiful mTOR promotes growth and protein synthesis; when they are scarce it steps back and allows repair processes such as autophagy to proceed. Chronic mTOR activation is associated with accelerated ageing in laboratory models, while inhibiting it extends lifespan in several species. This creates a genuine tension in practice, since building muscle requires mTOR activation, and the balance between growth and repair matters more than suppressing either.

AMPK

Also known as: AMP-activated protein kinase

AMPK is a cellular energy sensor that activates when energy is low, during exercise, fasting or energy restriction. Once active it promotes glucose uptake, fat oxidation, mitochondrial production and autophagy, broadly shifting the cell toward efficiency and repair. It acts roughly opposite to mTOR, and the two together form the core of what is often called nutrient sensing. Exercise and energy restriction are the most reliable ways to activate AMPK. Several compounds also influence it, though the evidence that supplementing to do so improves human outcomes is weaker than the mechanism suggests.

Senolytics

Also known as: senolytic therapy

Senolytics are compounds intended to selectively clear senescent cells, which accumulate with age and secrete inflammatory signals that impair surrounding tissue. In animal studies, removing senescent cells improves physical function, delays several age-related conditions and extends healthy lifespan, which makes this one of the more compelling areas in ageing biology. Human evidence is at an early stage, with small trials in specific conditions rather than broad use. Senolytics are not established clinical treatments and are not approved for slowing ageing, so anyone considering them should discuss the risks with a doctor.

Glycation and AGEs

Also known as: advanced glycation end products

Glycation is the process by which sugars attach to proteins and fats without enzymatic control, producing advanced glycation end products, or AGEs. These accumulate over time and stiffen tissues, contributing to arterial stiffness, reduced skin elasticity, kidney damage and cataract formation. Glycation increases with higher and more variable blood glucose, which is one reason glucose regulation matters beyond diabetes risk alone. AGEs also form in food during high-temperature dry cooking such as grilling and frying, though the contribution of dietary AGEs relative to internally generated ones remains debated.

Oxidative stress

Also known as: reactive oxygen species, free radicals

Oxidative stress describes an imbalance between reactive oxygen species produced during normal metabolism and the body's capacity to neutralise them, resulting in damage to DNA, proteins and cell membranes. It is one of the recognised contributors to ageing. However, the simple view that antioxidants should therefore be taken in quantity has not held up: reactive oxygen species also act as signalling molecules, and high-dose antioxidant supplementation can blunt beneficial adaptations to exercise. The evidence favours obtaining antioxidants from food and supporting the body's own antioxidant systems rather than large supplemental doses.

Sarcopenia

Also known as: age-related muscle loss

Sarcopenia is the progressive loss of skeletal muscle mass, strength and function associated with ageing. Muscle mass typically begins declining from the fourth decade and the rate accelerates thereafter, particularly during periods of inactivity or illness. Assessment is based on measured low muscle strength, usually grip strength or chair-stand performance, confirmed by low muscle quantity on body composition analysis. Because muscle is the body's largest site of glucose disposal and its structural reserve during illness, sarcopenia is associated with falls, fractures, longer hospital stays and loss of independence. Resistance training and adequate dietary protein have the strongest supporting evidence.

Visceral fat

Also known as: visceral adipose tissue, abdominal fat

Visceral fat is the adipose tissue stored deep within the abdomen, surrounding organs such as the liver, pancreas and intestines. It differs from subcutaneous fat, the layer directly beneath the skin, in being metabolically active: it releases inflammatory signalling molecules and free fatty acids into the portal circulation. Visceral adiposity is strongly associated with insulin resistance, type 2 diabetes, fatty liver disease and cardiovascular risk. Because body weight and body mass index cannot distinguish between fat compartments, a person of apparently normal weight may still carry a metabolically unfavourable amount, which is why direct body composition measurement is informative.

Insulin resistance

Also known as: reduced insulin sensitivity

Insulin resistance is a state in which cells respond less effectively to insulin, so the pancreas compensates by producing more of it to keep blood glucose within range. This compensation can continue for years, which is why a fasting glucose result often remains normal long after the underlying problem has begun to develop. Measuring fasting insulin alongside glucose, and calculating HOMA-IR from the two, reveals the compensation earlier. Insulin resistance sits upstream of type 2 diabetes, fatty liver disease and cardiovascular risk, and is influenced by visceral fat, physical inactivity, sleep loss and diet quality. It is substantially modifiable when addressed early.

HOMA-IR

Also known as: homeostatic model assessment

HOMA-IR, the Homeostatic Model Assessment of Insulin Resistance, is a calculated index that estimates insulin resistance from a single fasting blood sample using fasting glucose and fasting insulin together. It is derived by multiplying the two values and dividing by a fixed constant. Because it requires only a standard blood draw, it offers a practical way to identify insulin resistance earlier than fasting glucose alone, which can remain normal for years while the pancreas compensates. HOMA-IR is a screening and research tool rather than a standalone diagnostic test, and results should be interpreted in clinical context alongside other metabolic markers.

Metabolic syndrome

Also known as: syndrome X, cardiometabolic syndrome

Metabolic syndrome is a cluster of measurements that together indicate elevated cardiometabolic risk. It is generally identified when at least three of the following are present: increased waist circumference, raised triglycerides, reduced HDL cholesterol, elevated blood pressure and raised fasting glucose. The combination carries greater risk than any component alone, and is associated with type 2 diabetes and cardiovascular disease. Because each component is measurable in a routine assessment, metabolic syndrome is one of the more accessible early indicators of metabolic dysfunction, and its underlying drivers, particularly visceral fat and insulin resistance, are substantially modifiable.

HbA1c

Also known as: glycated haemoglobin

HbA1c measures the proportion of haemoglobin that has become glycated, reflecting average blood glucose over roughly the preceding two to three months. It is the standard test for diagnosing and monitoring diabetes and requires no fasting. Its limitation is that it is an average, so it can conceal considerable daily fluctuation, and it can be distorted by anaemia, kidney disease and conditions affecting red cell lifespan. For this reason it is best read alongside fasting glucose, fasting insulin, and where relevant continuous glucose data rather than treated as a complete picture.

Continuous glucose monitoring

Also known as: CGM

Continuous glucose monitoring uses a small sensor worn on the skin to measure glucose in the fluid between cells, typically every few minutes for one to two weeks. It reveals what a single fasting reading cannot: how particular meals, stress, sleep loss and exercise affect your own glucose in real time. Responses to identical foods vary substantially between people, which is why the data is personally useful rather than generic. Sensor readings lag blood glucose slightly and are less precise than laboratory testing, so patterns matter more than individual values.

Time in range

Also known as: glucose time in range

Time in range is the proportion of the day that glucose stays within a target band, measured using continuous glucose monitoring. It has become a preferred metric alongside HbA1c because it captures variability that an average conceals. Two people can share the same HbA1c while one is stable and the other is swinging between highs and lows, and those swings appear to carry their own metabolic and vascular consequences. Targets differ between people with and without diabetes, and interpretation should be clinical rather than based on consumer app defaults.

Metabolic flexibility

Metabolic flexibility is the ability to switch efficiently between burning carbohydrate and fat as circumstances change, using carbohydrate during intense exercise and after meals, and fat at rest or when fasting. Flexibility tends to decline with insulin resistance, inactivity and constant food availability, leaving the body relying heavily on carbohydrate and struggling between meals. It can be assessed through indirect calorimetry, which measures gas exchange, or inferred from glucose and lipid responses. Regular aerobic exercise, sufficient recovery and periods without eating all appear to improve it.

Ketosis

Also known as: ketone bodies, nutritional ketosis

Ketosis is a metabolic state in which the liver produces ketone bodies from fat as an alternative fuel, occurring during fasting, prolonged exercise or carbohydrate restriction. It is a normal physiological state and distinct from diabetic ketoacidosis, which is a medical emergency involving far higher ketone levels alongside high blood glucose. Ketogenic diets have established uses in epilepsy and show benefit for glycaemic control in some people, though long-term data on cardiovascular outcomes is limited and adherence is often the practical constraint rather than the underlying physiology.

Fatty liver disease

Also known as: MASLD, NAFLD, hepatic steatosis

Fatty liver disease is the accumulation of fat within liver cells in the absence of significant alcohol intake, now commonly termed metabolic dysfunction-associated steatotic liver disease. It affects a substantial proportion of adults, frequently without symptoms, and is closely tied to insulin resistance and visceral fat. Most cases remain stable, but a minority progress to inflammation, fibrosis and cirrhosis. It is detectable through liver enzymes, ultrasound and elastography, which estimates stiffness, and early disease is often substantially reversible through weight reduction and improved metabolic health.

ApoB

Also known as: apolipoprotein B

Apolipoprotein B, usually written ApoB, is a structural protein carried on every atherogenic lipoprotein particle, with one molecule per particle. Measuring ApoB therefore counts the number of particles capable of entering the arterial wall, whereas a standard LDL cholesterol result measures the cholesterol carried inside those particles. The two can disagree: a person may have an acceptable LDL cholesterol alongside an elevated particle count, particularly where there is insulin resistance or raised triglycerides. Because atherosclerosis is driven by particle number rather than cholesterol content, ApoB is increasingly regarded as the more informative marker of cardiovascular risk.

Lipoprotein(a)

Also known as: Lp(a)

Lipoprotein(a), written Lp(a), is a lipoprotein particle whose concentration is largely determined by inherited factors and changes little with diet or exercise. It is elevated in roughly one in five people and is an independent risk factor for atherosclerotic cardiovascular disease and aortic valve stenosis. Because levels remain relatively stable across life, Lp(a) generally needs measuring only once. Despite being inexpensive and widely available, it is absent from most routine lipid panels, which means a substantial proportion of people carry an inherited cardiovascular risk they have never been told about. Testing once is reasonable for most adults.

High-sensitivity CRP

Also known as: hs-CRP, C-reactive protein

High-sensitivity C-reactive protein, or hs-CRP, is a blood marker of systemic inflammation measured with an assay sensitive enough to detect the low concentrations relevant to chronic disease risk rather than acute infection. Persistently elevated hs-CRP is associated with cardiovascular events, metabolic dysfunction and several other chronic conditions, and it is one of the practical measures of inflammaging. Because levels rise temporarily with infection, injury and intense exercise, a single elevated result should be repeated before it is interpreted. It is inexpensive and widely available, yet is not routinely included in standard screening panels.

Homocysteine

Homocysteine is an amino acid produced during normal metabolism and cleared with the help of vitamins B12, B6 and folate. Raised levels are associated with cardiovascular disease, stroke and cognitive decline, and are often correctable by addressing those vitamin deficiencies. The association is well established; the causal question is less settled, since trials lowering homocysteine with B vitamins have shown limited effect on cardiovascular events, though some evidence suggests benefit for brain atrophy in people with elevated levels. It is inexpensive to measure and rarely included in standard panels.

Coronary artery calcium score

Also known as: CAC, calcium score

A coronary artery calcium score uses a brief CT scan to quantify calcified plaque in the coronary arteries, expressed as an Agatston score. It measures disease that already exists rather than estimating risk from proxies, which makes it one of the more decisive tests available for cardiovascular risk. A score of zero carries a very favourable short-term prognosis, while a high score substantially changes management. Its limitation is that it detects calcified plaque, so early soft plaque may be missed, which matters particularly in younger adults.

Omega-3 index

The omega-3 index measures EPA and DHA as a percentage of total fatty acids in red blood cell membranes, reflecting long-term intake rather than what was eaten recently. Lower values are associated with higher cardiovascular risk in observational studies, and the measure is also of interest for brain health and inflammation. Because it reflects membrane composition over months, it is more stable and informative than plasma measurement. Supplementation trials have produced mixed results on hard outcomes, which is why the index is best read as one marker among several.

Endothelial function

Also known as: endothelium

The endothelium is the single-cell lining of blood vessels, responsible for regulating vessel tone, blood flow, clotting and inflammation. Endothelial dysfunction is among the earliest detectable stages of cardiovascular disease, appearing before plaque is visible and before symptoms occur. It can be assessed non-invasively through techniques measuring how vessels dilate in response to increased flow. Function is influenced by blood pressure, glucose regulation, lipids, smoking, sleep and physical activity, and improves with the same interventions that reduce cardiovascular risk more broadly, which makes it an early and encouraging place to see change.

VO2 max

Also known as: cardiorespiratory fitness, aerobic capacity

VO2 max is the maximum rate at which the body can take in and use oxygen during intense exercise, and it is the standard measure of cardiorespiratory fitness. It is expressed in millilitres of oxygen per kilogram of body weight per minute. Cardiorespiratory fitness is among the strongest modifiable predictors of all-cause mortality: large cohort studies have found progressively lower mortality at higher levels of fitness, with no clear upper limit of benefit observed. It is also trainable at any age. Despite this, it is rarely measured in a standard health check, which makes it a valuable addition to screening.

Heart rate variability

Also known as: HRV

Heart rate variability, usually written HRV, is the variation in time between consecutive heartbeats, and it reflects the balance between the sympathetic and parasympathetic branches of the autonomic nervous system. Higher variability generally indicates greater parasympathetic activity and better recovery capacity, while a sustained decline can signal accumulated physiological load from training, illness, poor sleep or psychological stress. HRV varies substantially between individuals, so comparing absolute values between people is of limited value. It is most useful as a personal trend measured under consistent conditions across weeks, rather than as a daily verdict.

MCED

Also known as: multi-cancer early detection

Multi-cancer early detection, abbreviated MCED, refers to blood tests that screen for early signals shared across many cancer types from a single sample. These tests typically analyse cell-free DNA, fragments shed into the bloodstream by tumours, looking for methylation patterns or other features that may indicate the presence and possible tissue of origin of a cancer. MCED is designed to complement conventional single-cancer screening such as mammography and colonoscopy, not to replace it. Sensitivity varies considerably by cancer type and stage, and both false negatives and false positives occur, so results require clinical interpretation and confirmatory investigation.

Zone 2 training

Also known as: aerobic base training

Zone 2 refers to sustained aerobic exercise at an intensity where you could still hold a conversation, roughly corresponding to the point below which blood lactate begins to rise sharply. Training at this intensity is associated with improvements in mitochondrial density and fat oxidation, and it forms the base of most endurance training structures. Its popularity in longevity circles reflects the strength of cardiorespiratory fitness as a predictor of mortality. The precise zone definition varies between models, so the conversational test is usually more practical than a heart rate formula.

Lactate threshold

The lactate threshold is the exercise intensity at which lactate begins accumulating in the blood faster than it can be cleared, marking the transition from comfortably sustainable to progressively harder effort. It is measured through graded exercise testing with blood sampling, and it is a strong determinant of endurance performance, often more so than VO2 max in trained individuals. Threshold is highly trainable. For general health purposes the value of knowing it is mainly in setting training intensities accurately rather than guessing at effort, which makes structured aerobic work considerably more efficient.

Grip strength

Also known as: handgrip strength

Grip strength is measured with a handheld dynamometer and serves as a simple proxy for overall muscular strength. It is a consistent predictor of all-cause and cardiovascular mortality across populations, and is used as one criterion in assessing sarcopenia. Its value lies in being quick, inexpensive and reproducible, requiring no specialist facility. It is not that grip itself is critical, but that it correlates with total muscle function and reserve, which makes it a practical marker to track over years rather than a training target in itself.

Muscle protein synthesis

Also known as: MPS, leucine threshold

Muscle protein synthesis is the process by which the body builds new muscle protein, stimulated by resistance exercise and by dietary protein, particularly the amino acid leucine. Building or maintaining muscle requires synthesis to exceed breakdown across the day. The response to protein becomes less efficient with age, a phenomenon termed anabolic resistance, which is why older adults generally require more protein per meal than younger adults to achieve the same effect. Distributing protein across meals rather than concentrating it in one is usually recommended.

DEXA scan

Also known as: DXA, dual-energy X-ray absorptiometry

A DEXA scan uses two low-dose X-ray beams to measure bone mineral density and body composition, distinguishing bone, lean mass and fat, including an estimate of visceral fat. It is the reference standard for diagnosing osteoporosis and one of the more accurate accessible methods for tracking body composition. Radiation exposure is very low. Its main value in a longevity context is serial measurement: a single scan is a snapshot, while repeated scans show whether muscle is being preserved and where fat is actually changing, which weight alone can never reveal.

Bone mineral density

Also known as: BMD, T-score

Bone mineral density measures the amount of mineral in bone tissue, reported as a T-score comparing you with a healthy young adult reference. A T-score at or below minus 2.5 indicates osteoporosis, while values between minus 1 and minus 2.5 indicate osteopenia, a reduction that increases fracture risk without meeting the threshold for osteoporosis. Density declines with age and accelerates after menopause. Because bone loss is silent until fracture, measurement before symptoms is the only way the trajectory can be identified and addressed while loading, nutrition and hormonal health can still change it.

Circadian rhythm

Also known as: body clock

The circadian rhythm is the roughly 24-hour internal cycle governing sleep, hormone release, body temperature, digestion and alertness. It is coordinated by a master clock in the hypothalamus, synchronised primarily by light reaching the eyes, with peripheral clocks in organs including the liver influenced additionally by meal timing. Misalignment between internal timing and actual behaviour, as in shift work or persistent late nights, is associated with metabolic, cardiovascular and mood consequences. Morning light exposure and consistent timing of sleep and meals are the main practical levers.

Sleep architecture

Also known as: sleep stages, REM, deep sleep

Sleep architecture describes the structure of a night's sleep across its stages: light sleep, deep slow-wave sleep and REM sleep, cycling roughly every ninety minutes. Deep sleep dominates the first half of the night and is associated with physical restoration and memory consolidation, while REM concentrates in the second half and supports emotional and cognitive processing. Alcohol, illness, stress and some medications alter this structure. Consumer wearables estimate stages indirectly and are considerably less accurate than clinical sleep studies, so trends matter more than nightly figures.

Sleep regularity

Also known as: sleep regularity index

Sleep regularity describes how consistent your sleep and wake times are from day to day, as distinct from how long you sleep. Large cohort analyses using accelerometer data have found regularity to be a stronger predictor of all-cause mortality than duration, meaning a consistent shorter night may outperform an erratic longer one. The likely mechanism is circadian alignment, since irregular timing repeatedly shifts the internal clock. Of the available sleep levers, fixing wake time is usually the most controllable and has the widest downstream effect.

Chronotype

Also known as: morningness, eveningness

Chronotype is your natural tendency toward earlier or later sleep timing, substantially influenced by genetics and shifting predictably with age, with adolescents skewing later and older adults earlier. Later chronotypes living on early schedules experience what is termed social jetlag, a chronic mismatch between biological and social time that is associated with metabolic and mood consequences. Chronotype can be shifted modestly through light timing and consistent scheduling, but not reversed. Aligning demanding work with your natural peak, where circumstances allow, is usually more effective than fighting it.

Cortisol awakening response

Also known as: CAR

The cortisol awakening response is the sharp rise in cortisol occurring within thirty to forty-five minutes of waking, superimposed on the normal daily rhythm. It is a healthy and expected feature, preparing the body for the demands of the day, rather than a sign of stress. What matters clinically is the shape of the whole curve: a robust morning rise followed by a clear decline into the evening. A flattened slope, with blunted mornings and elevated evenings, is associated with worse cardiometabolic outcomes and often describes what people mean by feeling tired but wired.

Orthosomnia

Orthosomnia describes sleep disturbance caused by preoccupation with achieving perfect sleep data, a pattern clinicians began documenting as consumer sleep trackers became widespread. Anxiety about scores can itself delay sleep onset and fragment the night, and people sometimes report feeling unrested because a device said so despite sleeping adequately. It is a useful reminder that sleep tracking is helpful in aggregate and unreliable night to night. Where insomnia is genuinely present, cognitive behavioural therapy for insomnia is the established first-line treatment rather than more measurement.

IGF-1

Also known as: insulin-like growth factor 1

IGF-1 is a hormone produced mainly by the liver in response to growth hormone, mediating much of its effect on tissue growth and repair. It presents one of the clearer trade-offs in ageing biology: higher levels support muscle maintenance, bone density and recovery, while lower levels are associated with longevity in animal models and with reduced risk of some cancers. Both extremes appear unfavourable in human data, suggesting a middle range is preferable. It is measurable, and interpretation depends on age, sex and clinical context rather than a single ideal figure.

DHEA-S

Also known as: dehydroepiandrosterone sulfate

DHEA-S is an adrenal hormone that serves as a precursor to testosterone and oestrogen. Levels peak in early adulthood and decline steadily thereafter, which has made it a frequently cited marker of biological ageing and a popular supplement. Low levels are associated with poorer outcomes in observational studies, but supplementation trials have generally shown modest and inconsistent benefit in people without adrenal insufficiency. It is measurable and useful as part of a hormonal picture, though it is better interpreted as a marker than treated as a target.

SHBG and free testosterone

Also known as: sex hormone binding globulin

Sex hormone binding globulin binds testosterone and oestrogen in the blood, leaving only the unbound fraction biologically active. This matters because total testosterone can appear normal while the free, usable portion is low, or vice versa, depending on SHBG. Levels are influenced by insulin resistance, thyroid function, liver health, obesity and age, with insulin resistance typically lowering SHBG. Measuring total testosterone alongside SHBG, and calculating free testosterone, gives a considerably more accurate picture than a total measurement interpreted alone, and explains why some people with normal totals still have symptoms.

Perimenopause

Also known as: menopausal transition

Perimenopause is the transitional period preceding menopause, typically beginning in the forties and lasting several years, during which hormone levels fluctuate rather than simply declining. Because fluctuation is the defining feature, symptoms such as irregular cycles, sleep disruption, mood change, brain fog and hot flushes can appear while blood tests still read as normal, which is a common reason concerns are dismissed. Diagnosis is largely clinical and based on pattern and age rather than a single hormone result, and management decisions depend on symptoms and individual history.

Gut microbiome

Also known as: gut flora, microbiota

The gut microbiome is the community of bacteria, viruses and fungi living in the digestive tract, numbering in the trillions and carrying vastly more genes than the human genome. It influences digestion, immune regulation, inflammation, vitamin synthesis and, through several pathways, mood and metabolism. Composition is shaped by diet, medication, particularly antibiotics, sleep, stress and environment. The field is advancing quickly and the correlations are strong, though the ability to reliably reshape an individual microbiome toward a specific outcome remains considerably less developed than the marketing implies.

Dysbiosis

Dysbiosis describes an imbalance in the composition or diversity of gut microbes, typically reduced diversity or overgrowth of less favourable species. It has been associated with inflammatory bowel conditions, metabolic disease, allergy and mood disorders. The concept is genuinely useful, but it should be treated with some caution: there is no agreed definition of an optimal microbiome, so what counts as imbalance is partly a judgement. Interventions with the best evidence remain dietary, particularly fibre diversity and fermented foods, rather than targeted supplementation aimed at correcting a specific named imbalance.

Short-chain fatty acids

Also known as: SCFAs, butyrate

Short-chain fatty acids, principally butyrate, propionate and acetate, are produced when gut bacteria ferment dietary fibre. Butyrate is the primary fuel for the cells lining the colon and supports the integrity of the gut barrier, while all three influence immune regulation, appetite signalling and glucose metabolism. Their production depends directly on fibre intake and diversity, which is one of the more concrete mechanisms linking diet to systemic health. Increasing fibre from varied plant sources, rather than taking a single supplement, is the most reliable way to raise production.

Caloric restriction

Also known as: CR

Caloric restriction is a sustained reduction in energy intake without malnutrition. It is the most consistently reproducible intervention for extending lifespan across laboratory species, and it remains the reference point against which other longevity interventions are compared. In humans the CALERIE trial found that around two years of moderate restriction improved cardiometabolic markers and slightly slowed one measure of biological ageing. Long-term adherence is difficult and risks include muscle and bone loss, so it is generally approached through diet quality and protein adequacy rather than restriction alone.

Time-restricted eating

Also known as: intermittent fasting, TRE

Time-restricted eating confines food intake to a consistent window each day, commonly eight to ten hours, without necessarily changing what is eaten. It is one form of intermittent fasting. Evidence suggests benefits for glycaemic control and weight, though trials comparing it against equivalent calorie intake have often found the advantage comes largely from eating less overall. Timing appears to matter, with earlier windows aligning better with circadian biology than late ones. Adequate protein and resistance training remain important within any eating window, to avoid losing muscle alongside fat.

Polyphenols

Also known as: flavonoids

Polyphenols are plant compounds found in foods such as berries, olive oil, tea, coffee, cocoa and red wine, associated in observational research with lower cardiovascular and cognitive risk. They were once explained mainly as antioxidants, but current understanding emphasises other mechanisms, including favourable effects on the gut microbiome and mild hormetic stress responses. Absorption is often poor and varies considerably between individuals depending on gut bacteria. Evidence is stronger for polyphenol-rich foods within a whole dietary pattern than for isolated extracts taken in supplement form.

Polygenic risk score

Also known as: PRS

A polygenic risk score aggregates the small effects of many genetic variants into a single estimate of inherited susceptibility to a condition such as coronary artery disease or type 2 diabetes. It is a probability across a population rather than a prediction for an individual, and a high score does not mean the condition will develop. A significant limitation is that most scores were derived largely from European-ancestry populations, so accuracy is reduced in other groups, including Asian populations, which matters directly for interpretation in Malaysia.

APOE4

Also known as: apolipoprotein E

APOE is a gene with three common variants, of which the e4 form is the strongest known common genetic risk factor for late-onset Alzheimer's disease and also influences lipid handling. Carrying one or two copies raises risk substantially, but many carriers never develop dementia and many non-carriers do, so it is a risk factor rather than a diagnosis. Knowing your status can inform earlier attention to cardiovascular risk, sleep and metabolic health. Because the result cannot be undone, testing warrants genuine counselling beforehand about how you would use it.

Pharmacogenomics

Also known as: PGx

Pharmacogenomics studies how inherited variation affects response to medication, including how quickly drugs are metabolised and the likelihood of side effects. Variants in enzymes such as CYP2D6 and CYP2C19 meaningfully influence the handling of common medications including some antidepressants, cardiovascular drugs and painkillers. The evidence is strongest for a defined set of drug and gene pairs rather than across all medication. Where it applies, testing can shorten the trial-and-error period of finding an effective drug and dose, which is its main practical value and is most useful before starting a new medication.

Nutrigenomics

Also known as: nutritional genomics

Nutrigenomics examines how genetic variation influences the response to nutrients, and how diet in turn affects gene expression. Some findings are well established, such as lactase persistence determining dairy tolerance, or MTHFR variants influencing folate metabolism. Much of the wider consumer testing market is considerably less well supported, and trials of genotype-matched diets have often failed to outperform general dietary advice. It is best regarded as one input among several rather than a blueprint, with measured biomarkers such as glucose response or lipid levels usually more informative than genetically predicted responses.

Cell-free DNA

Also known as: cfDNA, liquid biopsy

Cell-free DNA consists of small fragments of DNA released into the bloodstream as cells die, including from tumours. Analysing it, often called liquid biopsy, underpins multi-cancer early detection testing and is also used in prenatal screening and in monitoring known cancers. Methylation patterns on these fragments can indicate the likely tissue of origin. Sensitivity depends heavily on how much DNA a tumour sheds, which varies by cancer type and stage, so early-stage detection remains substantially harder than later-stage, which is the main limitation of the technology at present.

Hormesis

Also known as: hormetic stress

Hormesis describes a biological response in which a mild stressor produces a beneficial adaptation, while the same stressor in larger doses causes harm. It is the organising principle behind much of biohacking: exercise, fasting, heat and cold all work partly by imposing manageable stress that prompts the body to strengthen its repair and resilience systems. The concept is well supported, but it is frequently used to justify extremes. The defining feature is dose, and the recovery that follows the stressor is as important as the stressor itself.

Cold exposure

Also known as: cold plunge, cold water immersion

Cold exposure through cold water immersion or cold showers triggers acute increases in noradrenaline, alertness and metabolic rate. Evidence is reasonably good for effects on mood and alertness, and for reducing perceived muscle soreness. One well-documented caveat matters for anyone training: cold immersion soon after resistance exercise appears to blunt muscle adaptation, so timing it away from strength sessions is advisable. Claims about substantial fat loss through brown fat activation are considerably weaker than the enthusiasm around them suggests, and the metabolic effect is small in practical terms.

Sauna and heat exposure

Also known as: heat therapy

Regular sauna use is associated in Finnish cohort studies with lower cardiovascular and all-cause mortality, with an apparent dose relationship by frequency. Plausible mechanisms include improved endothelial function, reduced blood pressure and heat shock protein responses, and the cardiovascular load resembles moderate exercise. The evidence is largely observational, so confounding by general health and lifestyle cannot be excluded. It is generally well tolerated, though caution applies in pregnancy, with unstable cardiovascular disease, and when combined with alcohol, and hydration matters more than most users expect.

Hyperbaric oxygen therapy

Also known as: HBOT

Hyperbaric oxygen therapy delivers oxygen at pressures above atmospheric, greatly increasing the oxygen dissolved in blood and tissue. It has well-established, approved indications including decompression sickness, carbon monoxide poisoning, certain non-healing wounds, diabetic foot ulcers and radiation tissue injury. Its use for ageing, cognition and general wellbeing is a separate matter: some small studies report changes in markers such as telomere length, but the evidence base is considerably smaller than for approved indications and should be described as preliminary rather than established, and courses marketed for general rejuvenation are not equivalent to treatment for an approved indication.

Photobiomodulation

Also known as: red light therapy, low-level laser therapy

Photobiomodulation uses red and near-infrared light, proposed to act on mitochondrial enzymes to improve cellular energy production. Evidence is reasonably supportive for certain skin applications, wound healing and some musculoskeletal pain, which is why it appears in dermatology and physiotherapy. Claims extending to fat loss, cognitive enhancement and systemic anti-ageing rest on much thinner ground. Device output varies enormously between consumer products, and dose parameters matter, so results achieved with clinical devices do not necessarily transfer to consumer home equipment bought on the strength of the same studies.

Rapamycin

Also known as: sirolimus

Rapamycin is an approved immunosuppressant used in transplant medicine, which inhibits mTOR. It extends lifespan in mice more consistently than any other pharmacological intervention tested, which has made it the most discussed candidate geroprotector. Human trials for ageing are ongoing, mostly small and short, and it is not approved for this purpose anywhere. Immunosuppression, metabolic effects and impaired wound healing are meaningful risks, and intermittent dosing protocols circulating informally are not established. Anyone considering it should do so with a doctor, not from online protocols.

Metformin

Metformin is a widely used, inexpensive and well-tolerated first-line medication for type 2 diabetes. Interest in it as a longevity intervention arose from observational data suggesting people with diabetes taking it had favourable outcomes compared with expectation. The TAME trial was designed to test this properly in people without diabetes. Current evidence does not establish benefit in people with normal glucose metabolism, and some studies suggest it may blunt some exercise adaptations. It is not approved for slowing ageing anywhere, and remains a prescription decision made for a specific clinical indication.

NAD precursors

Also known as: NMN, NR, nicotinamide riboside

Nicotinamide riboside and nicotinamide mononucleotide are supplement forms intended to raise cellular NAD+, which declines with age. Human trials consistently show they increase NAD+ measured in blood, and they appear well tolerated at studied doses. What remains unestablished is whether this translates into meaningful improvements in human health outcomes, since trials so far have been short, small and focused on surrogate markers rather than clinical endpoints. Regulatory status varies by country, and the gap between the striking animal evidence and the modest human evidence remains wide.

Peptide therapy

Also known as: therapeutic peptides

Peptides are short chains of amino acids, and several are legitimate approved medicines with strong evidence, including those used in diabetes and weight management, prescribed under medical supervision. The term is also used loosely to market a wide range of unapproved compounds for recovery, growth and anti-ageing purposes. For most of these, human evidence is limited or absent, manufacturing quality is unverified, and legal status is uncertain. The distinction between an approved, prescribed peptide medicine and an unregulated product is a substantial one worth insisting on.

Creatine

Also known as: creatine monohydrate

Creatine monohydrate is among the most extensively studied supplements available, with consistent evidence for improved strength, power and lean mass gains alongside resistance training. It works by supporting rapid energy regeneration in muscle. There is growing, though less definitive, evidence for effects on cognition and mood, particularly under sleep deprivation or in older adults. Safety data over long-term use is reassuring in healthy individuals, and concerns about kidney harm have not been substantiated outside pre-existing kidney disease, where individual medical advice applies before starting it.