A Working Reference

The Vocabulary of Longevity Science · Codeage

The Longevity
Glossary.

Defining the terms longevity science uses. Concepts, molecules, processes, pathways, practices, and biomarkers — with references to the primary scientific literature.

57 Entries 6 Categories 80+ Citations

The Premise

The terms collected here belong to the broader field of longevity science.

The studies and researchers cited throughout this glossary represent independent scientific work — conducted by laboratories, universities, and research institutions worldwide. None of the research referenced was conducted in connection with Codeage products or formulations. References appear here for educational and definitional context only, to ground the vocabulary used across the longevity field in its primary literature.

Section 01

Foundational concepts.

The framing terms — what aging, healthspan, lifespan, and longevity mean in the scientific literature.

01.01

Aging

The gradual accumulation of biological changes over time across cells, tissues, and systems. Described in the scientific literature as a multifactorial process involving genetic, epigenetic, metabolic, and environmental dimensions.

López-Otín, Blasco, Partridge, Serrano & Kroemer. Hallmarks of aging: An expanding universe. Cell, 2023.

01.02

Healthspan

The portion of a life spent in good health — distinct from total lifespan. The concept emphasizes years lived without significant chronic illness or functional decline.

Olshansky, S.J. From Lifespan to Healthspan. The Journals of Gerontology: Series A, 2018.

See also Lifespan · Longevity

01.03

Lifespan

The total number of years a person lives. Distinguished in longevity research from healthspan, which measures quality rather than duration. Both are studied together as the integrated measure of a long life.

Vaupel, J.W., Villavicencio, F. & Bergeron-Boucher, M.-P. Demographic perspectives on the rise of longevity. PNAS, 2021.

See also Healthspan · Longevity

01.04

Biological Age

An estimate of physiological aging based on molecular and cellular markers — distinct from chronological age (years since birth). Multiple measurement approaches exist, including DNA methylation-based epigenetic clocks.

Horvath, S. DNA methylation age of human tissues and cell types. Genome Biology, 2013.

See also Epigenetic Clocks · GrimAge · Methylation

01.05

Longevity

The condition of long life. In contemporary research, longevity is increasingly framed alongside healthspan — the integration of duration and quality across years.

Kennedy, B.K. et al. Geroscience: Linking aging to chronic disease. Cell, 2014.

01.06

The Hallmarks of Aging

A framework describing twelve cellular and molecular processes whose accumulation contributes to aging. Originally proposed as nine hallmarks in 2013, expanded to twelve in the 2023 update.

López-Otín, C. et al. The hallmarks of aging. Cell, 2013. Expanded in Hallmarks of aging: An expanding universe. Cell, 2023.

The Hallmarks of Aging — full reference →

Section 02

Key molecules & compounds.

Compounds, precursors, and molecules studied across the contemporary longevity literature.

02.01

NAD+ Nicotinamide Adenine Dinucleotide

A coenzyme central to cellular energy metabolism, redox balance, and the substrate for sirtuin enzymes. Tissue NAD+ levels have been observed to decline with age in published research.

Verdin, E. NAD+ in aging, metabolism, and neurodegeneration. Science, 2015. Imai, S. & Guarente, L. NAD+ and sirtuins in aging and disease. Trends in Cell Biology, 2014.

See also NMN · NR · Sirtuins · NAD+ Salvage Pathway

02.02

NMN Nicotinamide Mononucleotide

A nucleotide precursor in the NAD+ salvage pathway. NMN has been studied for its role in NAD+ biology, with published research examining bioavailability, kinetics, and downstream pathway effects.

Mills, K.F. et al. Long-term administration of nicotinamide mononucleotide mitigates age-associated physiological decline in mice. Cell Metabolism, 2016. Yoshino, M. et al. Nicotinamide mononucleotide increases muscle insulin sensitivity in prediabetic women. Science, 2021.

See also NAD+ · NR · NAD+ Salvage Pathway

02.03

NR Nicotinamide Riboside

A vitamin B3 form and NAD+ precursor. Studied in the same NAD+ research context as NMN, with distinct kinetics and metabolic pathways.

Trammell, S.A.J. et al. Nicotinamide riboside is uniquely and orally bioavailable in mice and humans. Nature Communications, 2016.

See also NAD+ · NMN · NAD+ Salvage Pathway

02.04

Sirtuins SIRT1 – SIRT7

A family of seven NAD+-dependent enzymes involved in cellular metabolism, DNA repair, and stress response. Studied extensively in the context of NAD+ biology and aging research.

Imai, S. et al. Transcriptional silencing and longevity protein Sir2 is an NAD-dependent histone deacetylase. Nature, 2000. Guarente, L. Sirtuins, aging, and metabolism. Cold Spring Harbor Symposia on Quantitative Biology, 2007.

See also NAD+ · Sirtuin Pathway · Resveratrol

02.05

Resveratrol

A polyphenol found in grapes, berries, and certain plants. Resveratrol has been studied extensively in connection with sirtuin pathway activation and metabolic processes in published research.

Howitz, K.T. et al. Small molecule activators of sirtuins extend Saccharomyces cerevisiae lifespan. Nature, 2003. Baur, J.A. et al. Resveratrol improves health and survival of mice on a high-calorie diet. Nature, 2006.

See also Pterostilbene · Sirtuins

02.06

Pterostilbene

A stilbene compound chemically related to resveratrol, found in blueberries and grapes. Studied for similar pathway interactions as resveratrol in published research, with distinct bioavailability characteristics.

McCormack, D. & McFadden, D. A review of pterostilbene antioxidant activity and disease modification. Oxidative Medicine and Cellular Longevity, 2013.

02.07

Fisetin

A flavonoid found in strawberries, apples, and certain other plants. Categorized in published research as a senolytic candidate — studied for its connection to senescent cell biology.

Yousefzadeh, M.J. et al. Fisetin is a senotherapeutic that extends health and lifespan. EBioMedicine, 2018.

See also Quercetin · Cellular Senescence

02.08

Quercetin

A flavonoid found in onions, apples, and certain berries. Studied in combination with dasatinib in published senolytic research and independently for its antioxidant properties.

Zhu, Y. et al. The Achilles' heel of senescent cells: from transcriptome to senolytic drugs. Aging Cell, 2015.

See also Fisetin · Cellular Senescence

02.09

Spermidine

A polyamine present in many foods and produced endogenously by gut microbiota. Spermidine has been studied for its connection to autophagy and cellular renewal in published research.

Eisenberg, T. et al. Cardioprotection and lifespan extension by the natural polyamine spermidine. Nature Medicine, 2016. Madeo, F. et al. Spermidine in health and disease. Science, 2018.

See also Autophagy

02.10

Sulforaphane

An isothiocyanate compound found in cruciferous vegetables (notably broccoli sprouts). Studied for its activation of the Nrf2 pathway in published research.

Vanduchova, A. et al. Isothiocyanate from broccoli, sulforaphane, and its properties. Journal of Medicinal Food, 2019.

02.11

Curcumin

The principal curcuminoid in turmeric (Curcuma longa). Studied in published research in connection with inflammation pathways and the NF-κB signaling cascade.

Hewlings, S.J. & Kalman, D.S. Curcumin: A review of its effects on human health. Foods, 2017.

02.12

CoQ10 Coenzyme Q10 / Ubiquinone

A lipid-soluble compound essential to mitochondrial electron transport. CoQ10 has been studied in published research in connection with mitochondrial function and cardiovascular biology.

Hernández-Camacho, J.D. et al. Coenzyme Q10 supplementation in aging and disease. Frontiers in Physiology, 2018.

See also Mitochondrial Biogenesis

02.13

Glutathione

A tripeptide antioxidant produced by the body, composed of glutamate, cysteine, and glycine. Studied in published research for its role in cellular redox balance and detoxification pathways.

Lu, S.C. Regulation of glutathione synthesis. Molecular Aspects of Medicine, 2009.

See also Oxidative Stress

02.14

Ergothioneine

A naturally occurring amino acid derivative found in mushrooms and some other foods. Studied as a mitochondrial antioxidant in published research, with a dedicated transporter (OCTN1) for cellular uptake.

Paul, B.D. & Snyder, S.H. The unusual amino acid L-ergothioneine is a physiologic cytoprotectant. Antioxidants & Redox Signaling, 2010.

02.15

Astaxanthin

A carotenoid pigment produced by certain algae and found in salmon, krill, and shrimp. Studied in published research for its antioxidant capacity and lipid-membrane interactions.

Ambati, R.R. et al. Astaxanthin: Sources, extraction, stability, biological activities and its commercial applications. Marine Drugs, 2014.

02.16

Omega-3 Fatty Acids DHA & EPA

Long-chain polyunsaturated fatty acids of marine origin (DHA, EPA) and plant origin (ALA). Studied extensively in published research for their role in cellular membrane composition, inflammation signaling, and cardiovascular biology.

Calder, P.C. Marine omega-3 fatty acids and inflammatory processes. Biochimica et Biophysica Acta, 2015. Mozaffarian, D. & Wu, J.H.Y. Omega-3 fatty acids and cardiovascular disease. Journal of the American College of Cardiology, 2011.

Section 03

Cellular processes.

The processes that govern what happens inside cells as they age — and the literature that describes them.

03.01

Autophagy

A cellular self-renewal process by which cells degrade and recycle damaged components. The Nobel Prize in Physiology or Medicine 2016 was awarded for autophagy research.

Mizushima, N. Autophagy: process and function. Genes & Development, 2007. Ohsumi, Y. Nobel Prize in Physiology or Medicine, 2016.

See also Mitophagy · mTOR Pathway · Spermidine

03.02

Mitophagy

A selective form of autophagy that removes damaged mitochondria. Studied in connection with mitochondrial quality control and the broader autophagy literature.

Pickles, S., Vigié, P. & Youle, R.J. Mitophagy and quality control mechanisms in mitochondrial maintenance. Current Biology, 2018.

See also Autophagy · Mitochondrial Biogenesis

03.03

Cellular Senescence

A state in which cells stop dividing while remaining metabolically active, often releasing inflammatory signals (the SASP — senescence-associated secretory phenotype). Recognized as one of the twelve hallmarks of aging.

Hayflick, L. & Moorhead, P.S. The serial cultivation of human diploid cell strains. Experimental Cell Research, 1961. Coppé, J.-P. et al. Senescence-associated secretory phenotypes reveal cell-nonautonomous functions of oncogenic RAS. PLoS Biology, 2008.

See also SASP · Fisetin · Quercetin

03.04

SASP Senescence-Associated Secretory Phenotype

The collection of cytokines, chemokines, growth factors, and proteases secreted by senescent cells. Studied in published research as a mechanism by which senescent cells influence surrounding tissue.

Coppé, J.-P. et al. The senescence-associated secretory phenotype: the dark side of tumor suppression. Annual Review of Pathology, 2010.

See also Cellular Senescence

03.05

Apoptosis

Programmed cell death — a regulated process by which cells are removed without releasing harmful contents. Distinguished from senescence (where cells persist) and necrosis (uncontrolled death).

Elmore, S. Apoptosis: A review of programmed cell death. Toxicologic Pathology, 2007.

03.06

Mitochondrial Biogenesis

The process by which new mitochondria are generated within cells. Studied as a component of mitochondrial quality control and metabolic regulation.

Ploumi, C., Daskalaki, I. & Tavernarakis, N. Mitochondrial biogenesis and clearance: a balancing act. The FEBS Journal, 2017.

See also Mitophagy · CoQ10

03.07

DNA Repair

The collection of cellular processes that identify and correct damage to DNA. Capacity for DNA repair has been studied in connection with aging biology and genomic stability.

Hoeijmakers, J.H.J. DNA damage, aging, and age-related conditions. New England Journal of Medicine, 2009.

03.08

Oxidative Stress

An imbalance between reactive oxygen species (ROS) and the body's antioxidant defenses. Studied in the context of cellular damage and aging mechanisms.

Sies, H. Oxidative stress: a concept in redox biology and medicine. Redox Biology, 2015.

See also Glutathione

03.09

Glycation AGEs — Advanced Glycation End Products

A non-enzymatic reaction between sugars and proteins or lipids that produces structurally altered molecules. AGEs have been studied in connection with tissue stiffening and aging biology.

Brownlee, M. The pathobiology of diabetic complications: a unifying mechanism. Diabetes, 2005.

03.10

Methylation

An epigenetic modification — the addition of methyl groups to DNA or proteins — that influences gene expression without altering the underlying DNA sequence. DNA methylation patterns form the basis of epigenetic clocks.

Horvath, S. DNA methylation age of human tissues and cell types. Genome Biology, 2013.

See also Epigenetic Clocks · Biological Age

03.11

Telomere Maintenance

The biological processes that preserve the protective caps at chromosome ends. Telomere length is studied in connection with cellular replicative capacity.

Blackburn, E.H., Greider, C.W. & Szostak, J.W. Nobel Prize in Physiology or Medicine, 2009. Aviv, A. & Shay, J.W. Reflections on telomere dynamics and ageing-related diseases in humans. Phil Trans R Soc B, 2018.

See also Telomere Length

Section 04

Pathways & signaling.

The cellular signaling architectures studied across the contemporary biology of aging.

04.01

mTOR Pathway

A nutrient and energy-sensing pathway central to cell growth and metabolism. Studied extensively in connection with caloric restriction and aging biology.

Saxton, R.A. & Sabatini, D.M. mTOR signaling in growth, metabolism, and disease. Cell, 2017.

See also AMPK Pathway · Caloric Restriction · Autophagy

04.02

AMPK Pathway

An energy-sensing pathway activated when cellular energy is low. Studied in connection with metabolic regulation and metformin's mechanism of action.

Hardie, D.G., Ross, F.A. & Hawley, S.A. AMPK: a nutrient and energy sensor that maintains energy homeostasis. Nature Reviews Molecular Cell Biology, 2012.

See also mTOR Pathway · Caloric Restriction

04.03

Sirtuin Pathway

NAD+-dependent enzymatic signaling involving the sirtuin family (SIRT1 – SIRT7). Studied in connection with metabolic homeostasis, DNA repair, and aging research.

Imai, S. & Guarente, L. NAD+ and sirtuins in aging and disease. Trends in Cell Biology, 2014.

See also Sirtuins · NAD+ · Resveratrol

04.04

Insulin / IGF-1 Signaling

Conserved growth-factor signaling pathways studied across organisms in connection with longevity research. Loss-of-function mutations in this pathway have been studied for lifespan extension in model organisms.

Kenyon, C. The genetics of ageing. Nature, 2010.

See also FOXO Transcription Factors

04.05

FOXO Transcription Factors

A family of transcription factors (FOXO1, FOXO3, FOXO4, FOXO6) studied in connection with stress resistance, metabolism, and longevity biology.

Salih, D.A.M. & Brunet, A. FoxO transcription factors in the maintenance of cellular homeostasis during aging. Current Opinion in Cell Biology, 2008.

See also Insulin / IGF-1 Signaling

04.06

Klotho

A protein and gene named for the Greek Fate. Discovered in 1997 in research describing a phenotype resembling accelerated aging in mice lacking the Klotho gene.

Kuro-o, M. et al. Mutation of the mouse klotho gene leads to a syndrome resembling ageing. Nature, 1997.

04.07

p53

A tumor suppressor protein involved in cell cycle regulation, DNA damage response, and apoptosis. Foundational to research on cell health across oncology and aging biology.

Vousden, K.H. & Prives, C. Blinded by the Light: The Growing Complexity of p53. Cell, 2009.

See also Apoptosis · DNA Repair

04.08

NAD+ Salvage Pathway

The metabolic pathway by which cells recycle NAD+ precursors (including NMN and NR) to maintain NAD+ levels. Central to NAD+ biology research.

Verdin, E. NAD+ in aging, metabolism, and neurodegeneration. Science, 2015.

See also NAD+ · NMN · NR

Section 05

Practices & interventions.

Lifestyle and behavioral practices studied across longevity research, with citations to the foundational literature.

05.01

Caloric Restriction

A reduction in calorie intake without malnutrition. The most studied longevity intervention across model organisms, with effects on lifespan documented in published research dating to McCay's foundational 1935 rat studies.

McCay, C.M., Crowell, M.F. & Maynard, L.A. The effect of retarded growth upon the length of life span and upon the ultimate body size. Journal of Nutrition, 1935. Mattison, J.A. et al. Caloric restriction improves health and survival of rhesus monkeys. Nature Communications, 2017.

See also Intermittent Fasting · mTOR Pathway · Sirtuins

05.02

Intermittent Fasting

Eating patterns that alternate periods of eating and not eating. Studied in published research for metabolic and cellular effects, including autophagy activation.

de Cabo, R. & Mattson, M.P. Effects of intermittent fasting on health, aging, and disease. New England Journal of Medicine, 2019.

See also Time-Restricted Eating · Caloric Restriction · Autophagy

05.03

Time-Restricted Eating

A form of intermittent fasting in which daily food intake is confined to a specific window (commonly six to twelve hours). Studied in published research in connection with circadian biology.

Manoogian, E.N.C. et al. Time-restricted eating for the prevention and management of metabolic diseases. Endocrine Reviews, 2022.

See also Intermittent Fasting

05.04

Zone 2 Exercise

Aerobic exercise performed at moderate intensity (approximately 60–70% of maximum heart rate). Studied in connection with mitochondrial adaptations and metabolic flexibility.

San-Millán, I. & Brooks, G.A. Assessment of metabolic flexibility by means of measuring blood lactate, fat, and carbohydrate oxidation responses to exercise. Sports Medicine, 2018.

See also High-Intensity Interval Training

05.05

High-Intensity Interval Training HIIT

Exercise alternating short periods of high-intensity effort with recovery. Studied in published research for cardiovascular and metabolic adaptations.

Gibala, M.J. et al. Physiological adaptations to low-volume, high-intensity interval training in health and disease. The Journal of Physiology, 2012.

See also Zone 2 Exercise

05.06

Resistance Training

Exercise performed against external resistance to build muscle strength and mass. Studied in published research in connection with the broader literature on muscle biology and physical function across age.

Westcott, W.L. Resistance training is medicine: effects of strength training on health. Current Sports Medicine Reports, 2012.

05.07

Sleep Architecture

The structural organization of sleep across REM and non-REM stages. Sleep is studied across longevity research as a foundational biological process.

Mander, B.A., Winer, J.R. & Walker, M.P. Sleep and human aging. Neuron, 2017.

05.08

Heat Exposure Sauna

Repeated exposure to elevated ambient temperatures. Studied in long-term Finnish cohort research in connection with cardiovascular outcomes.

Laukkanen, T. et al. Association between sauna bathing and fatal cardiovascular events and all-cause mortality. JAMA Internal Medicine, 2015.

See also Cold Exposure

05.09

Cold Exposure

Deliberate exposure to cold ambient temperatures (cold water immersion, cold showers, etc.). Studied for thermogenic and metabolic effects in published research.

van der Lans, A.A.J.J. et al. Cold acclimation recruits human brown fat and increases nonshivering thermogenesis. Journal of Clinical Investigation, 2013.

See also Heat Exposure

05.10

Microbiome Care

Practices that engage with gut microbial diversity and composition. The microbiome has been studied extensively in connection with aging research and inflammatory processes.

Wilmanski, T. et al. Gut microbiome pattern reflects healthy ageing and predicts survival in humans. Nature Metabolism, 2021.

Section 06

Biomarkers & measurement.

Quantitative measures used across longevity research to estimate biological age, inflammation, and cellular state.

06.01

Epigenetic Clocks

Computational models that estimate biological age from DNA methylation patterns at specific CpG sites. Multiple clocks have been developed since the original Horvath clock in 2013.

Horvath, S. DNA methylation age of human tissues and cell types. Genome Biology, 2013.

See also GrimAge · DunedinPACE · Methylation

06.02

GrimAge

An epigenetic clock developed in 2019 by the Horvath lab. Trained on plasma protein measurements and considered a strong predictor of aging-related outcomes in published research.

Lu, A.T. et al. DNA methylation GrimAge strongly predicts lifespan and healthspan. Aging, 2019.

See also Epigenetic Clocks

06.03

DunedinPACE

A methylation-based measure of the pace of biological aging, developed from longitudinal Dunedin Study data in 2022.

Belsky, D.W. et al. DunedinPACE, a DNA methylation biomarker of the pace of aging. eLife, 2022.

See also Epigenetic Clocks

06.04

Telomere Length

The length of the protective caps at chromosome ends, typically shortened with cell division. Measured as a longevity-research biomarker.

Aviv, A. & Shay, J.W. Reflections on telomere dynamics and ageing-related diseases in humans. Philosophical Transactions of the Royal Society B, 2018.

See also Telomere Maintenance

06.05

Inflammatory Markers CRP, IL-6, TNF-α

Serum measurements of inflammation. Chronic elevations have been studied in published research in connection with aging biology — the framework known as inflammaging.

Franceschi, C. et al. Inflamm-aging: An evolutionary perspective on immunosenescence. Mechanisms of Ageing and Development, 2007.

06.06

NAD+ Levels

Tissue or blood measurements of nicotinamide adenine dinucleotide concentration. Studied in published research, though measurement methodology varies across studies.

Mouchiroud, L. et al. The NAD+/sirtuin pathway modulates longevity through activation of mitochondrial UPR and FOXO signaling. Cell, 2013.

See also NAD+ · NAD+ Salvage Pathway

The Disclosures

A glossary,
responsibly stated.

Independence of References

The studies, researchers, and institutions cited throughout this glossary represent independent scientific work. None of the research referenced was conducted in connection with Codeage products or formulations. References appear here to ground the vocabulary used across the longevity field in its primary scientific literature, for educational and definitional context only.

Educational Purpose

This glossary defines the terms used across the contemporary longevity field. Definitions describe concepts as they appear in the scientific literature — they do not constitute medical advice, nutritional guidance, or claims about any product or formulation.

Citation Philosophy

Every entry includes a reference to a foundational paper or research group. Where multiple papers exist on a topic, foundational or widely-cited sources have been selected. Readers seeking depth on any term are encouraged to consult the original literature directly.

FDA Framework

The statements throughout this glossary have not been evaluated by the Food and Drug Administration. The terminology defined here belongs to the scientific literature — it is not a description of any product's effects, uses, or capabilities.

A Working Reference

The vocabulary of longevity science is the vocabulary of a living field. Terms are added, refined, and reconsidered as the science evolves. This glossary will be updated to reflect what the literature itself articulates.

For deeper reference, see The Hallmarks of Aging, The Literature, The Compounds Library, and the editorial work across The Longevity Code.