Aging in mainstream gerontology is treated as cumulative cell damage, hormonal decline, and loss of reserve capacity. The bioenergetic view ties visible aging directly to chronic stress chemistry instead: excess Estrogen relative to Progesterone, impaired Thyroid and mitochondrial respiration, and stored PUFA.[1][2]

Estrogen, at least when it is not opposed by a very large concentration of progesterone, creates all of the conditions known to be involved in the aging process.

— Ray Peat[3]

Ana Aslan, procaine, and stress amino acids

[edit]

Romanian gerontologist Ana Aslan treated elderly patients with Gerovital H3 (stabilized procaine). That clinical tradition sits beside Peat's interest in procaine versus polyamines and in diets that limit excess tryptophan and methionine (favor gelatin balance over pure muscle-meat protein). See Ana Aslan, Tryptophan, Methionine, Gelatin.

Aging spiral: mitochondrial decline, CO2, and the Bohr effect

[edit]

A 2025 hypothesis paper proposes a self-reinforcing "aging spiral": declining mitochondria produce less CO2, weakening the Bohr effect (CO2-driven oxygen release from hemoglobin) and impairing tissue oxygen delivery; the resulting hypoxia stabilizes HIF-1, which further suppresses mitochondrial biogenesis and shifts fuel use away from full oxidation, deepening the original ATP deficit. Cells stay able to recover through metabolic regulation as long as intracellular energy stays above the threshold needed for cell division; once energy falls below it, cells exit the spiral into a long-term, non-dividing (senescent) state.[4]

Mitochondrial energy as a unifying driver of intelligence, health, and aging

[edit]

A synthesis across evolutionary biology, medicine, and psychology proposes mitochondrial energy production as a common physiological substrate linking general intelligence, overall health, and the rate of biological aging, rather than treating these as independent traits.[5]

A multidimensional nutrient-intake analysis found higher protein, sugar, and vitamin E consumption associated with healthier aging trajectories, complicating simplistic "eat less of everything" dietary-restriction narratives around longevity.[6]

The same "aging as the common driver" logic has reached mainstream biotech commentary: an Andreessen Horowitz editorial argues that since age itself is the single biggest risk factor for Alzheimer's disease (risk roughly doubling every 5 years after 65), drug targets chosen from general aging biology, rather than Alzheimer's-specific amyloid/tau pathways alone, may be the more productive route to a treatment.[7]

Mitochondrial uncoupling and healthspan

[edit]

The mitochondrial uncoupler BAM15 extended lifespan 9% on normal diet and 25% on high-fat diet in Drosophila while improving locomotion and raising flight-muscle oxidative capacity without worsening the H2O2:O2 redox ratio.[8]

Mitochondria, lactic acid, and energy

[edit]

Mild cognitive impairment showed lower resting respiratory exchange ratio and greater fatty-acid oxidation than cognitively healthy elders, indicating cerebral hypometabolism with shifted substrate use.[9] Brief but sustained lactate elevation reduced mitochondrial oxidative capacity and promoted disease susceptibility in rodent models, supporting chronic lactate load as a driver of cardiometabolic aging phenotypes.[10] Lactate promotes mitochondrial fragmentation and ROS generation via ERK/DRP1 signaling, driving pulmonary fibrosis in a bleomycin mouse model.[11] Intense exercise damages cells in ways that accumulate: within five minutes, it measurably lowers the activity of the enzymes that oxidize glucose, and glycolysis's byproducts, lactic and pyruvic acid, directly suppress glucose oxidation in a self-reinforcing loop. Diabetes, Alzheimer's disease, and aging generally all involve this same pattern of rising lactic acid and accumulated mitochondrial damage.[12]

Adaptation toward carbon dioxide retention limits lactic acid formation instead: an adapted muscle runs about 50% more efficiently, since glucose (which produces more CO2 than fat per unit of oxygen used) becomes the more efficient fuel to oxidize.[12] Estrogen is directly harmful to mitochondria; progesterone is protective, and its brain-protective, restorative effects work partly through mitochondrial action. Thyroid hormone, palmitic acid (found in coconut oil and formed naturally in animal tissue), and light all activate the same key respiratory enzyme that suppresses lactic acid formation; unsaturated oils push in the opposite direction.[12]

Regeneration versus degeneration

[edit]

Creatine supplementation and improved mitochondrial transport both facilitated spinal-cord axon regeneration after injury by restoring ATP supply to damaged nerves.[13] Tissue stem cells partition older, respiration-competent mitochondria into differentiating daughters while retaining younger mitochondria in self-renewing stem cells; restricting mitochondrial respiration kept daughters in a stem-like state.[14] Human cartilage shows location-dependent regenerative capacity: ankle cartilage is molecularly "younger" than knee or hip cartilage and repairs faster, with microRNA programs resembling salamander-like tissue maintenance.[15] For about a century, the standard explanation for degenerative disease has been accumulated genetic mutation, "somatic mutation" distinct from the germline mutations behind conditions like Huntington's chorea. That theory of aging was shown to be false roughly 50 years ago.[16] The older, environment-based understanding of aging has returned to the foreground since: cells, tissues, and organs interact continuously with their environment and with each other, and an unsuitable environment becomes internally limiting for cells over time. The organism isn't fixed by its genes so much as by an environment that can itself be changed.[16]

Light and cumulative deterioration

[edit]

The chronic deficiency of such light is, I think, the best explanation for the deterioration which occurs with aging.

— Ray Peat[17]

Free-radical injury worsens specifically when energy production is already deficient, as in fasting or emotional stress, rather than accumulating as an unavoidable cost of being alive.[2]

Twelve hours daily blue-enriched light accelerates aging in Drosophila, cutting lifespan by more than half and causing retinal and brain neurodegeneration that can occur independently of the visual system.[18]

Lipid peroxidation and nuclear envelope aging

[edit]

Corvids with extended parental care, large brain-to-body ratios, and prolonged juvenile dependence show tool use and problem-solving comparable to apes; parental feeding during long juvenility supports cognitive development.[19] Developmental mitochondrial superoxide downregulates unsaturated-fatty-acid synthesis (SBP-1/SREBP), limiting membrane lipid peroxidation and preserving nuclear-envelope integrity into adulthood in C. elegans and mammalian progeria models.[20]

Fatty-acid oxidation and senescence

[edit]

Forcing higher mitochondrial fatty-acid oxidation in mice did not lower adiposity or raise energy expenditure; macronutrient fuel use shifted under Randle-cycle control rather than producing leanness.[21] Feeding cardiolipin to NFYB-1 mutant worms restored mitochondrial function and healthspan, linking lysosome–mitochondria lipid signaling (cardiolipin/ceramide) to aging phenotypes.[22] Pharmacologic activation of fatty-acid oxidation alone induces p16-dependent senescence in fibroblasts, endothelium, and mouse liver via the Randle cycle (PDH inhibition, reduced glucose-derived acetyl-CoA) and octanoate mimics doxorubicin-like senescent signaling.[23]

Viral suppression of Complex I

[edit]

SARS-CoV-2 infection selectively reduces nuclear-encoded Complex I mitochondrial proteins in human cells, diverting mitochondrial gene expression and weakening innate antiviral defenses; patients with pre-existing mitochondrial or metabolic dysfunction may be especially vulnerable.[24]

OXPHOS deficiency and glycolytic compensation

[edit]

In SURF1-deficient patient fibroblasts, ATP production shifts from roughly 64:36% OXPHOS:glycolysis to 23:77%, with shortened Hayflick limit, accelerated telomere erosion, and hypersecretion of stress cytokines, a hypermetabolic state driven by mitochondrial OXPHOS defects rather than ATP shortage alone.[25]

Simply diluting a portion of old mice's blood plasma with saline/albumin (no young-blood transfer at all) improved cognition and reduced neuroinflammation as effectively as heterochronic parabiosis, indicating that removing accumulated pro-aging factors, not adding young-blood "rejuvenating" factors, drives most of parabiosis's anti-aging effect.[26]

Endurance exercise and red blood cells

[edit]

After resistance exercise, lean pork raised post-workout muscle protein synthesis more than an isocaloric high-fat pork meal, which barely exceeded a carbohydrate control.[27] Elite endurance athletes show higher active tooth-decay prevalence than non-competing amateur athletes despite similar plaque scores and lower gingivitis, a confound to watch when interpreting athlete cohort studies.[28] Ultramarathon running stiffens red blood cells, accelerates their storage-like aging phenotype, and increases hemolysis (worst after 171 km versus 40 km), linking extreme endurance exercise to oxidative and mechanical blood-cell injury.[29]

Frailty and mitochondrial respiration

[edit]

Low serum vitamin K in older adults associated with faster progression to mobility limitation and disability, a frailty-relevant marker independent of other aging risk factors in the Health ABC cohort.[30] Chronic NMN supplementation delayed frailty and extended median and maximum lifespan in female mice; males showed delayed frailty and improved metabolism without a lifespan gain, supporting NAD+ repletion as a sex-dependent longevity lever.[31] Comparative physiology links higher membrane n-6/n-3 PUFA ratios to deeper torpor and shorter maximum lifespan across mammalian species, opposing simple rate-of-living explanations of aging.[32] Mild chronic complex I inhibition produced alternating manic and depressive states with mitochondrial OCR shifts, modeling bipolar disorder as a bioenergetic dysregulation syndrome.[33] Muscle-specific mitochondrial dysfunction and reduced oxidative capacity preceded atrophy and weakness in a model linking bioenergetic failure to sarcopenia.[34] TIF1γ transcriptionally controls coenzyme Q synthesis in erythroid precursors; CoQ10 repletion rescued anemia in zebrafish and linked mitochondrial metabolism to red-cell production.[35] Six weeks of nicotinamide mononucleotide raised aerobic capacity and skeletal-muscle oxygen utilization in amateur runners versus placebo.[36] Post-viral fatigue syndromes share impaired ATP generation and hypometabolism with acute infection biology, framing chronic fatigue as an energy-deficiency phenotype.[37] Cartilage-specific mitochondrial respiratory-chain disruption expanded and stiffened joint matrix, showing bone and cartilage integrity depend on oxidative metabolism.[38] IL-33 triggered macrophage mitochondrial uncoupling that let inflammatory cells sustain phagocytosis and resolve inflammation without mitochondrial overload.[39] Vitamin D receptor knockout caused skeletal muscle glycogen accumulation without usable glucose release, creating functional energy shortage, cortisol rise, and muscle wasting despite stored glycogen.[40] Exercise-induced selenium transport to the hippocampus activated quiescent neural progenitors and restored neurogenesis and cognition in aged mice; dietary selenium mimicked the effect without running.[41] Lifelong TLR4 knockout improved cognitive performance and brain structure in aged mice without reported deleterious immune consequences, supporting late-life TLR4 suppression as a brain-aging intervention target.[42] Niacinamide supplementation in obese mice increased mitochondrial biogenesis markers, fatty-acid β-oxidation, and CO2 production while lowering adipose acetylation, linking NAD+ salvage to systemic metabolic rejuvenation.[43] Adverse childhood experiences associated with older biological age across albumin, creatinine, HbA1c, CRP, and related blood biomarkers, with abuse showing the strongest effect.[44] Excess TNF-α in tuberculosis drives mitochondrial reverse electron transport and pathogenic ROS, killing infected macrophages and propagating bacterial spread.[45] Feeling unhappy, hopeless, or lonely accelerated biological aging more than smoking in a population biomarker model, with rural residence and single status as additional accelerants.[46] Successive birth cohorts show higher lifetime risk of early-onset cancers in multiple organs, consistent with accelerating environmental metabolic disruption rather than inherited susceptibility alone.[47] Adjusted basal metabolic rate in U.S. and European adults fell roughly 15% in men over three decades while physical activity rose, suggesting declining resting metabolism can explain much of the obesity epidemic.[48] A history of intermittent endotoxin challenges during the aging period in mice impaired learning, memory, and hippocampal synaptic plasticity weeks after the final inflammatory episode.[49] Older adults with highest dorsal-raphe serotonin synthesis capacity on PET showed greatest temporal-lobe cortical atrophy and rising depression symptoms over longitudinal follow-up.[50] A single non-toxic LPS dose shifted blackbirds to earlier dusk resting for up to three weeks after acute effects resolved, modeling how transient endotoxemia can produce lasting metabolic and behavioral suppression.[51] Adolescent stress-induced reductions in brain mitochondrial respiration persisted into adulthood and tracked behavioral deficits, linking early bioenergetic impairment to later psychiatric and cognitive aging phenotypes.[52] Lower hand-grip strength aligns with accelerated DNA methylation age on PhenoAge, GrimAge, and Dunedin Pace of Aging clocks.[53] Each additional adverse childhood event associated with lower maximal skeletal-muscle ATP production in older adults.[54] Cancer-cachexia muscle proteomics show age-like mitochondrial OXPHOS failure and NAD+ loss that track wasting severity.[55] In community-dwelling adults over 70, frail individuals show lower mitochondrial oxygen consumption in peripheral blood mononuclear cells, linking biological age (metabolic capacity) to frailty risk independent of chronological age.[56]

Cross-species mitochondrial interchange

[edit]

Mitochondria transplanted across species remain functionally interchangeable in composite pluripotent stem cells; human versus non-human mitochondria differ mainly in nuclear gene expression tied to brain development and neurological disease.[57]

Neurite growth and mitochondrial metabolism

[edit]

Human cortical neuron maturation rate is limited by mitochondrial respiration; pharmacologically accelerating mitochondrial metabolism in human neurons in vitro and in mouse xenografts speeds dendrite and synapse development to match faster-growing rodent neurons.[58]

SHMT2, glycine, and mitochondrial respiration

[edit]

Age-associated mitochondrial respiration defects in human fibroblasts trace to epigenetic downregulation of SHMT2 (one-carbon metabolism) rather than mtDNA mutation accumulation; SHMT2 knockout impairs hepatic mitochondrial respiration and erythropoiesis, and glycine or formate supplementation may restore one-carbon flux.[59]

A nested case-control in Chinese adults aged 80+ found non-meat diets associated with lower odds of reaching age 100 than meat-containing diets (observational; unmeasured confounders likely).[60]

Reproductive history and epigenetic aging

[edit]

The Finnish Twin Cohort followed 14,836 women and measured biological aging with a DNA-methylation clock in a 1,054-person subset. Women with no births and women with the most lifetime births (mean 6.8) both showed accelerated epigenetic aging and higher mortality risk after adjusting for lifestyle factors, while women with a moderate number of births (2-4) did not.[61] Nulliparous women carry more years of unopposed Estrogen exposure without the sustained progesterone of full-term pregnancy, while women with very high lifetime birth counts face repeated depletion of nutrient and hormonal reserves; a moderate number of pregnancies avoids both extremes.

Ovarian aging and inflammation

[edit]

Mitochondrial dysfunction in aged ovarian tissue drives pro-inflammatory cytokine release that accelerates follicle loss, with inflammation acting as a downstream metabolic signal rather than primary cause.[62]

Mitochondrial TSPO1 enzymatic activity depends on membrane cholesterol; loss of cholesterol coupling abolishes peripheral benzodiazepine-receptor protoporphyrin degradation, linking sterol–mitochondria coupling to stress-pathology signaling.[63]

Mifepristone, rapamycin, and mitophagy

[edit]

Mifepristone and rapamycin each extend mated female Drosophila lifespan through mitophagy activation and reduced mating-induced midgut hypertrophy; combined treatment is non-additive and can shorten lifespan relative to either drug alone.[64]

Reversing the aging signal

[edit]

In centenarian cohorts, inflammation markers, not telomere length, predicted successful aging and survival at extreme old age.[65] Cardiolipin supplementation restored mitochondrial function and extended lifespan in NFYB-1-deficient worms with defective lysosome–mitochondria lipid signaling.[66] Neuronal mitochondrial stress in C. elegans created a transgenerational memory of impaired respiration lasting more than fifty generations through germline mitochondrial signaling.[67] Transcranial 1068 nm photobiomodulation for four weeks improved memory, processing speed, and motor tapping in healthy adults, consistent with mitochondrial ATP restoration.[68] Adults free of major dementia risk factors such as smoking, diabetes, and hearing loss showed cognitive performance matching people decades younger, emphasizing lifestyle over chronological age.[69] Genetic and pharmacologic disruption of mitochondrial division or respiration in mice produced severe anemia refractory to iron, linking hematopoietic failure to bioenergetic collapse.[70] Dietary urolithin A restored mitochondrial function in aged hematopoietic stem cells, rejuvenating blood reconstitution and improving antiviral immune responses in old mice.[71] Enhanced MAO-dependent serotonin turnover in naked mole-rat cells promotes senescent-cell clearance through intracellular peroxide generation, linking monoamine catabolism to resistance against cellular aging.[72] Late-life dietary folate restriction in aged mice lowered anabolic biosynthesis and serum folate while preserving weight, adiposity, frailty scores, and metabolic flexibility without adverse healthspan outcomes.[73] Myeloid PGE2–EP2 signaling hoards glucose as glycogen rather than mitochondrial ATP, fueling age-related neuroinflammation; peripheral EP2 blockade restores youthful myeloid metabolism and hippocampal function in aged mice.[74] In nonagenarians followed for up to 11 years, each 1 ng/mL decrease in IGF-1 associated with roughly one additional week of survival; lower IGF-1 was especially protective in prior cancer survivors.[75] The same themes run through both the Estrogen and Light pages as the practical opposition to this whole process: Thyroid, Progesterone, adequate Salt, lower PUFA, Gelatin/glycine, and red light.[1][17] See Bioenergetics and Harm reduction for the fuller practical framework.

See also

[edit]

References

[edit]
  1. ↑ 1.0 1.1 "Not the "female hormone," but the shock hormone," Ray Peat article
  2. ↑ 2.0 2.1 "Fats, functions and malfunctions.," Ray Peat article
  3. ↑ "Not the "female hormone," but the shock hormone," Ray Peat article
  4. ↑ Hiki M. "The aging spiral hypothesis: mitochondrial decline, CO2 regulation, and the metabolic collapse of aging," Medical Hypotheses. 2025;205:111817. doi:10.1016/j.mehy.2025.111817.
  5. ↑ Geary DC. "The spark of life and the unification of intelligence, health, and aging," Curr Dir Psychol Sci. 2019. doi:10.1177/0963721419829719.
  6. ↑ Senior AM, Legault V, Lavoie FB, et al. "Multidimensional associations between nutrient intake and healthy ageing in humans," BMC Biol. 2022. doi:10.1186/s12915-022-01395-z.
  7. ↑ Pande V, Fortney K. "The Cure for Aging Might be the Cure for Alzheimer's," Andreessen Horowitz, 2020.
  8. ↑ Taylor AL, et al. "Bioenergetic uncoupling extends Drosophila lifespan," Aging Cell. 2024. doi:10.1111/acel.14107.
  9. ↑ Morris JK, et al. "Mitochondrial respiration in mild cognitive impairment," Function. 2021. doi:10.1093/function/zqab045.
  10. ↑ San-Millán I, et al. "Chronic lactate exposure decreases mitochondrial function by inhibition of fatty acid transport," Front Nutr. 2022. doi:10.3389/fnut.2022.809485.
  11. ↑ Sun Y, et al. "Lactate promotes pulmonary fibrosis via mitochondrial fission," J Transl Med. 2024. doi:10.1186/s12967-024-05289-2.
  12. ↑ 12.0 12.1 12.2 "Mitochondria and mortality," Ray Peat article
  13. ↑ Xu X, Sheng ZH, et al. "Creatine and axon regeneration," Cell Metab. 2020. doi:10.1016/j.cmet.2020.02.002.
  14. ↑ Döhla J, et al. "Metabolic determination of cell fate through selective inheritance of mitochondria," Nat Cell Biol. 2022. doi:10.1038/s41556-021-00837-0.
  15. ↑ Kraus VB, et al. "Analysis of 'salamander-like' regenerative capacity in humans," Sci Adv. 2019. doi:10.1126/sciadv.aax3203.
  16. ↑ 16.0 16.1 "Regeneration and degeneration - Types of inflammation change with aging," Ray Peat article
  17. ↑ 17.0 17.1 "Aging Eyes, Infant Eyes, and Excitable Tissues," Ray Peat article
  18. ↑ Nash TR, De Magalhaes JP, et al. "Daily blue-light exposure accelerates aging," npj Aging Mech Dis. 2019. doi:10.1038/s41514-019-0038-6.
  19. ↑ Griesser M, Uomini N, et al. "Extended childhood and corvid intelligence," Science. 2020. doi:10.1126/science.abd2209.
  20. ↑ Chen PX, Tian Y, et al. "Mitochondrial superoxide controls aging through lipids," Nat Metab. 2026. doi:10.1038/s42255-026-01452-9.
  21. ↑ Hoehn KL, et al. "Increased fatty acid oxidation does not reduce adiposity," Cell Metab. 2010. PMID 20074529.
  22. ↑ Schiffer TA, Antebi A, et al. "Cardiolipin and worm longevity," Nat Metab. 2020. doi:10.1038/s42255-020-0200-2.
  23. ↑ Lin Y, et al. "Fatty acid oxidation promotes cellular senescence," Sci Adv. 2024. doi:10.1126/sciadv.ado5887.
  24. ↑ Miller B, et al. "SARS-CoV-2 suppresses mitochondrial function in human cells," Sci Rep. 2021;11:2098. doi:10.1038/s41598-020-79552-z.
  25. ↑ Fellman SM, et al. "Hypermetabolism in mitochondrial disease," Commun Biol. 2023;6:22. doi:10.1038/s42003-022-04303-x.
  26. ↑ Mehdipour M, Mehdipour T, Skinner C, et al. "Plasma dilution improves cognition and attenuates neuroinflammation in old mice," Geroscience. 2021. doi:10.1007/s11357-020-00297-8.
  27. ↑ Zupančič N, Burd NA, et al. "Lipid-rich meat blunts postexercise MPS," Am J Clin Nutr. 2025. doi:10.1016/j.ajcnut.2025.09.001.
  28. ↑ Merle CL, Richter L, et al. "Oral health in elite endurance athletes," Scand J Med Sci Sports. 2022. doi:10.1111/sms.14143.
  29. ↑ Nemkov T, et al. "Ultramarathon red blood cell injury," Blood Red Cells Iron. 2026. PMID 42273167.
  30. ↑ Shea MK, Booth SL, et al. "Vitamin K status and mobility disability," J Gerontol A Biol Sci Med Sci. 2019. doi:10.1093/gerona/glz108.
  31. ↑ Kane AE, et al. "Long-term NMN increases lifespan and healthspan in mice," bioRxiv. 2024. PMID 38979132.
  32. ↑ Hochachka PW, et al. "PUFA ratios, torpor, and lifespan," Am J Physiol Regul Integr Comp Physiol. 2007. doi:10.1152/ajpregu.00688.2007.
  33. ↑ Damri O, et al. "Mitochondrial inhibitor model of bipolar disorder," Transl Psychiatry. 2021. doi:10.1038/s41398-021-01215-y.
  34. ↑ Peng M, et al. "Mitochondrial dysfunction and muscle atrophy," Skelet Muscle. 2021. doi:10.1186/s13395-021-00263-8.
  35. ↑ Rossmann A, et al. "TIF1γ and coenzyme Q in erythropoiesis," Science. 2021. doi:10.1126/science.aaz2740.
  36. ↑ Liao B, et al. "NMN supplementation and aerobic capacity in runners," J Int Soc Sports Nutr. 2021. doi:10.1186/s12970-021-00442-4.
  37. ↑ Paul BD, et al. "Redox imbalance in COVID-19 and ME/CFS," Proc Natl Acad Sci U S A. 2021. doi:10.1073/pnas.2024358118.
  38. ↑ Bubb K, et al. "Mitochondrial respiration and cartilage matrix integrity," J Biol Chem. 2021. doi:10.1016/j.jbc.2021.101224.
  39. ↑ Faas M, et al. "IL-33 and macrophage mitochondrial uncoupling," Immunity. 2021. doi:10.1016/j.immuni.2021.09.010.
  40. ↑ Das A, et al. "Systemic ablation of vitamin D receptor leads to skeletal muscle glycogen storage but energy deficiency," J Cachexia Sarcopenia Muscle. 2022. doi:10.1002/jcsm.12841.
  41. ↑ Leiter O, et al. "Selenium mediates exercise-induced adult neurogenesis and reverses learning deficits," Cell Metab. 2022. doi:10.1016/j.cmet.2022.01.005.
  42. ↑ Fei X, et al. "TLR4 deletion improves cognitive brain function and structure in aged mice," Neuroscience. 2022. doi:10.1016/j.neuroscience.2022.04.007.
  43. ↑ Luo C, et al. "Nicotinamide reprograms adipose cellular metabolism and increases mitochondrial biogenesis," J Nutr Biochem. 2022. doi:10.1016/j.jnutbio.2022.109056.
  44. ↑ Mian B, et al. "Adverse childhood experiences and biological aging," Psychoneuroendocrinology. 2022. doi:10.1016/j.psyneuen.2022.105821.
  45. ↑ Roca FJ, Ramakrishnan L, et al. "TNF and reverse electron transport in tuberculosis," Science. 2022. doi:10.1126/science.abh2841.
  46. ↑ Galkin F, et al. "Psychological factors and biological aging," Aging (Albany NY). 2022. doi:10.18632/aging.204264.
  47. ↑ Ugai T, Ogino S, et al. "Early-onset cancer as emerging global epidemic," Nat Rev Clin Oncol. 2022. doi:10.1038/s41571-022-00672-8.
  48. ↑ Speakman JR, et al. "Declining total daily energy expenditure," Nat Metab. 2023. doi:10.1038/s42255-023-00782-2.
  49. ↑ Sparkman NL, et al. "Intermittent LPS and cognitive aging in mice," Brain Behav Immun. 2023. doi:10.1016/j.bbi.2022.11.028. PMID 36549577.
  50. ↑ Holmes SE, et al. "Serotonin synthesis and aging trajectories," Mol Psychiatry. 2023. doi:10.1038/s41380-023-02177-x.
  51. ↑ Adelman JS, et al. "LPS and long-lasting rest behavior in birds," Proc Biol Sci. 2023. doi:10.1098/rspb.2023.0794.
  52. ↑ Gomes MV, et al. "Adolescent stress and mitochondrial respiration," Transl Psychiatry. 2023. doi:10.1038/s41398-023-02648-3.
  53. ↑ Peterson MD, et al. "Grip strength and epigenetic aging," J Cachexia Sarcopenia Muscle. 2023. doi:10.1002/jcsm.13110.
  54. ↑ Duchowny KA, et al. "Childhood adversity and muscle mitochondrial function," Sci Adv. 2024. doi:10.1126/sciadv.adj6411.
  55. ↑ Aho VTE, et al. "Cancer cachexia and muscle NAD+ metabolism," Mol Metab. 2020. doi:10.1016/j.molmet.2020.101046.
  56. ↑ Liabeuf G, Bravo-Sagua R, et al. "Decreased mitochondrial respiration associates with frailty in community-dwelling older adults," Front Cell Dev Biol. 2024;12:1301433. PMID 38778912.
  57. ↑ Schmitz TA, Wu JC, et al. "Mitochondrial influence on pluripotency via enforced mitophagy," Cell. 2025. doi:10.1016/j.cell.2025.05.020.
  58. ↑ Vanderhaeghen P, et al. "Mitochondrial metabolism controls the rate of cortical neuron maturation," Science. 2023;379(6629):133-138. doi:10.1126/science.abn4705.
  59. ↑ Hayashi JI, et al. "Age-associated epigenetic change in SHMT2 gene impairs mitochondrial respiration and induces senescence phenotypes," Sci Rep. 2019;9:16451. doi:10.1038/s41598-019-52372-6.
  60. ↑ Li Y, et al. "Vegetarian diet and centenarian likelihood," Am J Clin Nutr. 2025. doi:10.1016/j.ajcnut.2025.101136.
  61. ↑ Hukkanen M, Kankaanpää A, Heikkinen A, Kaprio J, Cristofari R, Ollikainen M. "Epigenetic aging and lifespan reflect reproductive history in the Finnish Twin Cohort," Nat Commun. 2026;17(1):44. doi:10.1038/s41467-025-67798-y. PMID 41507167.
  62. ↑ Ju X, et al. "Mitochondria in ovarian ageing inflammation," J Transl Med. 2025. doi:10.1186/s12967-025-06966-6.
  63. ↑ Qiu W, et al. "Cholesterol-dependent TSPO enzyme activity," Proc Natl Acad Sci U S A. 2025. doi:10.1073/pnas.2323045122.
  64. ↑ Landis GN, et al. "Mifepristone and rapamycin lifespan in Drosophila," Fly (Austin). 2024. doi:10.1080/19336934.2024.2419151.
  65. ↑ Arai Y, et al. "Inflammation predicts successful ageing at extreme old age," EBioMedicine. 2015. doi:10.1016/j.ebiom.2015.07.029.
  66. ↑ Tharyan RG, et al. "NFYB-1, lysosomes, and cardiolipin in longevity," Nat Metab. 2020. doi:10.1038/s42255-020-0200-2.
  67. ↑ Zhang Q, et al. "Inherited memory of neuronal mitochondrial stress," Nat Cell Biol. 2021. doi:10.1038/s41556-021-00724-8.
  68. ↑ Dougal A, et al. "Transcranial near-infrared light and memory performance," Photobiomodul Photomed Laser Surg. 2021. doi:10.1089/photob.2020.4956.
  69. ↑ LaPlume AA, et al. "Modifiable dementia risk factors and cognition," Alzheimers Dement (Amst). 2022. PMID 35845262.
  70. ↑ Ishikawa K, et al. "Mitochondrial dysfunction and severe anemia," Pharmacol Res. 2022. doi:10.1016/j.phrs.2022.106467.
  71. ↑ Hoffman E, et al. "Urolithin A rejuvenates aged hematopoietic stem cells," Nat Aging. 2023. doi:10.1038/s43587-023-00473-3.
  72. ↑ Miura M, et al. "Serotonin metabolism and senolysis in naked mole-rats," EMBO J. 2023. doi:10.15252/embj.2022111133.
  73. ↑ Blank HM, et al. "Late-life folate restriction and healthspan in mice," Life Sci Alliance. 2024. PMID 38260683.
  74. ↑ Minhas PS, Andreasson KI, et al. "PGE2-EP2 signaling drives brain aging," Nature. 2021. PMID 33473210.
  75. ↑ Graham T, Barzilai N, et al. "Low IGF-1 and exceptional longevity," Aging Cell. 2015. doi:10.1111/acel.12213.