Epigenetic clocks and biological age panels are the wellness industry’s newest anxiety product. They produce a single number – “your biological age is 38 but your chronological age is 45” – and send you into either celebration or despair. A single number invites more certainty than the research supports. A review of the field describes epigenetic clocks as highly accurate correlates of chronological age, while the work of turning them into dependable measures of an individual’s rate of aging is still ongoing, with open challenges the authors lay out.[1] It can also leave the impression that aging is one number you can fix with a protocol.
There are several types of epigenetic clocks, and the differences show why they are research tools more than personal dashboards. The Horvath clock uses DNA methylation at 353 sites and was built as a multi-tissue predictor of age.[2] It is accurate at telling you how old you are, which is information you already had. The PhenoAge clock started from a “phenotypic age” score built from nine routine blood biomarkers plus chronological age (including albumin, creatinine, glucose, and C-reactive protein), and then trained a DNA methylation predictor on that score. In the original work it predicted all-cause mortality, cancers, healthspan, and physical functioning.[3] The DunedinPACE clock was trained on two decades of change in 19 organ-system indicators in a birth cohort to estimate the pace of aging rather than a biological age. It was associated with morbidity, disability, and mortality in validation datasets.[4]
The underlying research is real and interesting. The question for an individual is usefulness. A different approach is to look at measurements that connect to a decision you and your clinician can make. Three worth asking about are ApoB, fasting insulin, and cardiorespiratory fitness.
ApoB – your cardiovascular particle count. Each atherogenic particle (LDL, VLDL, chylomicron, and lipoprotein(a)) carries one apoB molecule, and a narrative review concluded that apoB measures atherogenic risk more accurately than LDL cholesterol or non-HDL cholesterol.[5] Guidelines treat higher apoB as higher risk rather than reading it as a diagnosis. The 2019 ESC/EAS dyslipidaemia guidelines list apoB secondary goals of below 65, 80, and 100 mg/dL for people at very high, high, and moderate cardiovascular risk, respectively.[6] Which category applies depends on your overall risk, which your clinician estimates, so ask whether an apoB test makes sense for you and which goal applies.
Fasting insulin – one window on metabolic health. When tissues respond less to insulin, the normal response of the pancreatic beta cells is to secrete more insulin, and that extra insulin can keep fasting glucose in the normal range for a time.[7] Fasting insulin is not part of the ADA criteria for prediabetes, which are based on A1C, fasting glucose, and 2-hour glucose.[8] The sources cited here do not define a cutoff for fasting insulin, so ask your clinician how to read a result. No source cited here shows that testing fasting insulin changes decisions or outcomes, and insulin assays can vary between labs.
Cardiorespiratory fitness – your functional capacity. In a cohort of 6,213 men referred for treadmill exercise testing, peak exercise capacity (measured in metabolic equivalents, or METs) was the strongest predictor of death after adjusting for age, and each 1-MET increase went with a 12 percent improvement in survival. The authors concluded that exercise capacity was a more powerful predictor of mortality than other established cardiovascular risk factors.[9] That was an observational study of men, so it shows an association, not that raising your fitness will produce the same change in you. If you have heart disease or symptoms, talk to your clinician before any maximal exercise test.
Counterpoint: aren’t epigenetic clocks validated by research? In research cohorts, partly. PhenoAge and DunedinPACE were associated with mortality and other outcomes in the groups studied.[3][4] That is different from showing that one person’s score should change what they do. The review cited earlier lists open challenges in understanding what clocks measure and in using them as biomarkers, and raises ethical questions about predicting an individual’s aging trajectory.[1] Bettering Me’s view is that a clock result rarely changes the next step: you would still discuss your lipids, glucose, and fitness.
Before spending on a biological-age panel, Bettering Me suggests asking your clinician about ApoB and cardiorespiratory fitness, and whether fasting insulin adds anything for you. An epigenetic clock estimates how old your DNA methylation pattern looks. ApoB and fitness connect to things you can discuss and act on with your clinician; for fasting insulin, no source here shows that testing it changes outcomes.
References
↑︎ Bell CG, Lowe R, Adams PD, et al. DNA methylation aging clocks: challenges and recommendations. Genome Biol. 2019;20(1):249. DOI: https://doi.org/10.1186/s13059-019-1824-y
↑︎ Horvath S. DNA methylation age of human tissues and cell types. Genome Biol. 2013;14(10):R115. DOI: https://doi.org/10.1186/gb-2013-14-10-r115
↑︎ Levine ME, Lu AT, Quach A, et al. An epigenetic biomarker of aging for lifespan and healthspan. Aging (Albany NY). 2018;10(4):573-591. DOI: https://doi.org/10.18632/aging.101414
↑︎ Belsky DW, Caspi A, Corcoran DL, et al. DunedinPACE, a DNA methylation biomarker of the pace of aging. eLife. 2022;11:e73420. DOI: https://doi.org/10.7554/eLife.73420
↑︎ Sniderman AD, Thanassoulis G, Glavinovic T, et al. Apolipoprotein B particles and cardiovascular disease: a narrative review. JAMA Cardiol. 2019;4(12):1287-1295. DOI: https://doi.org/10.1001/jamacardio.2019.3780
↑︎ Mach F, Baigent C, Catapano AL, et al. 2019 ESC/EAS Guidelines for the management of dyslipidaemias: lipid modification to reduce cardiovascular risk. Eur Heart J. 2020;41(1):111-188 (apoB secondary goals: p. 132 and Table 7, p. 133). DOI: https://doi.org/10.1093/eurheartj/ehz455
↑︎ DeFronzo RA, Tripathy D. Skeletal muscle insulin resistance is the primary defect in type 2 diabetes. Diabetes Care. 2009;32(Suppl 2):S157-S163. DOI: https://doi.org/10.2337/dc09-S302
↑︎ American Diabetes Association Professional Practice Committee. 2. Diagnosis and classification of diabetes: Standards of Care in Diabetes-2025. Diabetes Care. 2025;48(Suppl 1):S27-S49. DOI: https://doi.org/10.2337/dc25-S002
↑︎ Myers J, Prakash M, Froelicher V, et al. Exercise capacity and mortality among men referred for exercise testing. N Engl J Med. 2002;346(11):793-801. DOI: https://doi.org/10.1056/NEJMoa011858
Kurt Greiner
Kurt is a digital strategist and IT professional blending emerging technology with practical application to help businesses and individuals streamline their digital presence. His current work focuses on the intersection of intentional living and technological resilience, exploring how individuals can leverage modern tools to navigate the second half of life with purpose.
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