Why You’re Aging Faster Than You Think & How to Slow It

Belsky emphasizes that DunedinPACE is a complement to standard labs, not a replacement. It integrates information across organ systems into a single number that patients find intuitive (a speedometer). He notes that in functional medicine, where the goal is whole-systems health, such a tool is particularly valuable for gauging whether the overall strategy is working. However, he cautions that the evidence base for using clock changes to guide individual patient care is still maturing; the FAST initiative aims to provide that validation by linking clock changes to hard outcomes in completed trials.

Belsky distinguishes between clinical use by trained professionals and hobbyist biohacking. He supports people's right to know their own data but stresses that the information requires nuanced interpretation. He points out that many competitors in the 'Rejuvenation Olympics' are actually working with healthcare professionals, which makes their self-experimentation safer. However, he worries about individuals who might see a high pace of aging and immediately adopt extreme diets or supplement stacks without addressing underlying health issues. He notes that in functional medicine, practitioners sometimes see patients who have optimized a trendy biohacking protocol while neglecting basic health needs like managing allergies or cardiovascular risk.

Belsky notes that the CALERIE trial achieved only about 12% restriction on average, not the 25% target, partly because the initial dietary models were imprecise. The intervention required a multidisciplinary team of internists, dietitians, nutritionists, and psychologists. He emphasizes that this is not a DIY intervention. The heterogeneity of response — some participants' aging accelerated — underscores the need for personalized approaches and better biomarkers to identify who will benefit. He also mentions that time-restricted feeding and intermittent fasting are being explored as potentially more sustainable alternatives to continuous caloric restriction.

Belsky draws an analogy to measuring CRP during an active infection — you wouldn't interpret that value as a stable indicator of systemic inflammation. Similarly, aging clocks may need 'fasting' from acute stressors. He suggests that as these tools move into clinical practice, we will develop guidelines for when to test and when to defer, much like we do for other lab tests. He also notes that some fluctuations might be useful — for example, measuring clocks during extreme stress could quantify the biological toll and justify interventions — but that's speculative.

Belsky explains that any measurement contains signal and noise. The original pace-of-aging phenotype, derived from repeated blood tests and physiological assessments, includes biological noise (e.g., day-to-day fluctuations, genetic background effects on biomarker levels). When they modeled that phenotype from DNA methylation data, the algorithm could only learn the systematic variance — the signal — because noise does not correlate with methylation across individuals. Consequently, the epigenetic surrogate became a cleaner readout of the underlying aging process. This is why it matched or exceeded the original phenotype in predicting functional deficits. He likens it to how a clinician knows that a single CRP value isn't a perfect readout of systemic inflammation; the methylation algorithm automatically performs that noise reduction.

Belsky borrows the metaphor from biologist Richard Miller. An odometer tells you how many miles you've traveled; a speedometer tells you your current speed. In aging terms, PhenoAge or GrimAge reflect accumulated damage and proximity to death, which may not change quickly even if you adopt a healthier lifestyle. DunedinPACE, by contrast, is designed to detect whether your rate of aging is slowing down in response to an intervention. This distinction is crucial for clinical trials and personalized medicine, where you want to know within a reasonable timeframe if a therapy is working. Belsky notes that this is why they encourage the term 'speedometer' — it sets appropriate expectations for what the test can and cannot do.

Belsky acknowledges that while his work focuses on the molecular breakdown of aging, there is a parallel process of psychological maturation that occurs with age. He notes that traits like delayed gratification and planfulness are exactly what help people adhere to diet, exercise, and medical regimens. Therefore, building these 'assets of aging' could be an important part of any geroprotective strategy. This is not just feel-good philosophy; it has practical implications for how we design interventions — for example, leveraging an older adult's natural tendency toward patience to improve adherence to a caloric restriction protocol.

Belsky emphasizes that as researchers they are trained to be conservative, but the real-world impact of even a 2–3% slowing is significant. He points out that the participants were already healthy at baseline, so the effect was on top of normal aging. He also notes that caloric restriction is extremely challenging and requires medical supervision to avoid nutrient deficiencies. The goal is to find interventions that achieve similar or greater slowing with less burden. This finding validates DunedinPACE as a surrogate endpoint that can detect clinically meaningful changes long before hard endpoints like death or disease onset.

Belsky explains that from an evolutionary perspective, natural selection cares less about maintaining the body after reproduction, so repair mechanisms are imperfect. Entropy — a physical principle, not just a biological one — ensures that molecular damage accumulates even under ideal conditions. Environmental factors like smoking, pollution, and stress accelerate this damage by making cells 'live harder.' He sees no qualitative difference between intrinsic and extrinsic aging; both contribute to the same entropic disintegration. This view has practical implications: interventions should focus on enhancing damage repair and reducing stressors, rather than trying to 'reprogram' aging.

Belsky explains that when you measure DNA methylation in whole blood, you're capturing a mixture of monocytes, lymphocytes, neutrophils, etc. These cell populations change dramatically during infection, injury, or pregnancy. So a clock change could simply reflect a shift in the proportion of cell types, not a change in the aging rate of any individual cell. While statistical methods exist to adjust for cell composition, it's not yet clear how well they work. He cautions that until we can disentangle these signals, short-term fluctuations should not be overinterpreted. This is why he advises against individuals using clocks to guide radical lifestyle changes without professional oversight.