We all know our chronological age, determined by the date we were born. It increases predictably every year, and we can’t change it (although some of us may prefer to stop counting at a certain point!). 

But chronological age doesn’t tell us the whole story about how we are ageing. 

Two people can both be 55 and have very different metabolic health, cardiovascular function, cognitive health, inflammatory profiles and physiological resilience. At a molecular and cellular level, they may also be ageing at different rates. 

This is where biological age becomes interesting. 

Healthy ageing isn’t simply about living longer. It’s about extending healthspan, the years we remain healthy, functional, cognitively well and able to do the things that matter to us. 

There is now a growing body of research investigating biological ageing itself, how we can measure it, why some people appear to age faster than others, and whether accelerated ageing can help predict future health and age-related disease risk. 

Biological age testing is now one of the most rapidly evolving areas of longevity and preventative health. But with that growth has come plenty of confusion. 

What exactly are these tests measuring? Are they actually validated? And does knowing someone’s biological age give us clinically useful information? 

The answer is more nuanced than a simple yes or no. 

First, there isn’t one biological age test

One of the most important things to understand is that biological age is not a single biological entity measured by one definitive test. 

Different tests capture different aspects of ageing. The same person may therefore receive different biological age results depending on the measure used.  

For example, biological age can be assessed using: 

• Physiological and functional measures – body composition, cardiovascular fitness, grip strength, heart rate variability and wearable data. 

• Blood-based algorithms – combinations of routine clinical biomarkers, such as Phenotypic Age. 

• Epigenetic clocks – patterns of DNA methylation associated with ageing and health outcomes. 

• Pace-of-ageing measures – particularly DunedinPACE, which asks a different question: how fast or slowly are you ageing? 

• Telomere length – one of the earliest molecular markers associated with ageing, although as a stand-alone measure it provides a narrower picture than many newer multi-marker approaches. 

• Organ- and system-specific measures – an emerging area looking at whether different organs and physiological systems may be ageing at different rates. 

That last area is particularly interesting. Newer commercial approaches include TruDiagnostic’s SYMPHONYAge and Generation Lab’s SystemAge, which attempt to move beyond a single whole-body age towards system- or organ-specific ageing. 

These newer approaches are promising, but the level of research behind them varies. In my review of SystemAge, I found good evidence supporting the biology and methodology behind the test. However, the SystemAge measures themselves have not yet been independently validated to the same extent as more established measures such as DunedinPACE, DNAm PhenoAge and GrimAge. 

I’m actually due to repeat my own biological age testing soon, including some of these newer measures. I’m genuinely interested to see how they compare with the Phenotypic Age and DunedinPACE measures I already track. 

So, are biological age tests actually valid?

For some measures, there is now a substantial and growing evidence base. 

The early first-generation epigenetic clocks, including Horvath and Hannum, were primarily developed to predict chronological age from DNA methylation. That was scientifically groundbreaking – but predicting someone’s calendar age isn’t necessarily the same as measuring their health or rate of ageing. 

Second-generation clocks, including DNAm PhenoAge and GrimAge, were developed to better capture physiological health, morbidity and mortality risk. Later pace-of-ageing measures, particularly DunedinPACE, ask a different question again: rather than estimating your biological age as a number, they aim to measure how fast or slowly you are ageing.[3] 

One of the more established blood-based measures is Phenotypic Age. Researchers initially considered 42 clinical biomarkers in almost 10,000 adults before narrowing the algorithm to nine routine blood biomarkers plus chronological age. The measure was then evaluated in more than 11,000 additional adults and was strongly associated with morbidity and mortality, even after accounting for chronological age.[1] 

There is an important terminology distinction here. Phenotypic Age refers to this blood-based algorithm, while DNAm PhenoAge is the later epigenetic clock developed using DNA methylation to predict the Phenotypic Age phenotype. DNAm PhenoAge uses methylation at 513 CpG sites and has been associated with a range of ageing-related outcomes.[2] 

You’ll often hear ‘PhenoAge’ used loosely for both and I’ll admit I’ve done this myself. Strictly speaking, though, they’re different measures: one uses routine blood biomarkers and the other DNA methylation. 

More recent work has tested Phenotypic Age in very large prospective cohorts. In more than 405,000 UK Biobank participants, accelerated Phenotypic Age was associated with incident cardiovascular disease, cancer and all-cause mortality; related mortality findings were also examined in NHANES.[4] 

The evidence extends strongly into metabolic health. A 2025 UK Biobank study followed 376,083 adults free of type 2 diabetes at baseline for a median of 13.7 years. Accelerated Phenotypic Age was associated with a higher risk of developing type 2 diabetes, progression to diabetes-related complications and mortality.[5] 

So yes, there is real science behind biological age assessment. 

But ‘validated’ doesn’t mean every commercially available age score is equally validated, or that every measure answers the same clinical question. 

What can biological age tell us about brain health?

This is one of the areas I find particularly exciting. 

Chronological age is the strongest risk factor for Alzheimer’s disease and related dementias, so an obvious question is whether accelerated biological ageing might give us additional information about brain and cognitive ageing. 

The emerging evidence is fascinating. 

In the Framingham Heart Study Offspring Cohort, researchers followed 2,296 people across approximately two decades of neuropsychological testing. Faster DunedinPACE was associated with poorer cognitive function at baseline and faster subsequent cognitive decline. Findings were similar for the PhenoAge and GrimAge epigenetic clocks.[6] 

Earlier work also linked faster DunedinPACE with age-related cognitive impairment and dementia-related outcomes, with findings tested across the Alzheimer’s Disease Neuroimaging Initiative and Framingham Heart Study.[7] 

A particularly interesting recent study examined 2,366 cognitively unimpaired older women, with 873 providing longitudinal data over approximately 15 years. Different epigenetic clocks were associated with different Alzheimer’s-related plasma biomarkers. Faster DunedinPACE at baseline was associated with faster subsequent increases in p-tau181, p-tau217, neurofilament light and GFAP – markers related to tau pathology, neurodegeneration and neuroinflammation.[8] 

Importantly, this does not mean DunedinPACE is an Alzheimer’s diagnostic test. But for someone like me who is particularly interested in cognitive health and healthy brain ageing, this is an exciting area to watch. 

There is prospective dementia evidence too. In 1,644 older participants from the Framingham Offspring Cohort, slower DunedinPACE was associated with lower subsequent dementia and mortality risk. Slower pace of ageing also statistically accounted for part of the association between greater adherence to a MIND diet and reduced dementia risk.[9] 

This is also personal for me. I have a family history of Alzheimer’s disease and carry a known genetic susceptibility, so the question of whether accelerated biological ageing can actually be influenced isn’t an abstract one for me. It’s a big part of why I’ve spent so much time in this field, and why I keep a close eye on my own biological age data rather than just my genetic risk on its own. 

I personally track both DunedinPACE and Phenotypic Age. I find them useful for different reasons, and I don’t expect all my biological age measures to tell me exactly the same thing. I’ve also managed to bring my own DunedinPACE down considerably over time, and right now it’s tracking very well – something I’m particularly happy about, given what’s at stake for me personally.  

Can we improve our biological age?

That question – whether biological ageing can actually be shifted – matters enormously to me personally, and I think it’s one of the most important messages we can give our clients. Biological age is dynamic, and research shows that different measures of biological age can and do change over time. 

We don’t necessarily age at the same rate throughout our lives. Periods of faster biological ageing can occur, but we can also experience periods of slower ageing. Also, importantly, some of the blood biomarkers, cellular processes and epigenetic changes associated with ageing can shift in a more favourable direction, resulting in a younger biological age. 

Our bodies are constantly responding and adapting. Cellular health, metabolism, inflammation and repair processes can change over time, and epigenetic mechanisms such as DNA methylation are influenced by ageing as well as environmental and lifestyle factors. 

We know this intuitively too. Our health isn’t static. We can go through periods of illness, chronic stress or poor metabolic health, and we can also recover, become fitter, improve our metabolic health and build greater physiological resilience. 

So it makes sense that at least some measures of biological ageing may be dynamic too. 

Plus, there is research demonstrating this. 

In a 2023 Cell Metabolism study, several biological-age measures increased during periods of substantial physiological stress, including major surgery, pregnancy and severe COVID-19, and moved back towards baseline following recovery.[10] 

I’ve seen this variability clinically too – in myself, my clients and across the three- and six-month follow-up periods of my biological age program. 

So, from my own experience and understanding of the biology, I believe we can influence aspects of biological ageing and there is a growing body of research supporting this. 

Studies led by Dr Kara Fitzgerald and colleagues have reported improvements in epigenetic age following an eight-week diet and lifestyle intervention in both men and women. Their initial randomised controlled trial in 43 healthy men found a significant reduction in Horvath DNA methylation age compared with controls.[11] A subsequent small case series in six women using a similar intervention also reported reductions in Horvath DNA methylation age.[12] 

The CALERIE randomised controlled trial studied 220 healthy adults without obesity who were assigned to caloric restriction or an ad-libitum control group for two years. Caloric restriction produced a small but significant slowing of DunedinPACE, but did not significantly change DNAm PhenoAge, GrimAge or the first-generation clocks.[13]

That finding is incredibly instructive: the clocks didn’t all move together.

More recently, the DO-HEALTH trial analysed 777 older adults over three years. Omega-3 supplementation was associated with small changes in several later-generation measures, including PhenoAge, GrimAge2 and DunedinPACE, while the pattern of response differed according to the biological-age measure used.[14] 

We saw this variability in our own published pilot program too.[15] Following a three-month nutrition, lifestyle and targeted supplementation protocol, we observed significant improvements in several DNA methylation measures of biological ageing, while others changed very little. We also collected six-month follow-up data as part of the program, which reinforced for me how dynamic these measures can be over time. 

For me, this is one of the most important lessons in the field. It isn’t enough to ask, ‘Did biological age go down?’ 

We need to ask: ‘Which measure changed, what was it designed to measure, and what might that change actually mean?’ 

Which biological age test should you actually use?

After looking at all this evidence, the question is: which biological age test should you actually use in clinical practice? 

There isn’t one answer. It depends on what you want to assess, the individual you’re working with, the evidence behind the measure, cost and accessibility – and accessibility can be particularly relevant for practitioners here in Australia. 

This is also where the practical questions start. Which tests can you order? How much do they cost? What results do you actually receive? When is epigenetic testing worthwhile? How often should you repeat testing? And what do you do with the information once you have it? 

If you’re interested in moving into this space and would like to understand these options – and have the opportunity to ask questions – I’ll be exploring them in my upcoming Biological Age Assessment in Clinical Practice live masterclass. 

We’ll look at the broader testing landscape, including access, ordering and approximate costs, particularly for practitioners in Australia. Then we’ll take a practical deep dive into Phenotypic Age, which I think is one of the easiest places for practitioners to start because it can be calculated from nine routine blood biomarkers you’re likely already assessing in clinical practice. 

I’ll show you how to calculate it, interpret the result, understand what may be driving it, and use it to help assess and track health and ageing. 

We’ll also have plenty of time for questions about epigenetic testing, the tests I use myself, and how I think about choosing between different biological-age measures in practice. 

Learn more about the masterclass happening in September 2026…

References 

1. Liu Z, Kuo P-L, Horvath S, Crimmins E, Ferrucci L, Levine M. A new aging measure captures morbidity and mortality risk across diverse subpopulations from NHANES IV: A cohort study. PLOS Medicine. 2018. 

2. Levine ME, Lu AT, Quach A, Chen BH, Assimes TL, Bandinelli S, et al. An epigenetic biomarker of aging for lifespan and healthspan. Aging (Albany NY). 2018. 

3. Belsky DW, Caspi A, Corcoran DL, Sugden K, Poulton R, Arseneault L, et al. DunedinPACE, a DNA methylation biomarker of the pace of aging. eLife. 2022. 

4. Li X, Cao X, Zhang J, Fu J, Mohedaner M, Danzengzhuoga, et al. Accelerated aging mediates the associations of unhealthy lifestyles with cardiovascular disease, cancer, and mortality. Journal of the American Geriatrics Society. 2024. 

5. Pan L, Liu Y, Huang C, Huang Y, Lin R, Wei K, et al. Association of accelerated phenotypic aging, genetic risk, and lifestyle with progression of type 2 diabetes: a prospective study using multi-state model. BMC Medicine. 2025. 

6. Savin MJ, Wang H, Pei H, Aiello AE, Assuras S, Caspi A, et al. Association of a pace of aging epigenetic clock with rate of cognitive decline in the Framingham Heart Study Offspring Cohort. Alzheimer’s & Dementia: Diagnosis, Assessment & Disease Monitoring. 2024. 

7. Sugden K, Caspi A, Elliott ML, Bourassa KJ, Chamarti K, Corcoran DL, et al. Association of Pace of Aging Measured by Blood-Based DNA Methylation With Age-Related Cognitive Impairment and Dementia. Neurology. 2022. 

8. Zhang B, McEvoy LK, Nguyen S, Espeland MA, Rapp SR, Horvath S, et al. Epigenetic clocks and longitudinal plasma biomarkers of Alzheimer’s disease. Alzheimer’s & Dementia. 2025. 

9. Thomas A, Ryan CP, Caspi A, Liu Z, Moffitt TE, Sugden K, et al. Diet, Pace of Biological Aging, and Risk of Dementia in the Framingham Heart Study. Annals of Neurology. 2024. 

10. Poganik JR, Zhang B, Baht GS, Tyshkovskiy A, Deik A, Kerepesi C, et al. Biological age is increased by stress and restored upon recovery. Cell Metabolism. 2023. 

11. Fitzgerald KN, Hodges R, Hanes D, Stack E, Cheishvili D, Szyf M, et al. Potential reversal of epigenetic age using a diet and lifestyle intervention: a pilot randomized clinical trial. Aging (Albany NY). 2021. 

12. Fitzgerald KN, Campbell T, Makarem S, Hodges R. Potential reversal of biological age in women following an 8-week methylation-supportive diet and lifestyle program: a case series. Aging (Albany NY). 2023;15(6):1833-1839. 

14. Bischoff-Ferrari HA, Gängler S, Wieczorek M, Belsky DW, Ryan J, Kressig RW, et al. Individual and additive effects of vitamin D, omega-3 and exercise on DNA methylation clocks of biological aging in older adults from the DO-HEALTH trial. Nature Aging. 2025. 

15. Furness D, Taylor P. Three-Month Nutritional and Lifestyle Intervention Reduces Biological Age: A Pilot Study Using DNA Methylation Clocks. Journal of the Australasian College of Nutritional and Environmental Medicine. 2025.