Dear readers,
I ran my own biological age last week. Chronologically, I am 44. The number that came back was 32.2.
My first reaction was not celebration but curiosity. As a physician, I do not trust a good number any more than I trust a bad one until I understand where it came from and what it actually measures. So before I tell you how to move your own number, I want to walk you through what this test is, how we calculate it here, and how much weight it deserves.
What biological age actually means
Chronological age is how long you have been alive. Biological age is an estimate of how well your body is holding up against the clock. Two people born the same year can sit a decade apart biologically, and that gap is where the interesting, actionable medicine lives.
There are several ways to estimate biological age. The most rigorous use DNA methylation, the chemical marks that accumulate on your genes over time. Those epigenetic clocks are powerful, but they require specialized testing. What I want to focus on is a method that runs on labs we already draw at the practice, using a validated tool called PhenoAge.
The other ways to measure it
PhenoAge is my starting point because it is accessible and validated, but it is not the only clock, and each method answers a slightly different question. It helps to know what else is out there so you can understand where PhenoAge fits.
Epigenetic clocks are the most talked-about category. These read DNA methylation patterns from a blood or saliva sample. The first-generation clocks, Horvath and Hannum, were built to track chronological age closely. The more clinically interesting second and third generation clocks, GrimAge and DunedinPACE, were designed instead to predict health outcomes and pace of aging. GrimAge in particular is one of the strongest single predictors of mortality risk we have. These are powerful tools, though they cost more, are not yet standardized across labs, and can vary between draws, so I treat them as a complement to blood-based measures rather than a replacement.
Telomere length testing measures the protective caps on your chromosomes, which shorten as cells divide. It is biologically meaningful and widely marketed, but the measurement is noisy and correlates loosely with health at the individual level, so I put less clinical weight on it than the marketing would suggest.
Functional and physiologic measures are the ones I never want to overlook, because they are cheap, repeatable, and closely tied to how you actually age. Grip strength, gait speed, VO2 max, body composition, and resting metabolic markers all track biological aging in ways that are visible year over year. VO2 max in particular is one of the most robust predictors of longevity we have, and unlike a lab clock, you can feel it improve as you train.
The realistic way to think about all of this: no single clock is the truth. Each is a different lens on the same underlying process. When two or three of them agree, I pay attention. When they disagree, that disagreement is itself useful information about what to investigate.
PhenoAge, and why I use it
PhenoAge was developed by Dr. Morgan Levine and colleagues and published in 2018. What makes it clinically useful is that it does not require anything exotic. It uses nine standard biomarkers plus your chronological age: albumin, creatinine, glucose, C-reactive protein, lymphocyte percentage, mean cell volume, red cell distribution width, alkaline phosphatase, and white blood cell count.
Every one of those sits on a routine metabolic panel and complete blood count with a CRP added on. In other words, the raw material for your biological age is already in the bloodwork most of my patients get anyway.
I want to be precise about one thing, because I see it misrepresented constantly. PhenoAge is not a number you can add up in your head. The formula weights each marker, feeds the result through a mortality-risk equation, and back-converts that risk into an age. We run it through a validated calculator with the published coefficients, and the units have to be exactly right or the answer is meaningless. So when I say we calculate it simply, I mean the inputs are simple and already in hand, not that the arithmetic is something you do on a napkin.
How accurate is it
This is the question that matters, and the answer has two parts.
PhenoAge is well validated as a predictor of mortality and age-related disease risk across large populations. In the original research and in independent studies, a higher phenotypic age relative to chronological age tracks with meaningfully higher risk of death and of conditions like cardiovascular disease and diabetes. That is a strong, reproducible signal. As a risk estimate expressed in the language of age, it earns its place in a longevity workup.
Here is the part I insist my patients understand. PhenoAge measures current physiologic risk, not some fixed biological truth carved into your cells. That is actually good news, because it means the number moves. But it also means the number is sensitive to what is happening the week you draw it. An acute infection, a recent hard training block, dehydration, or a flare of inflammation can push it up transiently. My own 32.2 reflects a genuinely favorable metabolic and inflammatory profile, but I would never treat a single reading as a verdict. I treat it as a data point on a trend line, which is how I would ask you to treat yours.
One distinction is worth drawing clearly. As a predictor of risk across large populations, PhenoAge is on solid ground. The idea that lowering your own PhenoAge through lifestyle change directly extends your lifespan is reasonable and supported by the underlying biology, but it is not the same as a clock you can wind back on command. That difference is not academic. It is the difference between chasing a cause and chasing a number.
What actually moves the number
When a biological age comes back high, the productive response is never to attack the score. It is to ask which of those nine markers is dragging it, and why. The markers themselves tell you where to look, and each one points to something you can genuinely influence.
Inflammation is usually the biggest lever. CRP carries real weight in the calculation, and chronically elevated CRP is one of the most modifiable inputs there is. Sleep, visceral fat, unmanaged dental or gut inflammation, and overtraining all show up here. Bringing inflammation down tends to move the number more than any single heroic intervention.
Glucose and metabolic health come next. Fasting glucose is in the formula, but it is a stand-in for a much larger story about insulin sensitivity. Reducing refined carbohydrate load, building muscle, walking after meals, and prioritizing protein all improve the metabolic markers that feed the score. This is the same ground we cover in body recomposition work, and it pays off twice.
The blood markers reward correcting quiet deficiencies. Red cell distribution width and mean cell volume rise with iron, B12, and folate issues and with alcohol intake. These are often silent, they are easy to test, and they are straightforward to correct once identified. Alcohol in particular touches several markers at once, which is why even a modest reduction tends to show up across the panel.
The practical foundations are unglamorous and they work. Consistent sleep, regular zone 2 and resistance training, a protein-forward and fiber-rich diet, muscle mass you actively protect as you age, and stress load you actually manage rather than endure. I would add, because it is central to how I practice, that emotional and spiritual health is not separate from any of this. Chronic stress is a physiologic input, and the markers know it.
The peptides I’m most excited about
This is the part patients lean in for, and I get it. Peptides are one of the most exciting frontiers in longevity medicine, and I use them a lot. I also use them carefully, so let me be clear up front: no peptide has been proven to lower a validated biological age score in humans, and I would be skeptical of anyone who tells you otherwise. What excites me is different. A handful of these peptides act right on the biology underneath the markers PhenoAge reads. Inflammation. Cellular repair. Mitochondrial function. Immune aging. That is where the real action is. I treat all of them as compounded therapeutics without FDA-approved indications for longevity, and always as one piece of a plan, never the whole thing.
Here are the four I am most excited about right now. For each, I have noted what it targets and what the evidence actually shows, so you can judge it the way you would any tool.
Epitalon: telomeres and cellular aging
Epitalon is a synthetic pineal peptide developed by Professor Vladimir Khavinson in St. Petersburg and studied for more than forty years. In human cells, it switches on telomerase and lengthens telomeres. That matters, because telomere shortening is one of the core drivers of aging, and here is a peptide that pushes back on it directly.
The human data is what sets it apart. In a group of 266 adults over 60, the pineal preparation it comes from cut deaths over six years by roughly a third to a half. Paired with a thymic peptide and dosed every year, the treated group had about four times fewer deaths than the untreated one. A separate 12-year study in heart patients showed lower cardiovascular and overall mortality, plus better metabolic and circadian markers.
Two caveats worth keeping in view. First, this is fewer deaths during the study, not a proven number of extra years for any one person. Second, nearly all of it comes from a single Russian program and has not been repeated in large Western trials. Still, very few longevity compounds have any multi-year human mortality data at all. This one does, and that is rare.
Why it matters for your number: better telomere maintenance, a steadier melatonin rhythm, and lower background inflammation all feed the cellular and inflammatory markers PhenoAge reads.
MOTS-c: mitochondria and metabolic fitness
MOTS-c is a peptide your own mitochondria make, and your levels drop as you age. The standout study (Nature Communications, 2021, from the Lee Lab at USC) is one of those results that stops you. Give mice MOTS-c and their treadmill capacity roughly doubles, at every age. The oldest mice, the equivalent of humans 65 and up, doubled their running capacity and outran untreated middle-aged animals. Late in life, it improved grip strength and gait and slowed the usual decline.
Here is the part I love. Exercise itself triggers MOTS-c. After a hard cycling session, muscle levels jump nearly twelvefold. So this is not some foreign compound. It is a signal your body already runs on, and we are simply topping it up. Earlier work also showed it reverses insulin resistance in mice, both the diet-driven kind and the kind that comes with age.
Why it matters for your number: it works at the mitochondrial and metabolic core that drives your glucose and inflammatory markers. The human treatment data is still early.
Thymosin alpha-1: immune aging
This is the one I reach for with the most confidence, because its evidence base is the strongest of the four. It is a real immune modulator, approved in more than 30 countries, and it restores the T-cell function and thymic output that fade steadily as we age. A meta-analysis in critically ill sepsis patients found it significantly cut 28-day deaths. Other work in older adults showed restored immune markers and fewer infections. And its close cousin thymalin is the peptide that was paired with epitalon in those long-term mortality studies above.
Why it matters for your number: immune drift and low-grade inflammation are two of the biggest engines of aging, and they sit right under the lymphocyte, white-cell, and inflammatory markers on your panel.
Pinealon: brain aging
Pinealon comes from the same Khavinson family, and its focus is the brain. In animal and cell studies, it protects neurons from low-oxygen and oxidative damage. What draws me to it is the target: brain aging, where we have so few good tools. Unfortunately, this has the thinnest human evidence of the four. I treat it as promising early science, not settled fact. But the direction is exciting, and I am watching it closely.
Why it matters for your number: the link is indirect, working through the broader inflammatory and cellular-stress biology of aging.
The pattern here is enthusiasm with discipline. These four act on the pathways that actually shape how we age, and yes, I am excited about them. But they earn their place only inside a plan, one where we watch your labs and your response over time, built on top of the sleep, training, food, and stress work that does the real heavy lifting. Used that way, they are powerful. Sold as a shortcut, they are a distraction from what moves your number.
The bottom line
My number was 32.2 against a chronological 44. I am glad it reflects years of the habits I ask my patients to build. But the value of the test was never the single figure. It was the confirmation that the levers I trust are pulling in the right direction, and the ability to watch that trend over time.
That is what I want this test to be for you. Not a grade, and not a source of anxiety, but a clear, repeatable readout of where your physiology stands and which specific inputs will move it. We can draw the panel, run the calculation, and sit down with what it shows. Then we do the far more interesting work of changing it.
If you are curious what your own number is, this is a conversation worth having at your next visit. Reach out to our office at 703-866-4144 or schedule a consultation with us and let’s get you sorted the right way.
Best wishes,
Dr. Gajer
The Gajer Practice – The Science of Health, The Art of Transformation.
