A river can get dammed by time and debris. Our blood might not be so different.
As we age, clotting happens faster, and the balance between clotting and clot breakdown can change. This might explain why we need to worry more about thrombosis, clumping inside a blood vessel, with age… Nothing good comes from that.
It would be easy to pin this age-related clotting on inflammation. We could technically end the article here. Everything aging is inflammation.
But inflammation alone might not explain why this age-related tendency to clot happens. It’s a phenomenon researchers have informally dubbed coagul-aging.
Understanding it may provide a new way to think about biology, and how we can intervene sooner.
Key takeaways
Coagul-aging: the process by which aging can increase the body’s blood clotting process.
Inflammation might only partially drive clotting. This phenomenon might also be deeply biological.
Clotting factors increase with age; it doesn’t mean you’ll develop a blood clot.
What aspect of aging do you think deserves a proper title?
What is coagul-aging?
Researchers use coagul-aging to describe the age-related shifts toward increased coagulation (ie, blood clotting). It’s an offshoot of inflamm-aging, the buzzy term for systemic inflammation that is both caused by (and a catalyst of) aging.
Now, clotting is a critical function, both for preventing excessive bleeding from minor injuries and for creating scabs to prevent infection. However, when these clotting factors become chronically activated, it could contribute to coagul-aging.
Inflammation certainly has a role to play. A review in Ageing Research Reviews explains that chronically activated inflammation and clotting factors engage in a type of “maladaptive crosstalk” that amplifies one another. That may worsen blood vessel function over time and drive disease.
Inflammation still might not be the only coagul-aging trigger.
The Molecular Triggers Behind Aging Blood
Aging is complex, so there’s probably more to aging blood vessels than inflammation.
In this case, research suggests that the aging/clotting link can also involve misplaced DNA and nucleic acids. This occurs when DNA, RNA, and other genetic material end up in the wrong location in cells.
As we age, senescent cells—inflammatory ‘zombie’ cells that cause aging—accumulate. This causes cellular stress and damage, which can also leave a paper trail of misplaced DNA or RNA.
What happens next? This genetic material can activate biological pathways (such as the factor XII-related pathways) that ramp up clotting activity.
As these misplaced molecules build up in aging tissue, they act like ‘molecular triggers’ that drive inflammation, aging, and coagul-aging. But what’s fascinating is that they trigger clotting without tuning into inflammatory pathways first.
This suggests that aging fundamentally alters clotting activity, and that coagul-aging is not simply a byproduct of inflammation. If that’s the case, doesn’t it mean we’re inevitably bound for blood clots? That’s not what the science suggests.
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The centenarian question
In 1995, a small study published in the journal Blood made a surprising discovery.
When researchers compared 28 healthy centenarians with younger and older healthy adults, the centenarians showed both markers linked to increased clotting (hypercoagulability). That included higher levels of enzymes, peptides, and other complexes linked to coagulation, and perhaps other more serious conditions.
Even though centenarians showed higher clotting markers, they also showed more signs of clot breakdown.
What became apparent is that clotting may be intrinsic to aging, but it doesn’t automatically increase the risk of vascular or clotting-related diseases.
This is just a small observational study, so it can’t fully explain why their blood vessels were protected. But the balance between clot formation and breakdown has led to new avenues of research.
Today, most evidence continues to point to metabolic health (managing blood sugar and other cardiovascular risk factors) as an important means to prevent clotting from becoming a clinical problem.
Before the clot: Getting ahead of cardiovascular aging
Cardiovascular disease remains the top killer globally, and most heart attacks occur from blood clots.
Beyond aging, hypercoagulation might be shaped by genetics, lifestyle, stress, and other health conditions. Reducing the accumulation of nucleic acids might slow vascular aging, but there’s not a lot of evidence for that, and ultimately, the best defense is going to be the advice you know:
Follow a heart-healthy diet. Consider an anti-inflammatory diet built around vegetables, fruit, beans, whole grains, nuts, and minimally processed foods. Look for foods rich in polyphenols, including foods like blueberries, apples, and leafy greens, says Dr. Frank Hu, professor of nutrition and epidemiology at the Harvard School of Public Health.
Move regularly. Try to increase your heart rate. A good benchmark is 150 minutes of moderate-to-vigorous exercise. Think brisk walks and bike rides.
Don’t smoke. (I think most of you are really good at this one!)
Know your numbers. Keep blood pressure, cholesterol, and blood sugar in a healthy range. Blood thinners can be lifesaving for some people.
Test if you need it. If you have a personal or strong family history of blood clots, ask a clinician if testing is appropriate for you. PT/INR or PTT is available to measure clotting time.
Senolytics: A promising (not proven) therapeutic
Senolytics are experimental compounds designed to target senescent (‘zombie’) cells. The theory goes that if senescent cells help drive inflammation, misplaced nucleic acids, and downstream vascular dysfunction, removing them could help.
Increasingly popular among biohackers—they are currently part of a four billion-dollar global market—there’s still little proof that senolytics can reverse aging and clotting in humans.
While researchers at labs like the Buck Institute of Aging study their potential, for now, they should not be considered a coagul-aging cure.
Big picture
I’d never heard of “coagul-aging” before this, but it could be a useful way to think about an often-overlooked part of getting older.
Healthy centenarians (if just part of a small study) show early evidence that blood changes do not automatically translate to disease. So, as researchers continue to sort out the “why,” the things within our control are familiar and accessible: watching how we eat, move, and sleep, monitoring our health, and working with clinicians when something feels off.
This might not be the last “-aging” term we’ll add to our longevity lists, but it marks the beginning of understanding more about how blood vessels shape a lifetime of health.
Poll response
This question comes from last week’s issue, Why nervous system resets don't feel like enough.
We asked: What’s keeping you “on” right now?
‘My own thoughts’ was the runaway answer. Maybe you’re “always thinking of how I can improve myself,” like one of our readers. Or maybe you’re more like the reader who caught himself “daydreaming about devouring a pint of Belgian chocolate ice cream from Häagen-Dazs.”
In the right context, either can inspire gratitude, balance, and connection for a good life.
Until next time!
Erin
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The information provided about wellness and health is for general informational and educational purposes only. We are not licensed medical professionals, and the content here should not be considered medical advice. Talk to a doctor before trying any of these suggestions.
