Dr. Nicholas Norwitz writes a best-selling science newsletter, StayCurious Metabolism, where he strives to empower readers with deep knowledge of cutting-edge health science.
In a recent trial, researchers put a popular weight-loss drug head-to-head with plain exercise to see which did more for the arteries. Over the course of a year, exercise reversed cardiovascular disease.
Exercise lowered inflammation and shrank arterial plaque on imaging. The drug did not.
The results, published in Nature Metabolism, point to something the cholesterol-and-drug model of heart disease tends to miss: Two of the most powerful tools for protecting your heart cost nothing, and they work through mechanisms most people have never had explained to them—including most doctors.
Medical school does not teach these mechanisms. Let’s dig into the data.
The Clones in Your Bones
The story begins in a place you may not associate with heart disease: your bone marrow, the spongy tissue inside your bones that manufactures blood cells.
Picture healthy marrow as a diverse ecosystem, with thousands of cell lineages coexisting. Now imagine one of those lineages picking up a random mutation that gives it a survival advantage. It stops playing nice, expands like an invasive species, and slowly crowds out its neighbors. Scientists call this “clonal hematopoiesis”—“clonal” for clones, and “hematopoiesis” for the production of blood cells. If that sounds a little like cancer, you are not wrong. It is not cancer, but it follows the same plot: a population of cells gains an edge and outcompetes the rest.
Here is why it matters for your heart. The lineages that tend to win this competition are the aggressive, inflammatory ones—and they do not stay in the marrow. They travel into the walls of your arteries, where they help drive atherosclerosis: the buildup of plaque that narrows and stiffens arteries and eventually leads to heart attacks and strokes.
An article published in Nature put the consequence bluntly: Clonal hematopoiesis stokes inflammation and raises the risk of atherosclerosis.
This is not some rare, exotic condition. It becomes more common with each decade of life and is quietly present in a meaningful fraction of older adults, almost all of whom have never heard of it. Think about it: You have probably spent years being told to fixate on your cholesterol number. Odds are, nobody ever mentioned the inflammatory cells that may be doing more of the actual damage.
That knowledge could be quietly empowering because it’s a process you can change—just not with a pill.
What Sleep and Exercise Do
Start with the human evidence. Researchers combined two very large databases—the UK Biobank and the All of Us Research Program in the United States—for more than 90,000 people. Physical activity was measured with wearable monitors rather than self-report, making the data more trustworthy.
Here’s the first reveal: More moderate-to-vigorous activity tracked with less clonal hematopoiesis.
A pattern that held in men and women and across both databases.
The obvious caveat is that people who exercise tend to be leaner and healthier to begin with, so of course their blood looks “cleaner.” Right? But the link held even after the researchers adjusted for body weight. Exercise was not simply working through the number on the scale; it appeared to be reaching the mutant clones themselves.
The biological story gets even more interesting. Exercise did not suppress blood-cell production across the board—and you would not want that. You would become anemic and immunodeficient. Instead, exercise showed precision effects—like a scalpel, not a sledgehammer. Exercise selectively held back certain harmful clones while leaving normal blood-cell production intact.
What about the other hallmark of healthy living, addressed by the study—the yin to exercise’s yang—sleep?
Sleep pulled in the same direction, from a complementary angle. Disrupted sleep makes clonal hematopoiesis worse. That aligns with what we know about night shift work, which is associated with about a 15 percent to 30 percent increased risk of cardiovascular events, such as heart attacks and strokes. Conversely, a good night’s sleep should control these clones in your bones and arteries.
So two of the most ordinary features of daily life—how you move and how you sleep—converge on the same hidden biology to protect your heart.
Before we get to our groundbreaking second study—the one we teased in the opening of this article- I want to give you a taste of how scientific researchers actually dissect these mechanisms. Let’s discuss the experiment in more detail.
How Can Running or a Good Night’s Sleep Target Mutant Cells?
First off, there are certain experiments you cannot do in humans for ethical reasons. In this case, you cannot ethically mutate the stem cells of living people. So we need to turn to animal models to better understand the mechanism. Here, the researchers engineered mice with about 10 percent mutant blood and then randomly assigned them to three conditions: sedentary, exercise, or fragmented sleep. Over 12 weeks, they tracked how far the mutant clones expanded.
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In the sedentary mice, the clones steadily grew.
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In the exercising mice, the expansion of some mutants stopped almost completely, with the share of mutant cells barely moving.
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In the sleep-fragmented mice, the clones grew faster than in any other group.
The effects did not stop in the marrow. Sleep and exercise also changed how these mutant inflammatory cells behaved once they reached the arteries.
Fragmented sleep raised levels of a receptor on the mutant clones that triggers an inflammatory cascade inside the artery wall. Exercise, for its part, activated neurons deep in the brainstem that adjust hormones such as noradrenaline. Those hormones bind to receptors on macrophages, the immune cells that patrol our tissues, and effectively tune down inflammation directly in the arteries.
So—and this is important, so do not miss it—sleep and exercise protect the arteries on two fronts each:
1. They slow the growth of inflammatory clones in the marrow.
2. They calm those clones once they have entered the artery wall.
In the mice, this translated into what you actually care about. Fragmenting sleep made arterial plaque worse. Adding exercise made it smaller. Again, there are limitations to the controlled experiments we can perform in humans; however, these pathways are conserved, and there’s no reason that this would not translate to us as well.
It’s very likely that sleep and exercise directly protect your arteries by changing the inflammatory and immune landscape throughout your body.
Do the Findings Hold Up in People?
We do have some gold-standard human data suggesting that, not only does exercise prevent cardiovascular disease, but it might even reverse it.
In the recent study published in Nature Metabolism, researchers randomly assigned 130 adults to 52 weeks of one of four programs: a placebo, structured exercise, a GLP-1 medication (liraglutide, from the same drug class as today’s popular weight-loss injections), or exercise plus the medication. To track arterial disease, they measured carotid intima-media thickness (cIMT), which uses ultrasound to measure arterial plaque.
The result? Exercise lowered inflammation and reduced plaque levels by 7 percent, as measured by cIMT, over the year. The drug on its own showed a hint of benefit that fell short of significance. The authors concluded that the artery wall responded more to the effects of exercise than to the medication.
What You Can Do
The practical advice is somewhat unglamorous.
Exercise
Aim for at least 150 minutes per week of moderate-to-vigorous physical activity. That’s not an arbitrary target. It’s the exact intensity range that was associated with fewer inflammatory clones in the large human datasets discussed above.
Practically speaking, that means that accumulating roughly 30 minutes per day, five days per week, of exercise that noticeably elevates your heart rate and breathing. Brisk walking uphill, jogging, cycling, rowing, swimming, and vigorous sports all qualify.
I would also strongly encourage incorporating resistance training two to four times per week. Building and maintaining muscle is one of the most powerful investments you can make in long-term health, and it complements the cardiovascular benefits of aerobic exercise.
Sleep
Start with the fundamentals before chasing gadgets and supplements.
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Keep your bedroom cool, dark, and quiet.
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Minimize bright light exposure—especially from screens—in the 60 to 90 minute window before bed.
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Try to maintain a consistent sleep and wake schedule, even on weekends.
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Develop a simple wind-down routine that tells your brain the day is over, whether that’s reading, stretching, journaling, breathing exercises, or some combination thereof.
If you want more advanced information on optimizing sleep efficiency, you can check out this newsletter.
The lesson here is bigger than sleep or exercise.
For decades, we have been taught to think about cardiovascular disease largely through the lens of cholesterol and pharmaceuticals. Those tools are useful. But they are only part of the story.
Deep inside your bones, a quiet evolutionary battle is unfolding. Mutant inflammatory clones compete for territory, spill into your arteries, and help shape your cardiovascular future. Two of the most powerful ways to influence that battle are not found in a pharmacy. They are found in your daily habits.
Every workout is a signal. Every night of quality sleep is a signal. Together, they help reshape the immune landscape of your body, slowing the expansion of harmful clones and reducing the inflammation that drives arterial disease.
That’s why I find this science so exciting. It reminds us that health is not simply something that happens to us. It’s something we can create, day after day, often through choices that seem far too ordinary to matter. Sometimes the most powerful medicines are the ones hiding in plain sight.
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