At Mount Sinai, researchers have uncovered something that feels almost too simple to be true: getting enough sleep and moving your body regularly can quiet the cancer-like mutations brewing silently in your blood cells. For the millions of people over 70 who carry these genetic glitches—and that's one in four of us—the finding offers something rare in medicine: a path forward that doesn't require a pill, just a lifestyle.
These mutations, collectively called clonal hematopoiesis, accumulate over decades in the bone marrow cells that manufacture white blood cells. When they occur, the mutant cells start multiplying too fast and become hyperinflammatory, damaging tissues throughout the body and accelerating atherosclerosis, the hardening of arteries that leads to heart disease. The condition is quietly widespread: it shows up in about a quarter of people over 70 and in half of all people over 80, yet rarely appears in younger, healthy people.
Until now, scientists had no clear answer to whether the way we live—how we sleep, whether we exercise—could actually change what these mutant cells do. Mount Sinai's Cardiovascular Research Institute, led by Dr. Cameron McAlpine, decided to find out. They analyzed data from nearly 83,000 participants in the UK Biobank and another 8,404 from All of Us, the National Institutes of Health's diverse dataset. They also ran extensive tests in mice, watching how sleep fragmentation and exercise affected cells carrying mutations in genes like Jak2 and Tet2.
What they discovered was striking: moderate-to-vigorous physical activity reduced the incidence of clonal hematopoiesis overall, and sufficient sleep actually "turned off" the harmful effects of certain mutant white blood cells. The mutant cells stopped proliferating so aggressively. They behaved more like normal, healthy cells. Dr. Teresa Gerhardt, the study's lead author, describes it plainly: "A healthy lifestyle can mitigate clonal expansion and the atherosclerotic consequences of mutations, making mutant cells behave like healthy, nonmutated cells."
The mechanism matters too. In immune cells called macrophages—which normally roam tissues looking for germs and damaged cells—those carrying a Jak2 mutation instead promote atherosclerosis and cardiovascular disease. But when people get adequate sleep, something remarkable happens: sleep represses the inflammatory pathways that make these macrophages dangerous. Healthy sleep appears to selectively target only the mutant cells, leaving normal ones untouched.
McAlpine put it this way: "We've discovered that healthy sleep and exercise can selectively influence immune cells with clonal hematopoiesis mutations, repressing their proliferative programming and expansion, as well as their ability to promote the formation of harmful plaque in the arteries of the heart." The surprise here is that these cells are not fixed, not destiny. They're malleable, responsive to how we live.
The study, published in Nature, reframes a piece of aging that felt inevitable—the accumulation of mutant white blood cells—as something we might actually influence. It's a reminder that the most powerful medicine is sometimes the simplest: rest and movement, repeated through the seasons of our lives. For aging people watching their health with growing concern, the message is hopeful. You are not powerless against your own mutations. How you live still matters.