When we think about heart disease, we usually blame things like high blood pressure, high cholesterol, diabetes, smoking, being overweight, or not getting enough exercise.
But scientists have now discovered another important risk factor that comes from inside our own bodies—mutations in our blood stem cells. This condition is called clonal hematopoiesis.
Clonal hematopoiesis happens when tiny changes, or mutations, appear in the stem cells that make our blood. These changes can give some cells an unfair advantage, helping them grow and spread more than normal blood cells.
Over time, a group of these mutated cells can grow in the bloodstream. Although most of these changes are harmless, some of them may cause health problems.
For a long time, researchers didn’t know whether these mutations caused heart disease or were just a result of it. But now, a new study from Spain has found that clonal hematopoiesis can actually lead to heart disease. This research was done by scientists at the National Center for Cardiovascular Research (CNIC) and was published in Nature Medicine.
The team studied more than 4,000 middle-aged people in the PESA-CNIC-Santander study, which has followed these healthy-looking volunteers since 2010. The researchers used advanced scans to check their arteries for a condition called atherosclerosis, where fatty deposits build up inside artery walls and raise the risk of heart attacks and strokes.
They also looked at the volunteers’ blood using sensitive DNA tests to find mutations linked to clonal hematopoiesis. The results showed that people with these mutations were more likely to develop atherosclerosis over time.
Interestingly, it didn’t work the other way around—having atherosclerosis did not cause the mutations. This means the blood mutations are likely a cause, not an effect.
In a related study, the scientists explored a possible treatment. They focused on one common mutation found in a gene called TET2. They worked with researchers in the U.S. to test colchicine, an old drug still used today to treat gout and inflammation.
They found that colchicine helped slow down artery damage in mice with the TET2 mutation. In people, those who had the same mutation and were already taking colchicine for other reasons had fewer heart attacks than those who weren’t taking the drug.
Colchicine is already approved for heart protection and is cheap and easy to find. This makes it a good option for helping people with certain blood mutations.
But the scientists warn that each mutation acts differently, so other treatments may be needed for different gene changes. They hope that more clinical trials will show whether colchicine really works to prevent heart disease in people with TET2 mutations.
This discovery changes how we think about heart disease. It shows that your genes—and how your blood cells behave—can also increase your risk, even if you live a healthy lifestyle. This could lead to new ways to treat and prevent heart disease by targeting the root causes hidden in our DNA.
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