They’re silent, invisible, and now—scientists say—genetically encoded. A groundbreaking discovery has linked specific gene variants to a dramatically increased risk of deadly blood clots, changing how we understand one of the world’s most overlooked killers.
Key Points at a Glance
- Three newly identified gene variants significantly raise blood clot risk
- Carriers of five variants face a 180% higher risk of venous thrombosis
- Unlike previous mutations, these variants appear across global populations
- Findings could revolutionize blood clot prevention and treatment strategies
Venous blood clots—those that form in veins, often in the legs—are one of the most common causes of death worldwide, yet remain overshadowed by their arterial counterparts. But new research out of Lund University in Sweden is casting a spotlight on the genetic drivers of this silent threat. Scientists have now identified three specific gene variants that sharply increase the risk of developing venous blood clots—especially when combined.
Using genomic data from nearly 30,000 participants in the Malmö Diet and Cancer Study, researchers pinpointed variants in the ABO, F8, and VWF genes. Each variant alone raises the risk of venous thrombosis by 10 to 30 percent. But in individuals with five of these variants, the risk jumps a staggering 180 percent. It’s the most significant genetic finding on the subject since the discovery of Factor V Leiden, a mutation found in about 10% of Swedes and long known to increase clotting risk.
“An individual with five of these gene variants has a 180 per cent higher risk of venous thrombosis,” explains lead researcher Bengt Zöller, professor of general medicine at Lund University and specialist at Skåne University Hospital. What’s especially significant is that—unlike Factor V Leiden—these newly identified mutations appear across global populations, making the discovery relevant to people worldwide.
Venous thrombosis typically occurs when blood flow slows or becomes stagnant, often during long periods of inactivity such as bed rest or extended travel. If a clot breaks loose and travels to the lungs, it can result in a pulmonary embolism—a life-threatening emergency. Age, obesity, and inactivity are known risk factors. But now, with the genetic puzzle becoming clearer, researchers hope to redefine risk profiles and treatment strategies.
“I think tailoring treatment based on risk assessment will become increasingly important,” says Zöller. The research opens the door to more personalized decisions about who should receive preventive blood thinners—especially during surgery, pregnancy, or extended immobility.
The study underscores a deeper evolutionary irony. Traits that once offered survival advantages—like reduced bleeding—can become liabilities in today’s sedentary lifestyles. This shift, Zöller notes, is especially relevant in modern societies where inactivity and obesity intersect with inherited risk factors to fuel a growing health crisis.
Beyond genetics, other factors play a role. Tall people, for instance, are more vulnerable to clots due to gravity’s impact on blood return from the legs. Overweight individuals often suffer from impaired venous circulation, and certain diets—especially those rich in ultra-processed foods—may further tip the scales toward clot formation. On the flip side, diets high in omega-3s, like those of commercial fishermen, appear to offer some protection.
As scientists continue to explore how genes influence the duration and intensity of anticoagulant therapy, this discovery marks a major leap forward. It reframes venous thrombosis as not just a lifestyle-related issue, but a genetically primed condition that can be predicted—and potentially prevented—before tragedy strikes.
In the near future, a simple genetic test could identify individuals who carry these risk variants and enable early, tailored interventions. It’s a vision of personalized medicine that could save thousands of lives—and change the way we think about blood clots forever.
Source: Lund University
