- Scientists have discovered why obesity causes high blood pressure.
- The loss of a beneficial type of fat called beige fat is key.
- This loss triggers a genetic program that stiffens arteries.
- An enzyme called QSOX1 drives this harmful process.
- Preserving beige fat could lead to new, targeted treatments.
Doctors have long known that carrying excess weight can lead to hypertension, a major driver of heart attacks and strokes, yet the precise biological reason why fat wreaks such havoc on blood vessels remained a frustrating mystery. Now, scientists at The Rockefeller University in New York have cracked a crucial part of the code. Their research reveals it’s not just any fat, but the loss of a specific, beneficial type called beige fat that can send blood pressure skyrocketing by directly stiffening our arteries.
The study, published in the journal Science, provides a long-sought mechanism for a deadly chain reaction. Cardiovascular disease is the world’s leading cause of death, and hypertension is a primary contributor. "We've known for a really long time that obesity raises the risk of hypertension and cardiovascular disease, but the underlying biology has never been fully understood," said Dr. Paul Cohen, head of the laboratory that conducted the research. His team’s work now suggests that preserving or activating our body’s beige fat could be a key to breaking that chain.
The power of thermogenic fat
Unlike white fat, which simply stores calories, beige fat and its close relative brown fat are metabolically active. They burn energy to generate heat. Humans are born with brown fat, which helps infants stay warm, and adults can develop beige fat through factors like cold exposure and exercise. Previous observational studies had hinted that people with more of this thermogenic fat had lower blood pressure, but correlation is not causation. To prove beige fat played a direct role, the Rockefeller team turned to genetically engineered mice.
They created mouse models that were otherwise healthy but completely lacked the ability to form beige fat. "We wanted the only difference to be whether the fat cells in the mouse were white or beige," explained study co-author Mascha Koenen, a postdoctoral fellow. "In that way, the engineered mice represent a healthy individual who just happens to not have brown fat." The change was far from minor. These mice developed hypertension and showed early signs of heart damage.
A cascade of stiffness
The consequences were clear in their blood vessels. The fat surrounding the arteries began acting like white fat, producing a precursor to a hormone that increases blood pressure. More strikingly, the vessels themselves became hypersensitive to pressure signals. The researchers found the loss of beige fat triggered a genetic program promoting fibrosis, a process where stiff, fibrous tissue builds up around blood vessels. This makes arteries less flexible, forcing the heart to pump harder and raising blood pressure.
The critical linchpin in this process turned out to be an enzyme called QSOX1. The team discovered that healthy beige fat normally suppresses QSOX1. When beige fat is lost, however, the enzyme is overproduced. To confirm, they engineered mice lacking both beige fat and the QSOX1 enzyme. These mice did not develop the vascular dysfunction or high blood pressure, pinpointing QSOX1 as the culprit.
The relevance to humans appears strong. The researchers noted that in existing clinical data, people with mutations in the PRDM16 gene—the same gene whose loss activates QSOX1 in mice—tend to have higher blood pressure. This translation from mouse models to human genetics strengthens the potential impact of the finding.
This work shifts the paradigm from viewing fat as a passive villain to understanding its complex types and functions. It underscores that the quality of our fat matters deeply. The findings open a new frontier for developing precise therapies. "The more we know about these molecular links, the more we can move towards conceiving of a world where we can recommend targeted therapies based on an individual’s medical and molecular characteristics," Cohen said.
For millions managing hypertension, often with generic dietary and drug advice, this research offers a more nuanced vision of the future. It suggests a day might come when treatment is tailored not just to a blood pressure reading, but to the specific biological profile of a patient’s own fat tissue. In the relentless fight against heart disease, understanding the protective color of our fat could finally provide a smarter path to turning down the pressure.
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