Scientists have uncovered a crucial biological mechanism linking a specific type of body fat to the dangerous rise in blood pressure, a discovery that could reshape our understanding of hypertension and heart disease. The research reveals that having insufficient amounts of so-called 'beige fat' can cause blood pressure to skyrocket, significantly elevating the risk of serious cardiovascular events like heart attacks and strokes.
The Vital Role of Beige Fat
While it has long been established that obesity can trigger hypertension, the precise biological pathways remained elusive. Now, a team spearheaded by experts at The Rockefeller University in New York has demonstrated how beige fat—a type of fatty tissue that helps burn energy—directly influences the body's blood pressure regulation.
Also known as brown adipose tissue, this fat's primary role is to convert food into body heat, a process activated in cold temperatures to keep us warm. It is typically found in areas like the neck, upper back, around the kidneys, and along the spinal cord. Although humans lose most of this fat after infancy, previous studies indicate it can be regenerated through exercise, quality sleep, and regular exposure to cold.
How Fat Loss Triggers Hypertension
In the study, published in the prestigious journal Science, researchers engineered otherwise healthy mouse models that completely lacked 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. This setup mimicked a healthy individual who simply does not possess brown fat.
The findings were stark. The loss of beige fat made the rodents' blood vessels hypersensitive to powerful pressure signals, driving up blood pressure. The fat surrounding these vessels began expressing markers of white fat, including a critical precursor called angiotensinogen, which is known to increase blood pressure.
All the engineered mice developed hypertension and showed early signs of heart damage, including fibrosis—a stiffening of connective tissue around blood vessels. This process restricts blood flow by making vessels less flexible, forcing the heart to pump harder.
A Molecular Chain Reaction
Advanced single-cell sequencing revealed that cells devoid of beige fat activated a genetic program promoting stiff, fibrous tissue. The researchers concluded that these fat cells release specific signalling enzymes into their environment, which switch on fibrosis-related genes.
One key enzyme, QSOX1—already implicated in cancer research for its role in tissue remodelling—was rapidly produced when beige fat was lost. In healthy conditions, beige fat normally suppresses QSOX1. Its unchecked production triggers a chain reaction culminating in high blood pressure.
Critically, the team highlighted that in existing human clinical cohorts, patients with mutations in the PDM16 gene—whose loss activates QSOX1 in mice—tend to have higher blood pressure. This suggests the mouse study findings translate directly to human biology.
Implications for Public Health and Future Treatment
The discovery comes at a critical time. An estimated 14 million UK adults now live with high blood pressure, a figure that continues to rise. While lack of exercise, poor diet, and excess alcohol are known contributors, the risk posed by chronic stress, particularly among the young, has been under-recognised.
Rates are climbing in younger demographics, with nearly 170,000 people aged 16 to 24 estimated to be living with undiagnosed hypertension. Alarmingly, the British Heart Foundation states that of the 16 million UK adults with high blood pressure, up to half are not receiving effective treatment, and as many as five million remain undiagnosed.
Dr Paul Cohen, the physician-scientist who led the study, said: "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."
The research paves the way for future investigations into how differences in perivascular fat influence disease development. It underscores that it is not just fat, but the type of fat, that critically affects vascular function and systemic blood pressure control, offering a new potential avenue for combating the hypertension epidemic.
