The male hormone testosterone causes arteries to harden and accumulate calcium deposits, explaining why heart disease is more prevalent among men, a new study has revealed.
Heart disease and strokes affect about one person in three and occur when arteries become narrowed and stiffened with calcium deposits. But how this occurs and why men are at increased risk wasn't known.
Now, writing in the journal Scientific Reports, University of Edinburgh researcher Vicky MacRae and her colleagues have shown that testosterone causes the muscle cells found normally in the walls of arteries to partially transform themselves into bone cells and lay down deposits of calcium salts similar to the substances found in the skeleton.
The net result is a thickening and stiffening of the artery wall and a higher risk for heart disease.
The team made the findings by studying samples of heart valve and arteries from human patients as well as cultures of the cells that make up the muscle in the walls of human arteries.
In the arterial specimens, the researchers were able to show that the muscle cells were expressing a chemical receptor that made them responsive to the effects of testosterone.
When the cells were then dosed with the hormone at the same concentrations that would be found in the blood, the cells began to display markers similar to bone cells complete with crystals of calcium salts. But if the testosterone receptor was deactivated in the cells the effect was markedly reduced.
"This shows that testosterone acting on the vessel wall and heart valves can lead to calcification and hardening of the tissue," explains MacRae.
Why the artery wall responds in this way isn't known, but it might be a protective response to injury.
"By laying down calcium, the tissue in the vessel wall may be trying to protect itself from further damage," MacRae says.
The new findings highlight why men are at increased risk of heart disease and may also lead to better screening tests that can predict the likelihood of heart attacks and strokes.
What the research cannot tell us yet is whether the calcification can be undone and the bone-like behaviour of the arterial cells reversed.
"That's the gold standard aim for this work," says MacRae. "But it's really difficult..."