Statin use associated with slower bone density decline in postmenopausal women
Statins are best known for lowering cholesterol. But new research shows that statin use is associated with a slower decline in bone mineral density in postmenopausal women, through a mechanism that has nothing to do with cholesterol.
After menopause, oestrogen levels fall sharply. This accelerates loss of bone density and can lead to osteoporosis. Hormone therapy is the standard treatment, but many women cannot use it. Researchers investigated whether statins might offer an alternative route to protecting bone.
Two cohorts, one finding
The study, published in Nature Aging, analysed two groups of postmenopausal women aged 55 to 65, one from a hospital in Beijing and one from a hospital in Suzhou. Women taking statins showed a significantly slower annual decline in bone mineral density compared to women receiving no lipid-lowering therapy. Importantly, women taking evolocumab, a different cholesterol-lowering drug, did not show the same bone effect, even though their cholesterol levels were comparable. This points to a mechanism beyond cholesterol reduction.
The pathway inside stem cells
In experiments with mice and with cultured human cells, the researchers traced the effect to a specific population of stem cells in the bone marrow. These cells give rise to the majority of bone-forming cells (osteoblasts) in adults. Atorvastatin promoted the maturation of these stem cells into osteoblasts, but specifically under oestrogen-deficient conditions.
Atorvastatin achieved this via a molecular route distinct from oestrogen signalling. Both pathways appeared to converge on the same bone-promoting growth factor, but by different mechanisms. The researchers emphasise that their findings identify an association and a possible mechanism; they do not yet constitute evidence that statins should be used as a bone therapy in clinical practice. Further research is needed to explore that question.
Search terms to explore further: statin osteogenic differentiation stem cells, oestrogen deficiency bone mineral density, skeletal stem progenitor cells postmenopause