Can statins (cholesterol-lowering drugs) affect your bones?

In laboratory and animal research, statins stimulate a protein that activates bone-forming cells, thereby promoting bone mineralisation. In rat studies following removal of the ovaries, bone density increased slightly in spongy bone, although compact bone remained unchanged. This mechanism sounds promising, but the question is whether it also occurs in humans.

In humans, the results are mixed. An Australian study of 1,375 women found a 60% lower risk of fractures in statin users, an effect too large to be explained by bone density alone. A systematic review with meta-analysis found a 23% lower fracture risk in observational studies. However, that same meta-analysis found no effect in randomised trials (odds ratio 1.03), and the authors explicitly point to bias from study design and possible publication bias as explanations for the positive signal seen in observational studies.

The largest study, the Women's Health Initiative with nearly 94,000 postmenopausal women, found no difference in hip, wrist, or other fractures between statin users and non-users, even with long-term use. Bone density of the hip and spine also did not differ meaningfully.

A likely reason why the laboratory effect does not carry over to humans is that statins are largely absorbed by the liver and barely reach bone tissue at a sufficiently high concentration. Multiple review authors therefore conclude that statins cannot currently be recommended as a means of preventing bone loss or fractures.