For at least eight years now, based primarily on animal studies, we have been told that statins provoke bone formation.
On this basis Christoph and others reported in the Journal of the American Medical Association, volume 283, 2000 that current exposure to statins is associated with a decreased risk of bone fractures in individuals age 50 years and older and that this finding has potentially important public health implications. Their study population included 28,340 men and women taking lipid-lowering drugs and was based on observing 3,940 fractures of all kinds.
The basis for my concern about this study has been the observation that, although most statins used in animal bone studies activate a gene promoter for bone osteoblast stimulation, this has never been proven in humans. The natural inclination has been to promote these animal study results in the marketing of statins. However, cooler heads have prevailed by revealing that in the animal studies the oral administration of statins is relatively ineffective.
Subcutaneous or topical administration results in 50 times the effectiveness on bone osteoblast activity than dosing orally.
For human use statins have been designed to selectively target the liver, since it is the primary site of cholesterol synthesis, and when taken orally, they undergo substantial conversion to inactive metabolites during their first passage through the liver. So because of this, the bone stimulating effect noted in animals is simply not significant in humans. With this in mind, one wonders how the study results were derived.
Now Ebru Alemdaroglu and colleagues from Ankara Numune Training and Research Hospital, Turkey report in Rheumatology International (Dec 2008) information that casts further doubt on the advisability of statin use in post-menopausal women.
They studied 107 post-menopausal women aged 45-79 years of age, finding that low levels of total cholesterol, triglycerides, and low-density lipoprotein (LDL) cholesterol are associated with fractures of the vertebrae. Although no mention was made of statin use, the finding that low serum cholesterol is associated with increased proneness for vertebral fractures argues strongly against the deliberate use of statins for lowering of cholesterol in older women.
Alemdaroglu and co-researchers report that neither osteoporosis or bone mineral density had any bearing on vertebral fracture risk - only the low serum lipid levels.
The researchers reason that since cholesterol is the substrate for sex hormones such as estrogen, testosterone and progesterone, decreased LDL levels would be associated with decreased stored estrogen that likely explains the relationship between vertebral fractures and reduced serum lipids. Statin drug use can only worsen this situation.
In support of this concept are the now well-known studies of statin associated erectile dysfunction in men of all ages, showing reduced levels of testosterone and positive response either to supplemental testosterone or elimination of the offending statin.
Duane Graveline MD MPH
Former USAF Flight Surgeon
Former NASA Astronaut
Retired Family Doctor