Osteoporosis: May Doping Cause It?

Abstract

Doping is defined as the use of substances or techniques to illegally improve athletic performance. Considering the relatively high prevalence of usage, and the pleiotropic actions exerted by doping agents, it is conceivable that chronic exposure might increase the risk of potential long-term complications, including osteoporosis, which is a frequent side effect of many substances, also used as doping agents. Nevertheless, with the exception of athletes using anabolic androgenic agents, which display an increased bone mineral content and density, and extremely low fracture rate, turning into increased osteoporosis, and hip or vertebral fracture rates, at withdrawal, scant investigation has been performed in athletes with the current use or history of doping. Conversely, other commonly used doping substances have been proven to negatively impact on bone status, in different pathological conditions which might be used as a surrogate model of doping in athletes. In particular, aromatase inhibitors use for the treatment of late-onset hypogonadism in elderly men might represent a suitable model to depict the potential adverse effects on bone of aromatase inhibitors used as performance-enhancing drugs, although partially controversial evidences are available concerning the effects on bone health. More convincing is the model of women with breast cancer administered with aromatase inhibitors, displaying increased bone resorption, decreased bone mineral density at the femoral neck and lumbar spine, and increased risk of fractures, although these effects seem to be reversible, at discontinuation of treatment. Growth hormone excess in acromegalic patients, leading to alteration of bone trabecular microstructure, might be responsible for the associated bone impairment, represented by osteoporosis, arthralgia, and osteoarthritis, and is associated to an increased risk of vertebral fractures, in acromegalic patients, compared to the general population, with a slight predominance in men. Moreover, a direct action of growth hormone on bone turnover is confirmed by the fact that bone markers are significantly higher in healthy volunteers treated with growth hormone, and are efficiently measured in blood as a marker for growth hormone abuse in athletes. Indirect evidences from studies on subjects using β2-adrenergic receptor agonists for respiratory disorders, or β-adrenergic receptor blockers for the treatment of cardiovascular diseases, and reporting increased or reduced risk for fractures, respectively, suggest that β2-adrenergic receptor agonists might decrease osteoblastic activity and increase bone resorption. Lastly, glucocorticoid doping, which is well modelled by the use of glucocorticoid as anti-inflammatory or immunosoppressive therapy and by the hypercortisolism in Cushing’s syndrome, might also determine bone status impairment, as suggested by osteopenia, osteoporosis, and skeletal fractures, which are frequently reported as disease comorbidities, and by the reduced bone mineral density, which successfully improves after hypercortisolism remission.