Effects of Smoking on Bone and Mineral Metabolism

Abstract

Many studies have confirmed Daniell’s observation in 1976 that postmenopausal women who smoke have more fractures and less bone than postmenopausal women who do not smoke. Comparison of the bone density of smokers with that of their nonsmoking twins perhaps makes the point most strongly. There are many potential causes of these differences, including less calcium and vitamin D intake and less physical activity in smokers compared with nonsmokers. There is also evidence for direct toxic effects of smoking on bone cells. Decreased new bone formation in smokers has been suggested by decreased biochemical bone marker levels in several studies. Impaired osteoblastic proliferation, differentiation, and function in vitro have also been described. A few studies found an increase in bone resorption but most did not. Several authors have reported decreased intestinal calcium absorption efficiency in smokers. This is most likely caused by low levels of serum calcitriol (1,25-dihydroxyvitamin D), the hormone that controls calcium absorption. Although many smokers also have low levels of the storage form of vitamin D, 25-hydroxyvitamin D [25(OH)D], this does not appear to be the cause of their low serum calcitriol. Most studies, but not all, indicate that serum parathyroid hormone (PTH) is suppressed in smokers, and this is most likely the cause of both the low serum calcitriol and decreased calcium absorption. Why PTH is decreased is not clear. It could be because of increased degradation or decreased production of PTH. Two studies report normal serum ionized calcium levels in smokers, but one suggests ionized calcium levels are increased, which might cause a secondary decrease in serum PTH. Management of the increased bone loss found in smokers will remain empirical until its causes are better understood.