Alcohol and bone disease

Alcohol is considered to be an important risk factor for various bone diseases but recent studies have shown that moderate alcohol intake can be beneficial to bone structure. Alcohol decreases osteoblastic activity, leading to decreased bone formation and defective mineralization. The changes reported in calciotropic hormones, mainly vitamin D and parathyroid hormone, are observed due in part to a deficient intestinal absorption of vitamin D and an inadequate synthesis of its hepatic metabolite, although greater emphasis has been given to dietary deficiencies or lack of exposure to sun. The changes in parathyroid hormone are not consistent and since there is no greater incidence of hyperparathyroidism in alcoholic patients, it suggests that alcohol does not have a long-term effect on the parathyroid glands. Alcohol increases calcitonin secretion acutely; calcitonin is an inhibitor of bone resorption and may be the mechanism by which moderate alcohol intake protects bone structure. Alcohol increases urinary calcium, magnesium and zinc excretion. Zinc deficiency has been postulated as a cause of oesteoporisis because it causes hypogonadism. The decrease in the levels of the gonadal hormones and the increase of cortisol, observed in chronic alcoholics, may indirectly cause osteopenia and aseptic necrosis. To these actions must be added the acidosis due to alcohol and the greater tendency of the alcoholic to fall, all of which influence bone changes and increase the incidence of bone fractures.