Low levels of carotenoids and retinol in involutional osteoporosis.

Previous epidemiological studies conducted in retinol-supplemented subjects showed an association between high serum levels or dietary intake of retinol and risk of hip fracture. On the other side, observational studies revealed that non-supplemented subjects with higher dietary intake of retinol lose less bone with age than subjects with lower intake. This discrepancy, currently unexplained, suggests that nutrition plays a major role in conditioning the effects of retinol on bone. Since retinol is derived from both retinoids--contained in animal food--and carotenoids--contained in vegetables and fruits--we evaluated a possible role of carotenoids in involutional osteoporosis. Therefore, plasma levels of beta-carotene and other carotenoids, in addition to those of retinol, were measured in free-living, non-supplemented, elderly women with or without severe osteoporosis. Plasma levels of retinol and of all carotenoids tested, with the exception of lutein, were consistently lower in osteoporotic than in control women. A weak association was found only between retinol and femoral neck bone mineral density in osteoporotic women. Our study suggests a bone sparing effect of retinol, to which the provitamin A activity of some carotenoids might have contributed.

Marked decrease in plasma antioxidants in aged osteoporotic women: results of a cross-sectional study.

Although recent epidemiological studies found a positive correlation between dietary vitamin C intake and bone mineral density, data on plasma levels of vitamin C or other antioxidants in osteoporotic subjects are scanty. The aim of this study was to evaluate whether antioxidant defenses are decreased in elderly osteoporotic women and, if this is the case, to understand whether osteoporosis is a condition characterized by increased oxidative stress. To answer these questions, plasma vitamins C, E, and A; uric acid; and the enzymatic activities of superoxide dismutase in plasma and erythrocytes and of glutathione peroxidase in plasma were measured in 75 subjects with osteoporosis and 75 controls. Dietary and endogenous antioxidants were consistently lower in osteoporotic than in control subjects. On the other hand, plasma levels of malondialdehyde, a byproduct of lipid peroxidation, did not differ between groups. Our results reveal that antioxidant defenses are markedly decreased in osteoporotic women. The mechanisms underlying antioxidant depletion and its relevance to the pathogenesis of osteoporosis deserve further investigation.