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Surprisingly little if any attention has been given to the role of copper in the aetiology of postmenopausal osteoporosis. For example, Freudenheim et al. (40). investigated relationships between usual intake of energy and 14 nutrients (but not copper) and the bone mineral content of US women 35-65 years of age in a longitudinal and cross-sectional study. They found interactions of bone loss with energy, calcium, phosphorus, protein, vitamin C, vitamin A, magnesium, zinc and a number of B vitamins. The omission of copper from previous investigations of dietary influences on post-menopausal osteoporosis is unwarranted given the well known defects in connective tissue leading to abnormalities of arteries and bone associated with copper deficiency in animals. These abnormalities include stiffness of gait, swelling of joints and lameness and an increase in the incidence of bone fractures.

Osteoporotic lesions in copper deficient sheep have been observed in both experimental studies and in the field . The most frequently described bone lesions in cattle have been attributed to reduced activity of the osteoblasts, which produced thin bone and overgrowth of cartilage. More recently significant decreases in rat bone calcium have been identified during long term dietary deficiencies of copper and manganese. Yuen et al. observed decreased density and fractures in the bones of copper deficient children and these changes in bone structure giving osteoporotic bone with expanded bone ends are probably the result of defective cross-linking of collagen and elastin in the bone. Bone changes which have been described in copper deficiency in children and in Menkes’ syndrome, a genetically determined defect in copper absorption and utilization, are similar to the changes seen in scurvy but the osteoporotic lesions are much more common and the extensive subperiosteal haemorrhage of vitamin C deficiency is missing.

An investigation, therefore, of a possible role of copper deficiency in the aetiology of postmenopausal osteoporosis is indicated especially in the light of the effect of oestrogens in increasing plasma caeruloplasmin – a multifactorial copper protein – two to three fold. An oestrogen effect on copper metabolism could explain the anomaly that despite the efficacy of oestrogens at retarding post menopausal bone loss, these hormones have an indirect or largely unknown effect on bone cells.

In addition prolonged glucocorticoid treatment may lead to a reduction in body copper status by stimulating biliary excretion of copper. The hypothesis that a mild dietary copper deficiency may be implicated in the onset and progression of osteoporosis is also consistent with the epidemiological evidence. Copper may be a limiting nutrient in many western diets . Milk and milk products are the poorest dietary sources of copper and moreover lactose may interfere with copper metabolism. Current recommendations, therefore, for the prevention of osteoporosis may actually be detrimental to health.

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