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Inhibition of bone turnover by milk intake in postmenopausal women

  • Jean-Philippe Bonjour (a1), Marion Brandolini-Bunlon (a2), Yves Boirie (a2), Françoise Morel-Laporte (a2), Véronique Braesco (a2), Marie-Claude Bertière (a3) and Jean-Claude Souberbielle (a4)...

Increased postmenopausal bone turnover leads to bone loss and fragility fracture risk. In the absence of osteoporosis, risk preventive measures, particularly those modifying nutritional lifestyle, are appropriate. We tested the hypothesis that milk supplementation affects bone turnover related to biochemical markers in a direction that, in the long term, may be expected to reduce postmenopausal bone loss. Thirty healthy postmenopausal women aged 59·3 (sd 3·3) years were enrolled in a prospective crossover trial of 16 weeks. After a 4-week period of adaptation with diet providing 600 mg calcium plus 300 mg ingested as 250 ml semi-skimmed milk, participants were maintained during 6 weeks under the same 600 mg calcium diet and randomized to receive either 500 ml semi-skimmed milk, thus providing a total of 1200 mg calcium, or no milk supplement. In the next 6 weeks they were switched to the alternative regimen. At the end of the each period, i.e. after 4, 10 and 16 weeks, blood and urinary samples were collected. The changes in blood variables between the periods of 6 weeks without and with milk supplementation were: for parathyroid hormone, − 3·2 pg/ml (P = 0·0054); for crosslinked telopeptide of type I collagen, − 624 pg/ml (P < 0·0001); for propeptide of type I procollagen, − 5·5 ng/ml (P = 0·0092); for osteocalcin, − 2·8 ng/ml (P = 0·0014). In conclusion, a 6-week period of milk supplementation induced a decrease in several biochemical variables compatible with diminished bone turnover mediated by reduction in parathyroid hormone secretion. This nutritional approach to postmenopausal alteration in bone metabolism may be a valuable measure in the primary prevention of osteoporosis.

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*Corresponding author: Professor Jean-Philippe Bonjour, fax +41 223829973, email
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