Abstract

A randomized clinical intervention trial to determine effects of lactation and 1 g of calcium (Ca) on bone remodeling was conducted in 15 women (calcium = 7, placebo [P] = 8) consuming 1.3–2.4 g of Ca/day from diet + prenatal supplement. Study periods were baseline, ≤2 weeks postpartum; lactation, 3 months lactation; and postweaning, 3 months postweaning. Bone mineral density (BMD) corrected for body weight was determined by dual‐energy X‐ray absorptiometry (DXA). Indicators of calcium metabolism, bone turnover, and lactation were measured: calcium metabolism, parathyroid hormone (PTH), 25‐hydroxyvitamin D (25[OH]D), 1,25‐dihydroxyvitamin D (1,25[OH]2D); bone turnover, formation, procollagen I carboxypeptides (PICP), osteocalcin, and bone alkaline phosphatase (B‐ALP), resorption, tartrate resistant acid phosphatase (TRAP); and lactation, prolactin (PRL). Mean BMD changes differed by site: baseline to lactation –4.3% (P) (p < 0.04) and –6.3% (Ca) (p < 0.01) at the lumbar spine (L2–L4) and 5.7% gains of the ultradistal (UD) radius (Ca) (p < 0.04); lactation to postweaning, –6% to –11% at all sites of the radius and ulna (Ca, P) (p < 0.04) +3% at L2–L4 (Ca) (p < 0.03); baseline to postweaning, (UD) radius –5.2% (P) (p < 0.03), UD radius + ulna –6% to –8% (Ca, P) (p < 0.04) but no significant loss of L2–L4 or total body. Bone turnover markers were higher at lactation than postweaning: PICP (+34%, p < 0.001), osteocalcin (+25%, p < 0.01), TRAP (+11%, p < 0.005) as was PRL (+81%, p < 0.001). Indicators of calcium metabolism were higher postweaning than lactation for PTH (+40%, p < 0.01) and 25(OH)D (+45%, p < 0.02) but not for 1,25(OH)2D. There were no differences between P or Ca for indices of calcium metabolism, bone turnover, or PRL. An increase in markers of bone turnover and a loss of BMD of the spine during lactation appears to be part of the physiological changes of lactation and not preventable by increasing calcium intake above the recommended dietary allowance (RDA). A return of BMD toward baseline of the spine but not the arm, was associated with an increase in PTH without an increase in 1,25(OH)2D postweaning. Loss of estrogen during lactation and a return postweaning may play an important role.

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