Bone mineral changes during pregnancy and lactation (original) (raw)
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The Effects of Pregnancy and Lactation on Bone Mineral Density
Osteoporosis International, 2001
We performed a prospective study of bone mineral density (BMD) in 38 women during their first full-term pregnancy until 12 months postpartum. BMD measurements at lumbar spine [L2-L4 (LS)] and forearm [distal 33% (RD) and ultradistal (RUD) region of the radius] were made within 3 months before conception, after delivery, and at 6 and 12 months postpartum. In mid-pregnancy the DXA examination was carried out only at the forearm. Patients were grouped according to duration of lactation as group I, II or III (0-1, 1-6, 6-12 months respectively). During pregnancy there was a significant difference between baseline and delivery (p< 0.001) in the LS, RUD and RD BMD values. In group I there was no statistically significant difference in LS BMD between visits following pregnancy. The RUD BMD loss was recovered by 6 months postpartum (PP6). Group II showed continuous bone loss from delivery until PP6 at LS and RUD. In group III the LS BMD loss continued throughout the lactation period. The RUD BMD dropped (4.9%) until PP6 then increased by 3.0% as measured at 12 months postpartum (PP12). There was no significant change in RD BMD in any of three groups during lactation. At LS bone loss between delivery and PP12 correlated well with the duration of lactation (r = 70.727; p<0.001). We suggest that calcium needed for fetal skeletal growth during pregnancy was gained from maternal trabecular and cortical sites and that calcium needed for infant growth during lactation was drawn mainly from the maternal trabecular skeleton in our patients. The effect of pregnancy and lactation on the maternal bone mass was spontaneously compensated after weaning.
Changes in Bone Mineral Density During Pregnancy and Postpartum: Prospective Data on Five Women
Osteoporosis International, 1999
Areal bone mineral density (BMD, g/cm 2 ) of five healthy women (aged 26-30 years) was measured at the lumbar spine, right femoral neck and dominant distal radius with dual-energy X-ray absorptiometry before pregnancy, immediately after delivery, 1 month after the resumption of menses and 1 year thereafter. Because of the small number of subjects, only individual changes in BMD that were greater than 2H2 times the short-term in vivo precision were considered as significant changes. To obtain a further perspective, the reproduction-related BMD changes were compared with twice the standard deviation (SD) of the BMD changes in healthy premenopausal women (about ± 5%), and with the SD of the BMD in a cross-sectional sample of young healthy women. The duration of postpartum amenorrhea (PPA) and of lactation in our subjects ranged from about 2 months to 1 year and from 5 months to almost 2 years, respectively. No clear association between PPA and lactation could be seen. The magnitudes of reproductionrelated BMD changes in general seemed not to differ substantially from about ± 5% variability in BMD changes in healthy nonpregnant and nonlactating women. There was, however, some tendency toward systematic bone loss at the lumbar spine (about -3%) during pregnancy and at the femoral neck during PPA (about -5% as compared with prepregnancy data). Some individuals can yet show large, systematic bone losses comparable to 1 SD in magnitude. The site-specific reproduction-induced bone loss and consequent recovery are apparently multifactorial phenomena that may be related not only to duration and magnitude of lactation and/or duration of postpartum amenorrhea, but also to prevailing biomechanical and dietary factors, and other yet unknown individually modulated factors.
Pregnancy and Lactation Confer Reversible Bone Loss in Humans
Osteoporosis International, 2001
The influence of pregnancy on bone mineral density (BMD) was evaluated by dual-energy X-ray absorptiometry (DXA) in 73 women (mean age 29 years, range 20-44 years) postpartum. Fifty-five age-matched women served as controls. The influence of lactation was evaluated in 65 of the delivered women who were followed with repeated measurements, a mean of 4.5 + 0.1 and 11.5 + 0.1 months after the delivery. The influence of multiple pregnancies was evaluated in 39 premenopausal women (mean age 38 years, range 31-54 years) with a minimum of four pregnancies (range 4-7). Fifty-eight age-matched healthy premenopausal women with a maximum of two pregnancies (range 0-2) served as controls. Data are presented as mean + SEM. BMD data are adjusted for differences in total fat mass and total lean mass. Lumbar spine BMD was 7.6 + 0.1% and total body BMD 3.9 + 0.1% lower in women postpartum compared with controls (both p<0.001). BMD did not decrease significantly in non-breastfeeding mothers. Mothers breastfeeding for 1-6 months decreased femoral neck BMD by 2.0 + 1.0% during the first 5 months postpartum (p<0.001). No further BMD loss was seen between 5 and 12 months postpartum. Femoral neck BMD 12 months after delivery was 1.3 + 0.8% lower than after delivery in mothers breastfeeding for 1-6 months (p = 0.05). Mothers breastfeeding for more than 6 months decreased Ward's triangle BMD by 8.5 + 1.0% and lumbar spine BMD by 4.1 + 0.8% during the first 5 months postpartum (both p<0.05). No further BMD loss was seen between 5 and 12 months postpartum. Femoral neck BMD 12 months after delivery was 4.0 + 1.1% lower and Ward's triangle BMD 5.3 + 1.9% lower than after delivery in mothers breastfeeding for more than 6 months (both p<0.05). BMD loss was higher during the first 5 months following delivery in the lactating women compared with the nonlactating women (p< 0.05 comparing lumbar spine BMD loss in lactating mothers versus non-lactating mothers). However, in women with a minimum of four pregnancies the BMD was no lower than in age-matched women with fewer pregnancies. Total duration of lactation was not correlated with the present BMD. In summary, pregnancy seem to confer a low BMD with additional BMD loss during 5 months of lactation. Even if complete restoration in BMD was not reached within 5 months of weaning, women with four pregnancies or more had a BMD no lower than women with two pregnancies or fewer. We conclude that neither an extended lactation period nor multiple pregnancies could be used as a risk factor when predicting women at risk for future osteoporosis.
The Journal of nutrition, 2000
The objective of this work was to compare long-term changes in bone mineral in lactating (L) and nonlactating (NL) women for 2 y postpartum. The 40 L women (mean duration of breastfeeding 345 +/- 177 d) and 36 NL women were enrolled during late pregnancy. Subjects were healthy and nonsmoking with a mean age of 28.8 +/- 4.1 y. Bone mineral content (BMC) was measured at 0.5, 3, 6, 12, 18 and 24 mo by dual-energy X-ray absorptiometry set for total body scan with regional analysis. BMC adjusted for bone area, weight and height (adj-BMC) decreased in L women at the lumbar spine (-3.1%, P < 0. 001) and pelvis (-0.9%, P = 0.03) by 3 mo, and at the total body (-0. 9%, P = 0.05) by 6 mo. Losses were recovered following onset of menses. Adj-BMC at the lumbar spine, pelvis, thoracic spine and total body increased over baseline by 24 mo in L women. In NL women, adj-BMC increased over baseline within 3 mo and continued to increase thereafter. Net total-body gains were greater in the 27 NL wom...
2000
The objective of this work was to compare long-term changes in bone mineral in lactating (L) and nonlactating (NL) women for 2 y postpartum. The 40 L women (mean duration of breastfeeding 345 Ϯ 177 d) and 36 NL women were enrolled during late pregnancy. Subjects were healthy and nonsmoking with a mean age of 28.8 Ϯ 4.1 y. Bone mineral content (BMC) was measured at 0.5, 3, 6, 12, 18 and 24 mo by dual-energy X-ray absorptiometry set for total body scan with regional analysis. BMC adjusted for bone area, weight and height (adj-BMC) decreased in L women at the lumbar spine (Ϫ3.1%, P Ͻ 0.001) and pelvis (Ϫ0.9%, P ϭ 0.03) by 3 mo, and at the total body (Ϫ0.9%, P ϭ 0.05) by 6 mo. Losses were recovered following onset of menses. Adj-BMC at the lumbar spine, pelvis, thoracic spine and total body increased over baseline by 24 mo in L women. In NL women, adj-BMC increased over baseline within 3 mo and continued to increase thereafter. Net total-body gains were greater in the 27 NL women who completed the final measurement than in their 26 L counterparts (ϩ2.3% vs. ϩ0.6%, P ϭ 0.001). Net regional gains differed at the head, legs, and ribs, but not at the lumber spine, pelvis or thoracic spine. Duration of breastfeeding, parity, onset of menses and maternal age affected bone changes in L women. These results indicate that lactation delays bone mineral accretion and temporarily alters its regional distribution in postpartum women. J. Nutr. 130: 777-783, 2000.
Factors Underlying Changes in Bone Mineral During Postpartum Amenorrhea and Lactation
Osteoporosis International, 2000
To determine the physiologic and habitual factors that may modulate changes in bone mineral density (BMD) postpartum, dual-energy X-ray absorptiometry was performed at the lumbar spine, right femoral neck and dominant distal radius immediately after delivery, after resumption of menses, and 1 year thereafter in a cohort of 41 healthy postpartum Finnish women aged 31.5 (SD 4.6) years. Mean durations of lactation and postpartum amenorrhea (PPA) were 7.7 (3.7) and 5.9 (2.9) months, respectively. After PPA, signi®cant bone losses of 2%±4% were observed at the lumbar spine and femoral neck. Duration of PPA and different lactational variables explained (adjusted R 2 ) from 21% to 27% of the variability in changes in BMD during PPA. A recovery to postpregnancy BMD levels was observed at the lumbar spine; in contrast BMD at the femoral neck showed only a partial recovery. The duration of unsupplemented lactation was weakly (adjusted R 2 = 0.13) associated with recovery at the lumbar spine, while a long duration of total lactation also showed a weak association (adjusted R 2 = 0.02) with delayed recovery at the femoral neck. In conclusion, a systematic bone loss occurs during PPA, and after resumption of menstruation BMD recovers despite continued lactation. However, the time of bony recovery back to postpregnancy level seems to be modulated slightly by lactation habits. It is obvious that the control of postpartum BMD changes is a multifactorial process that may be speci®c to the skeletal site of interest.
[Osteoporosis in pregnancy and lactation]
Medicina, 2000
Normal pregnancy and lactation lead to a combination of adaptive metabolic responses, the end result of which is to assure adequate delivery of mineral to the fetus while affording protection to the maternal skeleton. Elevated circulating levels of 1.25-OH vitamin D lead to increased efficiency of maternal intestinal calcium absorption and possibly lead to hypersecretion of calcitonin. Although serum concentrations of parathyroid hormone do not change during pregnancy, increased levels of a related hormone, PTH-related peptide, seem to contribute to a state of maternal functional hyperparathyroidism and maintain the fetal-maternal calcium gradient necessary to provide calcium to the fetus. Bone turnover increases during lactation and diminishes urinary calcium loss mobilizing mineral for the milk. Elevated levels of ionized calcium and phosphorus possibly correlate with increased bone resorption and decreased urinary excretion of these minerals. Bone mass is not normally lost during...
Pregnancy and lactation, a challenge for the skeleton
Endocrine Connections, 2020
In this review we discuss skeletal adaptations to the demanding situation of pregnancy and lactation. Calcium demands are increased during pregnancy and lactation, and this is effectuated by a complex series of hormonal changes. The changes in bone structure at the tissue and whole bone level observed during pregnancy and lactation appear to largely recover over time. The magnitude of the changes observed during lactation may relate to the volume and duration of breastfeeding and return to regular menses. Studies examining long-term consequences of pregnancy and lactation suggest that there are small, site-specific benefits to bone density and that bone geometry may also be affected. Pregnancy- and lactation-induced osteoporosis (PLO) is a rare disease for which the pathophysiological mechanism is as yet incompletely known; here, we discuss and speculate on the possible roles of genetics, oxytocin, sympathetic tone and bone marrow fat. Finally, we discuss fracture healing during pre...
Journal of Bone and …, 1995
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 [PI = 8) consuming 13-2.4 g of Ca/day from diet + prenatal supplement. Study periods were baseline, 5 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],D); 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-43% (P) (p < 0.04) and-63% (Ca) (p < 0.01) at the lumbar spine (L2-U) 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-U (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 (+ll%,p < 0.005) as was PRL (+81%,p < 0.001). Indicators of calcium metabolism were higher postweaning than lactation for PTH (+4wo,p < 0.01) and 25(OH)D (+45%, p < 0.02) but not for 1,25(OH),D. 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),D postweaning. Loss of estrogen during lactation and a return postweaning may play an important role.