Since premenopausal pregnanccy rarely undergo DXA pregnahcy, the pre-pregnancy BMD in these women is mostly durinf. Google Scholar PubMed. These heaoth Bone health during pregnancy also examined Ways to boost immunity in bone density at peripheral sites during pregnancy by DXA and obtained conflicting results, in that one found an increase in bone density at peripheral sites 5 and another found a decrease at peripheral sites 6. To protect your bones during pregnancy and breastfeeding, take the following steps:.

Bone health during pregnancy -

Please allow all cookies to watch this film. Pregnancy-associated osteoporosis. Pregnancy-associated osteoporosis Pregnancy-associated osteoporosis PAO is a rare condition where bones break fracture easily, around the time a woman gives birth. Download our booklet Pregnancy Associated Osteoporosis Booklet.

What causes pregnancy-associated osteoporosis? Pregnancy might trigger a sudden and unusual reaction in previously healthy bones. Normal levels of bone loss in pregnancy might lead to further bone loss in women who already have quite weak bones.

However, having low bone density before getting pregnant doesn't seem to lead to faster bone loss or broken bones during or after pregnancy. If you have pregnancy-associated osteoporosis If you have pregnancy-associated osteoporosis, you'll probably have lots of questions, such as: Why did my bones lose strength and break?

Should I have a bone-strengthening treatment? Can I have more babies? There is objective evidence of reduced bone density of the symptomatic femoral head and neck that has been shown by magnetic resonance imaging to be the consequence of increased water content of the femoral head and the marrow cavity; a joint effusion may also be present.

The symptoms and the radiological appearance usually resolve within 2—6 months postpartum. The typical daily loss of calcium in breast milk has been estimated to range from — mg, although daily losses as great as mg calcium have been reported.

Again, the mother could theoretically meet this demand by increasing the intestinal absorption of calcium, decreasing renal calcium losses, and increasing the resorption of calcium from the maternal skeleton.

A temporary demineralization of the skeleton seems to be the main mechanism by which lactating women meet these calcium requirements. This demineralization does not seem to be mediated by PTH or 1,dihydroxyvitamin D, but may be mediated by PTHrP in the setting of a fall in estrogen levels.

The mean ionized calcium level of exclusively lactating women is increased, although it remains in the normal range. Serum phosphate levels are also increased and may exceed the normal range.

Because reabsorption of phosphate by the kidneys seems to be increased, the increased serum phosphate levels may, therefore, reflect the combined effects of increased flux of phosphate into the blood from diet and from skeletal resorption in the setting of decreased renal phosphate excretion.

It rises to normal at weaning, but may rise above normal postweaning. Calcitonin levels fall to normal after the first 6 weeks postpartum.

In contrast to the high 1,dihydroxyvitamin D levels of pregnancy, maternal free and bound 1,dihydroxyvitamin D levels fall to normal within days of parturition and remain there throughout lactation.

PTHrP levels, as measured by two-site IRMAs, are significantly higher in lactating women than in nonpregnant controls. The source of PTHrP may be the breast, because PTHrP has been detected in breast milk at concentrations exceeding 10, times the level found in the blood of patients with hypercalcemia of malignancy or normal human controls.

Indeed, a small rise in the maternal level of PTHrP can be demonstrated after suckling 11 , The primary role of PTHrP in the breast or breast milk is not clear. Studies in animals suggest that PTHrP may have a primary role in the breast to regulate mammary development and mammary blood flow.

In addition, PTHrP may reach the maternal circulation from the lactating breast to cause resorption of calcium from the maternal skeleton, renal tubular reabsorption of calcium, and indirectly suppression of PTH.

In support of this hypothesis, PTHrP levels have been found to correlate negatively with PTH levels and positively with the ionized calcium levels of lactating women 11 , Also, PTHrP levels correlate with the loss of bone mineral density during lactation in humans Furthermore, observations in aparathyroid women may provide evidence of the impact of PTHrP in calcium homeostasis during lactation.

Calcitriol requirements of hypoparathyroid women fall early in the postpartum period, especially if the woman breastfeeds, and hypercalcemia may occur if the calcitriol dosage is not substantially reduced As observed in one recent case, this is consistent with PTHrP reaching the maternal circulation in amounts sufficient to allow stimulation of 1,dihydroxyvitamin D synthesis, and maintenance of normal or slightly increased maternal serum calcium This impact of lactation on calcium homeostasis does not occur in women with pseudohypoparathyroidism, who have resistance to the amino-terminal actions of both PTH and PTHrP.

The intestinal absorption of calcium is equal to the nonpregnant state and decreased from pregnancy. This change coincides with the fall in 1,dihydroxyvitamin D levels to normal. The GFR falls during lactation to a level below the pregnant and prepregnant value, and the renal excretion of calcium is typically reduced to levels as low as 50 mg per 24 h.

This suggests that the tubular reabsorption of calcium must be increased, to account for reduced calcium excretion in the setting of increased serum calcium.

Comparative histomorphometric data are lacking for humans, and, in place of that, serum markers of bone formation and urinary markers of bone resorption have been assessed in numerous cross-sectional and prospective studies of lactation. Some of the confounding factors discussed with respect to pregnancy apply to the use of these markers in lactating women.

In this instance, the GFR is reduced and the intravascular volume is more concentrated. Urinary markers of bone resorption h collection have been reported to be elevated 2- to 3-fold during lactation and are higher than the levels attained in the third trimester.

Serum markers of bone formation not adjusted for hemoconcentration or reduced GFR are generally high during lactation and increased over the levels attained during the third trimester. Total alkaline phosphatase falls immediately postpartum due to loss of the placental fraction, but may still remain above normal due to the elevation in the bone-specific fraction.

Considering the confounding variables, these findings suggest that bone turnover is significantly increased during lactation. Serial measurements of bone density during lactation by SPA, DPA, or DXA have shown a fall of 3— Loss of bone mineral from the maternal skeleton seems to be a normal consequence of lactation and may not be preventable by raising the calcium intake above the recommended dietary allowance.

Several recent studies have demonstrated that calcium supplementation does not significantly reduce the amount of bone density lost during lactation 17 — Not surprisingly, the lactational decrease in bone mineral density correlates with the amount of calcium lost in the breast milk output The mechanisms controlling the rapid loss of skeletal calcium content are not well understood.

The reduced estrogen levels of lactation are clearly important, but are unlikely to be the sole explanation. In the studies of lactational bone density changes, no study has adequately addressed the relative role of estrogen withdrawal during lactation in a definitive way, because no study has manipulated estrogen independently of lactation.

Such a study might, for example, require that lactating women be randomized to the use of an oral contraceptive vs.

a placebo. In the studies that have been done, earlier resumption of menses and, by implication, earlier restoration of estrogen levels is associated with smaller decreases in bone density during lactation; conversely, a longer duration of amenorrhea correlates with a greater degree of bone loss during lactation 14 , 19 , 20 , At first glance this might seem to solely implicate estrogen; however, it must also be remembered that the duration of amenorrhea correlates with the intensity of lactation.

Women who lactate more intensely i. infant exclusively breastfed, more frequent feedings, greater breast milk output, etc. can be expected to have greater net calcium losses and lose more bone, and that is not necessarily due to estrogen deficiency alone.

To estimate the effects of estrogen deficiency during lactation, it is worth noting the alterations in calcium and bone metabolism that occur in reproductive-age women who have estrogen deficiency induced by GnRH agonist therapy for endometriosis and other conditions. In lactation, women are not as estrogen deficient but lose more bone mineral density at both trabecular and cortical sites , have normal as opposed to low 1,dihydroxyvitamin D levels, and have reduced as opposed to increased urinary calcium excretion.

The difference between isolated estrogen deficiency and lactation may be due to the effects of other factors such as PTHrP that add to the effects of estrogen withdrawal in lactation Fig.

Acute estrogen deficiency e. GnRH analog therapy increases skeletal resorption and raises the blood calcium; in turn, PTH is suppressed and renal calcium losses are increased.

During lactation, the combined effects of PTHrP secreted by the breast and estrogen deficiency increase skeletal resorption, reduce renal calcium losses, and raise the blood calcium, but calcium is directed into breast milk. Kovacs and H. Kronenberg: Endocrine Reviews —, 1. The bone density losses of lactation seem to be substantially reversed within 3—6 months of cessation of lactation, irrespective of how much bone density was lost initially 1 , 10 , This corresponds to a gain in bone density of 0.

The mechanism for this restoration of bone density is uncertain and largely unexplored. A few studies have observed that levels of PTH and 1,dihydroxyvitamin D may be higher after weaning and during the time frame when bone mass is being accreted by the maternal skeleton 23 , but the significance of these observations is uncertain.

In the long-term, the consequences of lactation-induced depletion of bone mineral content seem clinically unimportant.

The vast majority of epidemiologic studies of pre- and postmenopausal women have found no adverse effect of a history of lactation on peak bone mass, bone density, or hip fracture risk.

Rarely, a woman will suffer a fragility fracture during lactation, and osteoporotic readings will be confirmed by DXA. Like osteoporosis in pregnancy, this may represent a coincidental, unrelated disease; the woman may have had low bone density before conception.

Alternatively, some cases might represent an exacerbation of the normal degree of skeletal demineralization that occurs during lactation, and a continuum from changes in bone density and bone turnover that may have occurred during pregnancy. For example, excessive PTHrP release from the lactating breast into the maternal circulation could cause excessive bone resorption, osteoporosis, and fractures in some of these cases.

PTHrP levels were high in one case of lactational osteoporosis and were found to remain elevated for months after weaning However, the extent to which PTHrP contributes to the reduction of bone density during lactation has yet to be established.

The studies of pregnant women suggest that the fetal calcium demand is met in large part by intestinal calcium absorption, which more than doubles from early in pregnancy. The studies of biochemical markers of bone turnover, DXA, and ultrasound are not conclusive, but are compatible with the possibility that the maternal skeleton does contribute calcium to the developing fetus.

In comparison, the studies in lactating women suggest that skeletal calcium resorption is a dominant mechanism by which calcium is supplied to the breast milk, while renal calcium conservation is also apparent. These observations indicate that the maternal adaptations to pregnancy and lactation have evolved differently over time, such that dietary calcium absorption dominates in pregnancy, whereas the temporary borrowing of calcium from the skeleton appears to dominate during lactation.

Lactation seems to program an obligatory skeletal calcium loss irrespective of maternal calcium intake, but the calcium is completely restored to the skeleton after weaning. The rapidity of calcium loss and regain by the skeleton of the lactating woman are through mechanisms that are at best, only partly understood.

A full elucidation of the mechanisms of bone loss and restoration in the lactating woman might lead to the development of novel approaches to the treatment of osteoporosis and other metabolic bone diseases.

Finally, although it is apparent that some women will experience fragility fractures as a consequence of pregnancy or lactation, the majority of women can rest assured that the changes in calcium and bone metabolism during pregnancy and lactation are normal, healthy, and without adverse consequences in the long term.

Kovacs CS , Kronenberg HM. Endocr Rev. Google Scholar. Kovacs CS , Lanske B , Hunzelman JL , Guo J , Karaplis AC , Kronenberg HM. Proc Natl Acad Sci USA.

Cornish J , Callon KE , Nicholson GC , Reid IR. Purdie DW , Aaron JE , Selby PL. Br J Obstet Gynaecol. Naylor KE , Iqbal P , Fledelius C , Fraser RB , Eastell R. J Bone Miner Res. The Memphis Obstetrics and Gynecological Association is proud to provide Memphis-area patients with leading care from experts in the field who prioritize patient outcomes over anything else.

We care about you, your baby, and your pocketbook! Give us a call today or schedule an appointment here to put yourself on the fast track to a successful pregnancy.

You can make sure your dental health stays strong during pregnancy with these easy steps: Brush your teeth twice a day with fluoride toothpaste. Use floss or interdental brushes to clean between your teeth daily. Consume a healthy diet and limit sugary foods and drinks.

Refrain from using tobacco products and minimize alcohol intake. Regularly visit your dentist every six to 12 months. Pregnancy and Bone Health Beyond its impact on oral health, pregnancy also holds a complex relationship with bone health. Pregnant woman having back pain.

About 30 years old, Caucasian brunette. Who Is Prone to Bone Health Problems? Nurturing Bone Health Motherhood comes with new responsibilities, and staying healthy is essential for both you and your baby.

Official websites use. durlng A. Bone health during pregnancy website belongs to an Dairy-free menu government organization in the United States. gov website. Share sensitive information only on official, secure websites. The amounts of calcium that women need do not change when they are pregnant or nursing. Christopher Duting. The primary cause for this bealth is, of course, the Bone health during pregnancy requirements of the rapidly mineralizing skeleton of the fetus and Recovery nutrition for team sports. The fetus and placenta actively pump calcium ptegnancy Bone health during pregnancy maternal circulation, heaalth hormonal duirng in the hralth ensure Bone health during pregnancy sufficient supply of calcium to the breast milk and, thereby, the nursing infant. Although the daily maternal calcium losses in the third trimester are similar to the daily calcium losses in breast milk of an exclusively lactating woman, it seems that the adjustments made in each of these reproductive periods differ significantly. This article summarizes what is currently known about altered calcium homeostasis in pregnancy and lactation; the interested reader is referred to a recent comprehensive review for more information and detailed references 1. This corresponds to a daily accretion rate of about — mg calcium by the fetal skeleton during the third trimester.