Calcium-enriched foods and bone mass growth in prepubertal girls: A randomized, double-blind, placebo-controlled trial

Division of Bone Diseases, WHO Collaborating Center for Osteoporosis and Bone Disease, Geneva, Switzerland.
Journal of Clinical Investigation (Impact Factor: 13.22). 04/1997; 99(6):1287-94. DOI: 10.1172/JCI119287
Source: PubMed


High calcium intake during childhood has been suggested to increase bone mass accrual, potentially resulting in a greater peak bone mass. Whether the effects of calcium supplementation on bone mass accrual vary from one skeletal region to another, and to what extent the level of spontaneous calcium intake may affect the magnitude of the response has, however, not yet been clearly established. In a double-blind, placebo-controlled study, 149 healthy prepubertal girls aged 7.9+/-0.1 yr (mean+/-SEM) were either allocated two food products containing 850 mg of calcium (Ca-suppl.) or not (placebo) on a daily basis for 1 yr. Areal bone mineral density (BMD), bone mineral content (BMC), and bone size were determined at six sites by dual-energy x-ray absorptiometry. The difference in BMD gain between calcium-supplemented (Ca-suppl.) and placebo was greater at radial (metaphysis and diaphysis) and femoral (neck, trochanter, and diaphyses) sites (7-12 mg/cm2 per yr) than in the lumbar spine (2 mg/cm2 per yr). The difference in BMD gains between Ca-suppl. and placebo was greatest in girls with a spontaneous calcium intake below the median of 880 mg/d. The increase in mean BMD of the 6 sites in the low-calcium consumers was accompanied by increased gains in mean BMC, bone size, and statural height. These results suggest a possible positive effect of calcium supplementation on skeletal growth at that age. In conclusion, calcium-enriched foods significantly increased bone mass accrual in prepubertal girls, with a preferential effect in the appendicular skeleton, and greater benefit at lower spontaneous calcium intake.

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    • "In contrast to our results, it has been previously reported that tibia BMD increased in 3-week-old WT and PTH-deficient mice fed by dams who received a high-calcium diet compared to those on a normal-calcium diet (Cao et al. 2009; Shu et al. 2011). Skeletal site selectivity in response to calcium supplementation is well-documented in human studies during childhood and adolescence , but the mechanism of this site-specific effect remains to be elucidated (Bonjour et al. 1997; Chevalley et al. 2005). Although lumbar BMD increased significantly in response to a high-calcium diet in both Cldn-18 KO and heterozygous control mice, we did not find a significant change in either the trabecular or cortical bone parameters at LV 5, as measured by lCT. "
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    ABSTRACT: We have recently demonstrated that mice with disruption of claudin-18 (Cldn-18) gene exhibited osteopenia due to increased bone resorption (BR). In this study, we found that gastric pH was significantly higher in Cldn-18 knockout (KO) mice compared to heterozygous control mice at 10 weeks of age. To test the possibility that the increased BR in the Cldn-18 KO mice fed a normal-Ca diet is a consequence of decreased Ca absorption caused by increased stomach pH, we subjected KO and control mice to a normal-Ca and high-Ca diet at birth. Serum Ca levels were significantly lower in Cldn-18 KO mice compared to control mice at a normal-Ca diet but not at high-Ca diet. Dual energy X-ray absorptiometry revealed that a high-Ca diet significantly increased lumbar bone mineral density (BMD), but had no effect on femur/tibia BMD in both Cldn-18 KO and control mice compared to a normal-Ca diet. While a high-Ca diet did not affect volumetric BMD, trabecular, and cortical parameters of the lumbar vertebra (LV) as measured by μCT, the size of the LV did increase, in both genotypes due to reduced BR. Comparison of the skeletal phenotype of high-Ca Cldn-18 KO and control mice revealed that an osteopenia phenotype seen at a normal-Ca diet was still maintained at different skeletal sites in the KO mice till 10 weeks of age. In conclusion, our findings suggest that increased BR is likely caused by direct effects of a lack of Cldn-18 on osteoclasts rather than gastric pH changes.
    01/2014; 2(1):e00200. DOI:10.1002/phy2.200
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    • "Another controversial area in LI research is whether this condition is associated with short stature. Although some investigators have suggested that adequate calcium intake during the growth period may be critical for reaching optimal bone growth during the growing years[9], others have provided evidence of short stature in children with LI, milk allergy, or those on milk-elimination diets[10-12]. Further studies in prepubertal children showed that long term avoidance of cow’s milk was associated with small stature and diminished bone health[6,10]. "
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    ABSTRACT: The health consequences of lactose intolerance (LI) are unclear. To investigate the effects of LI on stature and vitamin D status. LI subjects will have similar heights and vitamin D status as controls. Prepubertal children of ages 3-12 years with LI (n=38, age 8.61 ± 3.08y, male/female 19/19) were compared to healthy, age- and gender-matched controls (n=49, age 7.95±2.64, male/female 28/21). Inclusion criteria: prepubertal status (boys: testicular volume <3cc; girls: Tanner 1 breasts), diagnosis of LI by hydrogen breath test, and no history of calcium or vitamin D supplementation. Vitamin D deficiency was defined as 25-hydroxyvitamin D [25(OH)D] <50 nmol/L. Gender-adjusted midparental target height (MPTH) z-score was calculated using NCHS data for 18 year-old adults. Data were expressed as mean ± SD. There was no significant difference in 25(OH)D between the LI and non-LI subjects (60.1±21.1, vs. 65.4 ± 26.1 nmol/L, p = 0.29). Upon stratification into normal weight (BMI <85(th) percentile) vs. overweight/obese (BMI ≥85(th) percentile), the normal weight controls had significantly higher 25(OH)D level than both the normal weight LI children (78.3 ± 32.6 vs. 62.9 ± 23.2, p = 0.025), and the overweight/obese LI children (78.3±32.6 vs. 55.3±16.5, p = 0.004). Secondly, there was no overall difference in height z-score between the LI children and controls. The normal weight LI patients had similar height as normal controls (-0.46 ± 0.89 vs. -0.71 ± 1.67, p = 0.53), while the overweight/obese LI group was taller than the normal weight controls (0.36 ± 1.41 vs. -0.71 ± 1.67, p = 0.049), and of similar height as the overweight/obese controls (0.36 ± 1.41 vs. 0.87 ± 1.45, p = 0.28). MPTH z-score was similar between the groups. Short stature and vitamin D deficiency are not features of LI in prepubertal children.
    PLoS ONE 10/2013; 8(10):e78653. DOI:10.1371/journal.pone.0078653 · 3.23 Impact Factor
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    • "These effects of calcium are transient, however.[4748] Nevertheless, other studies have suggested that increasing calcium intake during childhood through dietary fortification with dairy sources may provide more long-lasting improvements in BMD.[4950] Optimal absorption of calcium from the gastrointestinal tract requires normal vitamin D homeostasis.[51] The primary source of vitamin D is the skin. "
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    ABSTRACT: During normal childhood and adolescence, the skeleton undergoes tremendous change. Utilizing the processes of modeling and remodeling, the skeleton acquires its adult configuration and ultimately achieves peak bone mass. Optimization of peak bone mass requires the proper interaction of environmental, dietary, hormonal, and genetic influences. A variety of acute and chronic conditions, as well as genetic polymorphisms, are associated with reduced bone density, which can lead to an increased risk of fracture both in childhood and later during adulthood. Bone densitometry has an established role in the evaluation of adults with bone disorders, and the development of suitable reference ranges for children now permits the application of this technology to younger individuals. We present a brief overview of the factors that determine bone density and the emerging role of bone densitometry in the assessment of bone mass in growing children and adolescents.
    12/2012; 16(Suppl 2):S205-12. DOI:10.4103/2230-8210.104040
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