Calcium supplementation increases bone density in adolescent
In a longitudinal calcium intervention study, bone density was assessed in pubertal girls for 18 months. Significant additional increases in total body bone mineral density (1.3%) and spine bone mineral density (2.9%) and content (4.7%) were noted in the calcium-supplemented group. Increasing bone mass during adolescence with adequate calcium intake, if maintained into adulthood, could decrease the risk of osteoporosis later in life.
Osteoporosis is a disease characterized by reduced bone density. A low bone density is a risk factor for osteoporosis, as demonstrated by the fact that the incidence of vertebral fractures is inversely proportional to bone mineral content in women over the age of 50.(1) Small differences in bone mass can be physiologically important; for example, there is a large difference in hip fracture rates between matched populations who differed in peak bone mass by only 6%.(2) Bone mineral density and content in later years is determined by both peak mass and the subsequent rate of bone mineral loss. Thus development of optimal peak mass is an important influence in reducing the incidence of osteoporosis.
An individual’s bone mass is primarily genetically controlled.(3) However, a variety of lifestyle factors can contribute to variations in bone mineral measures, such as dietary intake, smoking, and physical activity. Of the dietary factors, calcium has received the most attention. Most studies have examined the relationship between calcium intake and bone density in adults. A meta-analysis of these studies has shown a significant positive correlation between calcium intake and bone density, with a stronger relationship in premenopausal than in postmenopausal women.(4) However, adequate calcium intake may have an even greater impact during development of peak bone mass. For adolescents who are in linear growth, a calcium balance of intake equaling losses is not sufficient to meet the needs of growth. These individuals need to be in positive balance to meet skeletal demands. Determining the calcium requirements to optimize attainment of peak bone mass is therefore important to reduce the risk of low bone mass in later years. There are several techniques to assess the level of calcium required to achieve optimal calcium accretion or maximal peak mass, including balance studies or longitudinal studies, which use bone mass as the end point studied.
Lloyd et al.(5) assessed the effect o modest calcium supplementation on bone mineral measures in adolescent girls over an 18-month period. Caucasian girls aged 11.9 +/- 0.5 years were randomly assigned to treatment groups of placebo or calcium citrate malate supplementation (500 mg calcium/ day). Randomization was stratified with respect to body mass index (BMI) and spine bone mineral density. Since body mass index influences bone mineral density, stratification into treatment groups by BMI improved the ability to assess an effect of treatment on bone measures. Subjects were between 80% and 120o of ideal weight for height, had no known history of diseases or eating disorders that would affect bone development, and were not taking any medications regularly. Of 112 subjects initially enrolled in the study, 94 remained at its completion. Measurements were completed at baseline and at 6-month intervals up to 18 months. Medical history, height, weight, Tanner stages, percent body fat by caliper measurements, and urinary calcium, creatinine, estradiol, testosterone, cortisol, luteinizing hormone, and follicle-stimulating hormone were assessed using a 24-hour urine collection. Dietary intake of calcium was estimated from 3-day diet records at baseline and repeated every 6 months. Bone mineral density and content of the total body and lumbar spine were assessed with dual X-ray absorptiometry.
The subjects were similar at baseline and at completion of the study in regard to all the anthropometric measurements assessed. In addition, 65% of each group reached menarche by the end of the study. The urinary parameters measured were similar at baseline and at completion of the study with the exception of calcium. Upon completion of the study, significantly more calcium was excreted in the supplemented group (2.26 versus 1.82 mmol/ day [p = 0.02]). Calcium intake from supplementation alone was 354 +/- 90 mg/day. Intake of calcium from the diet was similar, with total intake for the supplemented and placebo groups measured at 1370 and 935 mg/day, respectively.
The increases in the supplemented group were significantly greater than the increases in the placebo group: spine bone mineral density (2.9%, 0. 14 versus 0.11 g/cm sup 2 , p = 0.03), spine bone mineral content (4.7%, 11.9 versus 10.4 g, p = O.05), and total body bone mineral density (1.3%, O.09 versus 0.07 g/cm sup 2 p = O.04). There was an increase in total body bone mineral content of 2.0% (404 versus 368 g); however, the difference in this measure did not reach significance (p = 0.13). Longitudinal models were applied to the data, and the linear coefficients reached significance for the spine (p = O.05) and total body 07 = 0.01) bone mineral density (Figure 1) and the spine bone mineral content (p = 0.03), but not total body bone mineral content (p = 0.07).(Figure 1 omitted) Unfortunately, although the linear models determined were presented graphically, the linear coefficients, intercepts, and the errors of the models were not available in the manuscript.
The study by Lloyd et al. was carefully designed and is the first to show that a modest increase in calcium intake can positively influence bone health in adolescents.(5) Matkovic et al.(6) studied pubertal girls with substantially different calcium intakes (750-1640 mg/day) and demonstrated a positive trend in bone accretion in those girls with the higher intakes. One other calcium intervention study was completed by Johnston et al.,(7) employing the unique model of identical twins. In this study, both boys and girls were studied across the age range of 6-14 years for 3 years with placebo or calcium supplementation (averaging 719 calcium mg/day). In pubertal subjects, no significant changes in bone measures were observed between treatment groups. The lack of effect of calcium intake on bone density in this age group, in contrast to the results of the study by Lloyd et al.,(5) may be due to the small sample size of only 19 twin pairs. However, in the prepubertal group with only 22 twin pairs, significant differences were noted in the spine and radial bone mineral density, and differences approached significance in the hip bone mineral density. Serum bone remodeling parameters (osteocalcin and tartrate-resistant acid phosphatase) suggested that bone turnover was lower in the calcium-supplemented group. This measure was not described by Lloyd et al. and would have been an interesting addition to the study.
As most studies suggest that peak mass of the femoral neck is attained at the early age of approximately 16 years,(8) it is unfortunate that Lloyd et al. chose to not use this measurement in their study. The authors also do not discuss the influence of other lifestyle factors, in particular, physical activity, on bone mineral measures.
Although the results of Lloyd et al. suggest that calcium intakes greater than 935 mg/day will allow greater increases in bone mineral measures, it is still unclear what level of calcium intake is required for achievement of optimal peak mass.(5) Balance studies are necessary to understand the mechanism of the increased retention, as well as calcium intervention studies at various levels of calcium intake to determine calcium requirements for optimal bone mass. Furthermore, it is not known whether increases in bone mass will be maintained in the absence of supplementation, or if calcium intakes must remain high to retain the extra bone mass. If maintained into adulthood, more bone could be resorbed without risk of fracture following menopause. The Recommended Dietary Allowance (RDA) for this age group is 1200 mg/day, and dietary intakes less than this in the studies by Lloyd et al. and Johnston et al. did not result in maximal bone accretion. Lloyd et al., however, have substantially contributed to the state of knowledge concerning the importance of the influence of dietary calcium on bone health during growth.
1. Smith DM, Khairi MRA, Johnston CC. The loss of bone mineral content with aging and its relationship to risk of fracture. J Clin Invest 1975;56:311-8
2. Matkovic V, Kostial K, Simonovic I, Buzina R. Brodarec A, Nordin BEC. Bone status and fracture rates in two regions of Yugoslavia. Am J Clin Nutr 1979;32:540-9
3. Johnston CC Jr, Slemenda CW. The relative importance of nutrition compared to the genetic factors in the development of bone mass. In: Burckhardt P, Heaney RP, eds. Nutritional aspects of osteoporosis. New York, NY: Raven Press, Serono Symposia Publication, 1991;85:21-6
4. Cumming RG. Calcium intake and bone mass: a quantitative review of the evidence. Calcif Tissue Int 1990;47:194-201
5. Lloyd TL, Andon MB, Rollings N, et al. Calcium supplementation and bone mineral density in adolescent girls. JAMA 1993;270:841-4
6. Matkovic V, Fontana D, Tominac C, Goel P, Chestnut CH III. Factors that influence peak bone mass formation: a study of calcium balance and the inheritance of bone mass in adolescent females. Am J Clin Nutr 1990;52:878-8
7. Johnston CC, Miller JZ, Slemenda CW, et al. Calcium supplementation and increases in bone mineral density in children. N Engl J Med 1992;327:82-7
8. Theintz G, Buchs B, Rizzoli R, et al. Longitudinal monitoring of bone mass accumulation in healthy adolescents: evidence for a marked reduction after 16 years of age at the levels of lumbar spine and femoral neck in female subjects. J Clin Endocrinol Metab 1992;75: 1060-5
This review was prepared by Dorothy Teegarden, Ph.D. and Connie M. Weaver, Ph.D. at the Department of Foods and Nutrition, Purdue University, West Lafayette, IN 47907, USA.
Copyright International Life Sciences Institute and Nutrition Foundation May 1994
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