Traditionally, calcium supplementation has been used to treat deficiency or prevent deficiency in high-risk conditions or people with increased calcium requirements such as pregnant women. Acute severe hypocalcaemic states are treated initially with IV infusion of calcium salts. In chronic cases, oral calcium supplements and occasionally vitamin D supplements are used.
Rickets and osteomalacia A deficiency of either calcium or vitamin D can produce these bone disorders. (See Vitamin D monograph for further information.) Infants The percentage and type of fats within an infant formula and their ability to bind calcium salts and increase excretion has been shown to influence the bone mineral content (BMC) of infants. One hundred 8-week-old infants given formulas considered to be more similar to breastmilk and less likely to form calcium soaps in the gut showed increased BMC after only 1 month's treatment compared with those infants on standard formula (Kennedy et al 1999).
BONE MINERAL DENSITY (BMD) AND OSTEOPOROSIS PROPHYLAXIS Children A 2006 Cochrane review of 19 trials including 2859 participants found there was no effect of calcium supplementation on femoral neck or lumbar spine BMD (Winzenberg et al 2006). There was a small effect on total body BMC and upper limb BMD; however, only the effect in the upper limb persisted after supplementation ceased. The effect is approximately equivalent to a 1.7% greater increase in supplemented groups, which at best would reduce absolute fracture risk in children by 0.1-0.2% annually. Additionally, there was no evidence of effect modification by baseline calcium intake, sex, ethnicity, physical activity or pubertal stage. Adolescents Peak bone mass is one of the main determinants of osteoporotic fracture in humans and therefore there is significant research dedicated to determining the influence of calcium status on the 40-50% peak bone mass accretion that occurs during adolescence. Overall, studies in adolescent girls have shown that calcium supplementation significantly improves bone mineral status. Numerous studies, including one by Stear in 2003 of 144 pubertal girls, have confirmed a synergistic relationship between mechanical load, through physical activity, calcium status and bone calcium accumulation; however, it is important to note that physical activity has a positive effect on BMD only at high calcium intakes, with no effect at calcium intakes < 1000 mg/day (Harkness & Bonny 2005).
Until recently, all clinical trials with calcium supplements in children and adolescents, demonstrating a positive effect on bone mass, were conducted over durations of 1-3 years. As such, it is uncertain whether supplementation and resultant increases in bone mass had a beneficial effect in the long-term. A 2005 © 2007 Elsevier Australia
placebo-controlled study addressed this Issue by using calcium supplements (670 mg/day) over a 7-year period. The study of 354 pubertal girls reported significant increases in BMD during growth spurts in the supplemented group; however, these gains did not uniformly persist into late adolescence and only girls of tall stature received long-lasting benefits. Interestingly, the placebo group exhibited a 'catch-up' in bone mineral accretion subsequent to the pubertal growth spurt (Matkovic et al 2005). These results introduce two novel concepts: the first being that dietary calcium requirement for skeletal development may be size dependent and secondly the possibility that a calcium mineral deficit may be a transient feature of the pubertal growth spurt, with a 'catch-up' possible during bone consolidation. In spite of these findings, the temporary gains in BMD may be important in the prevention of fractures during adolescence (Matkovic et al 2005).
A second study introduces other issues regarding the impact of variable calcium status in adolescents. The randomised, double-blind, placebo controlled study of 144 prepubertal girls used 850 mg/day of calcium over 1 year. After follow-up some 7 years later, in addition to positive effects on BMD outcomes, an inverse relationship became apparent between calcium supplementation and the age of menarche. The authors consequently speculate that higher calcium intake prior to menarche may favourably impact on long-term BMD through this dual mechanism (Chevalley et al 2005).
Postmenopausal women Numerous studies have confirmed an important role for calcium in the prevention of osteoporosis in postmenopausal women. Clinical studies have assessed its efficacy as a sole agent against placebo, in comparison with steroid hormones, antiresorptive drugs and as part of combination therapy.
Long-term calcium supplementation protects against bone loss according to a 2-year study involving 60 postmenopausal, non-osteoporotic women. The trial showed that in comparison with the 3% BMD loss evident in the placebo group, those consuming 1633 mg/day on average of supplemental calcium suffered no bone loss, as measured at the greater trochanter, and in fact their BMD improved at other sites tested (Storm et al 1998). A similar trend was demonstrated by Daniele et al (2004) in their study of 120 women, given only 500 mg of calcium and 200 IU of vitamin D per day over 30 months. In general though, the efficacy of calcium supplements in postmenopausal women appears to be largely dependent upon the baseline calcium intake. Those with an initial poor intake tend to achieve significant improvements over placebo, with more modest or no effect evident in groups with higher intakes at baseline (Daniele et al 2004, Fardellone et al 1998).
Whether calcium supplements are sufficient as a stand-alone preventative measure against osteoporosis is still being investigated. The results of one study suggest that the effects of calcium on BMD may require additional supplementation with the trace minerals zinc, manganese and copper (Strause et al 1994). However, the most impressive results obtained to date are for the combination of high-dose calcium with antiresorptive drugs such as oestrogen or calcitonin. A review of these studies highlights the gain in bone mass that resulted from the addition of calcium in contrast to the halt in BMD depletion commonly observed with use of calcitonin alone (Nieves etal 1998).
Other studies of both male (n = 50) and female (n = 200) populations using a combination of fluoride, as monofluorophosphate, and calcium over a 3-4-year period, found this combination to be superior to calcium alone in the prevention of BMD loss. Increased lumbar spine BMD and reduced risk of fractures was evident in both trials using the two minerals (Ringe et al 1998, Reginster et al 1998). The elderly A number of large studies investigating the preventative effect of calcium alone or in combination with vitamin D have produced mixed results in the elderly. Earlier studies by Chapuy et al (1992, 1994, 2002) and Dawson Hughes et al (1997) demonstrated a significant reduction in risk of fracture in the elderly, and Larsen et al in 2004 demonstrated up to 16% reduction in an open-label, 3-year intervention in 9605 community dwelling elderly people. However, the RECORD Trial in 2005 failed to yield positive results. It was a randomised, placebo-controlled trial of 5292 people aged 70 years or older who received either 1000 mg of calcium or 800 IU of vitamin D/day, alone or together, for 24-62 months (The RECORD Trial group 2005). The authors postulate that improved results in previous studies may be due to the increased age (>80 years) of study volunteers and poorer vitamin D status at baseline.
Glucocorticoid-induced osteoporosis Approximately one in six people with asthma receiving inhaled and/or systemic glucocorticoids developed fractures over 5 years. The interaction with calcium plays a small role in this process, with glucocorticoids directly inhibiting vitamin D mediated intestinal absorption of calcium. High vitamin D doses (50,000 IU twice weekly) in combination with 1.5 g calcium daily can overcome this interference (Wilson et al 1991), whereas a randomised study found that treatment with calcium alone or in combination with etidronate may not be effective. That study of 352 volunteers found that treatment for 5 years did not significantly reduce fracture rate (Campbell et al 2004).
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