A 2006 Cochrane review of 13 RCTs involving 485 volunteers found that when the results of all trials were combined, calcium supplementation produced a statistically © 2007 Elsevier Australia

significant reduction in SBP (mean difference: -2.5 mmHg), but not DBP (mean difference: -0.8 mmHg) compared with controls (Dickinson et al 2006). The authors temper their conclusion by stating that the quality of included trials was poor and the heterogeneity between trials means there is a tendency to overestimate the effects of treatment. Earlier, an extensive systematic review, updated in 1999 to include 42 randomised comparative trials, shows modest reductions in both SBP and DBP (-2 mmHg and -1 mmHg respectively) with 1-2 g/day calcium over a 4-14-week intervention (Griffith et al 1999). Although dietary calcium appeared to have a larger effect than supplementation, the difference was not statistically significant. The clinical significance of these small effects has been questioned and the recommendation of calcium as a therapy for all types of hypertension appears premature (Kawano et al 1998). Some studies have proposed that it is only a particular subset of hypertension that demonstrates the greatest improvement with calcium. A number of researchers, for example, have hypothesised a physiological correlation between 'salt sensitive' hypertension and responsiveness to calcium treatment (Coruzzi & Mossini 1997, Resnick 1999).

In recent years, ongoing international epidemiological data have continued to link low dietary calcium intake with a slightly increased risk of hypertension, such as the study by Geleijnse et al published in 2005. A recent prospective cohort study of 5880 Spanish adults free from hypertension and CVD at baseline found that with a 27-month follow-up period, low-fat, but not full-fat, dairy products could be found to be protective (Alonso et al 2005).

Additional findings that are attracting attention include epidemiologic links between markers of low calcium status or calcium metabolism abnormalities, hypertension and insulin resistance. In support of the possible link between these phenomena are the results of a Japanese study of 34 non-diabetic hypertensive and 34 non-diabetic normotensive women. Multiple assessments of the group revealed statistically significant increased urinary calcium, lower BMD, depressed serum calcium and elevated circulating PTH in the hypertensive sample (Gotoh et al 2005).

With another study implicating high serum calcium as an independent indicator of both increased coronary heart disease risk and its severity (Rasouli & Mohseni Kiasari 2006), it is clear that whatever calcium's relationship to cardiovascular disease, it is a complex one and more research with consistent findings is required before any conclusions can be drawn.

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