A population-based study of the relationship between salt intake, bone resorption and bone mass

Abstract

Objective: To explore the relationship between urinary sodium (the best measure of salt intake), urinary calcium, urinary deoxypyridinoline (DPYR) and bone mass. Design: Cross-sectional study. Setting: Population based sample of healthy Hobart residents. Subjects: One hundred and ®fty-four (M 34, F 120) subjects invited to take part from a systematic sample of the electoral roll and a single newspaper advertisement. Results: In both sexes, urinary sodium correlated moderately with urinary DPYR (r 0.32, P`0.0001) and urinary calcium (r 0.37, P`0.0001). In multivariate analysis, the combination of urinary sodium, total body bone area, age and sex explained 22% of the variation in log-transformed DPYR (P`0.00001). In univariate analysis, both urinary sodium and urinary DPYR were strongly associated with bone mineral content and bone mineral density at all sites but this association disappeared after adjustment for confounders particularly body weight. Conclusions: This study has shown that salt intake is associated with markers of bone resorption in a populationbased sample of males and females and appears likely to be a risk factor for osteoporosis despite the lack of a demonstrable association between bone mass and a single measure of urinary sodium excretion. Further studies are needed to de®ne the effect of salt intake on bone mass and fractures more clearly. These studies will need to be either longitudinal or interventional in design with repeated measures of urinary sodium so that habitual sodium intake can be accurately assessed and regression dilution bias can be minimised.

A 7-week reduction in salt intake does not contribute to markers of bone metabolism in young healthy subjects

“…This is in agreement with other studies, indicating that there are differences in the metabolic responses to sodium between the young and the elderly (Breslau et al, 1985;Itoh et al, 1999). Although the association between sodium intake and bone resorption in young subjects has been found in several studies (Goulding, 1981;Goulding & Lim, 1983;Chan et al 1992;Itoh & Suyama, 1996;Jones et al, 1997), opposite findings also exist (Castenmiller et al, 1985;Ginty et al, 1998).…”

“…Therefore, it could be postulated that a reduction in salt intake should be of benefit in the prevention of bone loss because it would decrease the urinary excretion of calcium and preserve bone. The correlation of r ¼ 0.45 between urinary sodium/creatinine and calcium/creatinine we found in the beginning of our dietary intervention is at the same level as previously shown in population studies (Goulding, 1981;Law et al, 1988;Itoh & Suyama 1996;Jones et al, 1997). The correlation disappeared by the end of the study, while both calcium intake and excretion remained constant.…”

“…It was concluded that no bone loss occurs when urinary sodium excretion is less than 92 mmol/day. In other population studies, no association between sodium and bone density has been found, but sodium intake has been assessed by a single urine specimen (Matkovic et al, 1995;DawsonHughes et al, 1996;Jones et al, 1997Jones et al, , 2001Carbone et al, 2003) or by a dietary recall (Greendale et al, 1994).…”

“…A commonly suggested strategy to diminish bone loss is to maintain positive calcium balance by consuming a diet containing adequate amounts of calcium and vitamin D. The positive relationship between urinary sodium and calcium excretion in humans has been established previously in both cross-sectional (Goulding, 1981;Law et al, 1988;Shortt et al, 1988;Chan et al, 1992;Matkovic et al, 1995;Dawson-Hughes et al, 1996;Itoh & Suyama, 1996;O'Brien et al, 1996;Jones et al, 1997) and experimental studies (Breslau et al, 1982;Goulding & Lim, 1983;Castenmiller et al, 1985;Law et al, 1988;McParland et al, 1989;Zarkadas et al, 1989;Chan et al, 1992;Evans et al, 1997). It could be hypothesised that sodium-induced urinary calcium loss decreases serum calcium concentration, which is compensated for increased excretion of parathyroid hormone (PTH) from the parathyroid glands (Evans et al, 1997).…”

A randomized controlled trial of phytoestrogen supplementation, growth and bone turnover in adolescent males

“…It is not possible to generalize to growing females; however, our results would suggest that supplementation may also be ineffective due their greater endogenous estrogen levels and hence greater competition for receptor binding. A time frame of 6 weeks may not be sufficient time to observe an effect on bone turnover; however, studies have shown a rapid response to both growth hormone (Lieuw-A-Fa et al, 1995) and estrogen (Kuiper et al, 1998) in children and markers of bone resorption change in line with daily salt intake ( Jones et al, 1997), and within 1 month in adult studies of antiresorptives (Ettinger et al, 1999;Schnitzer et al, 2000). Alternatively, it Phytoestrogens and bone turnover in boys G Jones et al may be that whole soy protein (containing isoflavones) may have biologically different actions to isolated isoflavones in a tablet formulation.…”