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SOFT DRINKS AND MILK AVOIDANCE

Carbonated beverage consumption has been linked with decreased BMD in girls but not boys [61,62] and with increased fracture risk in both sexes. Low milk intake and a higher consumption of carbonated beverages were independent fracture risk factors in children with recur­

rent fractures [8]. Other studies have reported increased fracture risk with higher cola intake but not non‐cola car­

bonated beverage intake [63,64]. It is unclear if this effect is due to milk replacement—two studies have demon­

strated that associations between fracture risk [5], pQCT measures [65], and cola drinks persist after adjustment for milk intake, suggesting independent effects. Milk avoidance also appears to have deleterious effects on chil­

dren’s bone. Prepubertal children who avoid milk have lower TB BMC and areal BMD [66] as well as an increased risk of childhood fracture [6]. There are limited and con­

flicting data examining whether milk consumption is beneficial in the long‐term for reducing fractures. Low milk consumption in childhood has been associated with higher risk of combined hip, wrist, and spine fracture in adult women [67] but in another long‐term cohort, for each additional glass of milk consumed daily between age 13 and 18 years, there was a 9% increase in hip

fracture risk in males and no association in women after age 50 years [68]. The effect in males appeared in part to be caused by the effect of dairy intake on height.

CONCLUSION

In conclusion, there is increasing evidence linking a number of nutritional factors with children’s bone devel­

opment. Calcium supplementation has been investigated to the greatest extent, but its effects are of limited public health significance. This makes the exploration of other nutritional approaches of key importance.

ACKNOWLEDGMENTS

Graeme Jones receives an NHMRC Practitioner Fellowship, which supported this work.

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19

INTRODUCTION

The basic morphology of the skeleton is determined genetically, but its final mass and architecture result from epigenetic mechanisms sensitive to mechanical factors. When subjected to loading, fracture resistance depends on bone mass, material properties, geometry, and tissue quality [1]. To determine if an intervention in children could reduce skeletal fragility in adults would require understanding of its effects on each mechanical determinant. Yet it is only recently that studies have moved beyond areal bone mineral density (aBMD) to include volumetric density and geometry [2]. None are yet able to determine if childhood adaptations translate into anti‐fracture efficacy in adults, but the latter varia- bles do provide surrogates of bone strength. There is con- vincing evidence that growing bone has greater capacity to respond to increased mechanical loading than the adult skeleton [2–9]. The question is what to prescribe,