The skeleton is a metabolically active organ that is continuously resorbed and rebuilt. With ageing, the balance shifts to increased resorption, leading to osteoporosis due to a reduction in bone mineral density (BMD) and disruption of bone microarchitecture. Bone metabolism is influenced by hormones such as oestrogen, thus post-menopausal women worldwide have a heightened risk of developing osteoporosis. Lifestyle factors also affect risk, with diet and exercise being the most important modifiable factors. Dietary calcium, vitamin D, fruit, vegetable and long chain polyunsaturated fatty acids (PUFAs) intake all correlate with bone health.
Osteoporosis is diagnosed using several methods. The measurement of BMD by dual energy X-ray absorptiometry (DXA) is the gold standard. Portable ultrasound heel scanners are practical for assessing bone health status in large population studies. Calcium and vitamin D serum levels provide valuable information about nutritional status. Changes in BMD occur very slowly, interventions can be monitored via blood levels of bone-turnover markers including c-telopeptide of type I collagen (CTX), osteocalcin, and receptor activator of nuclear factor kappa-B ligand (RANKL), with parathyroid hormone (PTH) as indicators of calcium balance.
Collaborative work with New Zealand and international research groups has focused on using foods and food components to intervene in the bone resorption process. Initial studies were carried out in vitro to identify cellular and molecular mechanisms as well as optimal dosages. Animal studies provided in vivo evidence, while human studies demonstrated efficacy at both individual and population levels.
In vitro studies demonstrated that the PUFA docosahexaenoic acid (DHA) from fish oil, β-carotene, and the oestrogen-like soy isoflavone daidzein reduced osteoclast formation, bone resorption, and osteoclast differentiation markers. These findings were extended to animal models. In ovariectomised (OVX) rats, which mimic the post-menopausal woman, dietary supplementation with DHA and other PUFAs significantly increased BMD and decreased serum PTH. Feeding β-carotene-rich kiwifruit and soy isoflavones significantly reduced CTX and RANKL serum levels and improved BMD in OVX rats and mice. Human studies similarly demonstrated the benefits of dietary supplementation. In healthy postmenopausal women, increasing vegetable and fruit intake reduced calcium excretion in the urine, kiwifruit consumption improved bone markers and fortified milk significantly reduced bone resorption.
However, human studies also revealed significant differences in genetic phenotypes, debunking long-held beliefs and leading to new paradigms in study design. A comparison of women in several Asian countries identified significant differences between the rate of decline in bone health in women in Vietnam compared to women in Indonesia and the Philippines. A study of black women in Africa demonstrated that higher proportions of body fat, once believed to protect against osteoporosis, did not correlate with bone health. Rural African women had higher 25 (OH)vitamin D levels but also higher bone turnover compared to urban women. Isoflavone interventions in Asian postmenopausal women have produced inconsistent bone health benefits, due in part to population heterogeneity in enteric bacterial metabolism of daidzein. Ongoing studies are now being specifically designed to assess genotype differences between Western, Malay, Chinese, African, and other phenotypes.
Funding sources: MBIE MAUX 1102; MBIE MAUX 1309; Fonterra Brands Singapore Ltd; Fonterra Cooperative Ltd; South African Medical Research Council; National Research Foundation South Africa, Institute for Food, Nutrition and Well-Being, University of Pretoria, South Africa.