Bone Mineral Density (BMD) is a key recognised predictor of fracture risk. This is evidenced by standards specified by the World health Organisation (WHO) in using absolute BMD for the diagnosis of osteoporosis. These standards stipulate that persons with a BMD value more than 2.5 standard deviations below the average specified for a 25-year-old Caucasian female are defined as having osteoporosis, while those between 1.0 and 2.5 standard deviations below the average are considered to have osteopenia (Shoback et el,2001,p.314).
Osteoporosis is a clinical term to imply reduced bone density; a condition associated with high morbidity and mortality. Where the reduction is mainly in the trabecular bone, the commonest complications are crush fractures of vertebrae, which may manifest as reductions in height and “dowager’s humps”. However, if cortical bone is involved, fractures of long bones such as those involving the neck of femur are likely; this is a major cause of death especially among older women (Longmore et al, 2004,p.698)
Compston and Rosen (2002, pp.10-18) outline the pathophysiology of low bone mass as a predisposing factor for osteoporotic fractures. They summarise that BMD is affected by Peak Bone Mass (PBM) and the extent of subsequent bone loss, both of which are regulated at the level of bone remodelling units. The function of such remodelling units in turn is influenced by interactions involving genetic and environmental factors.
PBM is achieved between the ages of 20 and 30 years, with remodelling favouring the formation of bone, resulting in a significant increase in bone mass (Compston and Rosen, 2002, p.12), which has lifelong implications. While most important factors that interact to regulate PBM are of genetic origin, studies in twins have suggested that this genetic regulation of PBM can be influenced by hormonal and environmental factors such as timely secretion of sex steroids in adequate volumes, supplemental calcium intake and balanced physical activity (Compston and Rosen, 2002, pp.12,13).
Whereas PBM is achieved by the age of approximately 30 years, bone loss is a process that occurs over a much longer duration. In outlining the relative importance of PBM and rates of bone loss in determining the BMD at any given, Compston and Rosen (2002) acknowledge that chronic loss of bone is a commonly recognised feature in many cases of osteoporosis. However, they emphasise that impairments in the acquisition of PBM are known to be responsible for “60-70% of the variance in bone mass at any age. Hormonal and environmental factors remain the strongest determinants of bone loss after the fourth decade in both men and women, whereas heritable influences, sex hormone status and dietary calcium are the principal regulators of PBM” (Compston and Rosen, 2002, p.13). Given below is a list of factors known to interact in the regulation of PBM, and thereby determine the risk of osteoporosis.
Factors known to interact in the regulation of PBM and therefore considered risk factors for osteoporosis (Compston and Rosen, 2002, p.14).
- Hypogonadism (including premature menopause)
- Glucocorticoid therapy
- Previous fragility fracture
- Low body weight
- Cigarette smoking
- Excess alcohol consumption
- Low dietary calcium intake
- Vitamin D deficiency
- Late menarche
- Physical activity
- High caffeine intake
- Maternal history of hip fracture
Rates of bone loss too are influenced by similar factors. Predominant among these are hormonal influences, especially linked to menopause, where oestrogen deprivation enhances the rate of bone dissolution, and the chronic ‘uncoupling’, or an imbalance, of resorption and formation of bone manifest as age-associated bone loss. Other factors associated with bone loss include calcium or vitamin D deficiency, secondary hyperparathyroidism, therapeutic use of glucocorticoids, immunosuppressant therapy, excess thyroid levels and chronic anticonvulsant therapy (Compston and Rosen, 2002, pp.14-16). Consideration of above reveals a significant overlap in the factors that influence PBM and bone loss.
Effects of calcium supplementation in younger women
The recognition of the importance of PBM and rates of bone loss in determining the risk of osteoporosis has led to a combination of preventative measures being identified in an attempt to minimise the mortality and morbidity associated with the condition. These include holistic measures such as fall avoidance and exercise, in addition to therapeutic measures such as high-calcium diet, calcium and vitamin D supplementation and oestrogen replacement therapy for postmenopausal women (Coble, 1995, p.118).
The rationale for calcium supplementation resides in its physiological action on bone modulation. The physiological effect of calcium, in bone modulation, manifests through the actions of osteoblasts and osteoclasts. Osteoclasts, when stimulated, work towards the resorption of bone mass with an increased release of calcium and a rise in plasma calcium levels. Osteoblasts, in comparison, have a bone-building effect leading to the incorporation calcium into the bone substance, resulting in a lower plasma calcium concentration. A low plasma calcium concentration due to chronic loss, or reduced intake, therefore, results in demineralization of bone substance leading to an increased risk of osteoporosis (Simonsen et al, 2006, p.316).
The optimal time for calcium supplementation, as means of preventing osteoporosis, has been a focus of much research. Coble (1195, p.124) outlined the need for calcium supplementation of all age groups based on the rationale that the daily requirement of calcium for young adults ranged between 1000 and 1500 milligrams, adults required a minimum of 1000 milligrams and postmenopausal women (especially those not receiving oestrogen) approximated 1500 milligrams. A recent issue of the British National Formulary (BNF) expands on this, recommending that calcium supplements should usually be indicated only in circumstances involving a deficiency in dietary intake. The recommendation highlights that calculation of the daily requirement is complex and multifactorial: for instance the requirement varies with age (greater in childhood) and during pregnancy and lactation, due, in both instances, to increased demand. Conversely, the requirement also increases in old age, due, in this instance, to impaired absorption (Joint Formulary Committee, 2008).
There is a consensus that research has already established the value of calcium supplementation in reducing osteoporotic fractures, as evidenced by a recent systematic review conducted by Gennari and Martini (2008). However, a majority of these studies have looked at supplementation targeted at postmenopausal women. The systematic review conducted by Gennari and Martini also looked only at studies involving participants over the age of 50 years. In comparison, is there sufficient evidence to suggest routine calcium supplementation of younger women would prevent later manifestations of osteoporosis? Understandably, the value of supplementation would be significantly influenced by the background levels of calcium intake in communities, which are subject to wide variation.
Barger-Lux et al (2005) reporting on a randomised controlled trial which looked at the augmentation of bone density following calcium supplementation of 152 post-adolescent healthy young women consuming a diet moderately low in calcium, concluded that the combined impact of increased dietary intake of calcium and the small quantity of calcium provided in the form of multivitamin tablets together, resulted in a mean increase in the control group (800 mg or 20 mmols per day) which was “possibly at or near the threshold beyond which additional calcium has no further effect on bone accrual” (Barger-Lux et al,2005). Woo et al (2007) reporting on a 2 year study involving 441 women between the ages of 20 and 35, looking at milk supplementation and bone health, also concluded that milk supplementation was not associated with consistent changes in BMD in that age group.
It seems reasonable therefore to conclude that the current scientific evidence does not support mandatory calcium supplementation of all young women, as means of reducing the longer term risk of osteoporosis. However, this should not be taken to mean that young women exposed to particularly lower levels of dietary calcium would not benefit from calcium supplementation, as indicated in the BNF quoted above.