The Role of Diet as a Modifiable Risk Factor in the Prevention of Osteoporosis
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Summary
This Position Stand provides an evaluation of diet as a modifiable risk factor in the prevention of osteoporosis. There is an abundance of scientific evidence, which demonstrates the significance of nutrition in the support of bone capital accumulation and wider skeletal health (Wood et al., 2013; Rizzoli, 2008; Ilich and Kerstetter, 2000). This text predominantly focuses on Calcium and vitamin D, as they are two of the most heavily revised nutrients within the context of skeletal system, however, the implications of wider nutrients are also considered. The effect size of diet is evaluated across the whole of the population, as some evidence has suggested that it can be more influential in sub-groups such as children, adolescents, the elderly, and menopausal women (Bianchi, 2007; Hannan et al., 2000; Neer et al., 2001). Thus, it was deemed appropriate to provide an individualistic evaluation of society. Findings from the current literature body are varied, consequently, few nutrients have universally accepted reference values. Position Stands are required to assess the clinical effectiveness of set nutrients at a specific point in time. Curre-ntly, there is enough evidence to make basic recomm-endations for calcium and vitamin D. On the contrary, there is inadequate evidence to make firm recommendations for other nutrients.
Potential Recommendations:
Calcium intake: >500 mg/d
Vitamin D intake: >400IU
The implications of wider modifiable risk factors such as physical activity and hormone regulation are also considered within this text. Some evidence has indicated such factors can alter the effects that certain nutrients have on the skeletal system (Winters and Snow, 2001; Turner and Pavalko, 1998). In light of these findings, it could be suggested wider considerations need to be made in the development of future reference values. Moreover, this text briefly considers a multi-factorial approach to controlling the effects of osteoporosis, as a method of yielding more substantial results.
Introduction
The skeletal system is continuously involved in a remodelling process, which involves the formation and resorption of bone (Courtney et al., 1994). This process is made possible by multicellular units, which aid in the production and removal of bone tissue (Francis, 2007). Osteoclast cells carry enzymes that penetrate the bone and erode segments of trabecular matter, whilst osteoblast cell aid in the remineralisation and formation of new bone mass (Frost, 1966). Osteoporosis occurs when regulated bone accretion is compromised and the structural integrity of the bone is reduced (Aaron, 1975).
Those who suffer with osteoporosis typically illicit few signs and symptoms, prior to encoun-tering problems such as fragility breaks and fractures (Izaks, 2007). Following problems that occur as a result of osteoporosis, individuals are likely to experience chronic pain and reduced functionality (Kanis, 1994). Across the United Kingdom, it is estimated that 300,000 people suffer with the disease (Kanis et al., 2012 cited in NHS Annual Reports). In terms of fracture rates, over 300,000 fragility fractures are recorded in the UK every year, with hip fractures alone accounting for over 1.3 million hospital bed days (Mitchell, 2009). Emergency hospital admissions for breaks and fractures in the UK, results in more bed days, than heart attack, heart failure, and stroke cases combined (Mitchell, 2009 cited in NHS Annual Reports). Treating osteoporosis is estimated to cost the National Health Service (NHS) £2 billion each calendar year, highlighting the scale of the problem (Mitchell, 2009 cited in NHS Annual Reports).
Although heritability contributes extensively in overall bone mass, other factors can have a notable impact on wider skeletal health (Macdonald et al., 2004). There is evidence that suggests diet can be used as a modifiable risk factor, which can minimise the effects of osteoporosis (Rizzoli, 2008). During adulthood, the main aim of nutritional adjustment should be to maintain existing bone mass (Francis, 2007). It remains unclear whether adults can actively increase bone mass with the adjustment of certain lifestyle factors (Wamoto, 2013). Meta-analyses have indicated dietary adjustment does not always result in significant developments of skeletal composition. However, diet remains an important factor in the maintenance of healthy bones (Cumming, 1990; Welton, Kemper, and Staveren, 1995).
There is significant debate surrounding the value of certain nutrients in the context of skeletal health (Prentice, 2004). Thus, such reviews need to analyse the literature body to assess the clinical effectiveness of certain nutrients.
Measuring Osteoporosis
A clinical diagnosis for osteoporosis is typically made when BMD is more than -2.5 SD below the young adult mean of the population (Kanis et al., 2009). A low BMD is a sign of sub-optimal bone mass, which can be acquired during puberty or as a result of accelerated bone loss later in life (Gafni and Baron, 2004). Low BMD readings are heavily associated with an increased prevalence of fragility fractures (Sabin et al., 1995). Thus, low BMD has remained one of the primary risk factors for osteoporosis.
Research has indicated BMD is capable of measuring 60-80% of bone strength variance (Courtney et al., 1994). However, the accuracy of BMD is often contested. Some studies report errors between 25%-41% when using BMD as a sole measure for osteoporosis (Glüer et al., 1995). Glüer et al. (1995) suggested BMD scores are heavily influenced by body size and composition, two factors unaccounted for during standard analysis. In addition, non-specific reference values exist for children and adolescents, as a result of this, it is unclear how usable current reference values are in younger populations (Gafni and Baron, 2004). Despite these caveats, a large evidence base exists that supports the use of BMD as a primary identification tool for osteoporosis (Preston, 2004).
Identifying genuine osteoporosis has previously been associated with relative error and difficulty (Winzenberg et al., 2003). This is often attributed to a lack of clarity in the definition and diagnosis of osteoporosis (Preston, 2004). Some research has suggested using wider measures in conjunction with BDM, so that the disease can be more competently identified within practice (Yasuda, Kaleta, and Bromme, 2005). A significant limitation of BMD, is that mineral content needs to be compromised before a diagnosis can be made (Winzenberg et al., 2003). In high-risk populations such as young individuals and female athletes, methods that detect problems at an earlier stage would provide a greater window for intervention to take place (Yasuda, Kaleta, and Bromme, 2005).
Blood and urinary analysis can detect certain chemical biomarkers, which can reflect the overall health of the skeletal system (Yasuda, Kaleta, and Bromme, 2005). One study reviewing female athletes, indicated that markers of bone turnover were between 33% and 71% lower in certain athletes (Garenero et al., 2013). Thus, such measures should be considered within the appropriate populations. However, as a result of the inequalities which exist in female sport, it seems unlikely methods with such expense will seriously considered by the relevant bodies (Heinonen et al., 1995). Research that surrounds “the female athlete triad”, has previously identified that more efficient measures for screening osteoporosis and secondary osteop-orosis need to be established. However, significant developments are yet to be put in place (Garenero et al., 2013). More precise methods for measuring osteoporosis, may be capable of providing a greater reflection of the impact certain nutrients have on skeletal health.
Calcium intake
Calcium intake is one of the most widely revised topics in the prevention of osteoporosis (Prentice, 2004). Furthermore, it is a key mineral used in the formation of bone mass, which is essential throughout all stages of life (Francis, 2007). Inadequate calcium intake is associated with secondary hyperparathyroidism, which leads to increased bone turnover and accelerated bone loss (Ilich and Kerstetter, 2000). Although it is generally agreed that sufficient calcium intake is an important part of skeletal health, universally accepted intake values are yet to be established. For example, the National Health Service (2016) in ...
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Calcium intake
Calcium intake is one of the most widely revised topics in the prevention of osteoporosis (Prentice, 2004). Furthermore, it is a key mineral used in the formation of bone mass, which is essential throughout all stages of life (Francis, 2007). Inadequate calcium intake is associated with secondary hyperparathyroidism, which leads to increased bone turnover and accelerated bone loss (Ilich and Kerstetter, 2000). Although it is generally agreed that sufficient calcium intake is an important part of skeletal health, universally accepted intake values are yet to be established. For example, the National Health Service (2016) in the UK recommend 700mg/d, whilst the Depa-rtment of Health and ageing (2016) in Australia and New Zealand recommend 1300mg/d. The Institute of Medicine in the US has developed more specific recommendations across the population (IOM, 2011).
Sub-population
RDA (mg/d)
19-50
1500
51-70 (men)
1000
51-70 (women)
1000
71+
1500
Pregnant/ lactating women
2000
Developed from IOM, 2011
Such inconsistency is reflective of the evidence base that surrounds calcium intake.
Epidemiological and prospective studies largely support the link between calcium intake and reduced fracture prevalence. Warensjo et al. (2011) conducted a longitudinal study on 61,000 women, using food frequency questionnaires, and found intake below 700mg/d was associated with increased fracture rates. However, the accuracy of self-administered food records is questionable. Schaefer et al. (2000) suggested such methods are highly vulnerable to both under-reporting and socially desirable reporting. Thus, such studies are unlikely to have accurately observed calcium intake at a population level. Thus, it is difficult to draw firm conclusions from this literature body.
Few studies have been able to observe significant benefits for calcium intake over 400mg/d-500mg/d (DOH, 1998; Dawson-Hughes et al., 1990). This was demonstrated by Hannan et al. (2000) who supplemented 800-mg/d in an elderly cohort during a 4-year longitudinal study; the only developments in bone loss and fracture rates, occurred in those who initially consumed an insufficient amount. Similar effects have been observed from studies in southern Europe, reviewing the effects of dietary calcium through milk and cheese consumption (Kanis et al., 1999). Taken together, the evidence body suggests whilst a calcium deficiency can be more heavily associated with fracture risk; there is limited evidence to suggest high levels of calcium results in lower than average fracture rates. However, fracture rates cannot be considered an absolute measure for osteoporosis. As identified by Rizzoli et al. (2009) fractures occur because of a multitude of factors. Thus, wider research is required to confirm the effects of calcium.
The link between calcium intake and BMD has been widely researched. Some studies have observed relative increases in BMD (up to 3%) when supplementing high levels of calcium (Dawson-Hughes et al. 1990). However, meta-analysis have concluded that on average the magnitude of effect is minimal (Cumming and Kleinberg, 2004). High-calcium intake trials have typically demonstrated an effect size of approx.-imately 1% on BMD (Welton, Kemper and VanStavrin, 2005). Although calcium is used extensively in bone capital accumulation, direct intake will not always have a significant impact on bone tissue. According to Jackson et al. (1995) calcium retention is limited, and thus, the body can only utilise a fraction of what it consumes. Although calcium is commonly recommended to enhance skeletal health, it may be more beneficial to identify methods that can yield greater calcium retention.
Some studies providing focus on specific parts of the population have yielded greater results. Hwadmin et al. (1994) found calcium intake was a significant predictor of peak bone mass in adolescents; it was also identified that participants consuming between 800mg/d-1200mg/d had a BMD 4.7% greater than those consuming less than 700mg/d. Furthermore, in a follow up study it was identified that peak BMD acquired during adolescence had a positive impact on BMD during adulthood (Hwadmin et al. 2004). Thus, the overall importance of calcium intake during puberty is considerably high. In addition, Rizzoli et al. (2013) found calcium intake over 800mg/d slowed bone resorption by 8.7% in menopausal women, and thus, reduced the likelihood of osteoporosis. In light of this evidence, the importance of individualised recommendations is apparent.
Some research has identified that physical activity is capable of improving mineral retention (Rizzoli et al. 2010). Weight-bearing exercises specifically, have been recognised a method for increasing mineral utilisation (Gardner, Rober-tson and Campbell, 2000). Thus, physical activity should be widely considered before recomm-ending certain nutrients. However, the research body that surrounds the effects of physical activity on individual nutrients is limited. As a result of this, it is difficult to make firm recom-mendations with relation to using exercise to maximise mineral retention. Future research could identify that calcium is capable of a greater effect size when combined with an exercise regimen.
Taken together, evidence suggests between 400mg/d and 500mg/d of calcium may provide some protective properties to the skeletal system. However, measures of BMD suggest the overall value of calcium intake across the general population is debatable. Wider studies on spec-ific parts of the population, yielded a greater effect size, and thus, calcium intake could be considered more important within these populations. Evidence indicated intakes greater than 800mg/d could be beneficial to adolescents and menopausal women. Furthermore, research on wider modifiable risk factors suggested calcium intake may be more beneficial when combined with physical activity.
Vitamin D
Vitamin D is identified as one of the key regulators of calcium and phosphate homeo-stasis, which makes it essential during bone turnover (Holick et al., 2011). Furthermore, vitamin D contributes extensively in mineral resorption and is essential to mineral retention (Burke, 2015). Severe Vitamin D deficiency (<200 IU) is heavily associated with bone disorders such as rickets in children and osteomalacia in adults (Litman, Ulstrom and Westin, 1957).
Epidemiological evidence indicates that groups which are less likely to achieve sufficient levels of vitamin D, such as the elderly people and dark-skinned people living in non-tropical environments, are more likely to suffer with osteomalacia (Bates et al., 2003). This evidence has prompted committees such as the Institute of Medicine, Food, and Nutrition board (1997) to advocate higher intake targets in certain pop-ulations. However, it is highly possible any bone-related disorders that are significant within these groups can be attributed to wider lifestyle, biological, and hereditary factors. Dore (1983) suggested epidemiological evidence is poor indicator of cause and effect in multifactorial disorders. Thus, more clinical evidence is requ-ired to confirm such effects.
Strong associations have been reported in some studies reviewing the effects of 25-hydroxyvitamin D on fracture prevalence. Peac-ock et al. (2000) reported a 29% reduction in hip fractures and a 24% reduction in non-vertebrae fractures, when comparing vitamin D intake trials against placebo groups. In addition, Holick et al. (2011) observed a significant reduction in vertebrae fractures whilst reviewing an elderly cohort, supplementing vitamin D during a longitudinal study. However, wider factors have also demonstrated an effect on fracture prev-alence, specifically in populations such as the elderly (Rizzoli et al., 2009). Thus, fracture rates cannot confirm the effectiveness of vitamin D, more clinical research is required.
Research revising the effects of vitamin D on BMD is inconsistent. Silk, Greene, and Baker (2015) found, when measuring males across multiple measurement sites, there was little evidence to support high vitamin D intake. In a sample of 867 participants the greatest increase of BMD was 0.64% at a single site (hip). Whist some participants displayed minor increases of BMD, the overall effect size was limited. Furthermore, increases of BMD where only observed in older males, whom already had lower than average measurements. Reid, Bolland, Grey (2014) conducted a meta-analysis, on current vitamin D trials across numerous measurement sites on predominantly female samples. They found increases of approximately 2% across the sample, however, similarly to the males, the minor effects were typically observed in older participants with already compromised BMD. Thus, there is some evidence that supports positive effects of vitamin D in older adults with already compromised BMD, this however, was not reflected across the rest of the population.
Some research has identified that children and adolescents that regularly consume the RDA for calcium and vitamin D, have greater BMD readings at the hip and lumbar section of the spine (Heaney, 2003). In addition, Lamberg-allardt et al. (2001) observed increased BMD and peak bone mass in adolescents who consumed > 400 IU of vitamin D. Such findings are important because bone capital accumulation acquired earlier in life, has demonstrated a relative effect on peak bones mass during adulthood (Brown et al. 1999). Similarly to the previous research, the overall effect size of vitamin D trials is small, however, the evidence base supporting the effect of vitamin D in children and adolescents is relatively consistent. Holick et al. (2006) concludes that there is an acceptable evidence base to support the requirements for vitamin D intake in children and adolescent, for purposes of skeletal health and growth.
Taken together, there is some evidence to suggest consuming >400 IU of vitamin D could result in reduced bone accretion. In addition, there is a strong evidence body associating adequate vitamin D consumption with reduced fracture risk. Thus, consuming over >400 may be advisable. However, the evidence linking vitamin D and BMD is inconsistent. Studies reviewing the effects of vitamin D on BMD indicated that the observable effects were minimal, although they were more significant in elderly individuals. Studies reviewing adolescents were more conclusive, and thus, consuming an adequate amount can be considered more important to this population.
Wider vitamins and minerals
Even though much of the research instils calcium and vitamin D are the most important nutrients in the context of skeletal health, several studies have suggested other vitamins and minerals play a role in bone metabolism, and thus, could impact an individual’s likelihood of suffering with osteoporosis. Nielsen et al. (2011) undertook a 2-year longitudinal (mineral) supplementation study, and found 2mg of copper and 12mg of zinc may have contributed to increases in BMD. However, Nielsen et al. (2011) concluded such effects were minor and only occurred in individuals with lower than average daily intakes. Furthermore, the study had a sample 50 participants making it hard to draw firm, generalisable recommendations from. Nielsen et al. (2011) suggested although only minor results were observed during this study, not enough emphasis has been placed on wider vitamins and minerals in academic research.
Although few studies have reported on the isolated effects of wider vitamins and minerals, some studies have revised the effects of nutrient rich foods such as fruits and vegetables. Fruits and vegetables are abundant in minerals such as calcium, potassium, and magnesium, each of which have been associated with stimulating osteoclast activity (Tucker et al. 1999). Further-more, fruits and vegetables are rich in vitamin C, Vitamin K, and certain B vitamins, which have also been associated with the maintenance of positive bone synthesis (Boeing et al., 2012). However, it is difficult to draw specific findings from such studies, as any effects that may have been observed, may have occurred as a result of holistic dietary choices rather than individual nutrients (wider review appendices A). Thus, this position stand cannot make recommendations for such nutrients.
Wider factors
Some evidence has suggested physical activity can affect the degree to which certain nutrients impact skeletal health (Tucker, 2009). Turner and Pavalko (1998) found mineral retention was superior in participants that regularly took part in weight-bearing exercise. Thus, the effect of diet, and furthermore individual nutrients, may be superior when combined with weight-bearing exercise. Branca and Silvia Vatueña (2004) suggested the anabolic effect of weight bearing exercise that occurs in bones after physical activity, relies heavily on adequate calcium and vitamin D intake. In addition, Prince et al. (1999) found in post-menopausal women, trials that utilised a comb-ination of calcium supplementation and exercise, resulted in superior increases of BMD. Future research should revise the effects of diet when used in conjunction with physical activity.
Recommendations
Mode
Weight bearing
Intensity
Moderate/ high
Frequency
3-5 x each week
Duration
30-60 minutes
Developed from ACSM Position Stand (2004)
Conclusion
There is relative error associated with the current methods for measuring osteoporosis (Winzen-berg et al., 2003). From a clinical perspective, this is problematic as it could result in patients not receiving sufficient treatment (Prentice, 2004). From a research perspective, this is problematic as it be difficult accurately follow the implications of risk factors such as diet and physical activity. In addition, there is a significant lack of knowledge on the usability of BMD values within children and adolescents (Gafni and Baron, 2004). Thus, it is difficult to know how valuable recomm-endations which are designed for the adult population are in younger individuals. In order to develop research on osteoporosis, it seems essential that methods that can identify the disease with a greater efficiency across the whole of the population are developed. In light of more accurate measurement techniques, research could also be developed within the context of nutrition and skeletal health.
In conclusion, calcium and vitamin D intake may act as a modifiable risk factor in the prevention of osteoporosis. However, the size of effect gained from these nutrients is debatable. Wider nutrients such as those identified in the position stand, are yet to be revised with enough focus to draw significant conclusions from. Future research needs to replicate the focus currently provided for calcium and vitamin D, so the isolated effects of other nutrients can be better understood. Bloomfield et al. (2004) suggested that a holistic approach controlling a multitude modifiable risk factors, could work with a greater effect size. Thus, future research could also look at controlling numerous factors such as, diet, physical activity, and hormone regulation simultaneously.
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Appendices A
Nutrient
Effect on bone health
Evidence base
Grade
Calcium
The skeleton stores 99% of the body’s` calcium; which is the main compound utilised in the production of new bone mass.
Largely supported by epidemiological and fracture prevalence studies with significant strength (Turner, Anderson and Morris, 2012). Generally support by clinical evidence, however, size of effect varies significantly.
A
Vitamin D
Contributes to calcium resorption and over-all bone synthesis. Further supports wider structures such as muscular skeletal.
Largely supported by epidemiological and fracture prevalence studies with significant strength (Turner, Anderson and Morris, 2012). Generally support by clinical evidence with varying levels of strength.
A
Vitamin K
Contributes to the carboxylation of glutamic acid, and thus, is used in the production of osteocalcin.
Numerous studies have reported elderly individuals that consume food rich in vitamin K are less likely to suffer with fragility fractures. Studies are yet to revise the isolated effects of vitamin K on fracture risk or BMD (Booth et al., 2000).
B
Vitamin C
Contributes to the hydroxylation of lysine and proline, and thus, is utilised during the cross-linking of fibrous collagen.
Some studies revising wider nutrient intake have suggested vitamin C could help maintain BMD. However, findings are both minimal and inconsistent (New et al., 2000).
C
B vitamins
Vitamins B6 and B12, are used during the synthesis of homocysteine and amino acids. Thus, they could have protective properties that act against osteoporosis.
Some studies revising wider nutrient bodies have linked lower vitamin B6, 12 intake with greater fracture risk in elderly populations. However, few studies have made substantial claims about vitamin B intake; and those which have typically demonstrate
C
Magnesium
Utilised during bone formation.
Some studies have reported that deficiencies in older individuals can potentially result in accelerated bone accretion in elderly populations (Tucker et al., 1999). Findings are scarce and largely based on wider studies revising fruit/ vegetable intake.
C
Zinc
Utilised during bone tissue renewal and mineralization.
Numerous studies have reported that deficiencies in older individuals can potentially contribute to impaired bone status (Nriagu, 2007). Findings are largely derived from wider studies, however, findings are more consistent than those observed in other nutrients.
B
Copper
Used in the formation of bone mass and collagen tissue. When combined with zinc also inhibits bone resorption.
Some studies have recently associated copper deficiencies with accelerated bone accretion. However, findings are recent and considered as preliminary (Lowe, Fraser and Jackson, M, 2002).
C
Grade A = strongest evidence body Grade B = relative evidence body Grade C = limited evidence body
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