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Osteoporosis - A Lifespan Approach

This article justifies nutritional strategies to maximize lifespan for an individual who is genetically prone to osteoporosis, throughout the complete life span, from preconception to later years.  


Information is provided on osteoporosis and genetic variations and how they may affect nutritional application. An overview is then given on bone development and considerations to be taken into account during the lifespan.  The nutritional strategy discusses the use of macro and micronutrients as well as pre/probiotics and phytochemicals. Lifestyle, costs, social and ethical considerations are discussed throughout. 



Osteoporosis (OP) is defined as a systemic disease characterised by a low bone mass and changes to the architectural structure within the bone tissue.  Low bone density can lead to bone fractures, which result in pain; restrictions to activities, disability and even death, with up to 20% women dying within a year after a hip fracture (Genius and Schwalfenberg 2006; Cech, 2012). Osteoporosis affects more than 200 million people worldwide and is a multi-factorial disease with genetics, endocrine function, exercise and nutrition playing a role in onset.

Bone strength relies on bone mineral content (BMC), this is determined by two interacting factors; peak bone mass (PBM) which is the uppermost amount of bone achieved in youth, compared to subsequent bone loss and bone quantity, which highlights the composition and structure. Dense bone is not necessarily strong bone.  A large part of growth in bone size and strength occurs in uterine, during childhood and through adolescence, it is usually completed by the age of 20.  Bone loss may occur at a slow rate after 35, in women when menopause occurs there is accelerated loss, as there is increased resorption of existing bone, due to declining levels of oestrogen (Genius & Schwalfenberg, 2007). 


Gender, ethnic and genetic differences

One in two women and one in five men, over the age of 50 will break a bone, mainly due to osteoporosis (National Osteoporosis Society, 2012).


Asians and Hispanic children have been shown to have a lower bone mass than Caucasian children and black children have the highest bone mass (Burrow et al., 2009; Baxter-Jones et al., 2010). Similar statistics have been shown in adults (Czech, 2012). 


More than 150 genes have been associated with osteoporosis (Aaseth, 2012; Mendoza et al, 2012). Some of the genes involved include:

  • COL1A1 – the primary protein matrix used for bone synthesis.  Polymorphisms lead to disordered collagen formation that can lead to reduced BMD and increased risk of osteoporosis (Genova Diagnostics, 2012).

  • CALCR – this mediates the hormone calcitonin, polymorphisms can lead to decreased bone density (Genova Diagnostics). Bone density is least for TT allele individuals and bone mineral density should be optimised when young (through calcium rich foods, sunlight exposure and regular weight bearing exercise) (Culp, 2004).

  • VDR – those with a TT allele are more likely to have decreased BMD, increased rate of bone turnover due to elevated osteocalcin, and may benefit from significantly increased Vitamin D and calcium supplementation where as those with a T/G allele may benefit from additional supplementation (Culp, 2004).


Other important factors include:

  • IL-6 – the G allele is associated with higher levels of IL-6 and cortisol.  GG and GC allele holders may benefit from a lower calorie, lower fat diet.  Fish oils, Siberian Ginseng and pinebark extract have all been shown to lower IL-6 (Culp, 2004) 

  • TNF-a – the A alleleis associated with higher levels of TNF-a which may be connected to increased bone loss, maintaining a normal weight, insulin and glucose levels all lower TNF-a.  Fish oils, green tea, NAC, lactobacillus and nettle leaf extract have all been shown to lower TNF-a (Culp, 2004). 

  • ESRa – Oestrogen receptor - significant increases in osteoporosis risk have been observed in those with CC alleles.  In postmenopausal women the risk decreased with moderate alcohol consumption. (Sonoda et al., 2012).



Phases of Lifespan


Preconception, Intrauterine, pregnancy and breastfeeding


Intrauterine environment affects the trajectory of subsequent bone development, with smoking, vitamin D, calcium, folic acid, potassium and magnesium intake having an impact on child’s bone health (Tobias et al., 2005). Maternal constraint (passing of environmental and nutritional information from mother to embryo or fetus) happens in all pregnancies and can limit foetal growth to a genetic potential, however this happens more frequently in women with short maternal stature, extremely young or old maternal age and in multiple pregnancies, excessively under or overweight women or those with an unbalanced diet (Holroyd et al., 2011).  Newborn total body BMC is lower among winter births than among infants born during the summer (Javaid & Cooper, 2002). One study (with 619 women at risk of post-menopausal osteoporosis) showed that the women who had their first pregnancy when they were 27 years or older and breastfed had a lower prevalence of OP compared to those who had a pregnancy before aged 27 and did not breastfeed  (Schnatz et al., 2010). Therefore if the mother knows she has a genetic risk for osteoporosis and is being proactive in prevention for her offspring, the timing of the pregnancy, and maternal nutritional weight and status is paramount. Lower social maternal class is also associated with reduced whole-body BMC, it is unlikely that a woman with a low income will have access to genetic testing, however even without testing it has been long known that daughters of osteoporotic mothers have low BMD (Aaseth et al., 2012). 


  • A daily practice of gentle weight-bearing exercise would be beneficial (e.g. yoga). 

  • Aim for vaginal delivery to support gut flora of child.

  • Ensure breastfeeding support in place prior to birth, and then aim to breastfeed.


Infancy and childhood


Bone growth occurs during infancy and the diaphysis of the long bones is ossified at birth while secondary ossification happens from infancy through to adolescence, with periods of rapid growth between 1-4 years (Ondrak & Morgan, 2007). Infants should be encouraged to play and move as movement against gravity contributes to muscle strength (Cech, 2012).  Weaning occurs now and the carer influences the infants diet.  This may be hard to achieve if the infant is in nursery full time, or if the child is one of many and the parents are unable to cook due to skills, time or money.  Children are susceptible to growth plate fractures as they enter a period of peak height growth (Caine et al., 2006) with overweight and obese children having impaired bone development (Goulding et al., 2000).


The website offers free resources for children and schools about the importance of bone health.


Puberty and Adolescent’s


It is estimated that between 33-60% of bone mass is acquired during the adolescent growth spurt, therefore maximizing bone mass during this life stage is very important (Bonjour et al., 2001). Bone density is strongly influenced by hormonal and metabolic factors associated with sexual development (NCSF, 2012). Trends affecting optimal bone health during adolescence include an increase in television viewing leading to less exercise, experimenting with smoking and alcohol as well as dietary changes.  Peer pressure and media are more likely to affect food choices.   Increased intake of soft drinks, which are high in phosphates, impairs calcification in growing bones and serum calcium is inversely correlated with numbers of soft drinks consumed each week (Tucker, 2009).




Bone growth and remodeling continue through adulthood with formation and resorption continuing at similar rates until 30-50 in men and 38-48 in women.  The age range differs depending on ethnicity.  After this time bone loss begins to exceed bone formation (Cech, 2012).  Oral contraceptive use is a risk factor and may prevent younger women attaining maximum peak bone mass contributing to osteoporosis in later life (Teegarden et al., 2005). The overriding factor for bone loss in menopausal women in their early 50’s is the hormonal response, that calcium intake over the first five years is not effective and pre/prebiotics appear not to modulate calcium absorption during this period (Coxam, 2007). EFA’s in menopausal women slowed bone loss and in some cases stimulated bone growth (Clayton, p259).




As oestrogen and testosterone decrease, so does bone mass.  The decline in these hormones influences the ability of the intestines to absorb calcium, triggering a depletion of bone calcium stores (Riggs et al., 2002).


Residential care has been correlated with hastened bone loss (Hansen & Vondracek, 2004).

  • As it is harder to eat, chew and digest foods, softer and easier to eat meals must be provided.  This may include; scrambled eggs, slow cooked meat and vegetable casseroles, steamed or flaked fish, such as fish pie, or fishcakes, soups including meats or beans and pulses, and whey protein could be incorporated into meals or snacks – pea protein can be added to savoury pancakes or soups.


Nutrients required for bone health


Further details are provided in one of my clinical handouts - showing specific recommendations for each life stage.


Protein - it is widely accepted that protein deficiency increases the risk of bone fragility and fracture; however diets high in protein have also been implicated in deteriorating bone health, in part due to high acid renal load with inadequate buffering by alkali foods or supplements.  According to the European Food Standards Agency Guidelines, evidence is insufficient to alter protein intakes for those with osteoporosis from that of the normal population (EFSA, 2012).  For those at risk of osteoporosis increasing the amount of fruits and vegetables is likely to be more useful than decreasing protein intake (Heaney & Layman, 2008), and focusing on plant proteins which decrease the risk compared to animal proteins which increase the risk, may be of benefit (Aaseth et al, 2012).


  • In all life stages good quality protein should be consumed at every meal.  Including meat, fish, pulses and soya products – organic is preferable.


Essential Fatty Acids (EFA’s) - increase absorption of calcium from the gut; prevent the abnormal deposition of calcium in soft tissue, and increases calcium content in the bone and enhance bone collagen synthesis this is due to a reduction in cytokine production and regulation of prostaglandins. The ratio of omega 6 to 3 is also important, with a ratio of 2:1 being ideal, however OP is reduced in Japan where the ratio is 4:1, and the general UK population has a ratio of 16:1. Deficiencies of omega 3 are a major contributor to OP and supplementing with omega 3 rich foods increases calcium absorption, bone calcium and BMD. (Albertazzi & Coupland, 2002; Genius & Schwalfenberg, 2006) A diet, which contains normal amounts of calcium, but is deficient in EFA’s, increases risk of osteoporosis (Clayton, p258).


  • Include essential fats in the diet daily.  Choose from oily fish, nuts, seeds, nut butters and oils or seed butters and oils.  Supplements may be useful in some population groups.


Calcium - is a major mineral involved in bone formation; however OP occurs more frequently in countries with high calcium intake indicating other factors may be involved, such a Vitamin D and Vitamin K synthesis (Aaseth et al., 2012).  This theory is supported with positive outcomes from trials using calcium with Vitamin D supplementation over calcium alone for reducing fracture risk (Tang, 2007; Reid et al., 2008). However with controversy over the use of high dose calcium supplements, due to increased risk for cardiovascular events or renal calculi (Reid et al., 2008; Bolland et al., 2010; Li et al., 2012), dietary sources are more preferable.


  • Including green leafy vegetables (spinach, pak choi, turnip or mustard greens, kale) broccoli and green beans, and using organic soy products would be advised.  Infants should include dairy products such as full fat milk, and yogurt (preferably organic).


During development the human foetus requires 30g of calcium for bone development, and much of this is acquired in the third trimester, therefore a lower maternal calcium intake may be a risk for lower bone mass in neonates (Holroyd et al., 2011).  Those with a COL1A1 TT allele respond well to increased dietary calcium, where as GG allele individuals may not respond significantly (Culp, 2004).


Vitamin D  – lower concentrations of serum 25(OH) – Vitamin D during late pregnancy have been associated with reduced whole-body and lumbar spine BMC, as well as BMD.  Supplementing with Vitamin D, especially during winter months, could lead to a decline in long-lasting osteoporosis risk (Holroyd et al., 2011).


Boron and Molybdenum – needed in tiny amounts to support enzymatic reactions which take place in bone growth.  Boron has been found to reduce urinary calcium loss and to increase serum levels of 17-beta estradiol both of these effects help bone health. The minimum daily dose of boron needed (2 mg per day) is easily met with a diet rich in fruits, nuts and vegetables; supplements can be taken up to 12 mg per day (Price et al., 2012).

  • ¼ cup prunes or almonds/1/3 cup apricots or peanuts or ½ avocado provides 1mg of Boron.


Fruits and vegetables - contain magnesium, potassium, manganese, vitamin C, and vitamin K all essential for bone health (Tucker, 2009).  Vitamin K has a profound impact on the bioavailability and transportation of calcium into bone tissue (Aaseth et al., 2012). It naturally occurs in two forms, VTK-1 which is abundant in green leafy vegetables, soya beans as well as olive oil and VTK-2 synthesised by gut bacteria.  It has been known for some time that deficiencies may be associated with lowered BMD (Shearer, 1997; Booth, 1997) The Nurses’ Health Study found that women with low VTK intake had higher rates of risk fracture (Feskanich et al., 1999) and The Framingham Osteoporosis study found that men and women with higher VTK consumption sustained 35% relative risk of hip fracture compared to those with low intakes  (Hanan et al., 2000).  Deficiencies occur due to insufficient intake or from a depletion of gut micro-flora, which commonly occurs following antibiotic use (Conley & Stein, 1994). Increase in plant fibres from fruits and vegetables are associated with increased BMD in elderly men and women (Tucker et al., 2002).


Phytoestrogens - published data is inconsistent which has led to many controversies (Lagari & Levis, 2010) however habitual intake of more than 5mg/day has positive effects on bone health (Kuhnle et al., 2011).  Organic and/or fermented soya products are advisable.


Supplements (vitamins, minerals, antioxidants, amino acids, phytonutrients, pre/probiotics).


The 2012 Canadian Combination Micronutrients for Bone (COMB) study had a total of 77 participants taking a daily combination of 250mg DHA, 2,000iu Vitamin D3, 100mcg Vitamin K3, 680mg Strontium citrate, 25mg magnesium, dietary calcium and daily exercise, for 12 months.  This is the first study reporting on multiple supplements in combination rather than individually.  They had compliance issues which led to the small number in the final sample however of those that did comply, the results were positive showing an increase in BMD of up to 8% in the lower spine (Genuis & Bouchard, 2012). This study has limitations but highlights the possibility of a nuetraceutical intervention for those unwilling or unable to use pharmaceutical preventions or treatments.  Larger studies of this kind would be very beneficial to clinicians.


Lycopene:  Roa et al., (2003) showed lycopene inhibits mineral resorption by inhibiting osteoclast formation and the production of ROS. In 2006 it was demonstrated that a higher lycopene intake correlated with lower bone turnover (Rao et al., 2006).  More recently lycopene given as tomato juice or as a supplement in postmenopausal women reduced risk of osteoporosis (Mackinnon et al., 2011).

Propolis regenerates bone tissue (Ang et al., 2009).


Pre/Probiotics - animal studies have demonstrated prebiotics stimulate the absorption of iron, calcium, magnesium and zinc in the short term, while longer term increasing BMC.  Data in human trials is conflicting with some studies finding no significant effect and others finding increased absorption in calcium and magnesium.  There are limited studies on probiotics and bone health in humans, however animal trials using Lactobacillus casei, Lactobacillus reuteri, Lactobacillus gasseri and Lactobacillus helveticus have seen positive results with BMC and calcium absorption (Scholz-Ahrens, 2007; Coxam, 2007).  Further studies in this area would be beneficial.  Optimising gut health should be of primary importance with any client at risk of osteoporosis, due to absorption and microbial metabolism, not only of vitamins but supporting beta-glucoronidation of isoflavones.  This is particularly important in aging populations (Yamaguchi, 2006).




Toxicity - aluminum, lead and cadmium block vitamin metabolism, organophosphate pesticides block Vitamin K metabolism, and many medications contribute to decreased bone density (Genuis & Schwalfenberg, 2006).

Smoking - is significantly associated with lower neonatal bone mass in both male and female offspring as well as being associated with reduced whole-body bone mineral content of children at the age of 9 (Holroyd et al., 2011).  Smoking depletes body of Vitamin C, essential for bone health, and increases risk of hip fracture by up to three times (Clayton, p248).  Smoking also affects MTHFR gene (5,10-methylenetetrahydrofolate reductase) leading to high serum homocysteine concentrations, which have adverse effects on bone (Lu et al., 2011).

Stress - maternal stress affects development of the HPA axis in the foetus, and high levels of circulating cortisol affect bone density and rates of bone loss (Holroyd et al., 2011). 




In 2005 the direct cost of osteoporosis in the USA was around $17 billion/year and in Europe around 13 billion Euros, this excludes costs due to lack of productivity (Lewiecki, 2004; Dennison et al., 2005). 


The cost of the supplements used in the COMB study was $2.26 per day ($824.90 per annum) compared to the cost of bisphosphonates, which range from $0.90 to $12.26 per day (Genuis & Bouchard, 2012). 


Using diet and nutritional supplements as a primary approach may be cost effective alternative. 



Ang E, Pavlos NJ, Chai LY, Qi M, Cheng TS, Steer JH, Joyce DA, Zheng MH, Xu J (2009) Caffeic acid phenethyl ester, an active component of honeybee propolis attenuates osteoclastogenesis and bone resorption via the suppression of RANKL-induced NF-κB and NFAT activity.  Journal of Cellular Physiology 221:3:642–649

[] Accessed: 27th August 2012.


Booth S (1997) Skeletal functions of vitamin K dependent proteins; not just for clotting anymore.  Nutrition Review 55:282-284. Available at: [].  Accessed: 26th August 2012.


Caine D, DiFiori J, Maffulli N (2006) Physical injuries in children’s and youth sports: reason for concern? British Journal of Sports Medicine 40:749-760. Available at: [].  Accessed: 20th August 2012.


Clayton P (2004) Health Defense: 2nd Edition. Accelerated Learning Systems Ltd. Bucks.

Conley & Stein (1994) Reductions of K2 concentrations in human liver associated with the use of broad scale antimicrobials. Clinical Investigative Medicine 17:531-539. 

Coxam V (2007) Current Data with Inulin Type fructans and calcium, targeting bone health in adults.  The Journal of Nutrition 2527S-2533S.  Available at: [].  Accessed: 24th August 2012.


Culp (2004) OsteoQuick Reference.


Aaseth J, Boivin G, Anderson O (2012) Osteoporosis and trace elements – An Overview.  Journal of Trace Elements in Medicine and Biology. Article In Press.  Available at: []. Accessed: 20th August 2012.


Baxter-Jone A, Burrows M, Bachrach L, Lloyd T, Petit M, Macdonald H (2010) International longitutinal pediatric reference standards for bone mineral content.  Bone 46:208-216. Available at: [].  Accessed: 20th August 2012.


Bolland MJ, Avenell A, Baron JA, Grey A, MacLennan GS, Gamble GD, Reid IR. (2010) Effect of calcium supplements on risk of myocardial infarction and cardiovascular events: meta-analysis. British Medical Journal 341:c3691. Available at: [].  Accessed: 12th August 2012.


Bonjour JP, Chevelley T, Ammann P, Slosman D, Rizzoli R (2001) Gain in bone mineral mass in prepuberatl girls 3-5 years after discontinuation of calcium supplements: a follow up study.  Lancet 358:1208-1212.  Available at: [].  Accessed: 20th August 2012.


Burrows M, Baxter-Jones A, Mirwald R, Macdonald H, McKay H (2009) Bone mineral accrual across growth in a mixed-ethinic group of children: are Asia children disadvantaged from an early age?  Calcified Tissue International 84:366-378.  Available at: [].  Accessed: 18th June 2012.


Cech D (2012) Prevention of osteoporosis: From infancy through older adulthood.  Hong Kong Physiotherapy Journal 30:6-12. Available at: [].  Accessed: 20th June 2012.


Dennison E, Cole Z, Cooper C, (2005) Diagnosis and epidemiology of osteoporosis.  Current Opinions in Rheumatology. 17:P456-61.  Available at: [].  Accessed: 15th August 2012.


Earl S, Harvey N, Cooper C (2010) The epigenetic regulation of bone mass.  IBMS BoneKEy 7:54–62 Available at: [].  Accessed: 18th June 2012.


European Foods Standards Agency (2012).  Dietary Reference Values for Protein. EFSA Journal 10:2:2557 Available at: [] Accessed: 19th June 2012.


Feskanich D, Weber P, Willett W, Rockett H, Booth S, Colditz G (1999) Dietary Vitamin K intakes are associated with hip fracture but not bone mineral density in elderly men and women.  American Journal of Clinical Nutrition 71:1201-1208.  Accessed: 26th August 2012.


Genova Diagnostics (2012) Available at: [].  Accessed: 12th June 2012.


Genuis & Bouchard (2012) Combination for Micronutrients for Bone (COMB) Bone Density after Micronutrient Intervention.  Journal of Environment and Public Health Article ID 354151. Available at: [].  Accessed: 27th August 2012.


Genuis & Schwalfenberg (2007) Picking a bone with contemporary osteoporosis management: Nutrient strategies to enhance skeletal integrity.  Clinical Nutrition 26:193-207.


Goulding A, Taylor R, Jones I, McAuley K, Manning P, Williams S (2000) Overweight and obese children have low bone mass and area for their weight. International Journal Obesity Related Metabolic Disorders 24:627-632.


Hanan M, Felson D, Dawson-Hughes B, Tucker K, Cupples A, Wilson P, Kiel D (2000) Risk Factors for Longitudinal Bone Loss in Elderly Men and Women: The Framingham Osteoporosis Study. Journal of Bone and Mineral Research 15:4:710–720. Available at: [].  Accessed: 18th June 2012.


Hansen L & Vondracek S (2004) Prevention and Treatment of non-postmenopausal osteoporosis.  American Journal Health System Pharmacy 61:2637-2654. Available at: [].  Accessed: 17th August 2012.


Heaney R & Layman D (2008) Amount and type of protein influences bone health.  American Journal of Clinical Nutrition 87:5:156S-157S. Available at: [].  Accessed: 15th August 2012.


Holroyd C, Harvey N, Dennison E, Cooper C (2011) Epigenetic influences in the developmental origins of osteoporosis.  Osteoporosis International 23:401-410.

Kuhnle G, Vogiatzoglou A, Ward HA, Khaw KT (2011) Dietary phytoestrogens and health – a population study. Proceedings of the Nutrition Society. 70:OCE4 Available at: [].  Accessed: 30th August 2012.


Lagari & Levis (2010) Phytoestrogens and bone health Current Opinion in Endocrinology, Diabetes & Obesity 17:6:546–553. Available at: []. Abstract only.  Accessed: 30th August 2012. 


Lewiecki E (2004) Management of osteoporosis. Clin Mol Allergy. 2:9.  Accessed: 15th August 2012.


Li K, Kaaks R, Linseisen J, Rohrmann S (2012) Associations of dietary calcium intake and calcium supplementation with myocardial infarction and stroke risk and overall cardiovascular mortality in the Heidelberg cohort of the European Prospective Investigation into Cancer and Nutrition Study. Heart 98:12:920-5. Available at: [].  Accessed: 17th August 2012.


Lu Y, Liuc YZ, Liub PY, Dvornykd V, Deng HW (2011) A bootstrap-based regression method for comprehensive discovery of differential gene expressions: An application to the osteoporosis study. European Journal of Medical Genetics 54: 6: e560–e564. Available at: [].  Accessed: 31st August 2011.


Mackinnon E, Rao A, Josse J, Rao L (2011) Supplementation with the antioxidant lycopene significantly decreases oxidative stress paramters and the bone resoprtion marker N-telopeptide of type 1 collagen in postmenopausal women.  Osteoporosis International 22:4:1091-1101.  [Abstract only]. Available at: []. Accessed: 21st August 2012.


Mendoza N, Quereda F, Presa J, Salamanca A, Sanchez-Borrego R, Vazguez F, Astorquiza T (2012) Estrogen-related genes and postmenopausal osteoporosis risk.  Climacteric.  [Abstract only]. Available at: [].  Accessed: 23rd June 2012.


Mlakar S, Prezelj J, Osredkar J, Marc J (2012) BMD Values and GSTM3 Gene Polymorphisms in Combination with GSTT1/GSTM1 Genes: A Genetic Association Study in Slovenian Elderly.  Gerentology 58:3:238-248. [Abstract only]. Available at: []. Accessed: 25th August 2012.


National Osteoporosis Society Available at: [].  Accessed: 15th August 2012.


National Council on Strength and Fitness (2012) Available at: []. Accessed: 15th August 2012.


Nutrition study (EPIC-Heidelberg) BMJ Heart 98:920-925 [] Accessed: 26th August 2012.


Office of Genomics and Disease Prevention: Centers for Disease Control and Prevention. Department of Health and Humans. Gene-Environment Interaction Fact Sheet, 2000.

Available at: [].  Accessed: 19th June 2012.


Ondrak & Morgan (2007) Physical activity, calcium intake and bone health in children and adolescents.  Sports Medicine 37: 587-600. Available at: [].  Accessed: 15th August 2012.


Prentice A (2004) Diet, nutrition and the prevention of osteoporosis. Public Health Nutrition 7:1A:227–243 . Accessed: 28th August 2012.


Rao LG, Krishnadev N, Banasikowska K, & Rao AV (2003) Lycopene I--effect on osteoclasts: lycopene inhibits basal and parathyroid hormone-stimulated osteoclast formation and mineral resorption mediated by reactive oxygen species in rat bone marrow cultures. Journal of Medicinal Food 6:2: 69-78. Available at: [].  Accessed: 15th August 2012.


Rao LG, Mackinnon ES, Josse RG, Murray TM, Strauss A, Rao AV (2007) Lycopene consumption decreases oxidative stress and bone resorption markers in postmenopausal women. Osteoporosis International 18:1:109-15. Available at: [].  Accessed: 15th August 2012.


Reid IR, Bolland MJ, Grey A. Effect of calcium supplementation on hip fractures. Osteoporos Int. 2008 Aug;19(8):1119-23. Epub 2008 Feb 20. Available at: [] Accessed: 26th August 2012.


Riggs B, Khosla S, Melton L (2002) Sex steroids and the construction and conservation of the adult skeleton.  Endocrine Reviews 23:279-302.


Schnatz P, Barker K, Marakovits K, O’Sullivan D (2010) Effects of age at first pregnancy and breastfeeding on the development of postmenopausal osteoporosis. Menopause 17:6:1161-1166.


Scholz-Ahrens K, Ade P, Marten B,Weber P,Timm W, A§il Y, Glu ̈er C, Schrezenmeir J (2007) Prebiotics, Probiotics, and Synbiotics Affect Mineral Absorption, Bone Mineral Content, and Bone Structure, The Journal of Nutrition.  137:838S-846S.


Shearer M (1997) The roles of vitaminD and K in bone health and osteoporosis prevention.  Proceedings of the Nutrition Society. Accessed:15th August 2012.


Sonoda T, Takada J, Iba K, Asakura S, Yamashati T, Mori M (2012) Intercation between ESR-a polymorphisms and environmental fctors in osteoporosis.  Journal of Orthopedic Research (Early View – online version of record before inclusion in an issue).  Wiley Online Library [Abstract only].


Tang BM, Eslick GD, Nowson C, Smith C, Bensoussan A. (2007) Use of calcium or calcium in combination with vitamin D supplementation to prevent fractures and bone loss in people aged 50 years and older: a meta-analysis. Lancet 25:370:9588:657-66. Available at: [].  Accessed: 26th August 2012.


Teegarden D, Legowski P, Gunther C, McCabe G, Peacock M, Kyle R (2005) Dietary calcium intake protects women consuming oral contraceptives from spine and hip bone loss.  Journal of Clinical Endocrinological Metabolism 5:127-5133.


Tobias J, Steer C, Emmett P, Tonkin R, Cooper C, Ness A (2005) Bone Mass in childhood is related to maternal diet in pregnancy.  Osteoporosis International 16:12:1731-1741. Available at: [].  Accessed: 18th June 2012.


Tucker KL, Hannan MT, Chen H, Cupples LA, Wilson PWF, Kiel DP (1999) Potassium, magnesium and fruit and vegetable intakes are associated with greater bone mineral density in elderly men and women.  American Journal of Clinical Nutrition 69:727-736.  Accessed: 15th August 2012.


Tucker KL, Chen H, Hannan MT, Wilson PW, Felson D (2002) Bone Mineral Density and dietary patterns in older adults.  The Framingham Osteoporosis Study. American Journal of Clinical Nutrition 76:245-252.  Accessed: 15th August 2012.


Tucker (2009) Osteoporosis Prevention and Nutrition.  Current Osteoporosis Reports 7:4:111-117.  Available at: [].  Accessed: 20th August 2012.


Yamaguchi M (2006) Regulatory mechanism of food factors in bone metabolism and prevention of osteoporosis. The Pharmaceutical Society of Japan 126:11:1117-1137. Available at: [].  Accessed: 17th August 2012.


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