Osteoporosis - The 'Silent' Disease


ION Archives

Year of publication: 

According to the UK National Osteoporosis Society, 1 in 3 women and 1 in 12 men will develop osteoporosis during their lifetime. Carolyn Moody Dip.ION examines this increasingly growing condition and provides a nutritional protocol for its prevention

The skeleton is a living structure, constantly reshaping itself, as old bone tissue is broken down and replaced with new. An adult skeleton is renewed every seven to ten years, while a child’s is renewed every two years. Bones are made up of a protein (collagen) matrix which provides a framework for calcium and other minerals in crystal form. The structure looks like a honeycomb, with blood vessels and bone marrow in the spaces between bone. Two types of cells - osteoclasts and osteoblasts - contribute to the process of bone remodelling and regeneration and are constantly dissolving and reforming the skeleton. Bone matter acts as a storage site for calcium and other minerals. When blood calcium levels fall, calcium is mobilised from the bones.

Osteoblasts and osteoclasts are influenced by two hormones which work to keep blood calcium levels at the desired concentration. The hormone calcitonin lowers serum calcium by increasing the activity of osteoblasts - cells that help build bone. This mechanism transports calcium, magnesium and phosphorous from the blood into bone tissue. Parathyroid hormone, on the other hand, raises blood calcium levels by increasing the activity of osteoclasts, cells that break bone down. Via this interplay of hormones and minerals the level of calcium in the blood is maintained.(1)

Osteoporosis, which literally means “porous bones”, occurs when the holes between bone matter enlarge, resulting in fragility and brittle bones. This increases the risk of bone fracture, particularly in the hip, spine, and wrist.(2) With more than 200,000 fractures occurring every year, osteoporosis is a disease that affects 1 in 3 women and costs the NHS and UK government over £1.5 billion. Men are also affected by loss of bone density, with estimates being as high as 1 in 12 men suffering from fractures due to osteoporosis.


Osteoporosis is often referred to as the “silent” disease because at the onset there are no obvious symptoms. The first sign that the condition may be present is when a fracture occurs, often in the wrist or spine, following a minor bump or fall. Osteoporosis causes the small vertebrae in the spine to crush or wedge, often resulting in chronic pain, curvature, and consequently a loss of height.


In women, bone mass begins to decline at 35 years of age, and bone loss accelerates rapidly for eight to ten years around the time of the menopause. Thereafter, bone loss continues at a slower rate. Those most at risk of developing osteoporosis are postmenopausal women. Bone loss at this time of life is caused by changes in the balance of hormones that control bone building and resorption, particularly parathyroid hormone, calcitonin, oestrogen and possibly progesterone.

Most studies have looked solely at the interaction between oestrogen, parathyroid hormone and calcitonin. Yet it is clear that this is not the only important interaction. Nutritionist, Henry Osiecki, in The Physicians Handbook of Clinical Nutrition (Bio Concepts), shows that yet another hormone plays a role in osteoporosis – cortisol. Produced by the adrenal cortex, cortisol appears to have several effects upon skeletal homeostasis, one of which is to increase the sensitivity of bone cells to parathyroid hormone, vitamin D and growth factors.

As oestrogen levels decline at menopause, the production of transcortin (protein binding hormone) decreases resulting in an increase in free cortisol. Stress (both acute and chronic) also increases cortisol levels. Raised cortisol levels block intestinal absorption of calcium and increase parathyroid hormone secretion, leading to an increase in loss of calcium in the urine and a block in new bone formation. Figure 1 illustrates the influence of stress and menopause on cortisol and its interaction with the hormones that affect bone strength.



Figure 1: Based on information obtained from Henry Osiecki’s, The Physicians Handbook of Clinical Nutrition, Bio Concepts, 1990.

Caucasian and oriental women over the age of 50 have a higher incidence of osteoporosis. US demographics show that people of African descent have higher bone mass and lower rates of fractures, while in Europe the highest rates of vertebral deformities are in Scandinavian countries.

Ageing men suffer a decrease in the hormone testosterone and since testosterone is converted into oestrogen, this hormone loss can cause similar problems for men as oestrogen loss does for women.
Other risk factors include: (3)

Early menopause or early hysterectomy (especially if both ovaries are removed), before age 45.
Family history of osteoporosis or maternal history of hip fracture.
History of over-active thyroid.
Hypercalcinuria (abnormally high amounts of calcium in the urine).
Medications: long term use of steroids, thyroid hormone, heparin, gonadotropin releasing hormone agonists, anticonvulsants and benzodiazepines.
Liver disease.
Long term immobility.
Malabsorption due to low stomach acid, inflammatory bowel disease and gastric surgery.
High alcohol and caffeine intake and smoking.
Low body weight and anorexia, which cause a reduction in oestrogen levels.


Although calcium supplementation alone has not been found to benefit the treatment of osteoporosis, it’s vital to obtain a sufficient amount of this mineral in the diet. Milk and milk products are often recommended as the main source of dietary calcium, but due to their poor magnesium content which is essential for proper calcium metabolism, they are best limited. In addition many people are lactose intolerant, so if dairy foods are not properly digested, the nutrients in them will be poorly absorbed. Yoghurt as a fermented milk product contains more easily absorbed calcium.(4) Non-dairy sources of calcium include broccoli, oysters, sardines, seeds, nuts, figs, beans, tofu and seaweed.(5)

Some foods actively cause the excretion of calcium, particularly those that are acid forming.(6) The pH level (measure of acidity or alkalinity) of the blood is vital and must be kept fairly constant or we would die. The body with its innate wisdom therefore draws alkaline minerals from the skeleton if we eat too many acid forming foods. It is therefore recommended that a healthy diet should be based on approximately 70-80% alkaline forming foods and 20-30% acid forming foods. Highly acid forming foods such as red meat, sugar, refined foods, caffeine and alcohol should be avoided.

Excess protein, as well as insufficient protein, have been found to influence the development of osteoporosis. When over 85,000 American women were followed for 12 years, those who ate the most animal protein (meat, poultry and dairy produce) had a significantly higher risk of osteoporotic fractures.(7) When dietary protein increases, so does the loss of calcium in urine, although this extra calcium loss is not always statistically significant.

Bone formation requires protein, so if too little protein is eaten, risks associated with osteoporosis may increase. In one trial of older women (average age 82) who had suffered an osteoporotic fracture, those given a 20 gram a day protein supplement had fewer complications, were less likely to die, and had much shorter hospital stays compared with women not assigned to receive extra protein.(8) However, under normal circumstances sufficient protein is best obtained from the diet. Similarly, in a three-year study of American women aged 50 to 69 funded by the National Dairy Council, those eating more animal protein had a lower risk of osteoporotic hip fracture compared with those eating less.(9) A related double-blind trial in older women who had recently suffered an osteoporotic hip fracture found that a 20 gram-a-day protein supplement reduced bone loss compared with those not receiving protein.(10)

Salt intake may increase bone loss. Researchers found that increasing dietary salt increases markers of bone loss in postmenopausal women (but not in premenopausal women).(11) Although a definitive link between salt intake and osteoporosis has yet to be proven, it may be wise to restrict dietary salt, or switch to unrefined sea salt that contains other minerals, including calcium.

A large study following American women for six years showed that caffeine consumption is linked to hip fractures due to its ability to increase urinary calcium loss. This is associated with caffeine’s diuretic properties.(12) The authors of this report concluded that two to three cups of coffee a day might speed up bone loss in women with calcium intakes of less than 800 mg a day. As caffeine is found in coffee, black tea and cola drinks, reducing the consumption of these may help to reduce loss of bone density.

Phosphoric acid, a substance found in many soft drinks, may be linked to abnormal calcium metabolism and calcium urinary loss. Studies show that young cola drinkers have an increased incidence of bone fractures and children drinking at least six glasses of carbonated drinks a day containing phosphoric acid had more than five times the risk of developing low blood calcium levels.(13,14)



Whole foods such as whole grains, vegetables, beans, pulses, tofu, fish, seeds, nuts (excluding peanuts), eggs and fresh fruit.
Calcium rich foods.
Plenty of water (approx. 11/2 -2 litres a day). Bottled or filtered water is preferable to tap water. Other liquids can include freshly pressed vegetable juices such as carrot, parsley, celery, watercress, and herbal teas. Horsetail tea, which is rich in silcon, is recommended.
Soya or oat milk may be preferable to cow's milk.


Foods that lack minerals such as refined carbohydrates.
Animal protein.
Foods that contain oxalic acid as this substance inhibits mineral uptake. Examples include rhubarb, Swiss chard and spinach.
Foods that are high in phytic acid such as wheat bran. This substance binds with minerals in the colon and carries them out of the body.
Salt. This causes increased amounts of calcium to be excreted from the body.
Foods that cause inflammation. These include red meat, dairy produce, fried food and saturated fats.
Stimulants such as sugar, spices, tea, coffee and alcohol.


Calcium, Magnesium and Vitamin D

Current medical treatments do not address the complexities of bone breakdown and regeneration or take into account all the factors that influence this on-going process. While calcium is the most abundant mineral found in bones, the main problem regarding osteoporosis seems to be associated with a lack of magnesium and vitamin D, both required for the absorption of calcium. In several studies, calcium intake has not correlated with protection against osteoporosis, for example, in men,(15) or in women shortly after becoming menopausal.(16)

Women with osteoporosis lack the bone enzyme, alkaline phosphatase. This enzyme, activated by magnesium, helps to form calcium crystals in bones. It therefore serves as a good indicator of whether new bone is being laid down or not. A study carried out by Dr John McLaren Howard at BioLab in London showed that the lowest levels of alkaline phosphatase were in the women with osteoporosis on HRT.(17)

Dr Guy Abraham conducted a trial based on magnesium therapy in postmenopausal women who were given dietary advice, vitamins and minerals, 600mg of magnesium oxide and 500mg calcium citrate – an unusual ratio. The control group received HRT only. The magnesium therapy group achieved an 11% increase in bone density in eight to nine months compared to the control group with only a 0.7% increase. Dr Abraham believes that osteoporosis is a sign of magnesium deficiency rather than calcium deficiency.(18)

Vitamin D3 (calciferol) is required for the absorption of calcium in the intestines and is made by the action of sunlight on the skin. Vitamin D is particularly deficient in those who live in sunless northern climates. Office workers spending most of their time indoors can soon become low in this vitamin. Magnesium is needed to convert vitamin D to its active form, 1,25-dihyroxyvitamin D3.(19)
Bones also need vitamins B6, C, K, folic acid, manganese, boron, strontium, silicon, zinc and copper for their health and strength.(20)

Vitamin B6 and Folic Acid

Vitamin B6 and folic acid are required for the detoxification of the toxic compound homocysteine produced in the body as a result of the breakdown of the amino acid methionine. Too much homocysteine damages bone tissue. Vitamin B6 is also a co-factor in the production of collagen which increases the strength of connective tissue in the protein matrix of bone. Smoking, alcohol, the Pill and HRT reduce B6 and folic acid levels.


Just 1 to 3 mg of boron a day slows down the excretion of calcium in urine and increases the level of naturally occurring oestrogens, particularly 17ß-estradiol, the most biologically active form of naturally occurring human oestrogen. In countries where the diet contains as much as 41mg of boron a day, no side effects have been reported.(21)

Unlike conventional HRT, boron is thought to reduce the risk of cancer due to its ability to increase oestriol levels, a form of oestrogen known to prevent certain types of cancer. All good quality multi vitamin and mineral supplements should now contain boron, especially if they are aimed at women.(22)

Vitamin K

Vitamin K is needed for the synthesis of osteocalcin, a protein found in large amounts in bone matter. Octeocalcin is the protein matrix upon which calcium crystallizes. A lack of vitamin K increases excretion of calcium through the kidneys. As this vitamin is normally found in vegetables, people eating fewer than five servings of vegetables a day may be susceptible to deficiency. Vitamin K can be manufactured in the body if there are sufficient “friendly” bacteria in the intestines.


Manganese is required for bone mineralisation and for the synthesis of connective tissue in cartilage and bone. Manganese deficiency leads to smaller, less dense bones with less resistance to fractures.


Zinc is essential for normal bone formation and for enhancing the biochemical action of vitamin D3.


Non-radioactive strontium occurs naturally in food and water and appears to reduce the incidence of dental caries and bone resorption.


Silicon is found in high concentrations at calcification sites in growing bone. It appears to strengthen the connective tissue matrix by cross-linking collagen strands. Horsetail is a useful herb as it is a rich source of silicon.


Copper is needed for normal bone synthesis. It is best obtained from food sources rather than a food supplement. Copper rich foods include nuts, legumes, whole grains and potatoes.

Natural Progesterone

Dr John Lee, an American physician, has done much to promote the use of natural progesterone in conjunction with a healthy diet, an exercise programme and vitamin and mineral supplementation to reverse osteoporosis.(23) However, two double-blind studies using natural progesterone cream for one and three years were unable to reproduce these results. It is not clear if these studies also recommended dietary changes, more exercise and a vitamin and mineral programme to accompany the natural progesterone cream.(24)

Essential Fatty Acids

In one study, the essential fatty acids from fish oil, notably EPA (eicosapentaenoic acid) and DHA (docosahexaenoic acid), and GLA (gamma linoleic acid) from evening primrose oil, were shown to help improve calcium metabolism. After taking fish oil and evening primrose oil with a 600mg calcium supplement, women with osteoporosis who were deficient in essential fatty acids, had a significant 3.1% increase in spinal bone mineral density compared to control groups.(25,26)


Ipriflavone is a synthetic flavonoid derived from the soya isoflavone, diadzein, and is now registered in Europe, Japan and Argentina, as a drug for osteoporosis, as well as being available over the counter in the UK. Unlike other isoflavones, ipriflavone does not possess oestrogenic activity. Nevertheless, it appears to enhance oestogen’s effect, making it a useful alternative to conventional hormone replacement treatments. Ipriflavone increases bone density by enhancing the absorption of calcium and phosphorus in the bone. It does this by stimulating bone-building osteoblast cells while inhibiting osteoclasts, cells which break down bone tissue. Ipriflavone is also thought to enhance the secretion of calcitonin, the primary bone-building hormone, and increase the production of bone matrix proteins.(27,28)

However, a potentially dangerous side effect of ipriflavone has been highlighted. Participants taking the supplement in two studies showed a significant drop in lymphocyte (white blood cell) count. Women who experienced the most severe drop in lymphocyte count took a year or more to recover. The main difference between these trials and other more successful studies was the amount of calcium taken with the ipriflavone. It may be that ipriflavone needs a higher quantity of calcium (1000 mg) to work properly.(29) Ipriflavone should probably be taken under medical supervision and avoided by anyone who is already immune compromised, such as individuals with HIV or those taking drugs to suppress the immune system.

Caucasian and oriental women over the age of 50 have a higher incidence of osteoporosis. US demographics show that people of African descent have higher bone mass and lower rates of fractures, while in Europe the highest ratesof vertebral deformities are in Scandinavian countries


Lifestyle changes that have been shown to influence bone density include the reduction of caffeine and alcohol intake, avoiding cigarettes, and taking regular weight bearing exercise (30) such as walking.

Excess body mass also helps protect against osteoporosis. As a result, researchers have been able to show that people who successfully lose weight have greater loss of bone compared with those who do not lose weight.(31) Therefore, people on weight loss regimes need to be more vigilant about
preventing osteoporotic fractures.


Vander Arthur J. Human Physiology, The Mechanisms of Body Function, Fourth Edition, McGraw-Hill International, 1988.
UK National Osteoporosis Society. Camerton, Bath BA2 0PJ.
Ott, Susan MD, Associate Professor Department of Medicine University of Washington.
The UK Vegetarian Society. Parkdale, Dunham Road, Altrincham, Chesire WA14 4QG.
Lactose Intolerance: A Resource including Recipes, Food Sensitivity Series, American Dietetic Association, 1991.
Holford, Patrick, The Optimum Nutrition Bible, Piatkus, 1997
Feskanich D, Willett WC, Stampfer MJ, Coldtiz GA. Protein consumption and bone fractures in women. Am J Epidemiol1996;143:472-9.
Schürch M-A, Rizzoli R, Slosman D, et al. Protein supplements increase serum insulin-like growth factor-I levels and attenuate proximal femur bone loss in patients with recent hip fracture. A randomised, double blind, placebo-controlled trial. Ann Intern Med 1998;128:801–9.
Tkatch L, Rapin C-H, Rizzoli R, et al. Benefits of oral protein supplementation in elderly patients with fracture of the proximal femur. J Am Coll Nutr 1992;11:519–25.
Munger RG, Cerhan JR, Chiu BC-H. Prospective study of dietary protein intake and risk of hip fracture in postmenopausal women. Am J Clin Nutr 1999;69:147–52.
Zarkadas M, Geougeon-Reyburn R, Marliss EB, et al. Sodium chloride supplementation and urinary calcium excretion in post menopausal women. Am J Clin Nutr 1989;50:1088-94.
Hernandez-Avila M, Colditz GA, Stampfer MJ, et al. Caffeine, moderate alcohol intake, and risk of the hip and forearm in middle-aged women. Am J Clin Nutri1991;54:157-63.
Wyshak G, Frisch RE. Carbonated beverages, dietary calcium, the dietary calcium/phosphorous ratio, and bone fractures in girls and boys. J Adolescent Health 1994;15:210-5.
Mazariegos-Ramos E, Guerrero-Romero F, Rodriquez-Moran F, et al. Consumption of soft drinks with phosphoric acid as a risk factor for the development of hypocalcaemia in children: a case-control study. J Pediatr 1995;126:940-2.
Owusu W, Willett WC, Feskanich D, et al. Calcium intake and the incidence of forearm and hip fractures among men. J Nutr 1997;127:1782–7.
Hosking DJ, Ross PD, Thompson DE, et al. Evidence that increased calcium intake does not prevent early postmenopausal bone loss. Clin Ther 1998;20:933–44.
CurRes in Osteo and Bone Mine Meas II, British Institute Radiology, London, 1992.
Abrahm GE, Grewal H. A total dietary programme emphasizing magnesium instead of calcium. J Reprod Med1990;35:503-7.
Rude RK, Adams JS, Ryzen E, Endres DB, Niimi H, et al. Low serum concentrations of 1,25-dihyroxyvitamin D in human magnesium deficiency. J Clin Endocrinol Metab 1985; 61:933-40.
Gaby, Alan R, MD and Wright, Jonathan V, MD. Nutrients and osteoporosis. Review Article. Journal of Nutritional Medicine 1990;1:63-72.
Weir RJ Jr, Fisher RS. Toxicologic studies on borax and boric acid. Toxicol Appl Pharmacol 1972;23:351-64.
Lemon HM, Wotiz HH, Parsons L, Mozden PJ. Reduced estriol excretion in patients with breast cancer prior to endocrine therapy. JAMA 1966;196:1128-36.
Lee, John R. MD, Natural Progesterone, BLL Publishing, California, USA, 1993.
Leonetti HB, Longo S, Anasti JN. Transdermal progesterone cream for vasomotor symptoms and postmenopausal bone loss. Obstet Gynecol. 1999;94:225-228.
Van Papendorp DH, Coetzer H, Kruger MC. Biochemical profile of osteoporotic patients on essential fatty acid supplementation. Nutr Res 1995;15:325-34.
Kruger MC, Coetzer H, de Winter R, et al. Calcium, gamma-linolenic acid and eicosapentaenoic acid supplementation in senile osteoporosis. Ageing 1998;10:385-94.
Gennari C, Agnusdei D, Crepaldi G, et al. Effect of ipriflavone – a synthetic derivative of natural isoflavones – on bone mass loss in the early years after menopause. Menopause 1998;5(1):9-15.
Agnusdei D, Buffalini L. Efficacy of ipriflavone in established osteoporosis and long term safety. Calcif Tissue Int 1997;61 :142-147.
Alexandersen P, Toussaint A, Christiansen C, et al. Ipriflavone in the treatment of postmenopausal osteoporosis: a randomised controlled trial. JAMA.2001;285:1482-1488.
Chow R, Harrison JE, Noorarius C. Effect of two randomised exercise programmes on bone mass of healthy postmenopausal women. Br Med J 1987;295:1441-4.
Salamone LM, Cauley JA, Black DM, et al. Effect of a lifestyle intervention on bone mineral density in premenopausal women: a randomised trial. Am J Clin Nutr 1999;70:97–103.




Carolyn Moody is a nutritional therapist practicing in the heart of the European Union in Brussels.



The Institute for Optimum Nutrition is an independent educational charity.
Registered company number 2724405, registered charity number 1013084