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Osteoporosis: Definition, Description and Overview

Sunday, March 06, 2011   (0 Comments)
Posted by: Leah Dean
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Cathy L. Zanker, PhD

Article for F.E.A.S.T. March 2011

Osteoporosis: Definition, Description and Overview

The term osteoporosis, derived from Latin, literally means ‘porous bones’. It is caused by a deterioration of the internal structure of bones which leaves them fragile and more vulnerable to fracture. The development of osteoporosis involves the progressive loss of both protein and mineral salts. This loss reduces bone mass and strength - and hence puts the person at risk of breaking bones, even without an injury.

Approximately one in three women and one in ten men will ultimately develop osteoporosis. The onset usually occurs after the age of 50 years and is related to both hormonal changes and age-related loss of muscle mass. Osteoporosis is more common in older women than in older men. In post-menopausal women, bone is broken down faster than it is reformed, which leads to bone loss.

Osteoporosis can also occur in young children and adolescents if they have inherited bone diseases, physical disabilities which limit movement, intestinal malabsorption, corticosteroid use or suffer from  malnutrition. In healthy children, bone mass increases gradually with age . There is an accelerated acquisition of bone during the pubertal growth spurt, with continued increases in bone mass and strength through the teenage years.  Peak bone mass is usually acquired between the ages of 18 and 23 years. Optimisation of bone growth and development during childhood and adolescence may be achieved through the consumption of a well balanced, nutritious diet in conjunction with the maintenance of a healthy weight and regular weight bearing exercise.

Osteoporosis in Eating Disorders

People with low weight anorexia nervosa are at special risk of  developing osteoporosis, and at a much younger age than people with no history of eating disorder (Klibanski et al., 1995; Hotta et al., 1998). Osteoporosis is less common in individuals with bulimia nervosa than in those with anorexia nervosa, primarily because weight history tends be significantly higher in bulimic individuals. Fractures are also more common in people with anorexia nervosa, or those with a history of the illness (Biller et al., 1989; Klibanski et al. 1995).

The reason why people with a history of anorexia nervosa often have osteoporosis is two-fold:

  • First, anorexia nervosa usually starts during the teenage years when bones are still growing and developing both their structure and strength. Malnutrition and low weight slow or halt bone development and growth.
  • Second, anorexia nervosa frequently continues, or follows a relapsing course during a person’s 20s and beyond - i.e. after normal linear growth has ceased. This causes the individual to lose bone prematurely and often from an already fragile skeleton.

People who develop anorexia nervosa at a younger age (especially pre-puberty) are at risk of both failing to build bone during growth and also losing bone prematurely (Soyka et al. 2002). These individuals usually have the most fragile bones and are most vulnerable to fracture. If recovery from anorexia nervosa occurs during the teens and early 20s, and bone mass deficits are quite small, it may be possible to ‘catch up’ and achieve a normal, healthy bone mass (Bass et al. 2005). The potential to increase bone mass with combined re-feeding and normalisation of body weight is probably reduced with increasing age. The extent of any increase in bone mass (with weight gain and the maintenance of a healthy weight) will also depend upon such factors as: the amount of bone accrued before the onset of low weight anorexia nervosa, the amount of bone lost as a consequence of low weight anorexia nervosa, the rate and severity of weight loss, and the duration of low weight (Zanker and Hind 2007).     

Causes of Osteoporosis in Eating Disorders

In the early 1980s it was assumed, without substantive evidence, that osteoporosis in young women with anorexia nervosa is caused by an oestrogen deficiency, as is the case after the menopause (Rigotti et al. 1984). Oestrogen deficiency is typical in girls/women with anorexia nervosa who do not have a menstrual cycle and are not taking oestrogen replacement (e.g. the oral contraceptive pill). In the past, women with anorexia nervosa were often prescribed oestrogen, usually in the form of the oral contraceptive pill with the objective of protecting their bone density. However, subsequent extensive research has shown that few anorexic women benefitted from this hormone treatment and many still continued to lose bone (Mehler and MacKenzie 2009). These findings suggested that the causes of osteoporosis in anorexia nervosa are different to the causes of osteoporosis in post-menopausal women.

It is now known that osteoporosis occurs in anorexia nervosa not just because of a deficiency of sex hormones , but also on account of malnutrition (Zanker and Cooke 2004; Mehler and MacKenzie 2009). Over the past 10-15 years there have been many studies of the mechanisms of low bone density  or osteoporosis in women with anorexia nervosa which suggest that the main cause is malnutrition and low weight (Zanker and Hind 2007; Mehler and MacKenzie 2009). Underweight runners, especially those with amenorrhoea also have osteopenia or osteoporosis (Zanker and Cooke 2004). It seems that when the body is not receiving enough energy and nutrients, and has little reserves of both fat and muscle (due to low weight loss and the maintenance of a low weight), there are many hormonal changes which slow bone formation and/or accelerate bone loss. These hormonal changes include high levels of cortisol, and low levels of IGF-1 and leptin (Zanker and Cooke 2004; Zanker and Hind 2007). The only way to normalise the levels of these 'nutritional' hormones is to reverse malnutrition and for the individual to achieve and maintain a healthy weight (Zanker and Hind 2007, Mehler and MacKenzie 2009). Research has shown that in girls and women with anorexia nervosa or exercise-associated (low weight) amenorrhoea, bone mass usually increases during and after weight gain, especially if periods start (or return) and remain regular (Zanker and Hind 2007, Mehler and MacKenzie 2009).

In comparison with the large amount of research that has explored the causes of osteoporosis in girls and women with eating disorders, there has been relatively little research undertaken with boys and men. However, the small amount of recent research that has been conducted with males suggests that as with females, osteoporosis is caused by both sex hormone deficiency and abnormal synthesis or metabolism of 'nutritional' hormones (Misra et al. 2008). Thus, the same treatment is advised for males as for females; i.e. reversal of malnutrition and weight gain.

Diagnosis of Osteoporosis in Eating Disorders

Osteoporosis is usually diagnosed using a procedure called dual energy x-ray absorptiometry (DXA). DXA measures areal bone mineral density (BMD) - i.e. the amount of mineral in a given area of bone. The sites of measurement for diagnostic purposes are the lumbar spine and the hip. A DXA scan provides an indication of a person’s BMD in relation to normal, healthy values for a male or female of a particular age. It is a painless procedure which requires the person to lie on a couch for 5-10 minutes while the scanner moves above the body. Doctors treating individuals with anorexia nervosa usually recommend a DXA scan, especially if body weight has been low for some time. However, as described next, there is currently no effective drug treatment for osteoporosis caused by anorexia nervosa and so the use of DXA scans in untreated anorexia nervosa is questionable.

Treatment of Osteoporosis in Eating Disorders    

The only really effective treatment of osteoporosis in anorexia nervosa is weight gain. Bone cells, like all other cells in the body function optimally when a person is of a healthy weight for their height, sex and age. This weight usually amounts to a body mass index (BMI) between 19 and 25 kg.m-2 for adults. The greatest concern about osteoporosis and fracture is in girls who develop anorexia nervosa before their periods start, and in boys who should still be growing in height. In these children there is a risk of permanently stunted growth.

Treatment with hormones or other drugs that are used to treat osteoporosis in older people is not normally advised - especially for younger people with eating disorders. This is because such treatments are not very effective - and may even exacerbate disturbances of bone metabolism (Zanker and Hind 2007; Mehler and MacKenzie 2009). Instead, good nutrition and weight gain, which are known to be far more effective, is recommended. Indeed, weight gain is usually essential to prevent irreversible damage not only to bones but to all other tissues. If anorexia nervosa develops after periods have already started in girls, or growth is near complete in boys, bone that has been lost may be regained, provided the illness hasn’t continued for more than 2-3 years. The longer the duration of low weight and the lower the weight attained in anorexia nervosa, the greater the risk of irreversible osteoporosis.

Exercise and calcium supplements are often recommended for older people with osteoporosis related to the menopause or their older age; however, neither of these treatments is very effective in low weight anorexia nervosa. This is because abnormal bone metabolism and osteoporosis develop as a direct consequence of negative energy balance and weight loss (Zanker and Hind 2007; Mehler and MacKenzie 2009). The recommended treatment is a nutritious, well balanced diet that leads to normalization of weight and body composition  and the maintenance of a healthy weight.

Although exercise helps to maintain bone health in children and adults of a healthy weight, it may pose a serious risk to people with anorexia nervosa. In particular, intense or prolonged exercise at a low weight increases the widespread complications of starvation on all organs and should definitely be avoided. Once BMI has increased to above approx. 18 kg.m-2 with re-feeding, carefully prescribed weight-bearing exercise may help to build bone as the weight normalization process continues. However, advice should be taken from an eating disorder professional before starting an exercise programme during recovery from anorexia nervosa. Factors such as electrolyte balance, heart health and bone mass density will need to be considered.

Calcium supplements are unlikely to bring about significant benefits to bone health when weight is low and may even worsen metabolic complications in people with very low weight (e.g. by further lowering blood phosphate levels and inducing other electrolyte disturbances).

Key points:

  • Girls and women with anorexia nervosa are at high risk of developing osteoporosis
  • Osteoporosis in anorexia nervosa is usually caused by inadequate bone growth and development during adolescence, sometimes in conjunction with premature bone loss.
  • The most severe cases of osteoporosis occur in women who develop anorexia nervosa pre-puberty and have a long duration of illness.
  • Osteoporosis in anorexia nervosa is rarely reversible, but bone mass/density usually increases with weight gain and the maintenance of a healthy body weight.
  • Osteoporosis in anorexia nervosa is refractory to treatment with most drugs, including the oral contraceptive pill, HRT and bisphosphonates.
  • The primary, and most effective treatment for osteoporosis in anorexia nervosa is weight gain to BMI > 19, which also leads to regular menses
  • There are no specific dietary recommendations for treatment of osteoporosis in anorexia nervosa apart from a well balanced diet that promotes weight gain. However, an adequate intake of calcium and protein is essential, and any vitamin deficiencies should be corrected, using supplements if necessary (e.g. Vitamin D3).

 

References

Bass SL, Saxon L, Corral AM, Rodda CP, Strauss DL, Reidpath D, Clarke C. Near normalization of lumbar spine bone density in young women with osteopenia recovered from adolescent onset anorexia nervosa: a longitudinal study. Journal of Pediatric Endocrinology and Metabolism 2005: 18; 897-907.

Biller BM, Saxe V, Herzog DB, Rosenthal DI, Holzman S, Klibanski A. Mechanisms of osteoporosis in adult and adolescent women with anorexia nervosa. Journal of Clinical Endocrinology and Metabolism 1989: 68; 548-554.

Hotta MT, Shibasaki K, Sato K, Demura H. The importance of body weight history in the occurrence and recovery of osteoporosis in patients with anorexia nervosa: evaluation by dual X-ray absorptiometry and bone metabolic markers. European Journal of Endocrinology 1998: 139; 276-283.

Klibanski A, Biller BMK, Schoenfeld DA, Herzog DB, Saxe VC. The effects of estrogen administration on trabecular bone loss in young women with anorexia nervosa. Journal of Clinical Endocrinology and Metabolism  1995: 80; 898-904.

Mehler PS, MacKenzie TD. Treatment of osteopenia and osteoporosis in anorexia nervosa: a systematic review of the literature. International Journal of Eating Disorders. 2009: 42; 195-201.

Misra M, Katzman DK, Cord J, Manning SJ, Mickley D, Herzog DB, Miller KK, Klibanski A. Bone metabolism in adolescent boys with anorexia nervosa. Journal of Clinical Endocrinology and Metabolism  2008: 93; 3029-36.

Rigotti NA, Nussbaum NR, Herzog DB, Neer RM. Osteoporosis in women with anorexia nervosa. New England Journal of Medicine 1984: 311; 1601-1606.

Soyka LA, Misra M, Frenchman A, Miller KK, Grinspoon S, Schoenfeld DA, Klibanski A. Abnormal bone mineral accrual in adolescent girls with anorexia nervosa. Journal of Clinical Endocrinology and Metabolism 2002;87:4177-4185.

Zanker CL, Cooke CB. Energy balance, endocrine function and bone health. Medicine and Science in Sports and Exercise 2004: 36; 1372-1381.

Zanker CL, Hind K. The effect of energy balance on endocrine function and bone health in youth. Book chapter in ‘Optimizing Bone Mass and Strength: The Role of Physical Activity and Nutrition during Growth. Karger International Series in Medicine and Sport Science 2007: 51;  81-101.  



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