If you are:

• a women under 50 years old
• have not yet reached menopause and
• recently learned that your bone density is low

We would like to hear your story. We are looking for women to be confidentially interviewed about their experiences of having low bone density.

Young Osteoporosis Women (Y.O.W.)

Y.O.W. is a group of younger women throughout B.C. who have low bone density, osteoporosis or osteopenia. Since osteoporosis is viewed by the general public and the medical professions as a largely “old women’s disease”, Y.O.W. has started a project to research our situation and begin changing this perception. By bringing younger women together to collectively analyze their stories and circumstances, the project aims to fill critical gaps in information and create educational materials for both the general public and for health care providers. As importantly, connecting with women in similar circumstances is one way that young women with low bone density can find the support that is needed for healing.

The Research Project is co-directed by Dr. Jerilynn C. Prior and Francis Kirson. You are invited to call us and tell us your story. If you wish more information or simply want to connect with other women in your situation please call Francis Kirson, at (604) 833-8856, or email: fkirson@telus.net.

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As a society we have become more aware of the implications of our food choices with regards to our general health. We are taught by media and health professionals to think before we eat and to make “healthy food choices”. In many ways, watching what we eat has become an important step in achieving and maintaining a healthy lifestyle. For many individuals, however, the choice of what and how much to eat is an almost constant stress. Extreme dieting behavior and the prevalence of severe eating disorders such as anorexia nervosa are increasing.

It is well-established that malnutrition and clinical eating disorders such as anorexia nervosa are negative for bone health. Adolescents and adults with anorexia have very low bone mass and high risk for fracture (1). Weight loss through dieting or illness causes rapid bone loss (2,3). In anorexia nervosa, multiple factors cause bone loss and/or lack of bone gain including inadequate nutrition, decreased mechanical load on bone (due to low muscle mass and low body weight), lower reproductive hormone levels, and stress-related increases in cortisol levels.

In the general population, many generally healthy individuals, consciously try to limit their food intake in order to achieve or maintain a desired body weight or size. This is referred to as dietary restraint. In our research at the University of British Columbia, we have evidence from three different groups of girls or women that dietary restraint, as well as dieting behavior, influence how much bone is gained during adolescence and increase the risk for fracture. In this article we will define eating attitudes and dieting behavior, describe how stressors act to influence bone mass, and finally summarize key studies showing negative effects of dietary restraint and dieting on bone mass.

Eating attitudes and dieting behavior

Eating attitudes are assessed in both clinical and research settings with well established questionnaires. Two of those questionnaires, which we have used in our research, include the Three Factor Eating Questionnaire (TFEQ) (4) and the children’s Eating Attitudes Test (chEAT) (5). Both include questions used to define behaviors including dieting and bulimia (meaning self-induced vomiting). They also have questions designed to determine how much an individual thinks about or attempts to restrict food intake – termed “Dietary Restraint” on the TFEQ and “Oral Control” on the chEAT. Although these two terms are not identical, they are highly related and the terms will be used interchangeably for the purposes of this article.

Dietary restraint is defined as “a conscious attempt to limit food intake to regulate body weight”. Individuals scoring high on the restraint scale are extremely aware of the amount and type of food they consume (6). An example question used to assess restraint is: “how likely are you to consciously eat less than you want?”. Answers are scored from 1-5 ranging from not at all (1) to extremely (5). It is important to note that, although someone may score high on the restraint scale, they do not necessarily exhibit different patterns of eating behavior. In other words, many individuals who are extremely conscious and concerned about what they eat, do not actually eat less than those who happily eat what they want. In contrast, dieting behavior is an actual limiting of caloric intake resulting in weight loss. Weight loss schemes are often ineffective over the long-term and a rapid re-gain of weight is common. This loss and re-gain of weight is referred to as weight-cycling. We will discuss the effects of both eating attitudes/dietary restraint, and weight-cycling (or dieting) behavior. In our research, we have also studied individuals who score within what is considered to be the “normal” range for eating attitudes.

How could eating attitudes or dieting behavior influence bone mass?

Threats / Stresses:

• Physical — cold heat etc.
• Emotional — relationships
• Nutritional — undernutrition, fasting
• Overtraining — excess exercise

Figure 1. Process through which physical, emotional, or nutritional challenges cause increased release of CRH from the hypothalamus. These factors suppress the reproductive system and stimulate the adrenal axis. Abbreviations: ACTH = cortiotrophin; LH = lutenizing hormone. Adapted from Prior JC. Exercise associated menstrual disturbances. In: Adashi EY, Rock JA, Rosenwaks Z (eds). Reproductive Endocrinology, Surgery, and Technology. Raven, New York, 1996, pp. 1077-1091

Eating restraint and dieting behavior can be chronic stressors for many individuals. We hypothesized that bone loss occurs due to subtle decreases in reproductive hormones and increases in cortisol (a stress hormone) – both of these changes negatively effect bone mass.

In order to understand these relationships, it is important to discuss how the endocrine system responds and adapts to perceived stressors. In women, physiological adaptation to a number of stressors often results in changes in menstrual cycle function. These alterations range from subtle changes including shortened luteal phase length and anovulation in the presence of normal cycle length, to long cycles or amenorreha (lack of menstruation(. Menstrual cycle and ovulatory disturbances are often protective and necessary adaptations to increased stress (Figure 1).

The hypothalamus, which controls reproductive function and stress hormone release, receives information from several areas of the brain and functions to maintain homeostasis in response to internal and external demands. In situations of high stress, the body may adapt to prevent pregnancy for women or decrease libido and reproductive hormones in men, as a protective mechanism to conserve energy. Psychological or physiological stresses such as life changes, loss of a loved one, college stresses, inadequate energy intake, eating restraint, or rapid increases in exercise training, have all been associated with menstrual cycle disturbances.

These may be mediated by increased release of corticotrophin-releasing hormone (CRH) from the hypothalamus, which is hypothesized to suppress lutenizing hormone (LH) pulses through GnRH, possibly via the B-endorphin system, leading to suppressed reproductive capacity (7). Increases in cortisol also directly affect bone mass by increasing bone resorption. Thus, bone mass is negatively affected by both the increase in cortisol and the decrease in reproductive hormones (progesterone and estrogen) (Figure 1).

Similarly, dieting or other life stresses stimulate an increase in cortisol and a decrease in reproductive function (8-10).

What is the evidence that eating attitudes influence bone mass and fracture risk?

This section will summarize the results of a series of studies conducted at the University of British Columbia looking at the effects on bone mass of eating attitudes in university-aged women and adolescent girls, and of dieting behavior on fracture risk in adult men and women. Together these data provide important information about the role of eating attitudes and dieting behavior on bone mass and fracture risk.

Eating restraint and adult bone mass

Dr’s Susan Barr, Judy McLean and Jerilynn Prior have made a number of important observations about eating restraint in a series of studies in university-aged women (20-35y). The first of these studies showed that women with high restraint scores were more likely to have subtle menstrual cycle disturbances including short luteal phase lengths and anovulatory cycles (despite normal cycle lengths) (11). Women scoring high on the restraint scale also had higher cortisol levels in a 24 hour urine sample (12). Although the cortisol levels were within what is considered to be the normal range, these women also had a 1-3% lower bone mass at the spine and total body compared with women with low restraint (13). There were no other differences between the groups to explain the differences in bone mass. Interestingly, high eating restraint appeared to over-ride the positive benefits of exercise on bone mass (13). Taken together, these important data support the hypothesis that eating restraint, or a related aspect of restraint, is perceived as a stressor by the hypothalamus leading to subtle changes in the menstrual cycle, increased cortisol and decreases in bone mass.

Weight cycling and fracture risk Eating attitudes and bone mineral accrual

Childhood and adolescence are critical for the attainment of an optimal peak bone mass at adulthood (14). Peak bone mass is considered critical to preventing osteoporosis in later life. Thus, lifestyle factors should be optimized during these years. Therefore, we examined the role of eating attitudes in adolescent girls followed over 2 years (15). Girls were aged 9-12 years at the beginning of the study and were generally healthy, with adequate caloric and calcium intakes and were moderately active. Oral control scores, assessed using the children’s version of the Eating Attitudes Test, did not change during the two year study suggesting eating attitudes are established very early in life. Although we did not assess the parents’ eating attitudes, a previous study showed that 5-year old girls whose mothers dieted had high restraint scores (16). In our study, girls exhibiting high oral control had 3-5% lower bone mass at baseline and after 2 years (15). As in the studies of university-aged women, we could find no other factors to explain the differences between the groups.

Weight cycling and fracture risk

Figure 2. Proposed mechanism for bone loss with dietary restraint (from Dr. Judy McLean). Body weight is a well-established predictor of bone mineral density. People with higher body weights have higher bone mass (17) and weight gain protects against hip fracture (18). In contrast, with weight loss bone loss is inevitable (3). Individuals who diet to lose weight commonly regain what they have lost, and often more. This phenomenon, known as “weight cycling” is associated with lower spine and radius bone mineral density in premenopausal women (19) and with increased fracture risk (20).

We have recently looked at the role of weight cycling in 337 men and 728 women ages 25-96 years from British Columbia enrolled in the Candian Multicentre Osteoporosis Study (CaMOS).

In this study, men and women with 4 or more episodes of weight cycling (defined as weight loss and re-gain of 10 lbs or more) in their lifetimes had 1-3% lower bone mineral density at the hip and spine (common fracture sites) than individuals reporting no weight cycling episodes (21).

Men with more weight cycling also experienced more low-trauma fractures in their life time. This is despite the fact that the people with more weight cycling also had higher body weight – which is generally protective of bone.

There are some complicated issues in this study that we are currently examining. However, these data support the earlier work from the large Norwegian study suggesting that repeat dieting has a negative effect on bone health.

Summary

In summary, our studies and those of others suggest that:

• Dietary restraint and weight-cycling behavior can decrease bone mass and increase risk of fracture.
• Eating attitudes are established early in life and partially influenced by parental dieting behavior.
• Concern about food may prevent optimal gain of bone mass during adolescence.
• The negative influence of eating restraint on bone is at least partially mediated through a common stress mechanism due to the constant stress and worry about food intake.
• The effects of chronic stress on bone may over-ride the beneficial effects of exercise or other lifestyle factors on bone mass.

Conclusions

Although we have made great strides over the past decade in developing pharmecutical interventions for the prevention and treatment of osteoporosis and fractures, much less research has looked at lifestyle factors. New research suggests that stress and worry about food intake, attitudes towards eating, and “yo-yo” dieting behavior negatively affect bone mass and increase fracture risk. Eating attitudes are formed very early in life and associated to some extent with parental dieting behavior. It is important to encourage healthy eating attitudes and behaviors from a very early age. In addition to eating attitude and dieting behavior, reducing other life-stressors is also important for optimizing bone mineral accrual early in life, and slowing bone loss in later life.

Moira Petit is a post-doctoral research fellow at BC Women’s and Children’s Hospital and with the UBC Bone research group. Her research focuses on the role of physical activity, lifestyle, and endocrine factors in the prevention of osteoporosis. Jerilynn Prior is a Professor of Endocrinology at the University of British Columbia and an internationally known expert on women’s health.

References

1. Bachrach LK, Guido D, Katzman D, Litt IF, Marcus R 1990 Decreased bone density in adolescent girls with anorexia nervosa. Pediatrics. 86: 440-7.
2. Compston JE, Laskey MA, Croucher PI, Coxon A, Kreitzman S 1992 Effect of diet-induced weight loss on total body bone mass. Clin Sci. 82: 429-432.
3. Pritchard JE, Nowson CA, Wark JD 1996 Bone loss accompanying diet-induced or exercise-induced weight loss : A randomized controlled study. Int J Obes. 20: 513-520.
4. Stunkard AJ, Messick S 1985 The Three Factor Eating Questionnaire to measure dietary restraint, disinhibition and hunger. J Psychosom Res. 29: 71-83.
5. Maloney MJ, McGuire J, Daniels SR, Specker B 1989 Dieting behavior and eating attitudes in children. Pedatr. 84: 482-489.
6. McLean JA 1999 Cognitive dietary restraint, food intake and cortisol excretion in premenopausal women: Ph.D. Thesis. In:: Barr SIs (ed.). University of British Columbia, Vancouver, B.C.
7. Prior JC, Vigna YM, McKay DM 1992 Reproduction for the athletic woman: new understandings of physiology and management. Sports Med. 14: 190-199.
8. Alvero R, Kimzey L, Sebring N, Reynolds J, Loughran M, Nieman L, Olson BR 1998 Effects of fasting on neuroendocrine function and follicle development in lean women. J Clin Endocrinol Metab. 83: 76-80.
9. Berga SL 1996 Stress and ovarian function. Am J Sports Med. 24: S36-S37.
10. Petit MA, Prior JC 2000 Exercise and the hypothalamus: Ovulatory disturbances. In: Warren MP, Constantini N (eds.) Sports Endocrinology. Humana Press.
11. Barr SI, Prior JC, Vigna YM 1994 Restrained eating and ovulatory disturbances : possible implications for bone health. Am J Clin Nutr. 59: 92-97.
12. McLean JA, Barr SI, Prior JC 2000 Cognitive dietary restraint is associated with higher cortisol excretion in healthy premenopausal women. Am J Clin Nutr. In Press.
13. McLean JA, Barr SI, Prior JC 2000 Dietary restraint, exercise and bone density in young women: are they related? Med Sci Sports Exerc. In Press.
14. Bailey DA, McKay HA, Mirwald RL, Crocker PRE, Faulkner RA 1999 The University of Saskatchewan Bone Mineral Accrual Study: A six year longitudinal study of the relationship of physical activity to bone mineral accrual in growing children. J Bone Miner Res. 14: 1672-1679.
15. Barr SI, Petit MA, Vigna YM, Prior JC 2001 Eating attitudes and habitual calcium intake in peripubertal girls are associated with initial bone mineral content and its change over two years. J Bone Miner Res. In Press for May, 2001.
16. Abramovitz GA, Birch LL 2000 Five-year-old girls’ ideas about dieting are predicted by their mothers’ dieting. J Am Diet Assoc. 100: 1157-1163.
17. Felson DT, Zhang Y, Hannan MT, Anderson JJ 1993 Effects of body mass index on bone mineral density in men and women: The Framingham study. J Bone Miner Res. 8: 567-573.
18. Meyer HE, Tverdal A, Falch JA 1995 Changes in body weight and incidence of hip fracture among middle aged Norwegians. BMJ. 311: 91-92.
19. Fogelholm M, Sievanen H, Heinonen A, Virtanen M, Uusi-Rasi K, Pasanen M, Vuori I 1997 Association between weight cycling history and bone mineral denisty in premenopausal women. Osteoporos Int. 7: 354-358.
20. Langlois JA, Visser M, Davidovic LS, S. M, Li G, Harris TB 1998 Hip fracture risk in older white men is associated with change in body weight from age 50 years to old age. Arch Intern Med. 158: 990-996.
21. Petit MA, Kramer L, Hitchcock C, Barr SI, McKay HA, Vigna YM, Prior JC 2000 Weight cycling – A population risk factor for osteoporosis: Baseline data from the B.C. centre of the Canadian Multicentre Osteoporosis Study (abstract). J Bone Miner Res. 15: S140.

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Bones are truly amazing. A unique combination of flexible collagen and brittle calcium phosphate makes them incredibly strong and durable.

Part of the durability has to do with the fact that our bones are under constant maintenance, being partially broken down and rebuilt on a daily basis. Special bone cells called osteoblasts take calcium and phosphorus from the blood and deposit it as calcium phosphate crystals in the bone. In order for this to happen effectively a second set of cells, termed osteoclasts, must make some space for the new bone.

Figure 1. Relationship between total bone mass and age (from Kamen, 1996)

Osteoclasts remove the crystals and return them to the blood as calcium and phosphorus. It is the outer layer of the bones that are susceptible to these ongoing processes. We build up an optimum bone mineral (calcium phosphate) density (BMD) for the first 25-30 years of our life and spend the remainder of our lives gradually losing it, more quickly in women than in men.

(Figure 1). That is one reason why it is important to maximize your bone density when you are young improving your chances of avoiding or at least delaying osteoporosis.

Why all the fuss about calcium?

Calcium is responsible for nerve cell communication, contraction of muscle cells, function of important enzymes, protein synthesis, blood clotting efficiency and bone formation. Calcium levels in the blood are so important that the body will do almost anything to maintain an optimum concentration. If adequate calcium is not available from the diet then calcium will be removed from the bones and delivered to the blood. Unfortunately for your bones, blood calcium levels take priority.

Figure 2. Typical daily flow of calcium in and out of bone tissue (from Kamen, 1996)

You can imagine, perhaps, a blood calcium budget in your body being run by an accountant who insists on a balanced budget at all costs. The only external source of calcium is the diet (income). Since the digestive tract isn’t 100% efficient we must consume more calcium than our bodies really need. In addition some calcium gets excreted in the urine. So if we use 1000 mg as an example (Figure 2). of a typical daily calcium intake then it is estimated that only about 300 mg of that will enter the blood, and of that 300 mg about 150 will be excreted in the urine and another 150 returned to the digestive tract and eliminated in the feces.

In this budget there is a constant daily input and output of calcium to and from the gastrointesinal tract, the blood, the bones and the body’s other cells. With this in mind think of your bones as your nest-egg of calcium savings (sort of a calcium RRSP to be used when you’re older or on a rainy day). If calcium income at a given time is not adequate to maintain the blood calcium balance then the accountant will borrow from the bones to ensure a steady blood calcium level. Under ideal circumstances this calcium debt will be repaid to the bones.

So what’s the problem?

The problem is that the ideal conditions for repaying the calcium debt to the bones, are too infrequent in many people’s lives. Imagine if you made frequent withdraws from your RRSP and never repaid them. When it came time to retire you would be in for an awful shock. A poor lifestyle, inadequate diet, increased stress and insufficient exercise make it almost impossible for the blood calcium accountant to replace the bone calcium savings. Too many rainy days over an extended period of time and a calcium deficit is created in the bones and they become weak increasing the risk of fracture.

“Well”, says the accountant, “we need more income!” Yes, increased dietary calcium and calcium supplements may help slow the loss of BMD but the majority of research studies show that supplements don’t prevent the loss and they certainly don’t increase your BMD (Kamen, 1996).

Why? Because increasing available calcium for bone formation is complex and many other variables come into play. Certain aspects of diet and lifestyle are almost like having embezzlers within the company (your body) who keep sneaking off with potential “profits” (improved BMD). You can boost calcium “income” as much you wish but if a thief is stealing the profits how do you solve the problem?

Let’s get rid of the thieves!

Coffee, alcohol and smoking all lead to an increase in the acidity of the blood and one way the body compensates for this is by using calcium from the bones, as a buffer to reduce the acidity. Reducing or eliminating these items from your diet would be wise, especially smoking since it causes so much other damage to your body besides brittle bones. These are not the only delicacies that increase blood acidity. Dr. Susan Brown provides an excellent review of this subject (Brown and Jaffe, 2000) and a comprehensive list of a variety of foods and their affect on blood pH (alkalinity/acidity).

A diet that is too high in protein, for example, can increase the acidity of the blood and result in increased urinary excretion of calcium. This is one reason why excessive consumption of meat is not good for the bones (Marsh et al., 1988). As a general rule a 70 kg person only requires about 70 grams of protein per day and there are many other options besides meat. Be wary of milk, which is very high in protein, fat and sugar, and therefore may not be the ideal source of dietary calcium. Green leafy vegetables are your best source of calcium; chard, dandelion, alfalfa and parsley to name just a few.

Soft drinks are typically loaded with phosphoric acid which is a nightmare for pH balance and the high phosphorus content can throw off the calcium:phosphorus ratio and result in poor calcium assimilation. Most soft drinks are also high in sugar and caffeine making for a quadruple whammy. This one form of junk food is impairing healthy bone development in a significant number of young men and women as some studies are already showing (Wyshak and Frisch, 1994).

Calcium is only part of the picture

Calcium may be a key building material but other nutrients are critical to enabling your body to make the most efficient use of the available calcium, including adequate amounts of vitamin D3, magnesium, HCl, zinc and also key minerals such as boron and silicon.

Exercise, especially outdoor weight bearing exercise is essential as well. The benefits of exercise start as early as childhood and continue into our 70’s and 80’s with benefits resulting no matter when the exercise program has begun. Exercise, yoga or meditation will all help to reduce stress leading to healthier bones.

Space does not permit a discussion of all the nutrients that play a role in bone development but they are all consistent with an approach to diet that is nutritionally complete and benefits the entire body, not just the bones. It seems appropriate that if we take good care of the body as a whole, healthy bones and a healthy heart will follow.

Eric Norman is a research scientist investigating heart disease in post-menopausal women using ovarian hormone therapy and in type II diabetics.

References

1. Brown, S.E. and R. Jaffe. Acid-alkaline balance and its effect on bone health. International Journal of Integrative Medicine Vol. 2: No.6, 2000.
2. Chalmers, P. Geographical variationsin Senile Osteoporosis. J of Bone and Joint Surgery. 1970; 52B:667
3. Kamen, B. Hormone Replacement Therapy: Yes or No? Fourth Ed.. Pub. Nutrition Encounter, Novato, Cal. 1996
4. Marsh, A.G. et al..Vegetarian lifestyle and bone mineral density. Amer J Clin Nutr. 1988:48:837.
5. Wyshak, G. and R.E. Frisch. Carbonated beverages, diettary calcium/phosphorus ratio, and bone fractures in boys and girls. J Adolesc Health 15:210-215. 1994)

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If you are under 50 years old and recently learned that your bone density is lower than it should be, you may be feeling confused, worried or frightened. You are not alone. Osteo Juniors is a group of younger women throughout BC who have osteoporosis or osteopenia.

The problem with diabetes is that if blood sugar is allowed to be significantly above normal for many years irreversible damage to the eyes, kidneys, nerves and blood vessels may result leading to significant disability or even death. If blood sugar can be kept close to normal throughout life, not only will you have very good quality of life but your life expectancy should be no different to people who do not have diabetes. The key to controlling diabetes is to learn to closely regulate diet, exercise, insulin administration and blood glucose testing.

By bringing younger women together to collectively analyze their stories and circumstances, the project aims to fill critical gaps in information and create educational materials for both the general public and for health care providers. As importantly, joining the Osteo Juniors is one way that young women with low bone density can connect to each other and find the support that is needed for healing.

The Research Project is co-directed by:

• Dr. Jerilynn C. Prior, Professor of Endocrinology at the University of British Columbia, and Director of the Vancouver Centre of the Canadian Multicentre Osteoporosis Study (CAMOS). Dr. Prior’s Research has examined the connections among ovulation disturbance, exercise, stress of eating restraint and bone health.
• Frances Kirson, B.A.(Sociology), M.A.(Planning). As a community development planner with 10 years experience and over 15 years experience as an educator and coach, Francis has worked extensively on gender issues. Frances discovered she had osteoporosis when she fractured her hip at the age of 33. Over the last decade she has explored and used a variety of conventional and alternative treatments to improve her health.

You are invited to join us. We will explore and discuss the unique experiences of premenopausal women who have poor bone health.

If you wish more information, would like to get involved in this exciting project, or simply want to connect to other women in your situation, please call Frances Kirson, at (604) 833-8856, or email

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