Many women still believe that osteoporosis is a condition that only affects bone density later in life, regardless of recent efforts of medical experts to establish otherwise. In the most recent issue of Women’s Health Orthopedic Edition, Rebecca J. Locke and Michelle P. Warren, MD from Columbia Presbyterian Medical Center in New York discuss the relationship between nutrition, hypothalamic amenorrhea (HA), osteopenia and osteoporosis, a link which clearly puts many young women at increased risk of low bone density. Recognizing that bone loss can occur early in a woman’s life is a crucial step in the prevention of this process.
Hypothalamic amenorrhea (HA), or secondary amenorrhea, is the absence of menstruation in women who previously had regular periods. The term hypothalamic refers to the hypothalamus, an area at the base of the brain that acts as a hormone control center for the body, regulating, among other things, a woman’s menstrual cycle. In certain situations, such as anorexia, excessive exercise and stress, the flow of hormones is interrupted. This results in the failure of the body to produce enough estrogen and progesterone, the suppression of ovulation, and ultimately, the loss of menses. (Mayo Clinic. Amenorrhea: When Menstruation Goes Away.)
Hypothalamic amenorrhea (HA) due to anorexia, excessive exercise and stress can be extremely damaging to the body in many ways. Low body weight, inadequate body fat and energy deficiency contribute to the suppression of hormones in cases of anorexia and excessive exercise, including gonadotropin-releasing hormone (GnRH), luteinizing hormone (LH) and follicle stimulating hormone (FSH) that eventually leads to the loss of menses. Stress-related amenorrhea, also known as psychogenic HA, can affect normal weight, nonathletic women due to high levels of cortisol (a stress-related hormone) and accompanying endocrine and metabolic changes in the body.
Because hypothalamic amenorrhea is the body’s hormonal reaction to a number of different issues, it is usually seen as a red flag that whatever has lead to the loss of menstruation needs to be addressed. Furthermore, long-term amenorrhea has significant complications of its own, such as a significantly increased risk of osteopenia and osteoporosis. Osteopenia is literally defined as “poverty of bone”, and refers to any decrease in bone mass below the normal. The more commonly used term, osteoporosis, is an advanced version of osteopenia, meaning that the loss of bone mass is more significant. (Johns Hopkins. Osteoporosis. www.intelihealth.com)
Because the loss of estrogen at menopause has been implicated in the acceleration of bone loss, some have concluded that targeting the lack of estrogen production associated with amenorrhea is the most effective route to recovery in the pre-menopausal population. However, Locke and Warren point to recent evidence that highlights nutritional deficiency as a common precursor to the loss of estrogen in all types of HA. Women with eating disorders suffer from nutritional insult, low body weight and inadequate body fat, all of which clearly play a role in the loss of estrogen, the development of HA and the subsequent increased risk of osteoporosis. Athletes and excessive exercisers often expend enormous amounts of energy without adding to their diet to make up for this deficit, leading to a form of malnutrition which can trigger the hormonal suppression that leads to amenorrhea.
Finally, in key studies, restrictive eating patterns and subclinical eating and exercise disorders, such as very low fat intake, high fiber intake and more calories expended in aerobic activity daily, were found in normal weight, non-athletic women with amenorrhea, even though overall caloric intake was not significantly altered. Thus, even in the absence of blatant dietary restrictions or excessive exercise, nutritional deficiencies still played a role in their development of amenorrhea. From this evidence, which identifies nutritional deficiency as a common underlying cause of estrogen loss leading to amenorrhea in young women, it seems that targeting nutrition may be a more effective route to recovery than trying to replace estrogen without addressing the cause for loss. (Journal of Clinical Endocrinology & Metabolism, March 1999, p. 873-877).
Other evidence supporting nutrition as a common denominator for HA has been substantiated by the role of the hormone leptin, which is normally secreted by adipose tissues. Studies have shown that levels of leptin fall rapidly with severe nutritional restriction, regardless of body weight, fat, or body mass index. Low levels of leptin are a signal to the brain to shut down other “unnecessary” hormonal pathways, such as ovulation and reproduction, and to slow down cellular metabolism to protect the body’s fat stores. Furthermore, it has been shown that menstruation cannot occur beneath a certain level of leptin in the body. Thus, because lower leptin levels have been found in both normal and underweight women with HA, it can be concluded that nutritional deficiencies, regardless of overall caloric intake or body fat percentage, play a major role in the development of amenorrhea.
By identifying nutritional deficiency as a common, underlying cause for all three types of HA, it is possible to develop preventive measures to minimize bone density loss due to amenorrhea, such as screening for restrictive eating patterns regardless of weight. Patient education efforts must also be increased to ensure that young women realize that the detrimental effects of amenorrhea, such as osteoporosis, extend past the point of the recovery of menses. Peak bone mass can and must be reached through nutrition and exercise into a woman’s late 20’s and possibly early 30’s. After age 40, regardless of what level of density was reached, bone mass begins to decline. Thus, by reaching peak bone mass in the first place a young woman can minimize the amount of bone density decline due to the aging process.
Once a woman has developed hypothalamic amenorrhea, treatment must be pursued as soon as possible. The overall goal of treatment is to restore menses as soon as possible to minimize the loss of bone mass. According to Locke and Warren, this is most effectively accomplished by treating the cause for hormonal suppression (nutrition) instead of merely replacing the lost estrogen. Treatment options also include behavioral and psychiatric counseling to address individual reasons for excessive stress, exercise and eating disorders. As a last resort, oral contraceptives can be used to minimize the loss of bone density caused by a prolonged lack of estrogen, but unless the causes for hormonal loss are addressed, estrogen replacement has not been shown to be very effective.
Women need to be made aware of the role that nutrition plays in the loss of estrogen, the development of amenorrhea, and the subsequent increased risk of osteopenia and osteoporosis. By understanding what initiates the cycle that leads to osteoporosis, it is possible that women at risk can minimize or even avoid substantial bone loss.
Locke, Rebecca J. and Warren, Michelle P. How to Prevent Bone Loss in Women with Hypothalamic Amenorrhea. Women’s Health Orthopedic Edition. 2000; 3: 82-88.
Warren MP, Voussoughian F, Geer EB, et al. Functional Hypothalamic Amenorrhea: Hypoleptinemia and Disordered Eating. Journal of Clinical Endocrinology and Metabolism. 1999; 84: 873-877.
Mayo Clinic. Amenorrhea. www.mayohealth.com
Johns Hopkins. Osteoporosis www.intelihealth.com