Reuters reported on a study that was published in the American Journal of Clinical Nutrition that suggests the restoration of normal menstrual periods in anorexic women to be necessary for normal bone metabolism and prevent osteoporosis.
One of the limitations of this study is the small sample size: when I checked out the abstract, the study contained only 28 women. Additionally, there may be other confounding effects, including the role of dietary intake in bone metabolism. The study suggests that anorexic women form bones at a normal rate, but break down bones faster than they make bones to result in net loss of bone mineral density.
Recently I wrote about a pill that would stop menstrual periods altogether, and my concern about the long term side effects of modulating hormones, especially if the pill gets marketed as a “lifestyle” drug for women rather than for a diagnosed medical need. Additionally, menstrual periods may signal other health states in the female body, as evidenced by the loss of menses in anorexic women and in women who over-exercise.
American Journal of Clinical Nutrition, Vol. 86, No. 1, 92-99, July 2007
© 2007 American Society for Nutrition
“Treatment of anorexia nervosa is associated with increases in bone mineral density, and recovery is a biphasic process involving both nutrition and return of menses”
Jennifer Dominguez, Linnea Goodman, Surupa Sen Gupta, Laurel Mayer, Sarah Fischer Etu, B Timothy Walsh, Jack Wang, Richard Pierson and Michelle P Warren
Background: Recovery from osteoporosis in anorexia nervosa (AN) is uncertain.
Objective: The purpose of this study was to understand the changes in bone mineral density (BMD) in women with AN and the mechanisms of recovery from osteopenia.
Design: We studied BMD and markers of bone formation and resorption, osteocalcin and N-telopeptide (NTX), in patients with AN (n = 28) who were following a behavioral weight-gain protocol.
Results: Anorexic patients experienced significant percentage increases in BMD (4.38 ± 7.48% for spine; 3.77 ± 8.8% for hip; P < 0.05 for both) from admission until recovery of 90% ideal body weight, achieved over 2.2 mo. NTX concentrations were higher in patients with AN at admission than in healthy control subjects (n =11; 69.0 ± 31.09 and 48.3 ± 14.38 nmol/mmol creatinine, respectively; P < 0.05) and in reference control subjects (n = 30; 69.0 ± 31.09 and 37.0±6.00 nmol/mmol creatinine, respectively; P < 0.001). In weight-recovered subjects with AN, osteocalcin increased (from 8.0 ± 3.05 to 11.2 ± 6.54 ng/mL; P < 0.05), whereas NTX remained elevated (from 69.0 ± 31.09 to 66.7 ± 45.5 nmol/mmol creatinine; NS). A decrease in NTX (from 70.7 ± 40.84 to 45.9 ± 22.72 nmol/mmol creatinine; NS) occurred only in the subgroup of subjects who regained menses with weight recovery. Conclusions: Nutritional rehabilitation induces a powerful anabolic effect on bone. However, a fall of NTX and a shift from the dominant resorptive state, which we postulate involves full recovery, may involve a hormonal mechanism and require a return of menses. Nutritional rehabilitation appears to be critical to bone recovery and may explain the ineffectiveness of estrogen treatment alone on BMD in the cachectic state.