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Using the Activity-based Anorexia Rodent Model to Study the Neurobiological Basis of Anorexia Nervosa
Published on: October 22, 2015
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Osteoporosis in anorexia nervosa.
1a Division of Adolescent Medicine, Stanford University School of Medicine, 770 Welch Road, Suite 433, Palo Alto, CA 94034, USA. ngolden@stanford.edu.
Expert Review of Endocrinology & Metabolism
|February 16, 2019
Summary
Anorexia nervosa leads to low bone mass and fragility, with limited treatment options. This review discusses fracture risk assessment and management strategies for bone health in affected children and adolescents.
Area of Science:
- Pediatric Endocrinology
- Bone Metabolism
- Eating Disorders
Background:
- Anorexia nervosa (AN) is linked to decreased bone mass and increased fracture risk.
- Adolescence, a critical period for peak bone mass accrual, is the typical onset for AN.
- Multifactorial causes include poor nutrition, low body weight, hormonal deficiencies, and hypercortisolism.
Purpose of the Study:
- To review fracture risk assessment in pediatric AN.
- To summarize evidence on low bone mass and fracture risk in AN.
- To discuss management strategies for low bone mass in AN.
Main Methods:
- Literature review of recent recommendations for fracture risk assessment.
- Synthesis of evidence regarding bone density and fragility in AN.
- Discussion of therapeutic approaches for managing low bone mass.
Main Results:
- AN is associated with reduced bone formation and accelerated resorption, leading to low bone mass.
- Weight gain and hormonal normalization may partially improve bone mass but often not to normal levels.
- Oral estrogen therapy is ineffective; bisphosphonates show promise but have safety concerns.
Conclusions:
- Effective treatments for bone loss in AN are lacking.
- Bisphosphonates, alongside nutritional rehabilitation, may offer a potential therapeutic avenue.
- Further research is needed to optimize bone health management in AN patients.
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