Anorexia Nervosa (AN) is a severe psychiatric illness characterized by self-induced starvation and a pathologically low body weight. Chronic energy deficit and malnutrition cause widespread damage across multiple body systems. One of the most serious long-term medical complications of AN is its profound impact on skeletal health. The intense restriction associated with AN is strongly linked to a significant decrease in Bone Mineral Density (BMD). This bone thinning often leads to the development of osteopenia and, in more severe cases, osteoporosis.
Establishing the Link to Low Bone Mass
Up to 90% of individuals with AN exhibit some degree of low bone mineral density, significantly increasing their lifetime risk of fracture, which is approximately three times higher than for a healthy individual. The damage is particularly concerning when AN begins during adolescence, a timeframe of critical bone accrual when most people reach their peak bone mass. Disrupting this process means the patient may never achieve their full bone strength potential. Low body weight, specifically a low Body Mass Index (BMI), is consistently identified as the strongest predictor of low BMD in patients with AN. The resulting bone loss can be difficult to reverse, even after weight restoration.
Key Physiological Drivers of Bone Density Loss
The loss of bone density in AN is a complex process driven by multiple hormonal and metabolic disruptions caused by chronic caloric deprivation. Starvation triggers a defensive state in the body that prioritizes immediate survival functions over long-term processes like bone maintenance.
A major factor is severe hormonal imbalance, particularly estrogen deficiency. In females, low body weight often causes functional hypothalamic amenorrhea, leading to drastically reduced estrogen levels. Estrogen normally protects the skeleton by inhibiting osteoclasts (cells that break down bone tissue). With low estrogen, bone breakdown increases and the function of osteoblasts (bone-building cells) is impaired, resulting in a net loss of bone mass.
In addition to sex hormones, the body’s stress response contributes to bone degradation. The chronic stress of starvation leads to elevated levels of the stress hormone cortisol. High cortisol accelerates the process of bone resorption, further tipping the balance toward bone loss.
Furthermore, the nutritional deficit directly impacts bone construction. Low intake of essential micronutrients, such as Calcium and Vitamin D, means the body lacks the raw materials necessary to form a strong bone matrix. Insufficient protein intake also hinders the formation of the organic scaffolding upon which bone minerals are deposited.
Another key mechanism is the suppression of Insulin-like Growth Factor 1 (IGF-1). Starvation leads to growth hormone resistance, dramatically lowering circulating IGF-1 levels. IGF-1 is a powerful anabolic hormone that directly stimulates osteoblasts to build new bone. Its suppression severely limits the body’s ability to repair or replace bone tissue.
Diagnosis and Measurement of Bone Health
The primary diagnostic method is the Dual-Energy X-ray Absorptiometry (DEXA) scan. This non-invasive test uses low-dose X-rays to determine bone mineral density, typically focusing on the hip and lower spine.
For adults, a T-score is used, comparing the patient’s BMD to that of a healthy young adult. A T-score of -1.0 to -2.5 indicates osteopenia, while a score of -2.5 or lower confirms osteoporosis.
For adolescents and young adults who have not yet achieved peak bone mass, the Z-score is the relevant metric. The Z-score compares the patient’s BMD to that of age- and sex-matched peers; a score of -2.0 or lower indicates a significant bone density deficit. Blood work complements the scan, providing information on hormone levels and bone-building nutrients like Vitamin D and calcium.
Intervention Strategies for Recovery
The most effective and fundamental intervention for addressing bone loss in AN is achieving weight restoration and comprehensive nutritional rehabilitation. Restoring a healthy body weight and consistent energy intake is the necessary first step to normalizing the hormonal environment. As weight improves, the body can resume normal menstrual cycles, which leads to an increase in estrogen and a subsequent reduction in bone breakdown.
Targeted supplementation is an immediate and necessary component of treatment. Adequate daily intake of Calcium and Vitamin D is required to provide the body with the necessary building blocks for bone repair. However, supplementation alone is not sufficient to reverse the damage without addressing the underlying malnutrition.
Weight-bearing exercise is beneficial for stimulating bone growth, but it must be approached cautiously and with medical clearance. Exercising too intensely or without sufficient caloric intake can be counterproductive, potentially worsening the energy deficit and increasing the risk of fracture in already fragile bones.
Pharmacological treatments are generally reserved for adults with severe osteoporosis or those who have not responded sufficiently to nutritional recovery. Bisphosphonates, a class of drugs that slow bone breakdown, may be used in select adult cases. These medications are used sparingly in younger individuals due to concerns about their long half-life and potential long-term effects. For adolescents, transdermal estrogen delivery can improve bone density, but it serves as an adjunct to, not a replacement for, full nutritional recovery.