At many inpatient eating disorder treatment centers patients with anorexia nervosa are required to restore their weight quickly; I’ve had patients that were forced to gain 20 pounds in 21 days! Not coincidentally, 21 days was the amount of time that managed care would cover. There are numerous reasons as to why gaining weight this quickly actually sets the patient up for relapse. Let’s look at what gaining weight at a rapid rate does to leptin levels.
In the malnourished, underweight anorexic, leptin levels are typically very low, due to low fat reserves. Usually, leptin levels reach normal levels during weight restoration. However, when weight is gained too quickly, leptin levels rise too quickly and may exceed the normal range. Of course this has the opposite effect needed for refeeding and individuals experience suppressed appetite and suppressed energy expenditure. As a result, it becomes increasingly difficult for the patient to eat, often interfering with the refeeding process. Many of the patients who have had this experience, were told, in effect, that they were at fault, or “not trying”. The reason that this happens is that not enough practitioners know about Leptin and the role that it plays in re-feeding. For someone who already has control issues, this is an extremely painful and often damaging experience.
At the Norton Center, our anorexic patients are helped to restore their weight slowly, but steadily. This, along with other important nutritional factors, plays a major role in our high success. It is important to note that many treatment programs use weight gain at the conclusion of treatment as the measure of success. This is a distortion in as much as the 20 pound weight gain is often gone in a matter or months, and sometimes in a matter of weeks. We measure success as weight gain that is maintained for a at least one year post treatment. Currently, our success rates for those patients that remain in treatment is about 90%; in comparison, many inpatient treatment centers experience a much lower success rate, or about 30 to 40%.
How Low Leptin Effects the Physical Complications and Behaviors Typical of Anorexia Nervosa
Low leptin plays a significant role in many of the physical complications and behaviors that are typically associated with anorexia nervosa; amenorrhea, hypothyroidism, hypercortisolism, osteopenia, immune changes, and increased physical activity.
Leptin levels of less than 1.85 µg suggests amenorrhea and subnormal luteinizing hormone (a hormone that stimulates ovulation) in women with anorexia nervosa. As leptin levels normalize through weight restoration, the hypothalamic-pituitary-gonadal axis may be activated. Not all patients with anorexia nervosa resume menses upon weight restoration.
The majority of women with anorexia nervosa exhibit osteopenia. Low leptin levels are also associated with a reduction in bone formation rate. Although there are other endocrine changes that contribute to osteopenia, low leptin levels appear to play a significant role.
Individuals with anorexia nervosa, often experience a compromised immune system. This could also be due, in part to low leptin levels although most of the compromised immunity is due to increased cortisol levels. Cortisol is the hormone that we associate with stress. Patients who are gaining weight too rapidly, are under considerably more stress, and may also be experiencing increased cortisol levels
Finally, up to 80% of patients with Anorexia Nervosa tend to engage in excessive physical activity. It is believed that there is an inverse correlation between food intake and physical activity during the weight loss phase. In other words, the lower the leptin levels, the more drive there is to exercise excessively, which causes more weight loss or less weight gain. One study demonstrated that patients reported a decreased feeling of restlessness or hyperactivity (need to exercise) as leptin increased during the refeeding/weight restoration phase of treatment.
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Sources: Monteleone P. Di Lieto A. Castaldo E, et al. Leptin functioning in eating disorders. CNS Spectrums. 2004;9:523–529. [PubMed]