To describe the hormonal adaptations and alterations in anorexia nervosa. Many of the studies were also conducted in Europe and the US, limiting generalizability regarding the results to other regions of the world. This heterogeneity likely reflects differences in study populations and differences in the use of laboratory assays. Several limitations need to be acknowledged such as the high between-study heterogeneity in several pooled analyses. The adrenal cortex is an important source of androgen production.38 The zona reticularis secretes DHEA, DHEA-S, androstenedione, testosterone, and other C19 steroids including androstenediol and the 11-oxoandrogens39 (Figure 11).
Thyroid hormones (thyroxine (T4) and triiodothyronine (T3)) are important regulators of metabolism that affect the function of organs throughout the body. Some studies have suggested that CRH hypersecretion may also play a role in the pathophysiology of the disorder, as central injections of CRH in animals leads to anorexia and increased motor activity , which can be reversed by CRH antagonists . This is a critical unmet need as pregnancies in women with AN, whether planned or unplanned, are at higher risk for adverse outcomes for both mother and fetus, including miscarriage, cesarean delivery, premature birth, low birth weight, and perinatal mortality . When seeking medically assisted reproduction, the majority of women with a history of an eating disorder do not report it to their providers, and the majority of providers do not screen for a history of an eating disorder 17, 18. Given the paucity of data on the efficacy and safety of testosterone therapy in men with chronic illnesses such as AN, the Endocrine Society does not provide general recommendations for testosterone therapy in patients with chronic illness. Although weight recovery is generally thought to restore GnRH pulsatility, inter-individual differences exist in the sensitivity of the hypothalamic–pituitary–gonadal axis to weight gain (and loss).
Starvation leads to impaired pulsatility of gonadotropin-releasing hormone, which suppresses the secretion of gonadotropins, particularly LH, and leads to anovulation, prolonged follicular phase with luteal phase deficiency, and hypoestrogenism (7). Sexual orientation was not fully assessed in our patients, although the majority had reported being in heterosexual relationships. Similar to previously reported studies (13,14), depression, psychosis, and personality disorders were highly evident in our cohort, which parallels the high prevalence of comorbid psychiatric illness in females with AN.
Pituitary growth hormone (GH) pulsatility and secretion are higher in states of chronic starvation such as AN , which may be mediated in part by increased levels of ghrelin, a GH secretagogue . In addition, T4 and/or T3 supplements have the potential to be abused by patients with AN since they increase basal metabolic rate and can cause weight loss. In more severe disease, levels of thyroid stimulating hormone (TSH) from the anterior pituitary and free T4 from the thyroid may fall into the low-normal range due to general suppression of the hypothalamic-pituitary-thyroid axis.
AN is especially damaging to bone health in adolescents, as malnutrition during these formative years interferes with the accumulation of peak bone mass (12). Hepatic IGF-1 production is inhibited by malnutrition, and low IGF-1 levels stimulate increased GH secretion. One could postulate that as hypercortisolemia reflects responsiveness to stress, it may also reflect adrenal reserve, which could explain the potential use of cortisol levels as a marker for menstrual recovery. Patients with AN and high cortisol levels do not typically display features of Cushing syndrome, as they have low baseline levels of adipose tissue and cortisol resistance (5,30). Vasopressin has a greater involvement in hypercortisolemia of depression, while corticotropin-releasing hormone appears to have a dominant role in hypothalamic-pituitary-adrenal axis hyperactivity in AN (36). The poor cortisol response to corticotropin-releasing hormone is suggestive of hypersecretion of corticotropin-releasing hormone as a means of overcoming cortisol resistance.

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