The endocrine manifestations of anorexia nervosa: mechanisms and management

Abstract

Anorexia nervosa is a psychiatric disorder characterized by altered body image, persistent food restriction and low body weight, and is associated with global endocrine dysregulation in both adolescent girls and women. Dysfunction of the hypothalamic-pituitary axis includes hypogonadotrophic hypogonadism with relative oestrogen and androgen deficiency, growth hormone resistance, hypercortisolaemia, non-thyroidal illness syndrome, hyponatraemia, and hypooxytocinaemia. Serum levels of leptin, an anorexigenic adipokine, are suppressed and levels of ghrelin, an orexigenic gut peptide, are elevated in women with anorexia nervosa; however, levels of peptide YY, an anorexigenic gut peptide, are paradoxically elevated. Although most, but not all, of these endocrine disturbances are adaptive to the low energy state of chronic starvation and reverse with treatment of the eating disorder, many contribute to impaired skeletal integrity, as well as neuropsychiatric comorbidities, in individuals with anorexia nervosa. Although 5–15% of those affected by anorexia nervosa are men, only limited data exists regarding the endocrine impact of the disease in adolescent boys and men. Further research is needed to understand the endocrine determinants of bone loss and neuropsychiatric comorbidities in anorexia nervosa in both women and men, as well as to formulate optimal treatment strategies.

Increased lipid and lipoprotein concentrations in anorexia nervosa: A systematic review and meta‐analysis

“…Additionally, stress increases epinephrine, cortisol, growth hormone (GH), and glucagon, and has been observed in combination with low triiodothyronine (T 3 ) concentrations in AN (Schorr & Miller, 2017). Furthermore, GH is elevated in AN (Schorr & Miller, 2017) and may have a direct lipolytic effect independent from insulin-like growth factor 1 (IGF-1), increasing especially LDL concentrations (Misra et al, 2006). It shows significantly higher activity in AN compared with HC (Ohwada et al, 2006).…”

“…Adipose tissue plays an important role in the regulation of insulin sensitivity, and cross-talk between glucose and lipid metabolism occurs (Saltiel & Kahn, 2001). Additionally, stress increases epinephrine, cortisol, growth hormone (GH), and glucagon, and has been observed in combination with low triiodothyronine (T 3 ) concentrations in AN (Schorr & Miller, 2017 (Ohwada et al, 2006). However, high T 3 (Rigaud et al, 2009;Weinbrenner et al, 2004;Zák et al, 2005) and low T 3 (Matzkin et al, 2006) have been associated with increased HDL, but one study showed no association (Ohwada et al, 2006), rendering results inconclusive.…”

“…However, high T 3 (Rigaud et al, 2009;Weinbrenner et al, 2004;Zák et al, 2005) and low T 3 (Matzkin et al, 2006) have been associated with increased HDL, but one study showed no association (Ohwada et al, 2006), rendering results inconclusive. Furthermore, GH is elevated in AN (Schorr & Miller, 2017) and may have a direct lipolytic effect independent from insulin-like growth factor 1 (IGF-1), increasing especially LDL concentrations (Misra et al, 2006). Another potential explanation is that steroid hormones such as cortisol and estradiol (for which cholesterol is the precursor) are associated with lipid alterations and, in AN the hypoestrogenic state is differentially associated with increased cholesterol in premenarchal and postmenarchal female patients (Swenne, 2016).…”

Hypothalamic Structural and Functional Imbalances in Anorexia Nervosa

“…One of the most questioning features of individuals with AN is their ability to chronically restrict energy intake, whereas they are in an emaciated condition often for many years, and not rarely to the point of death. These alterations of interoception clearly illustrate a communication breakdown between the body and the brain, that is, the inability of the brain to translate circulating factors that signal the energy state of the organism into the appropriate adaptive behavior [4]. In fact, recent genome-wide association studies provide evidence of a genetic predisposition for a lower body weight set-point in AN and also indicate that it is not merely a psychiatric but also a metabolic disorder [5,6].…”

Does UK medical education provide doctors with sufficient skills and knowledge to manage patients with eating disorders safely?

“…This is in stark contrast with the common misperception that eating disorders are trivial and self-imposed problems 8. The physical complications of eating disorders are partially to malnutrition, including acute metabolic or electrolyte disturbances, gastrointestinal or cardiac complications,9 10 fertility and perinatal complications,11 bone metabolic12 or endocrine13 problems, growth and developmental delay in children. In addition, certain physical illnesses are associated with eating disorders.…”