Eating Disorders and Gastrointestinal Diseases

Abstract

Eating disorders (ED) are frequently associated with a wide range of psychiatric or somatic comorbidities. The most relevant ED are anorexia nervosa (AN), bulimia nervosa (BN), and binge eating disorders (BED). Patients with ED exhibit both upper and lower gastrointestinal (GI) symptoms. Evidence of alterations throughout the GI tract in ED will be analyzed given the role of the GI tract in food intake and its regulation. It remains a matter of debate whether GI disorders are inherent manifestations of ED or the results of malnutrition occurring from ED. Moreover, recent clinical studies have highlighted the growing role of intestinal microbiota in the pathogenesis of ED, making it possible to hypothesize a modulation of intestinal microbiota as a co-adjuvant to standard therapy. The aim of this review is to analyze the link between ED and GI diseases and to present, where known, the potential key factors underlying these conditions. Conclusions: The presence of GI disorders should be investigated in patients with ED. Screening for ED should also be encouraged in individuals seeking treatment for unexplained GI complaints to better address therapeutic issues that surround these difficult medical conditions. Nutrients 2019, 11, 3038 3 of 17 ED can be associated with anxiety or mood disorders; insomnia; as well as somatic complications such as cardiac alterations, hormonal imbalances and also a wide range of gastrointestinal (GI) symptoms [3].Prevalence estimate of lifetime AN is 0.8% [4]. The overall incidence rate of AN is around 7 per 100,000 persons; however, it is higher in 15-19 year old girls reaching 109.2 cases per 100,000. The incidence is increasing in Italy and other Western countries probably due to earlier diagnosis or earlier onset [5,6].The prevalence of BN is 0.28% [4]. The highest incidence rate of BN is 300 per 100,000 persons in women aged between 16 and 20 [7], although the age at onset is decreasing [5].BED are described in 0.85% of the population [4,8] and are frequently associated with medical comorbidities, especially obesity and its complications such as Type II diabetes mellitus, hypertension, and dyslipidemia [9]. Furthermore, BED may occur in a subset ranging from 27% to 47% in severely obese persons undergoing bariatric surgery [10].The previous edition of DSM (DSM-IV) [11], classified as "Eating Disorders Not Otherwise Specified (EDNOS)", is the ED that does not satisfy all the diagnostic criteria for AN or BN. Previously, EDNOS contained a huge and varied group of individuals and was the most commonly diagnosed ED. However, the DSM-V revised this ED type and called it "Other Specified Feeding or Eating Disorder" (OSFED). Moreover, the DSM-V introduced the definition of Avoidant/restrictive food intake disorder (ARFID) that was distinct from AN and BN in that there is no body image disturbance [2].The first description of AN in the 19th century revealed that the sufferers' reasons for self-starvation generally were strictly connected to inappetence, feelings of fullness and abdominal ...

Eating Disorders During Gestation: Implications for Mother's Health, Fetal Outcomes, and Epigenetic Changes

“…EDs impair gastrointestinal function leading to esophageal acidic damage for self-inducing vomiting, gastric distension, dysphagia, increased intestinal motility and chronic diarrhea. Clinician should detect such symptoms and practice the differential diagnosis with intestinal disease like celiac disease, gastroesophageal reflux, and inflammatory bowel diseases (196).…”

Characteristics of avoidant/restrictive food intake disorder in a general paediatric inpatient sample

“…Thereby, restrictive eating disorders can be confused with GI diseases—suggesting that the diagnosis of ARFID is easily overlooked and the specific clinical consequences can be missed (Bern & O'Brien, 2013). This may be detrimental as eating disorders among children and adolescents are likely to co‐occur with physical illnesses like type 1 diabetes mellitus (Colton et al, 2015; Jones, Lawson, Daneman, Olmsted, & Rodin, 2000; Kelly, Howe, Hendler, & Lipman, 2005; Peducci et al, 2019; Young et al, 2013), diseases of the digestive system, autoimmune diseases, and seizures (Leffler, Dennis, Edwards George, & Kelly, 2007; Makhzoumi et al, 2019; Santonicola et al, 2019; Tegethoff, Belardi, Stalujanis, & Meinlschmidt, 2015; Zerwas et al, 2017). The refusal to eat may be conditioned to avoid food‐induced symptoms of these diseases (Carlson, Moore, Tsai, Shulman, & Chumpitazi, 2014; Gerasimidis, McGrogan, & Edwards, 2011).…”

Backstage of Eating Disorder—About the Biological Mechanisms behind the Symptoms of Anorexia Nervosa

“…The vagus nerve and non-vagal splanchnic mesenteric nerves form the peripheral extrinsic component of the gut-brain axis [109], and primarily project to the nucleus of the solitary tract localized in the brainstem [95]. The stimulation of mechano-sensitive vagal or spinal afferent fibers through distension of the gastric wall is responsible for the perception of fullness, and consequently controls the meal size [95,[110][111][112][113][114][115]. Additionally, macronutrients influence motility and appetite regulating molecules, and further affect energy intake, but do not reach consciousness [114].…”

“…Additionally, macronutrients influence motility and appetite regulating molecules, and further affect energy intake, but do not reach consciousness [114]. Dysregulation of these complex physiological processes negatively affects eating behaviors, and might provoke the most frequent gastrointestinal symptoms observed in AN (further discussed in the following sections), including excessive postprandial fullness, bloating, nausea, vomiting, or regurgitation) [115,116]. Microbiome dysbiosis and microbial metabolites as well as entero-endocrine alterations (also further discussed) contribute, as major etiological factors, to the gut-brain dysregulation and negatively impact satiation and satiety in AN.…”

“…And indeed, more than 60% of AN patients suffer from delayed colonic transit and around 40% from pelvic floor dysfunction [ 210 ]. According to Santonicola et al (2019) the correlation between pelvic dysfunction and a history of an eating disorder (including AN) might be explained as a combination of prolonged evacuation efforts, laxative abuse, enforced vomiting together with extreme exercise, and subsequently lead to the structural damage of pelvic floor muscles in addition to atrophy and rhabdomyolysis (skeletal muscle breakdown) due to starvation [ 115 ].…”