Frostad Stein
Division of Psychiatry, Haukeland University Hospital, 5021 Bergen, Norway.
Microorganisms. 2022 Jul 24;10(8):1486. doi: 10.3390/microorganisms10081486.
Anorexia nervosa (AN) is a disabling, costly, and potentially deadly illness. Treatment failure and relapse after treatment are common. Several studies have indicated the involvement of the gut microbiota-brain (GMB) axis. This narrative review hypothesizes that AN is driven by malnutrition-induced alterations in the GMB axis in susceptible individuals. According to this hypothesis, initial weight loss can voluntarily occur through dieting or be caused by somatic or psychiatric diseases. Malnutrition-induced alterations in gut microbiota may increase the sensitivity to anxiety-inducing gastrointestinal hormones released during meals, one of which is cholecystokinin (CCK). The experimental injection of a high dose of its CCK-4 fragment in healthy individuals induces panic attacks, probably via the stimulation of CCK receptors in the brain. Such meal-related anxiety attacks may take part in developing the clinical picture of AN. Malnutrition may also cause increased effects from appetite-reducing hormones that also seem to have roles in AN development and maintenance. The scientific background, including clinical, microbiological, and biochemical factors, of AN is discussed. A novel model for AN development and maintenance in accordance with this hypothesis is presented. Suggestions for future research are also provided.
神经性厌食症（AN）是一种致残、代价高昂且可能致命的疾病。治疗失败和治疗后复发很常见。多项研究表明肠道微生物群-脑（GMB）轴与之相关。这篇叙述性综述假设，AN是由易感个体中营养不良引起的GMB轴改变所驱动。根据这一假设，最初的体重减轻可能是通过节食自愿发生的，也可能是由躯体疾病或精神疾病引起的。营养不良引起的肠道微生物群改变可能会增加对进食期间释放的诱发焦虑的胃肠激素的敏感性，其中之一是胆囊收缩素（CCK）。在健康个体中实验性注射高剂量的其CCK-4片段会诱发惊恐发作，可能是通过刺激大脑中的CCK受体。这种与进食相关的焦虑发作可能参与了AN临床表现的形成。营养不良还可能导致食欲降低激素的作用增强，这些激素似乎也在AN的发生和维持中起作用。本文讨论了AN的科学背景，包括临床、微生物学和生化因素。提出了一个符合这一假设的AN发生和维持的新模型。还提供了对未来研究的建议。
