Eating Disorders: An Evolutionary Psychoneuroimmunological Approach

Abstract

Eating disorders are evolutionarily novel conditions. They lead to some of the highest mortality rates of all psychiatric disorders. Several evolutionary hypotheses have been proposed for eating disorders, but only the intrasexual competition hypothesis is extensively supported by evidence. We present the mismatch hypothesis as a necessary extension to the current theoretical framework of eating disorders. This hypothesis explains the evolutionarily novel adaptive metaproblem that has arisen when mating motives conflict with the large-scale and easy availability of hyper-rewarding but obesogenic foods. This situation is exacerbated particularly in those contemporary environments that are characterized by sedentary lifestyles, ever-present junk foods, caloric surplus and the ubiquity of social comparisons that take place via social media. Our psychoneuroimmunological model connects ultimate-level causation with proximate mechanisms by showing how the adaptive metaproblem between mating motives and food rewards leads to chronic stress and, further, to disordered eating. Chronic stress causes neuroinflammation, which increases susceptibility to OCD-like behaviors that typically co-occur with eating disorders. Chronic stress upregulates the serotonergic system and causes dysphoric mood in anorexia nervosa patients. Dieting, however, reduces serotonin levels and dysphoric mood, leading to a vicious serotonergic-homeostatic stress/starvation cycle whereby cortisol and neuroinflammation increase through stringent dieting. Our psychoneuroimmunological model indicates that between-individual and within-individual variation in eating disorders partially arises from (co)variation in gut microbiota and stress responsivity, which influence neuroinflammation and the serotonergic system. We review the advances that have been made in recent years in understanding how to best treat eating disorders, outlining directions for future clinical research. Current evidence indicates that eating disorder treatments should aim to reduce the chronic stress, neuroinflammation, stress responsivity and gut dysbiosis that fuel the disorders. Connecting ultimate causes with proximate mechanisms and treating biopsychosocial causes rather than manifest symptoms is expected to bring more effective and sophisticated long-term interventions for the millions of people who suffer from eating disorders.

The Gut Microbiome in Anorexia Nervosa: Friend or Foe?

“…This can lead to aberrant immune responses, such as the development of a chronic state of low-grade inflammation, which is increasingly acknowledged to contribute to psychiatric pathology ( 35 ). Indeed, increased levels of pro-inflammatory cytokines have been found in acute AN ( 36 ), but it unclear whether this is a consequence of dysbiosis, or whether other factors, such as starvation-induced stress, upregulate inflammatory pathways and exacerbate intestinal dysfunction ( 37 ).…”

A systematic review on the role of microbiota in the pathogenesis and treatment of eating disorders

“…In a transdiagnostic view of EDs [88], the hypothesis of neuroinflammation and gut dysbiosis in the aetiology of EDs should be screened. Recently, a new a continuum model was presented, suggesting that changes in proinflammatory cytokines, serotonin levels and microbiota cause shifts in EDs [89].…”

Women’s socioeconomic position in ontogeny is associated with improved immune function and lower stress, but not with height

“…This interpretation is consistent with many studies that indicate a negative effect of high stress and cortisol on health, causing cardiovascular diseases [76][77][78] , acute myocardial infarction 72 and type 2 diabetes 73 as well as predicting cancer survival [81][82][83] . Overall, a well-regulated cortisol stress response is an essential component of adaptive cognitive, emotional and behavioral responses to stress, which in turn influence long-term health outcomes 10,[84][85][86][87] . A possible limitation of the current study was that cortisol was measured only within a narrow time period in a single day.…”