LF313 - Systems Interactions In Humans
Eating disorders
Eating disorders take many forms
- Avoidant/restrictive food intake disorder (ARFID) - restrictive specific foods
- Purging disorder - reduce caloric intake by ridding the body of food
- Anorexia nervosa - Restrictive, restrictive-purging, binge-purge
- Bulimia nervosa
- Binge eating disorder
- Rumination disorder
- Orthorexia nervosa
- Pica
82% of eating disorder patients have a co-morbid mood disorder.
- Depression - most common: MDD and dysthymia, worsens eating disorder severity, increases rates of suicide attempts and suicides. Genetic contribution ~35%, bidirectional
- Anxiety - mostly OCD and social phobia. GAD and panic disorder are increased in both anorexics and bulimics. Phobias are increased in bulimics, genetic contribution 50-80%
Serotonin is involved in eating disorders. Serotonin reuptake drives eating disorders with a bingeing component. Bingeing symptoms reduced by antidepressant drugs, not dependent on antidepressant effect, no effect on anorexia.
Dopamine and HVA are reduced in anorexia vs bulimia. Functional polymorphisms of DRD2 affect receptor transcription and translation efficiency. Striatal DA dysfunction might contribute to altered reward and affect, decision making, executive control and food ingestion. Reduced dopamine returns to normal levels after recovery from anorexia and bulimia. Dopamine is positively correlated with bingeing but negatively correlated with purging. Elevated noradrenaline levels normalise following recovery from bulimia. Noradrenaline is normal in anorexia but falls following long-term recovery.
Brain atrophy in anorexia includes enlarged ventricles and reduced grey and white matter. Anorexia is associated with grey matter change, increased somatosensory cortex and precuneus, decreased hippocampus thalamus, supramarginal gyrus and primary motor cortex.
Bulimia is associated with gray matter changes, increased somatosensory cortex and precuneus, left insula and putamen, decreased thalamus, caudate nucleus.
Anorexics have more activity in the left caudate, bulimics have more activity in the SMA, left insula,l eft postcentral gyrus, left supramarginal, left lingual, right fusiform, left occipital and temporal cortex and thalamus.
Anorexia is associated with altered connectivity, more connectivity in the left insula bilateral temporal pole and posterior cingulate cortex, less connectivity in the parietal lobe. Anorexics show hyper-excitability in specific brain areas: BA9, BA40 and IPS.
Calorie fear in anorexia is controlled by the temporal and frontal lobes.
Eating disorders are developed as coping strategies for aberrant emotional responses to anxiety.
- Abnormal emotional response
- Autonomic hyperreactivity - fight or flight, averse physiological sensations
- Behavioural modifications - ritualistic behaviours as a coping mechanism, safety behaviours to control anxiety
Eating disorder patients use cognitive dissociation to tolerate their behaviours. Disruption in integration of consciousness, memory, identity or perception of the environment. Cognitive narrowing excludes conflicting information - switch focus to immediate environment, avoid emotional distress by avoiding aversive self-awareness, perceptional changes to make abhorrent acts acceptable.
Eating disorders can precede depressive symptoms and vice versa. Temporal relationships between eating disorders and anxiety disorders depend on the disorder. OCD, social phobia and other specific phobias predate eating disorders. Generalised anxiety disorder (GAD) occurs around the same time as an eating disorder. PTSD, panic disorder and agoraphobia follow an eating disorder.