Underlying metabolic disturbances are often ignored when treating psychiatric disorders and can even be exacerbated with treatments, but it is becoming more apparent that these metabolic issues may not arise a result of treatment, but may instead be pre-existing in psychosis. This session echoed the theme of schizophrenia and its co-morbidity with eating disorders that was touched on during the plenary session on the previous day.
The first talk by Professor Janet Treasure from Kings College London was titled “Eating disorders as developmental psychosomatic disorders: building new models with evidence from genetics and epidemiology”. The presentation was a comprehensive update of the genetic, metabolic and behavioural risk factors for eating disorders, but as a researcher with a background in behavioural psychopharmacology, I was particularly interested in the latter. For example, I was surprised to learn that the prevalence of anorexia nervosa (AN) shows a high correlation with trait neuroticism, and also with high levels of empathy, a trait commonly found in extroversion.
Janet described how difficult it is to conduct large prospective studies in AN patients, since the disorder is relatively rare, however retrospective studies have revealed that problems with eating habits in early childhood (such as picky eating and conflict over meals) is linked to the development of eating disorders in later life. Of great interest was the apparent relationship between AN and autism spectrum disorder (ASD), since both disorders share similar traits, including obsessive behaviours and social issues, as well as the higher prevalence of eating disorders in patients with ADHD. It also became clear throughout the talk that AN is no longer considered a disease of the middle-class white girl and is in fact much more diverse in its epidemiology than (at least I had) first believed.
The second half of the talk focused more on binge eating and bulimia, and how the information provided by epidemiological studies could be translated into new explanatory models of these disorders. The use of new questionnaires to identify aspects of food addiction, a transdiagnostic trait in clinical populations, has been a useful tool, and food addiction has begun to be incorporated into models of cognitive behavioural therapy in treating eating disorders.
Lastly, Janet outlined a new maintenance model of binge eating, where the rate of change of glucose is a key factor in driving abnormal eating behaviours in patients. The key underlying hypothesis still needs to be tested to monitor these changes in glucose, however it may be useful in developing personalised models to understand and manage eating disorders.
Secondly, Professor Stephen Cooper from the Royal College of Psychiatrists spoke for the second time on the subject of metabolic dysfunction in schizophrenia (previously during the plenary session), in “A clinical perspective on the association between schizophrenia and obesity: risk factors and interventions”.
Since 2004 there has been a widening gap in mortality between people with mental disorders like schizophrenia and the normal population, with the life expectancy of patients sitting at over 20 years lower. The largest cause of death in patients is cardiovascular, and the presentation focused on the modifiable factors in the management of schizophrenia patients at risk of cardio-metabolic problems.
Stephen described how the risk of cardiovascular disease in patients receiving antipsychotic treatment is driven by early weight gain, with more than a 5% increase within the first month of treatment being a strong predictor of longer term issues. In addition, whilst the rates of smoking in the general population have fallen in recent years, this is not reflected amongst those with schizophrenia, and attempts to reduce smoking in patients have so far proved largely unsuccessful. However SCIMITAR, a pilot study of a new smoking cessation programme designed to provide bespoke interventions for those with severe mental illness, has yielded some promising results and is now being funded for a longer term study. Stephen went on to describe the relationship between cardiovascular problems and issues around diet, physical activity and deprivation present in patients with schizophrenia.
The prevalence of metabolic syndrome (indicated by the presence of a combination of symptoms including hypertension, dyslipidaemia, obesity and raised glucose) in patients with psychosis is associated with an increased risk of Type-II diabetes and cardiovascular disease in patients. Interestingly recent studies have shown that these metabolic abnormalities are present in antipsychotic-naïve patients, suggesting that they are present at the onset of psychosis, rather than as a result of treatment.
The second part of this symposium focused more on the relationship between eating disorders and other psychiatric disorders such as depression and ADHD, and began with Dr Ciara McCabe from the University of Reading and her talk titled “What can brain responses to food tell us about depression and eating disorders?”.
While up to 80% of patients with AN also suffer from depression and report high rates of anhedonia, there have so far been only three major studies investigating anhedonia in AN patients, and Ciara critiqued the poor measures that these studies employed to adequately disseminate the numerous components of anhedonia.
In her research, Ciara uses an fMRI task to measure neural responses to anticipation and consummation of a food reward and has previously shown that these responses are decreased in patients suffering with depression. Interestingly, in recovered AN patients, she has found that both anticipatory and consummatory responses are enhanced in key areas of the brain. Whilst it is not possible to link these changes to symptoms since the subjects were in recovery, these findings may represent a trait vulnerability for AN. Furthermore, it was found that in sisters of AN patients, there were lower reports of wanting and liking of the food reward, indicative of behavioural differences in at-risk participants.
The second part of Ciara’s talk asked the question of whether introducing an effortful component to the task would help to separate out the distinct aspects of reward processing. She found that sisters of AN patients put in less effort to obtain reward and to avoid aversion than controls, and that this blunted behavioural response was correlated with higher anhedonia scores.
In conclusion Ciara suggests that anhedonia isn’t necessarily something that should be considered exclusive to reward, but that perhaps the drive to avoid something also effects one’s experience of anhedonia. She proposed that diminished drive may be a much better predictor of depression than the current DSM anhedonia criteria.
Professor Suzanne Higgs from the University of Birmingham then closed the morning’s session with her talk on “New developments in our understanding of the relationship between specific symptoms of ADHD and binge eating behaviour”.
The beginning of the presentation formed a brief introduction to ADHD as a neurodevelopmental disorder characterised by age inappropriate impulsiveness, inattention and hyperactivity, and there is a wealth of evidence to suggest that many forms of eating disorders are associated with ADHD, in particular binge eating and overeating behaviours. However very few studies have looked at the specific mechanisms mediating the relationship between specific symptoms of ADHD and disordered eating behaviours.
Suzanne then presented results of a multidimensional study that recruited adults across a range of severity of ADHD symptoms (measured with a combination of online and lab-based studies), focusing on binge-like eating and disinhibited eating in response to food cues. The aim of this study was to investigate hypothesised mediators of disordered eating behaviour, such as negative mood, lack of awareness of interceptive signals (internal satiation cues) and altered food-reward processing. The data showed that both inattentive and hyperactive/impulsive symptoms of ADHD are associated with binge-like eating, and negative mood was a significant mediator of this relationship. Specifically, inattentive, but not hyperactive/impulsive, symptoms of ADHD were associated with lower levels of awareness and reliance on internal satiety cues, which in turn were associated with disordered eating behaviours, especially binge and disinhibited eating. In addition, Suzanne presented data from an fMRI study looking at neural reactivity to visual food cues and showed greater activation in reward-related brain regions in response to food pictures in participants with ADHD symptom scores.
Together these findings help us to move forward in our understanding of the causal mechanisms underlying the relationship between ADHD and eating disorders, and their potential interaction, and puts us in a better position to identify those individuals with ADHD who may be particularly at risk for developing eating disorders.