Psychology & Psychophysiology of Disordered Eating & Eating Disorders Claus Vögele Institute for Health and Behaviour University of Luxembourg

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1 Psychology & Psychophysiology of Disordered Eating & Eating Claus Vögele Institute for Health and Behaviour University of Luxembourg 1

2 Don t worry, eat happy!

3 Eating as emotion-regulation strategy but what if it fails? Binge eating Comfort eating Emotional eating Restrained eating

4 Feeding and Eating are characterized by a persistent disturbance of eating or eating-related behavior that results in the altered consumption or absorption of food and that significantly impairs physical health or psychological functioning. (American Psychiatric Association, 2013) 4

5 Types of Feeding and Eating Pica Rumination Disorder Avoidant/Restrictive Food Intake Disorder Other Specified Feeding and Eating Unspecified Feeding and Eating Anorexia Nervosa Bulimia Nervosa Binge-eating Disorder Not in the DSM-5: Obesity 5

6 Anorexia nervosa (prevalence: 0.4%) BMI < 17.5 kg/m 2, rigid control of food intake Bulimia nervosa (prevalence: 3.5%) BMI normal range, alternating binge episodes and fasting / purging Binge Eating Disorder (prevalence 3.5%) binge eating episodes without purging behaviour: BMI > 25 kg/m 2

7 Anorexia Nervosa (I) Diagnostic Features persistent energy intake restriction intense fear of gaining weight disturbance in self-perceived weight or shape maintainance of a low body weight (BMI < 17,0 kg/m 2 ) Types: Restricting type Binge-eating/Purging type Prevalence young females: ±0,4% ratio: 10:1 female-to-male Development and Course onset: adolescence or young adulthood recover after a single episode with relapse or chronic course over many years complications: e.g., dehydration, amenorrhea, osteoporosis, abdominal pains mortality rate: 5% per decade (DSM-V American Psychiatric Association, 2013) 7

8 Anorexia Nervosa (II) Functional Consequences social isolation and/or failure to fulfill academic or career potential Differential Diagnosis Medical conditions Major Depressive disorder Schizophrenia Substance use disorder Social anxiety disorder, OCD, body dysmorphic disorder Bulimia nervosa Avoidant/restrictive food intake disorder Comorbidity Bipolar, depressive, anxiety disorders OCD Alcohol use disorder (DSM-V American Psychiatric Association, 2013) 8

9 Bulimia Nervosa (I) Diagnostic Features recurrent episodes of binge eating recurrent compensatory behaviors to prevent weight gain self-evaluation that is unduly influenced by body shape and weight Prevalence young females: 3.5% ratio: 10:1 female-to-male Development and Course onset: adolescence or young adulthood persists for at least several years course: chronic or intermittent long-term: symptoms can diminish with or without treatment mortality rate: 2% per decade (DSM-V American Psychiatric Association, 2013) 9

10 Functional Consequences affects social-life domain Differential Diagnosis Bulimia Nervosa (II) AN, binge-eating/purging type Binge-eating disorder Kleine-Levin syndrome Major depressive disorder, with atypical features Borderline personality disorder Comorbidity increase of depressive symptoms, bipolar and depressive disorders increase of anxiety symptoms or anxiety disorders substance use disorder Personality disorders (DSM-V American Psychiatric Association, 2013) 10

11 Diagnostic Features Binge-Eating Disorder (I) recurrent episodes of binge eating at least 3/5 features must occur: Prevalence o eating much more rapidly than normal o eating until feeling uncomfortably full o eating large amounts of food when not feeling physically hungry o eating alone because of feeling embarrassed by how much one is eating o feeling disgusted with oneself, depressed or guilty afterward females: 1.6% males: 0.8% 11

12 Binge-Eating Disorder (II) Development and Course onset: adolescence, young adulthood or later adulthood persistent course comparable to that of BN Functional Consequences social role adjustment problems impaired health-quality of life and life satisfaction medical morbidity and mortality increased health care utilization risk for weight gain and obesity 12

13 Binge-Eating Disorder (III) Differential Diagnosis BN Obesity Bipolar and depressive disorders Borderline personality disorder Comorbidity Bipolar disorder Depressive disorders Anxiety disorders Substance use disorders (DSM-V American Psychiatric Association, 2013) 13

14 Etiological Models Biological Models and Findings Inherited biological and genetic factors contribute a risk of up to 56% for developing an eating disorder Hypothalamus abnormalities (eating regulation) Neurotransmitters Serotonin BN: low levels causes binge eating episodes AN: high levels stress, anxiety starvation reduces levels and leads to calmness Dopamine AN: dopamine disruptions cause hyperactivity, anhedonia, repetition of behaviour; affect reward-motivated behaviour, which explains the lack of pleasure when losing weight Cortisol AN and BN: high levels eating after stress cause or result of eating disorders? Leptin regulation of reproduction, appetite, metabolism and bone formation losing a lot of body fat decrease in Leptin levels amenorrhea, bone loss, impaired metabolism 14

15 Current models Risk factors Risk factors General Factors Premorbid experiences Premorbid characteristics Female Adolescence, early adulthood Averse parenting (low contact, high expectations, parental discord Sexual abuse Low self-esteem Perfectionism (AN, BN lesser extent) Living in Western Society Family dieting Anxiety & anxiety disorders Individual-specific factors Critical comments (eating) Obesity (BN) Family history ED of any type Depression Substance abuse (alcohol, BN) Obesity (BN) Shape, weight of family and others Occupational and recreational pressure to be slim Early menarche (BN)

16 Current models Risk factors Treatment methods Treatment Methods Pharmacological (e.g. SSRIs or MAOIs) Family based treatment Cognitive Behavioural Therapy (CBT) Starting point: CBT in Bulimia Nervosa (Fairburn, Marcus & Wilson, 1993) 16

17 Current models Risk factors Treatment methods Cognitive Behavioral Therapy Meta-Analyses Results These quantitative results correspond to qualitative reviews and suggest that CBT is the treatment of choice for BN. (Whittal, Agras & Gould, 1999) (...) results suggest that the use of a cognitivebehavioral therapy will result in favorable treatment outcomes (Lewandowski et al., 1997) Cognitive behavioral therapy (CBT) is the best established treatment for binge-eating disorder (BED) (Grilo et al., 2011)

18 Current models Risk factors Treatment methods Treatment Methods Cognitive Behavioural Therapy (CBT) Nevertheless: with 25% of treated AN patients developing a chronic form of the condition and the conclusion drawn by Hay et al. (2009, Cochrane) that Psychotherapy alone is unlikely to reduce or change body weight in people with bulimia nervosa or similar eating disorders.. the search for alternative treatment approaches goes on. Physiological approaches (TMS, vagus nerve stimulation, DBS) 18

19 Heart rate variability-biofeedback reduces craving in chocolate addicts Meule et al., 2012

20 Cardiac autonomic control PFC Central Autonomic Network + Sinus node N. vagus

21 Model of Neurovisceral Integration Thayer & Lane (2009)

22 Vagus nerve and disinhibition in bulimia nervosa Bulimic behaviour may disregulate the vagal nerve (Faris et al., 2008). Binge-purge episodes bring the vagal nerve back to its normal role. This retraining of the vagal nerve has long term effects on the brain s reward circuitry.

23 Food addiction?

24 Summary Amongst the available, evidence-based forms of psychotherapy, CBT is currently the most efficacious. Nevertheless, success rates are modest at best. There is a need for alternative treatments: physiological approaches are promising. DBS has been performed at a range of locations (e.g. bilateral Nucleus Accumbens, subcallosal cingulated region) with varying success. We need studies investigating testable hypotheses on dysfunctional circuits on patient groups with similar inclusion and exclusion criteria.