Getting to the fundamentals of eating disorders. Professor Janet Treasure www.eatingresearch.com Janet.email@example.com
Conflict of Interest • Pharma- Nil • Books-Several books for patients/carers and professionals. • NICE guideline committee • World federation of biological psychiatry guidelines.
Talk Map • What are eating disorders? • The history • The prevalence of eating disorders • The clinical features. • Treatment
Spectrumof EDs Binge-purging AN Restricting AN Purging BN Purging Disorder Non-purging BN Simple obesity Binge-eating Gull 1873 Lasegue 1873 Volkow 2007 Stunkard Russell 1979
Orphan Disorders • What are they? • Physical or psychological? • Body image or eating? • Neurotic or psychotic? • Developmental or Environmental ?
Cases presenting to primary care in UK (Micali et al 2012) EDNOS BED most common diagnosis
Epidemiology: Lifetime prevalence)(Hudson et al 2007, Jacobi et al 2004, Preti et al 2009, Field 2011)
Anorexia Nervosa • Illness defined 1860 • Teenage onset • Avoid eating • Excess exercise • High mortality (up to 20%) & disability I had a voice in my head that criticised me. It told me I was dreadful and did not deserve food. It became harder to ignore the voice.
1979: Defined by Russell Core Behaviours: Binge >1000cal out of control Compensatory Behaviours eg Vomit, laxatives, exercise, drugs Teenage onset Bulimia nervosa I used to go to the kitchen and eat as much as I could as quickly as possible to fill the hole I felt inside. I felt horrid afterwards and would make myself sick
Binge Eating Disorder: History Recurrent distressing binges • No food restriction • No compensatory behaviours • Obesity Prevalence: 1-3% • Men & women affected equally Peak age onset: 13-15 and early 20s I spent all my time thinking of food. I would wake in the night and want to eat
What is the Health and Psychosocial Burden? • ↑ Morbidity (Johnson et 2002, Striegel Moore et al 2003,Patton et al 2008). • Education: interruptions and lower level for AN. (Byford et al 2007). • Vocational: 21% on state benefits (Hjern et al 2006). • Social networks small (Tiller et al 1997). • Communication Skills impaired (Takahasi et al 2006).
The evolution of eating disorders Anorexia Nervosa Bulimia Nervosa Bulimia nervosa Drug & alcohol abuse, social anxiety Binge eating disorder Obesity Lewinsohn et al 2000, Brukner et 2010, Field et al 2011, Tozzi et al 2005, Milos et al 2005
Learning Memories of food reward & metabolic consequences Self regulation system Embeds eating into social context & individual values Hedonic centre Reward from food (limbic system Homeostatic centre Regulates input and output of energy supply
The effect of Nutritional Problems on the brain Brain needs 500kcal/day. Brain needs 7 X caloric intake of muscle Brain function can be damaged by irregular pattern eating as well as amount.
Breeding (impulsive) Early adversity A period of under nutrition. Divert food stomach Intermittent availability of highly palatable food Stress. (Rada et al 2005, Lewis et al 2005, Avena et al 2005, Corwin 2006, Corwin & Hajnal 2005, Boggiano et al 2005; Avena & Hoebel 2003, Avena & Hoebel 2007, Boggiano et al 2007, Jahng 2011). Animals models of binge eating
Restriction from cognitive control Damaged by starvation Self regulation system Embeds eating into social context & individual values Hedonic centre Reward from food (limbic system Over sensitive reward centre ↑ binging Starvation ↑ reward Fast/feast ↑ reward Homeostatic centre Regulates input and output of energy supply Brain areas implicated in eating disorder symptoms Secondary problems
The interpersonal perpetuating cycle Kyriacou et a 2008 Sepulveda et al 2009 • (Zabala et al, Eur Eat Rev 2009)
Amy’s line manager phoned you saying that she was worried that Amy had anorexia nervosa. Amy comes to see you reluctantly saying that nothing is wrong.
Opening Moves • Normalise ambivalence about attendance. Who is the prime mover, peers, self, line manager? • Elicit concerns: physical, psychological, spiritual, family, social, education/career, forensic. • Elicit readiness to change. • Assess medical risk. • Ethical responsibility: Discuss issues of confidentiality. If high risk need to involve others, professionals.
Is it Anorexia Nervosa? • Usually the history from self or informants is clear. • Atypical cases ie with no overt concern about eating, shape & weight do occur • Differential Diagnosis: examine over time (can they gain weight?), ESR, C reactive protein, platelets, TFT , albumin are useful screening tests
Physical Signs • Parotid or submandibular gland enlargement • Eroded teeth • "Russell's sign" callus on back of hand • Cold blue hands, nose and feet • Lanugo hair
What is the Risk?The Brief Medical Risk Assessment www.eatingresearch.com • Skeletal power to examine for myopathy which is a good marker of severity. • Blood pressure and HR to measure cardiac function and circulation. The fall in BP between sitting & standing & dizziness is a measure of dehydration. • Core temperature- level of metabolism. • Blood markers of organ failure: liver, marrow, kidney.
Danger Signs Fits, Coma Arrythmias, Syncope PR<40bpm BP<80mmHg Postural drop>20mmHg LFT’s Tetany Difficulty arising from squat/sit up Na K Glucose Hb WCC platelets Rapid Rate Weight loss Petechial rash Ulcer
New Tools for Eating Disorder Treatment Perkins, S Cochrane Systematic Reviews 2006 Issue 3 Books Web base Mobile Games More effective if used with guidance
Guided Self Help (GSH) • BN: GSH= CBT (Thiels et al 1998) , GSH > CBT for sustained benefit (Mitchell et al 2011). • BN adolescents. GSH>FT (Schmidt et al 2007). • BED: GSH> BWL (Grilo et al 2005) GSH>IPT post Px & 2 y (Wilson et al 2010). • BN EDNOS: GSH>TAU (Streigel Moore et al 2010), GSH> wait list (Traviss et al 2010). • AN : GSH> TAU: pre admission (Fichter et al 2008) post admission (Fichter et al 2011)
The Long Term Outcome of Anorexia Nervosa (Stoving et al 2011) 20-25% Persistent illness N=351, Male %% Median recovery 7 years
The outcome of Bulimia Nervosa (Stoving et al 2010) N=361, Male 1% 40% Chronic Illness Median Recovery 12 years
Conclusion • Eating disorders are increasing and they have a persistent course. • Genetic, environmental and developmental factors contribute to causes. • Eating disorders have profound effects on brain, body and social network. • Biological, psychological and social process maintain the disorders. • Early intervention before secondary effects become entrenched is essential to avoid harmful costs. • A collaborative approach with individual and family is essential.