1. Getting to the fundamentals of eating disorders.
Professor Janet Treasure

2. Conflict of Interest Pharma- Nil
Books-Several books for patients/carers and professionals.
NICE guideline committee
World federation of biological psychiatry guidelines.

3. Talk Map What are eating disorders? The history
The prevalence of eating disorders
The clinical features.
Treatment

4. Spectrum of EDs Gull 1873 Volkow 2007 Lasegue 1873 Russell 1979
Binge-purging AN
Restricting AN
Purging Disorder
Purging BN
Non-purging BN
Simple obesity
Binge-eating
Gull 1873
Lasegue 1873
Volkow 2007
Stunkard
Russell 1979

5. Orphan Disorders What are they? Physical or psychological?
Body image or eating?
Neurotic or psychotic?
Developmental or Environmental ?

7. Cases presenting to primary care in UK (Micali et al 2012)
EDNOS BED most common diagnosis

8. Epidemiology: Lifetime prevalence) (Hudson et al 2007, Jacobi et al 2004, Preti et al 2009, Field 2011)
All F M AN
0.6%
0.9%
0.3% BN 1%
1.5%
0.5%
BED 3%
3.5%
2.0%
EDNOS
(PD)
15%
10% 5%

9. Clinical Features

10. 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.

11. Bulimia nervosa 1979: Defined by Russell
Core Behaviours: Binge >1000cal out of control
Compensatory Behaviours eg Vomit, laxatives, exercise, drugs
Teenage onset
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

12. Binge Eating Disorder: History
Recurrent distressing binges
No food restriction
No compensatory behaviours
Obesity
Prevalence: 1-3%
Men & women affected equally
Peak age onset: and early 20s
I spent all my time thinking of food. I would wake in the night and want to eat

13. What is the Health and Psychosocial Burden?

14. 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).

15. 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

16. The Brain Causes

17. Memories of food reward & metabolic
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

18. Consequences of malnutrition on the brain

19. 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.

20. Consequences of fast/feast/ vomiting on the brain

21. Animals models of binge eating
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).

22. Brain areas implicated in eating disorder symptoms
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

23. Consequences on other people

24. The interpersonal perpetuating cycle
Kyriacou et a 2008
Sepulveda et al 2009
First step in getting treatment, important throughout the course of the eating disorder and after
NICE Guidelines – in the UK guidelines stipulate that sufferers should be treated as outpatients as much as possible. Only 15-30% receive inpatient treatment in the UK therefore much of the care involved falls upon their carers, namely parents, siblings, partners etc.
Carers have high distress and unmet needs: poor quality of life, high levels of caregiver burden (the impact of the illness on their daily functioning/routines/life), high levels of general health concerns, distress and anxiety. Whitney et al (2005) : Guilt, fear, anger, hostility and self blame are common (40 ED carers)
A maintenance model of ED has been proposed. It has 4 factors of which interpersonal factors is one of them. This component suggests that interactions, communication patterns, and carers’ response to the illness can have an impact on the course of the ED. This includes aspects of expressed emotion – CC and EOI. We know that EE has a negative impact on outcome in many mental illnesses, including schizophrenia and ED. Accommodation and enabling are responses of carers that perpetuate ED symptoms by allowing them to carry on.
We wanted to develop an intervention that targeted carer distress and interpersonal maintaining factors of EE and accommodation.
(Zabala et al, Eur Eat Rev 2009) 24

25. 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.

26. 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.

27. 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

28. 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

29. WWW.eatingresearch.com-health professionals

30. 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.

31. Danger Signs Fits, Coma Arrythmias, Syncope PR<40bpm LFT’s 
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

32. Treatment

33. Systematic reviews: AN
Outpatient
psychotherapy
Specific >non specific
Hay et al 2008
Family therapy
Probable effect
Fisher et al 2010
Antidepressants
Little effect
Claudino et al 2006
Antipsychotics
In progress
Claudino et al

34. Systematic reviews: BN
Outpatient
psychotherapy
CBT large
Hay et al 2003
Self help
Small effect
Perkins 2006
Antidepressants
TCA, SSRI, Large effect
Bacaltchuk 2003,
Aiger, Treasure WFBP 2011
Antidepressants & therapy
Large effects
Bacaltchuk 2001

35. Systematic reviews: BED
Outpatient
psychotherapy CBT, IPT< DBT
Moderate binge
Nil-small weight
Vocks 2009
Self help
Small effect
Orlistat, topiramate
Moderate weight
Antidepressants
SNRI> SSRI
Aiger, Treasure WFBP 2011

36. Perkins, S Cochrane Systematic Reviews 2006 Issue 3
New Tools for Eating Disorder Treatment
Books
Web base
Mobile
Games
More effective if used with guidance
Perkins, S Cochrane Systematic Reviews 2006 Issue 3

37. 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)

38. Outcome

39. The Long Term Outcome of Anorexia Nervosa (Stoving et al 2011)
20-25% Persistent illness
N=351, Male %%
Median recovery 7 years

40. The outcome of Bulimia Nervosa (Stoving et al 2010)
N=361, Male 1%
40% Chronic Illness
Median Recovery 12 years

41. 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.