Getting to the fundamentals of eating disorders.

Professor Janet Treasurewww.eatingresearch.comJanet.treasure@kcl.ac.uk

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

Spectrum of EDs

Increasing tendency to fatness

Gull 1873Lasegue 1873 Russell 1979

Volkow 2007

Purgi

ng D

isord

er

Stunkard

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)

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%

Clinical Features

Anorexia NervosaAnorexia 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.

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

Binge Eating Disorder: History

Recurrent distressing Recurrent distressing bingesbinges

• No food restrictionNo food restriction• No compensatory No compensatory

behavioursbehaviours• ObesityObesityPrevalence: 1-3%Prevalence: 1-3%• Men & women affected Men & women affected

equallyequallyPeak age onset: 13-15 and Peak age onset: 13-15 and

early 20s 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?

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

The Brain Causes

Self regulation systemSelf regulation systemEmbeds eating into social context & Embeds eating into social context & individual valuesindividual values

Hedonic centreReward from food (limbic system

Homeostatic centreHomeostatic centreRegulates input and output of Regulates input and output of energy supplyenergy supply

LearningMemories of food

reward & metabolic consequences

Consequences of malnutrition on the brain

The effect of Nutritional Problems The effect of Nutritional Problems on the brainon 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.

Consequences of fast/feast/ vomiting on the brain

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).

Self regulation systemSelf regulation systemEmbeds eating into social context & Embeds eating into social context & individual valuesindividual values

Hedonic centreReward from food (limbic system

Homeostatic centreHomeostatic centreRegulates input and output of Regulates input and output of energy supplyenergy supply

Restriction from cognitive control

Damaged by starvation

Over sensitive reward centre ↑

binging Starvation ↑ rewardFast/feast ↑ reward

Brain areas implicated in eating disorder symptomsSecondary problems

Consequences on other people

The interpersonal perpetuating cycle

Distressing EDSymptoms

And Behaviours

Carers concernedAnd anxious at ED

symptoms

Carers respond:Expressed emotion

AccommodateEnable

•(Zabala et al, Eur Eat Rev 2009)

Kyriacou et a 2008Sepulveda et al 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 SignsPhysical Signs

Parotid or submandibular gland enlargement

Eroded teeth "Russell's sign" callus on back of hand

Cold blue hands, nose and feet

Lanugo hair

WWW.eatingresearch.com-health professionals

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

Difficulty arising from squat/sit up

Tetany

LFT’s

Na K

Fits, Coma

Glucose

Arrythmias, SyncopePR<40bpmBP<80mmHgPostural drop>20mmHg

Rapid Rate Weight loss

Hb WCC platelets

Petechial rashUlcer

Treatment

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

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

Systematic reviews: BED

Outpatient

psychotherapy CBT, IPT< DBT

Moderate binge

Nil-small weight

Vocks 2009

Self help Small effect Vocks 2009

Orlistat, topiramate Moderate binge

Moderate weight

Vocks 2009

Antidepressants

SNRI> SSRI

Moderate binge

Nil-small weight

Vocks 2009

Aiger, Treasure WFBP 2011

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

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)

Outcome

The Long Term Outcome of Anorexia Nervosa (Stoving et al 2011)

20-25% Persistent illness

Median recovery 7 years

N=351, Male %%

The outcome of Bulimia Nervosa (Stoving et al 2010)

40% Chronic Illness

Median Recovery 12 years

N=361, Male 1%

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.