Transcript Getting to the fundamentals of eating disorders.

Getting to the
fundamentals of
eating disorders.
Professor Janet Treasure
www.eatingresearch.com
[email protected]
Conflict of Interest
• Pharma- Nil
• Books-Several books for patients/carers
and professionals.
• NICE guideline committee
• World federation of biological psychiatry
guidelines.
Talk Map
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What are eating disorders?
The history
The prevalence of eating disorders
The clinical features.
Treatment
Spectrum of EDs
Increasing tendency to fatness
Gull 1873
Lasegue 1873
Russell 1979
Stunkard
Volkow 2007
Orphan Disorders
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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 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
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?
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
Lewinsohn et al 2000, Brukner et 2010, Field et al 2011,
Tozzi et al 2005, Milos et al 2005
Obesity
The Brain Causes
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
Learning
Memories of food
reward & metabolic
consequences
Consequences of
malnutrition on the brain
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.
Consequences of fast/feast/
vomiting on the brain
Animals models of binge eating
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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 system
Embeds eating into social context &
individual values
Restriction from
cognitive control
Damaged by
starvation
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
Consequences on other
people
The interpersonal perpetuating cycle
Distressing ED
Symptoms
And
Behaviours
Carers respond:
Expressed emotion
Accommodate
Enable
Kyriacou et a 2008
Sepulveda et al 2009
Carers concerned
And anxious at ED
symptoms
•(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
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
LFT’s 
Fits, Coma
Arrythmias,
Syncope
PR<40bpm
BP<80mmHg
Postural drop>20mmHg
Tetany
Na K 
Difficulty arising
from squat/sit up
Glucose 
Hb WCC
platelets
Rapid Rate
Weight loss
Petechial rash
Ulcer
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
Claudino et al
In progress
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 Large effects
& therapy
Bacaltchuk 2001
Systematic reviews: BED
Outpatient
psychotherapy
CBT, IPT< DBT
Self help
Moderate binge
Nil-small weight
Vocks 2009
Small effect
Vocks 2009
Orlistat, topiramate Moderate binge
Moderate weight
Vocks 2009
Antidepressants
SNRI> SSRI
Vocks 2009
Aiger, Treasure
WFBP 2011
Moderate binge
Nil-small weight
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
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)
N=351, Male %%
Median recovery 7
years
20-25% Persistent
illness
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.