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Eating disorders Flashcards

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1
Q

Define eating disorders

A
  • Definite disturbance in eating habits or weight control behaviour;
  • Core ED features ( disturbed eating + overevaluation of the control of eating, weight, shape) resulting in clinically significant impairment in health/psychosocial function;
  • Not secondary to any general medical or psychiatric condition.
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2
Q

Describe how EDs are classified

A

classified by the DSM-V as:

  • anorexia nervosa
  • bulimia nervosa
  • binge eating disorder,
  • otherwise specified feeding/eating disorders (OSFED) -c.f. DSM-IV eating disorder not otherwise specified (ED-NOS
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3
Q

What is the lifetime prevalence of any ED?

A

5%

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4
Q

What is AN chcaracterised by?

A

relentless self-starvation with dramatic physiological and psychological effects, especially critically low body weight; AN is associated with low rates of recovery (Berkman et al., 2007), and has the highest mortality rate of any psychiatric disorder (Arcelus et al., 2011); [however, it has a lower incidence than bulimia nervosa]

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5
Q

To be diagnosed with AN, a person must display…

A
  1. Persistent restriction of energy intake leading to significantly low body weight (in the context of what is minimally expected for age, sex, developmental trajectory and physical health)
  2. Either an intense fear of gaining weight or becoming fat, or persistent behaviour that interferes with weight gain (even though significantly low weight)
  3. Disturbance in the way one’s body weight or shape is experienced, undue influence of body shape and weight on self-evaluation, or persistent lack of recognition of the seriousness of the current body weight
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6
Q

What are the subtypes of AN?

A

Restricting type:
- during the last three months, the person has not engaged in recurrent episodes of binge eating or purging behaviour (ie., self induced vomiting or misuse of laxatives, diuretics or enemas)

Binge/purge type:
- during the last three months, the person has engaged in recurrent episodes of binge eating or purging behaviour (ie., self induced vomiting or misuse of laxatives, diuretics or enemas)

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7
Q

Prevalence of AN

A

0.3% in teenage girls

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8
Q

Incidence of AN

A

90% female, 19 cases in females and 2 in males per 100,000 per year

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9
Q

Describe BN

A
  • Recurrent binge-eating – episodes of uncontrolled overeating at least > weekly > 3 m
  • Extreme weight control behaviour – self-induced vomiting, laxative misuse, extreme exercise, strict dieting
  • Over-evaluation of shape and weight
  • Diagnostic criteria for anorexia nervosa not met (e.g. not underweight, possibly overweight) - makes it more difficult to diagnose
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10
Q

What can BN vomiting cause?

A

Electrolyte imbalances and cardiac dysrhythmias

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11
Q

Which of AN and BN has a greater incidence?

A

BN

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12
Q

Prevalence of BN

A

1-2% in 16 to 35 yr olds

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13
Q

Incidence of BN

A

Mostly female, 29 cases in females and 1 in males per 100,000 per year

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14
Q

Mortality rate and percentage with chronic illness with AN

A

10-15% mortality rate

Chronic illness in 50%

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15
Q

When are the peak onsets of AN and BN?

A

Adolescent/ young adult

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16
Q

Describe binge eating disorder

A
  • Recurrent episodes of binge eating > weekly for > 3 months
  • Causes impairment and / or distress
  • No compensatory behaviours
  • No over evaluation of control of eating, weight and shape
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17
Q

Describe onset of BED

A

Later onset
50% binge eat before dieting begins
Around 65% are morbidly obese

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18
Q

Describe incidence of BED

A

more balanced distribution between men and women - still more frequent in women (c.f. BN and AN which are mostly women)

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19
Q

Describe otherwise specified feeding/eating disorder

A

Eating disorders of clinical severity that do not conform to the diagnostic criteria for anorexia nervosa or bulimia nervosa, or atypical forms (comparable to ED-NOS in DSM-IV).

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20
Q

Describe temporal movement between EDs

A

It is polarised - more common to move from AN to BN rather than from BN to AN

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21
Q

Describe obesity as a ED

A

Controversial (eating disorder or disordered eating?) - CURRENTLY NOT CLASSIFIED AS AN ED

  • ‘eating addiction’ vs ‘food addiction’ - much debated construct → behavioural addiction vs substance abuse
  • hypometabolism of hypophagia
  • public health issues: societal and social-lifestyle factors
  • genetics/ centeaal obesity - neural mechanisms: e.g. prader will, leptin deficiency
  • obesity can be secondary to binge eating, other psychiatric disorders, medication side effects, and other medical conditions - diabetes
22
Q

What is striking about AN, BN and OSFED?

A

How much they have in common, rather than what distinguishes them:

  • characteristic behavioural forms of attempted and actual under-eating; binge-eating; self-induced vomiting, laxative misuse, driven exercising
  • a common core psychopathology the over-evaluation of control or eating, weight, and body shape, body checking and body avoidance, feeling fat, etc-;
23
Q

What is a difference between AN and others?

A

Different physiological features - e.g. due to effects of starvation

24
Q

What is a significant barrier to AN recovery?

A

Individuals with AN view the compulsive nature of their behaviour as central to the maintenance of their disorder, and as a significant barrier to recovery.

25
Q

What is compulsivity?

A

Compulsivity = a trait leading to behaviour that is inappropriate to the situation, persists despite having no relationship with any overall goal, and often results in undesirable consequences (Dalley et al., 2011).

26
Q

Describe compulsivity in AN

A
  • Dietary restriction tends to take on a driven and compulsive quality in AN
  • May be motivated by an aberrant sense of reward, specifically the perceived rewards of extreme dietary control and thinness
  • Compulsive over-exercising common - 80% in restrictive AN, 43% of B/P AN
  • Parallels with other compulsive disorders- OCD, SUDs-addictions
27
Q

Describe Godier 2015

A

The themes that emerged from qualitative analysis (Godier 2015) show parallels with the DSM-V criteria for SUDs (substance use disorders), (and OCD).

These 8 themes were:

  • Compulsivity central in AN
  • Escalating compulsions
  • Emotional triggers
  • Impaired control
  • Negative reactions to prevention
  • Role in recovery
  • Detrimental continuation
  • Functional impairment
28
Q

What study showed the effects of starvation?

A

Minnesota study (keys et al, 1950)

29
Q

Describe the set-up of the Minnesota study

A
  • Recruited 36 young healthy men
  • A 3-month baseline was obtained, followed by a 6-month period of severe dietary restriction (50% prior intake)
  • And a 3-month re-feeding phase
30
Q

What was observed in the Minnesota study?

A
  • Subjects experienced preoccupation with food and eating it became the subject of conversation, reading and dreaming; three became chefs afterwards.
  • Their eating habits changed: eating became planned, ritualistic and prolonged; food was smuggled out of meals to be consumed later in private; there was increased use of salt and spices; coffee and tea; odd food concoctions.
  • Overeating also occurred: some experienced episodic loss of control (resembling binge eating) during the restriction phase, and in a minority this persisted for months; many overate “more or less continually” during the refeeding phase.
  • Changes in mood were marked: extreme in 20%-increase in anxiety and depression; lability of mood, marked irritability. Severe dysphoria occured on refeeding - one man cut fingers off.
  • Subjects engaged in hoarding, compulsive behaviours towards food and other items.
  • Decrease in outside interests occurred with initial sociability changed to social withdrawal, general apathy, decreased sexual interest, impaired concentration and alertness.
31
Q

What are the implications of the Minnesota study?

A
  • Many features of eating disorders are compounded by starvation, and some are reversed by re-feeding;
  • Some are likely to maintain the eating disorder;
  • An essential component of treatment is therefore weight restoration.
  • It follows that other clinical features are not due to starvation; rather, some are responsible for it;
  • Treatment needs to involve much more than weight regain.
32
Q

Look at the flow charts from lecture

A

Lecture/notes

33
Q

Examples of rules to control weight, shape and eating

A

 Gym 2 hours every day (Compulsive exercise)
 Delay eating as long as possible/ only eat one meal
 Only eat fruit and vegetables; avoided foods
 Eat less / more slowly than others around me
 Limit bulky foods that make my stomach fat
 Stomach must not stick out- ever: body checking
 I should be thinner than my friends
 My thighs should not touch –ever
 I should wear the lowest clothes size
 Weight should go down- never up

34
Q

Pathogenesis of AN and BN

A

research shows it is multifactorial → genetic predisposition -as well as epigenetic modifications- and a range of environmental risk factors have been identified

35
Q

What physiological changes may occur in AN and BN?

A

altered serotonergic and dopaminergic function (exacerbated by weight loss) and altered interoception -i.e. internal perception of your body- and (possibly reward processes in AN); [Kaye, 2009, 2013; Park et al-, 2011, 2014]

36
Q

What is the genetics of ED supported by?

A

o Eating disorders and traits run in families; traits confer vulnerability
o Cross-transmission of AN, BN and EDNOS
o Twin studies: AN 55%:5% MZ:DZ, BN: 35%:30% MZ:DZ
o Heritability estimates 50-80%
o Evidence for 3 genetic loci involved in both AN risk and variation of BMI

37
Q

General risk factors for ED

A

o Female
o Adolescence/early adulthood
o Living in Western society
 “No woman can be too rich or too thin” Duchess of Windsor

38
Q

Individual-specific risk factors

A 
Family history
o	Eating disorder of any type
o	Depression
o	Substance misuse, especially alcoholism (for BN)
o	Obesity (for BN)
o	Early menarche (for BM) 
•
Premorbid experiences: 
o	Adverse parenting (low contact, high expectations, parental discord)
o	Sexual abuse
o	Family dieting
o	Critical comments about eating/weight/shape from others
o	Occupational pressure to be slim

Premorbid characteristics:
o Anxiety and anxiety disorders
o Perfectionism (for AN)
o Low self-esteem

39
Q

Describe Watson 2019 GWAS

A

Identified 8 risk loci and implicates metabo-psychiatric origins for AN

  • 16,992 cases of AN and 55,525 controls
  • Genetic architecture of AN mirrors its clinical presentation,
    significant genetic correlations with
    • psychiatric disorders,
    • physical activity,
    • metabolic (including glycemic), lipid and anthropometric traits,
    independent of the effects of common variants associated with BMI.
    encourage a reconceptualization of AN as a metabo-psychiatric disorder
40
Q

How specific features might link to abnormalities in neuropsychological systems

A

Corticostriatal [ventral striatum and mOFC] dysregulation => compulsivity (rules such as 2h gym/every day; avoided foods; body checking rituals)

41
Q

What are the key aspects of management of AN

A

• Helping patients to see they need help to fight the ED ‘motivation’
• Helping patients reverse starvation, restore weight( OP, DP, IP)
• Addressing over-evaluation of shape, weight and control over eating; eg ED
family therapy CBT-E/MANTRA/SSCM
• Compulsory treatment only relevant in a few cases
• Drug treatment does not currently have an established role

42
Q

Describe BN management

A

Research base –more than 60 randomised controlled trials
NICE guidelines:
• Grade A: A specific form of CBT is the treatment of choice – a
third to a half make a complete and lasting recovery, others
improve
• Grade B: Interpersonal psychotherapy a possible alternative
• Grade B: Evidence based self-help and /or a trial of anti-depressant
drugs may be offered as first step
No consistent predictors of outcome
Combining CBT with anti-depressant drugs results in few added
benefits

43
Q

Describe a form of treatment for the full range of EDs

A

A transdiagnostic form of CBT , CBT-E developed in Oxford (Fairburn et al 2012) for the full range of eating disorders
• Based on a transdiagnostic theory of maintenance
• Evidence from controlled evaluation indicates that
outcome for ED-NOS exactly the same as for BN;
(all talking treatments of limited efficacy in low weight AN)

Focuses on specific maintaining factors: - low weight ( AN)
- institute regular eating , self monitoring  reduce binges
- reduce body checking
- relax dietary rules and increasing flexibility  guidelines
Using behavioural experiments
Mood management skills

44
Q

Management of BED

A

BED – strongest support is for a form of CBT- guided self-help is also very promising.

45
Q

Describe Godier & park 2014, Robbins 2012 - a transidagnostic approach to compulsivity

A
  • Dysfunction of cortico-striatal circuitry results in compulsive behaviour
  • Abberent reward processing underpins compulsive behaviour
  • Abnormalities in activity and volume of striatum (caudate) and FC across compulsive disorders: Eating disorders, OCD and Addictions
46
Q

What did Fladung 2009 and 2012 do?

A

Showed high ventral striatal activity in acute AN vs controls
VS is a neural marker in AN → develops with illness durations (2012)

47
Q

Cowdrey et al 2011

A

showed increased ventral striatal response to chocolate taste in women recovered from AN compared to healthy controls.

48
Q

Cowdrey et al 2013

A

preference for high-calorie foods is lower in AN patients and recovered AN patients than healthy controls, and preference for low-calorie foods is greater

They also showed that weight-restored AN and current AN patients have sig higher implicit wanting for high-cal foods compared to healthy controls, and lower implicit wanting than healthy controls for low-cal foods

49
Q

Read through the experiments from lecture - don’t really understand

A

Lecture

50
Q

novel medications acting on reward/compulsivity pathways

A
  • Characteristic neural circuits – state of the art neuroimaging
  • Intervening with neural circuits? – neuromodulation – DBS, TMS

Psych (12 decks)

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