26.11 - Eating Disorders Flashcards

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1
Q

What are the main eating disorders?

A
  • Anorexia nervosa
  • Bulimia nervosa
  • Binge eating disorder
  • (Other conditions that do not fit exactly into these categories)
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2
Q

What is the lifetime prevalence of any eating disorder?

A

5%

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3
Q

Define eating disorders.

A

Definite disturbance in eating habits or weight control behaviour with a core psychopathology that leads to disturbed eating and overevaluation of the control of eating and weight. It results in clinically significant impairment in health/psychosocial function and is not secondary to any general medical or psychiatric condition.

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4
Q

What is anorexia nervosa?

A
  • A severely debilitating psychiatric disorder characterised by relentless self-starvation with dramatic physiological and psychological effects.
  • It has low rates of recovery (<50%) and the highest mortality rate of any psychiatric disorder.
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5
Q

What is the prevalence of anorexia nervosa?

A
  • 1-4% in women
  • 0.3% in men
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6
Q

What is the heritability of anorexia nervosa?

A

50-60%

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7
Q

When is the onset of anorexia nervosa most common?

A

Adolescence

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8
Q

What are the outcomes of anorexia nervosa?

A
  • 10-15% mortality rate
  • Chronic illness seen in 50% of cases -> No effective therapies for these patients
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9
Q

What are some common features of anorexia nervosa?

A
  • Strict dietary rules, such as counting calories
  • Rigidity of eating and ritualistic behaviour
  • Body checking and weighing
  • Compulsive exercise
  • Obsessive preoccupation with (control of ) eating shape and weight
  • Parallels with OCD (and a high comorbidity OCPD)
  • Body image dysphoria and distortion
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10
Q

What is bulimia nervosa?

A
  • Similar to anorexia nervosa, but w/ lapses in control -> periods of binge eating (>weekly >3 months)
    • different diagnostic criteria (don’t need low BMI)
  • Extreme weight control behaviour including extreme exercise, strict dieting + compensatory behaviours (laxative misuse/ self-induced vomiting)
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11
Q

When is the onset of bulimia nervosa most common?

A

Adolescence and young adulthood

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12
Q

What is binge eating disorder?

A
  • Recurrent episodes of binge eating > weekly for > 3 months
  • It leads to impairment and/or distress
  • NO compensatory behaviours + NO over evaluation of control of eating, weight and shape.
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13
Q

When is the onset of binge eating disorder most common?

A

It has a later onset than anorexia and bulimia.

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14
Q

Can people switch between different types of eating disorder?

A

Yes, it is relatively common.

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15
Q

What is the common feature in the psychopathology of anorexia nervosa and bulimia nervosa?

A

Overevaluation of control of eating based on shape and weight (too much importance placed on body weight when evaluating self-worth).

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16
Q

Experimentally, describe the Minnesota starvation study and its results.

[EXTRA]

A

(Keys et al, 1950)

Study plan:
36 young healthy men
* 3-month - baseline feeding
* 6-month - severe dietary restriction (50% prior intake)
* 3-month - re-feeding phase

Results:

  • Preoccupation with food and eating
  • Eating habits changed
    • Eating became planned, ritualistic and prolonged
    • Food smuggled out of meals to be consumed later in private
    • Increased use of salt and spices; coffee and tea; odd food concoctions
  • Overeating
    • 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
    • Extreme in 20%-increase in anxiety and depression
    • Lability of mood, marked irritability
    • Severe dysphoria on refeeding (one man cut fingers off)
  • Hoarding, compulsive behaviours
  • Decrease in outside interests
  • Impaired concentration and alertness
    Full recovery was not experienced by all after refeeding.
17
Q

What are some implications about anorexia and bulimia that we can learn from the Minnesota starvation experiment?

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 weight restoration
  • Corollary is that other clinical features are not due to starvation; rather, some are responsible for it
  • Treatment needs to involve much more than weight regain
18
Q

Describe the cycle that keeps anorexia nervosa going.

A

There are two cycles:

  • “Starvation syndrome”, where the starvation itself makes you preoccupied with weight, so you exert greater control over eating, etc.
  • Perverse rewards, where losing weight leads to social reinforcement and euphoria
19
Q

Describe the cycle that keeps binge eating disorder going.

A
20
Q

Describe how eating disorders are treated in general.

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 bulimia nervosa
  • But all talking treatments of limited efficacy in low weight anorexia nervosa
21
Q

Describe how anorexia nervosa can be treated.

A
  • In adolescents, there is good evidence for the Maudsley model eating disorder family therapy (for patients will less than 3 years illness)
  • In adults, there is moderate evidence for all treatments (less than 50% recover)
  • Early intervention is most effective since behavioural patterns get stuck
  • Key aspects to management:
    • Helping patients to see they need help to fight the ED ‘motivation’
    • Helping patients reverse starvation, restore weight
    • Addressing over-evaluation of shape, weight and control over eating
    • Compulsory treatment only relevant in a few cases
    • Drug treatment does not currently have an established role
22
Q

Describe how bulimia nervosa can be treated.

A

NICE guidelines:

  • Grade A treatment (treatment of choice): A specific form of CBT
  • Grade B treatment: Interpersonal psychotherapy
  • Grade B treatment: Evidence-based self-help and/or a trial of anti-depressant drugs
23
Q

What are some risk factors for anorexia/bulimia nervosa?

[IMPORTANT]

A

There are both genetic and environmental factors -> 50-60% heritability, highest for anorexia nervosa. Cross-transmission between eating disorders.

Some example risk factors:

  • Being female
  • Adolescence and early adulthood
  • Living in western society
  • Family history of: Eating disorders of any type, depression, substance abuse and obesity
  • Adverse parenting
  • Sexual abuse
  • Family dieting
  • Critical comments about eating, weight and shape from others
  • Occupational pressure to be slim
  • Obesity
  • Early menarche
  • Low self-esteem
  • Perfectionism
  • Anxiety and anxiety disorders
  • Altered 5-HT and dopaminergic function that is exacerbated by weight loss
24
Q

Give some experimental evidence for the genetic component of anorexia nervosa.

[EXTRA]

A

(Watson, 2019):

  • GWAS of 16,992 cases of anorexia nervosa and 55,525 controls
  • Identified eight loci significant to anorexia nervosa
25
Q

Is anorexia nervosa purely an psychiatric disorder?

A

It has been proposed that it should be considered a metabo-psychiatric disorder, since it shares significant genetic correlations with psychiatric disorders, physical activity, metabolic (including glycemic), lipid and anthropometric traits.

26
Q

Give some experimental evidence for the relevance of the gut microbiome in anorexia nervosa.

[EXTRA]

A

(Ghenciulescu, 2021):

  • Reviewed research about the gut microbiome in patients with anorexia nervosa
  • Studies show considerable low divergence and altered taxonomic abundance of the anorexia nervosa gut microbiome
  • It is uncertain whether this is causative of the symptoms of anorexia nervosa or simply a result of the calorific restriction
  • Fecal transplants and other therapies show potential for treatment
27
Q

What are some neuropsychological abnormalities that may explain anorexia nervosa?

[EXTRA]

A

Imbalance in top-down cortical control and bottom-up striatal control:

  • In most people, the sight of food triggers the reward pathways driving the urge to satisfy hunger in the short term
  • In people with anorexia nervosa, the sight of food triggers activation of the amygdala and prefrontal cortex, leading to a dominant desire to stay thin in the long-term, rather than satisfy hunger
  • In other words, the prefrontal cortex, which is involved in decision making and control, does a lot of work to ensure that the individual does not want to eat the high calorie food by overruling their desires (i.e. the PFC weighs up a lot of evidence against eating high calorie food in order to decide that this outweighs the benefit of eating it)
  • Dysfunction of cortico-striatal circuitry can also explain why patients with anorexia nervosa experience aberrant reward upon starvaing themselves -> (Fladung, 2009) showed that patients with anorexia nervosa had higher ventral striatal activity compared to controls when shown a picture of an underweight person

Decreased connectivity in regions associated with somatosensory processing and abnormalities in body/object recognitions areas:

  • Explains reduced interoceptive awareness and misperception of body image
28
Q

Is anorexia nervosa driven by “liking” or “wanting” low calories foods?

[EXTRA?]

A
  • “Liking” is explicit, while wanting is “implicit”
  • (Cowdry, 2013):
    • “The aberrant responses to food that characterize AN may be driven more by altered motivational salience (“wanting”) than by explicit liking responses.”