Eating Disorders: Anorexia Nervosa Flashcards

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1
Q

Anorexia nervosa

A

“Nervous loss of appetite” sufferers do feel hungry but do not respond to hunger by eating,

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2
Q

Summary of symptoms from DSM-5

A
  • Persistent restriction of energy intake leading to significant low body weight
  • An intense fear of gaining weight
  • Disturbance in the way ones body shape is experienced
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3
Q

Two types of anorexia

A
  • Restricting type: self starvation not associated with purging
  • Binge-purging: involves losing weight through self induced vomiting

(Bulimia nervosa is different, involves binge-purging, but does not involve symptoms from DSM-5)

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4
Q

What percentage of suffers are female?

A

-About 90% of suffers are female, it is on the increase among males.

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5
Q

Typical age of onset

A

-Typically 13 to 18 (although can be earlier or later)

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6
Q

The incidence of the disorder in young females is between…

A

0.5% and 1%

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7
Q

Davey (2008)

A

-Between 5% and 8% of people diagnosed die as a result of the physical problems it causes

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8
Q

Minnesota starvation study

A
  • The aim of the study was to starve some subjects (young men volunteers) to then work out the best way to re-feed them during world war 2.
  • After halving the mens daily intake the men showed remarkable decline in health and energy and they also complained a lot about their fatigue.
  • They showed similarities between anorectics as they grew to have an obsession with food and it was due to their starvation
  • However afterwards they were able to recover fully; suggest there is psychological differences in anorectics
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9
Q

Hoek’s research

A

-Research into anorexia by Hoek highlighted cultural differences of body image. He went to the island of Curacao where it is considered to be beautiful to be overweight, and he found only 8 cases of anorexia on the island. This shows that while there is obviously a considerable impact of the media and culture to want to be thin, even in a place where it is considered to be beautiful if you are overweight, there is still a small number of anorexia cases, suggesting their must be other (psychological) factors.

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10
Q

Which gene is more common in anorectics?

A

-A variation in a serotonin receptor gene is more common in anorectics than among the general population

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11
Q

Kaye

A
  • The serotonin system is involved both in eating and in obsessional behaviour.
  • For eating disorder sufferers high levels of serotonin cause high anxiety. Often suffers say they feel btter when they don’t eat.
  • Serotonin is made from tryptophan, which comes from food. Starvation reduces the amount of tryptophan, and therefore the amount of serotonin.
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12
Q

Cycle of serotonin

A
  • > Less food
  • > Less tryptophan
  • > Less serotonin
  • > Less receptor activity
  • > Less anxiety
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13
Q

Holland et al (1988)

A

-They investigated concordance rates of anorexia nervosa for MZ and DZ twins.
-They found that there was a much higher concordance rate for MZ’s then DZ’s.
->MZ’s = 67% and DZ’s = 7%
(and mz share 100% of genes compared to dzs share 50%)
-Compared to 1% of teenage girls generally.
-In cases where the non-diagnosed twin did not have anorexia they were diagnosed with other psychiatric disorders

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14
Q

If asked about bio explanations for eating disorders…

A

Include genetics as a separate explanation

-Can also use the study as indirect supporting evidence

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15
Q

How does Holland et al. indirectly support Kaye’s neural explanation?

A
  • Serotonin receptors are controlled by genes
  • If serotonin receptors are faulty (e.g overactive), would expect to find evidence of a genetic basis for AN.
  • If there was no difference in concordance rates then would cast doubt on neural explanation
  • Holland shows that genes play a role, but doesn’t show would gene plays a role so is indirect supporting evidence.
  • Then Kaye shows that the specific gene 5HT is different in anorectics than the general population
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16
Q

Garfinkel & Garner suggest that AN may result from a defect in the lateral hypothalamus, the part of the brain which ‘Switches on’ eating is supported by…

A
  • Anand & Brobeck as they lesioned the hypothalamus of rats and the rats starved themselves to death.
  • This shows that the damaged LH leads to a decrease in hunger
17
Q

Kaye proses that increase serotonin activity in areas of the brain which regulate mood and cognitions such as anxiety and fear. This may predate the onset of AN contributing to anxious, obsessional and perfectionistic childhood traits, this is supported by…

A
  • Kayes research into anxiety, obsessiveness and perfectionism, also hormonal changes in puberty worsen serotonin dysregulation, and as the typical age of onset is between 13 to 18 this shows that this is about the age that girls reach puberty and so their dysregulation in serotonin may lead to AN.
  • The incidence of the disorder among young females is between 0.5% and 1%, compared to 0.04% of the general population.
  • Supports the idea that self-starvation may lead to a reduction in anxiety and suggests that dysregular serotonin activity causes anorexia.
18
Q

Serotonin in made from tryptophan which comes from food. Starvation reduces the amount of tryptophan, and therefore the amount of serotonin and in turn reduces anxiety levels. This is supported by…

A

-Bailer et al. did a PET scan. A chemical tracer travels to the brain and the drug shows up as brightly lit on the scan. Studying women from recovering AN, Bailer found the highest levels of serotonin in those who showed the most anxiety.
Therefore supports the idea that serotonin causes high anxiety levels.

19
Q

However, Bailer et al, does not sow any direct evidence that disorder itself reduces serotonin levels and so reduces anxiety. This is then shown by Kaye…

A
  • Keya used an experimental procedure called acute tryptophan depletion; this is where levels of tryptophan are artificially lowered (14 ill AN women and 14 recovered AN and a healthy control group.)
  • The ill AN and rec AN had a significantly higher baseline of tryptophan and they had a greater reduction compared to the control group. Both the ill AN and rec AN had a significant reduction in anxiety on the day compared to placebo day. (came in twice but only received ATD once)
  • This is direct evidence that those who suffer from AN have a greater amount of tryptophan and so anxiety, and will try to reduce this by not eating.
20
Q

Over activity of dopamine receptors in the basal ganglia (reward centre). If the system is overactive it may fail to respond o natural pleasure giving stimuli. This is supported by Kaye et al. (2005)…

A
  • Used a PET scan to compare dopamine activity in the basal ganglia of 10 women recovering from AN, and 12 healthy women. Activity was significantly higher in the recovering anorectics. Kaye notes that AN have been ‘able to deny themselves most comforts and pleasure in life.’
  • This shows that over activity in reward centre leads to failure to respond to pleasure stimuli and as AN have extreme over activity they may not experience the same pleasure from food as everyone else.
21
Q

Practical application from Kayes PET scan (2005)

A

-Because it shows that even recovered anorectics still have overactive functioning, it shows that it must be something that it always present in anorectics and so psychologists can use this as a premorbid symptom to help diagnose the illness and prevent it because it progresses.

22
Q

On the contrary (Kayes PET scan)…

A

-If the anorexia is a fully functioning disorder, then the participants should have lower serotonin levels to everyone else as they are not eating and so reduces there levels of tryptophan and subsequently serotonin.

23
Q

Methodological issues from PET scan studies…

A
  • Strengths: its physical biological evidence that certain parts of the brain are more active than others, objective evidence, and also easier to generalise results as people have similar brain structures.
  • Weakness: causality issues as it could be the illness that effects the dopamine activity rather than the dopamine activity causing the illness.
24
Q

Weakness and strength with studying recovered anorectics…

A
  • S: you can compare to anorectics and prove that the dysregulation is the cause of the disorder because they still have the dysregulation even after they have recovered.
  • W: however it could be that as a result from the disorder the dysregulation has resulted in damaged pathways and so they still have over activity, but doesn’t necessarily mean that it causes the disorder.
25
Q

Further general evaluation points relating to neural explanations…

A
  • Neural explanations offer the possibility of drug treatments to normalise neurotransmitter levels.
  • If as Kaye suggests, there is a link between genetic and neural explanations, it may be possible to use an individuals genetics profile to indicate risk level. Then specially tailored prevention programmes could be developed for those most susceptible to developing anorexia.
  • A further implication is that these explanations reduce guilt caused by psychodynamic explanations , which suggests that parents are to blame for their children’s anorexia.
26
Q

IDA

A
  • Biological explanation: deterministic, ignores free will (PA- parents may feel that they can’t recover so don’t deal with the disorder.
  • Nature vs. Nurture: Doesn’t take into account nurture and that psychological damage from up bringing could’ve cause it.
  • Social- approach: pressure form society and the media
  • PA: Helps treat anorexia and find cures
  • Deterministic: Lead a passive response o the disease.
27
Q

Causality

A
  • A further point regarding causality is that Collier found that there is a variation in the serotonin receptor gene which is more common in anorectics.
  • As the gene lays down a ‘template’ for the body to make the receptor, this would suggest that serotonin dysregulation is more likely to be a cause than a result of the disorder.