Near explanations of AN

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  • Created by: imanilara
  • Created on: 03-06-16 22:29

Neural Theory 1: issues w NT levels

Serotonin: 

-disturbances in serotonin levs seems to be characteristic of those w EB
-Bailer et al 2007- higher levs of sero in women recovring from restrictive eating by binge purge periods, than in healthy controls 
-highest levs found in those recovering who show the most anxiety
-suggests...persistent disruption of SE levs= anxiety= AN symptoms 

Dopamine:

-over-activity in DA receptors in basal ganglia in women recovering from AN compared to healthy controls in PET scan - Kaye et al- 10 women in recovery, 12 controls 
-role of DA in b. gang. = interpretation of harm+pleasure- increased DA activity alters the way ppl view reward, +find it difficult to associate good w what others find pleasurable, eg FOOD. Cause could be genetic, or environmental effects eg infection/traumatic experience. 

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AO2- research evidence

Support that high DA in AN:

Castro Forneiles et al (2006) : adolescent girls w AN had higher levs of homovanillic acids than controls - this is a waste product of dopamine metabolism 
- supports bc fits hypothesis that high DA in AN 
also.. improvement in weight levs associated w normailisation of homovanilic levs- 
-supports idea that DA is associated w AN! 

Wang et al 2001- found lower than norm levs of DA receptors in the brains of obese ppl. 
-suggests that DA levels inversely relate to weight, more evidence for DA as a chemical involved w EB. 

However..
- disruption of DA a cause/effect?? could be down to psych cause (cognitive) which leads to disruption of DA levels in the brain. 

Only way to test: To see if NT levels are raised before onset- this would take longitudinal study but difficult bc AN has low prevalence!

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Problems w theory

Selective serotonin reuptake inhibitors (SSRIs) class of drugs used to prevent relapse in patients, but they increase SE levels in the brain - Kaye et al 2001
-confused picture- high SE levs = AN, than SSRIs should lead to relapse? Inconsistent and invalid. In order to explain - suggestsed that malnutrition related changes in SE function may be responsible 

Issues of causality- bc they are used in recovery, does this mean they caused the disorder, or are they an effect of restrictive eating and AN? no causal conclusion 

IDA:
- most evidence on girls/women-beta bias so neural explanations for AN can only be generalised to them- we should enrich our understanding of how biochemistry effects mens susceptibility to AN- different? would perhaps help treatment - and is needed as 25% of AN sufferers are MEN. we need research in this area . 

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Neural theory 2 : issue w neuroanatomy in the hypo

One neural exp looks at the role of the hypo in the regulation of appetite. 

When an indi restricts theyir eating despite physical harm, could be hypothalamus dysfunction which is causing issues w appetite + EB.

Lateral hypo- feeding centre- damage could mean that person stops feeling hungry + reduces intake dramatically 

Ventromedial hypo- satiety centre- damage could lead person feeling full when they are not - restricted eating . 

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AO2 research evidence

Teitelbaum et al (1957)- lesions to LH in rats caused them to avoid eating + lose weight dramatically 

Langhans 2001- when noraadrenaline/serotonin injected into LH/VMH- stop eating+ starvation occurs 

Commentary-
reasonable to suggest that similar probs w hypothalamus cause AN food restriction, but sig generalisation from animale, in that humans would be able to understand that not eating would lead to death- they are not solely guided by appetite like rats. 

Human evidence: 
- Weller+Weller (1982)- humans suffering from hypothalamic tumours - suffered from AN
-supports idea that damage to hypo leads to AN sympotms, but doesnt prove that AN people dont feel hunger. 
Also why mainly teenage girls (western, middle class) if hypothalamic dysfunction??? 

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