Biological explanations for anorexia nervosa

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Anorexia nervosa (AN)

Obsessive desire to lose weight by refusing to eat. Several theories - biological, psychological, may apply in diff circumstances. Can occur at diff times, diff degrees. 

3 main symptoms:
 - severe weight loss
 - fear of weight increase
 - refusal to eat sufficiently to maintain body weight

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Genetic explanation

Sees AN as transmitted through hereditary means - genetic material. Evidence - increased risk for 1st degree relatives w/ disorder. Genetics seen as only partly contributing - whaat genes may do is give level of inherited vulnerability - when they develop AN dependent on presence of other factors, eg environmental stress.

Study methods eg twin studies.

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Neural explanation

Idea AN linked to defective brain structures. Early research - focus on damage to hypothalamus, more recent research - identifying specific brain mechanisms. Area of interest - insula dysfunction hypothesis (IDH) - bio root of AN. Sees insula brain area (part of cerebral cortex), developing diff in anorexics. Various symptoms associated w/ dysfunction in brain areas, common factor - insula, responsible for neural connections. 

Involve idea faulty biochemistry related to development of AN. Serotonin linked w/ AN. Noradrenaline area of interest - role in maintaining restriction of eating by influencing anxiety levels.

Leptin - interest. Anorexics can have low L levels, due to low fat levels. Thought L influences regulation of neuroendocrine system during starvation. Low levels known to affect hypothalamic-pituitary-gonadal axis, -> periods stopping - seen in anorexics.

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Main study

Oberndorfer et al (2013) - participants 14 female recovered anorexics, 14 non-anorexic F's. Fasted overnight, standardised breakfast of 604 calories before fMRI as control for satiety state. 

AN participants reduced reponses to sweet tastes in right anterior of brain.

Confirm earlier studies - suggests relationship between AN + neural processes in insula brain region. Altered functioning of neural circuitry contributes to restricted eating - occurs b/c brain fails to accurately recognise hunger signals. Anorexics appear to have altered balance/sensitivity in brain mechanisms that signal calorific content of food.

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Main study - Evaluation

Findings may offer practical app in development of effective AN treatments eg enhancing insula activity in anorexics by using biofeedback to adjust brain's response to food stimuli. Medications could be manufactured that enhance reward response of food/decrease inhibition to food consumption in brain's reward circuitry.

Research doesn't determine whether faulty brain mechanisms cause anorexic behaviour/whether anorexic behaviour -> changes in brain mechanisms. Could scan brains of at-risk children to see whether brains exhibit faulty mechanisms.

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Genetic explanation - Strengths

Bulik et al (2006) - sample of 31,406 Swedish twin pairs, found incidence of AN 1.2% for females, 0.29% for males w/ heritability of disorder calculated as 56% suggesting significant genetic influence in development of disorder.

Scott-Van Zeeland et al (2014) compared 152 genes in 1205 women w/ AN, 1948 w/o - found variants of EPHX2 gene, involved w/ cholesterol function in body, more common in those w/ AN. Findings suggest contributory role for gene. 

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Genetic explanation - Weaknesses

Fact that multiple genes involved + environmental factors, makes it diff to identify + quantify role of individual genes - many involved, diff levels of influence. Genes may exert diff levels of influence on diff people.

If genes solely responsible, concordance rates b/ween MZ twins would be 100%, but not. Suggests interaction.

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Neural explanation - Strengths

Nunn et al (2012) - abnormal noradrenaline functioning seen as being genetically determined -> high anxiety + insula brain area dysfunction results in neg body image distortion. Gives rise to intense dieting, helps reduce anxiety in ST. Anxiety increases again, shows how noradrenaline -> cycle of AN being maintained. Link b/ween genetic + neural.

Mayo-Smith et al (1989) found leptin + body fat mass levels higher in healthy low-weight F's than in AN F's, supports idea L levels related to low amounts body fat in ANs rather than actual body weight.

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Neural explanation - Weaknesses

Research - female participant, findings not generalisable to males - differ physiologically from females. Eg, males diff distribution + amounts of body fat, relationship b/ween male ANs + neurotransmitter levels may be diff than female sufferers.

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