Research project

Biological explanations

Generally explained via two factors:
Genetic inheritance
Biochemistry
Eating disorders seen as originating from biological dysfunction therefore treated medically

1

Genetic factors
APA reports increased risk among first-degree relatives – prevalence rates higher than in general population
Family studies – first-degree relatives 4-5 times more likely to suffer from eating disorder (Strober & Humphrey, 1987)
Twin studies – higher concordance for MZ vs DZ pairs; MZ = 55% DZ = 7% (Holland, 1988)

2

Twin studies
Kendler et al (1991) – study on bulimia found 23% for MZ’s vs 9% for DZ’s
Results suggest higher concordance rates, but fail to distinguish genetics from other factors (eg, shared environment, common personality traits)
Cannot explain why 45% of Holland’s MZ’s were discordant

3

Biochemistry
Evidence for role of hypothalamus from Keesey & Corbett (1983) – lateral hypothalamus (LH) & ventromedial hypothalamus (VMH) provide “weight thermostat”; act as stop/start mechanism for hunger & maintain weight homeostasis (Garfinkel & Garner, 1982)
When activated LH produces hunger, VHM depresses hunger

4

LH & VMH
Evidence from animal studies show that when LH damaged rats starve themselves; when VMH damaged they overeat
In humans LH should be activated when weight drops below set point & VMH activated when it rises above set point
Therefore hypothalamic dysfunction implicated in eating disorders

5

Endocrine system & amenorrhoea
Amenorrhoea can occur prior to weight loss – suggests primary disorder of low endocrine levels – associated with hypothalamus dysfunction
Endocrine levels of 19yr old anorexics reported to be similar to those of normal 9 yr old

6

Serotonin & cortisol
Starvation decreases tryptophan > low levels of serotonin produced > depression occurs > hunger suppressed
Stress hormones (eg, cortisol & adrenaline) produced by hippocampus – high levels suppress appetite (fight or flight response)
Many anorexic & bulimic sufferers have acute, chronic levels of arousal/anxiety

7

Evaluation of biological approach
Twin & family studies inconclusive – concordance rates not 100% so other factors must be involved
Cannot separate environmental influences
Genetics may predispose rather than cause the condition
Genes cannot explain recent rapid increase in eating disorders

8

Evaluation of biochemistry
Cause, effect or correlate? Difficult to interpret biochemical imbalances
Low levels of serotonin may be due to lack of food – so a symptom of disorder
Research has not found conclusive evidence of physical cause
Reductionist – motivation & cognition can override biology; deterministic – free will

9

Behavioural explanations
Classical conditioning – anorexia originates when eating is associated with anxiety (fear of weight gain) (Leitenberg et al, 1968)
Operant conditioning – weight phobia reinforced as food avoidance is rewarding (negative reinforcement) – weight gain avoided (Rosen & Leitenberg, 1985)

10

Conditioning
Positive reinforcement – attention/compliments on weight loss or concern about eating behaviour
Anxiety caused by binging is reduced via compensatory behaviours – reduced anxiety reinforces purging – perpetuates binge-purge cycle

11

SLT & Modelling
More than 15% of Miss America contestants below expected body weight (Barlow & Durand, 1985)
Nasser (1986) compared Egyptian women studying in Cairo & London – no ED’s seen in those in Cairo, but 12% of those in London developed an ED
Cooper (1994) Western norms > women admired for being slim

12

SLT & culture
Lee et al (1992) – bulimia rare in Chinese populations of Singapore, Malaysia & Hong Kong
Success linked more to family than appearance
Suggests eating disorders may be culture-bound syndrome

13

Evaluation of behavioural approach
Does not account for individual differences in vulnerability
May explain maintenance rather than cause – OC to perpetuate eating disorders makes sense, but causation by association of anxiety harder to explain
Does not explain why onset tends to be during adolescence (AN)

14

Behaviourist
Fails to explain why anorexics continue to diet when compliments and/or attention no longer received
SLT explains role of vicarious learning – may account for cultural bias – but cannot explain cases in non-western cultures
Cannot explain why only some women in Western cultures develop ED’s
May explain gender bias

15

Psychodynamic approach
Link to fear of sexual development (such as becoming pregnant)
Emaciated body is an attempt to remain pre-pubescent
Wonderlich et al (1996) linked BN to childhood abuse – reflection of dislike of body
McLelland (1991) 30% of clients had history of sexual abuse – ED seen as way of repressed trauma rejecting own body

16

Abuse, gender & ED’s
Females taught to be subservient/self-critical so repressed trauma turns inward
Males encouraged to be dominant – hostility more outwardly focused
Carlat (1997) –study of 135 anorexic/bulimic males; 42% of bulimic groups either homosexual or bisexual; 58% or anorexics identified as asexual
Concluded sexual orientation major factor in male ED’s

17

Family systems theory
Minuchin et al (1978) – CORE = conflict, overprotectiveness, rigidity, enmeshment
Enmeshed family is smothering – difficult to develop own identity & achieve independence
ED’s seen as way of achieving control, identity & independence; may also be act of rebellion against dysfunctional family
AN & BN’s use body to take control as family situation is beyond control

18

Autonomy & identity confusion
Bruch (1971) – food used as currency of affection – given as comfort but controlled by mother
Mother serves own needs – AN is a rejection of food as a reward & a struggle for autonomy & establishment of own identity & internal needs
Halmi (1995) bulimics unable to distinguish between hunger & other bodily needs and/or emotions – food/eating as inappropriate response

19

Evaluation of psychodynamic
Conflict – cause or consequence? Family conflict may arise as result of family member with ED
Many families have conflict but this does not result in ED or other disorders
Family conflict cannot explain gender bias
Does not account for recent increase

20

Evaluation
Psychodynamic theories seen as dated
Evidence based on case studies & clinical interviews – lack objectivity
Many people abused in childhood do not develop eating disorders
Theories difficult to prove
When family conflict is resolved why does disorder continue?

21

Cognitive explanation
Distortion of body image – anorexics typically over-estimate body size
Distorted view of own & ideal body image
Too much emphasis on importance of weight & body image
Similar discrepancy found in bulimics between desired body size & actual estimation of own size (Cooper & Taylor, 1988)

22

Cognitive dysfunction
Obsessive thinking & perfectionism common in sufferers of ED’s
Fairburn et al (1999) found perfectionism & negative self-evaluation high-risk factors for both AN & BN
Individuals tend to set impossibly high standards
Failure to recognise dangers of illness

23

Evaluation of cognitive model
Does account for the way sufferers think about their bodies
Suggested therapies designed to develop more realistic ways of thinking about themselves
But cause/consequence unclear – cannot explain where thinking stems from nor where/when breakdown in cognitive processes occured

24

Cognitive bias
If cognitive biases exist before onset of ED they may play a part in its development
If biases occur after the onset of ED they cannot be a causal factor
Minnesota starvation study – starvation caused obsession with food – so suggests consequence rather than cause

25

Bibliography
Cardwell, M., Clark, L, & Meldrum, C. (2003) “ for AS-Level” (3rd Ed). HarperCollins:London
Cardwell, M., Clark, L, & Meldrum, C. (2008) “ for AS For AQA A” (4th Ed). HarperCollins:London
Eysenck, M. (2005) “ for AS Level” (3rd Ed). Press: East Sussex