biological explantions for anorexia nervosa Flashcards
genetic expantion for anorexia
anorexia runs in families
evidence for the genetic explanation for anorexia nervous a coems form twin studies
MZ and DZ twins
concordance rate indicates the proportion of twin pairs which both have AN
relative pairs in which only one indivual has it
MZ twins share 100% of their genes
DZ share 50%
higher concordance rate for MZ is strong evidence of a genetic component to AN
Holland et al
45 pairs of female twins and one set of triplets
found concordance rate of 56% for MZ
5% for DZ
candidate genes
zealand et al
carried out candidate gene association study
compared 1205 people with AN
1948 control particant
sequencing 152 candidate genes suspected to be linked with features of AN
discovered only one gene was signifanctly associated with AN
Ephx2
codes for an enzyme involved in cholesterol metabolism
many people in the acute phase of AN when symptoms are severe do have abnormally high levels of cholesterol
genome-wide association studies
look at the entire collection of human genes rather than just indivual ones
GWAS of anorexia are rare
Boraska et al
conducted one with 5551 people with AN
21080 matched contorls
7 separate genetic variations were identified
none of them were significantly related to AN
researchers argued that this was not because genetic influences on AN are non existent
because study was no sentive enough to detect them
limitation
Limitation of twin studies
lack validity
in every pair assumption is made that twins share the same environment as each other
but do DZ twins share the same environment to the same extent as MZ
assumption is wrong because DZ can be treated differently as they look different
MZ are treated very similarly because they look identical and act in the same way
means genetic influences on AN may not be as great as twin studies suggest
Strength
polygenic basis
gene studies have highlighted the true genetic nature of AN are
such strides have been unsuccessful in identifying gnese that contribute to AN are such
main contribution of these studies is to show that rhe search for a single gene is futile
widely accepted that no one gene can be
responsible for the wide variety of physical anf psychological symptoms that characterise AN
therefore gene studies have shown that AN is polygenic
many genes make importnat contributions to the disorder
neural epxlantion for anorexia
neurotransmitters
serotonin and dopamine
researchers measure levels of metabolites (chemical byproducts)
main metabolite of serotonin is 5-HIAA
main metabolite of dopamine is HVA
serotonin
Bailer and Kaye
low levels of 5-HIAA in people with AN is evident
these levels return to normal after short term weight recovery and increase beyond normal levels after long-term revpvery
Attia et al
studied indivuals with AN who had not returned to their pre-illness weight
responded less well to drugs that stimulate serotonin activity than people with AN who had restored a healthy weight
pattern of results clearly indicated under activity of the serotonin system in AN
dopamine
Kaye et al
lower level of HVA in recovered AN patients compared with contorls
suggest lowered levels of dompaine associated with AN
Bailer at al
injecting particant with amphetamine - increases dompaone
control particant with no history of eating disorders expoenrec euphoria / pleasure associated with dopamine increase
participants with AN experienced anxiety instead
eating increases dopamine release
therefore people with AN may restrict their food intake to reduce their anxiety levels
strength
research support
support the tole of dopamine dysfunction in AN
many studies have rested CSF for HVA
Kaye et al
compared women diagnosed with AN and severely underwiueght
with women who had no history of eating disorders (control)
HVA level of the women with AN were 30% lower than for the non AN women
strongly suggest that a disturbance of dopamine metalblism may contribute to symptoms of AN Bailer at
limitastion
oversimplified
neural explanations can be simplistic
Nunn et al
argued that serotonin on its own does not distinguish between people who have AN and those who do not
AN is better explained in considering the interaction between serotonin and another neurotransmitter - noradrenaline
researchers claim that other neurotransmitters such as GABA are also involved
important reminder that neurotransmitter systems fo not operate in isolation but in compared ineractions
