anorexia- neural explanation Flashcards
what 3 things may there be an imbalance of
leptin
serotonin
dopamine
what are other biological issues that could enhance vulnerability
birth complications and premature birth
poor maternal nutrition (during pregnancy)
why is this a double disadvantage (assuming mother has AN)
Double disadvantage: You both inherit an AN mother’s genes, then she restricts food during pregnancy – so your genetics are triggered
not a flashcard:
all of these things (in 1,2 and 3) lead to AN
whats the limbic system (for your understanding and to use)
involved in generating and processing emotional responses
who studied this
lipsman (2015)
what did he conclude
AN correlates to dysfunction in parts of limbic system
Lead to deficits in emotional processing
Creates the pathological thoughts/behaviors associated with AN
These neural abnormalities can help account for the extreme anxiety around food, distorted reward processing, and persistent fear of gaining weight that characterize the disorder.
who studied the effects of dopamine and serotonin
kaye (2005)
what did kaye say about dopamine
Dopamine: overactivity in dopamine receptors in basal ganglia
If increased, it alters the way people interpret rewards
so an increase in dopamine in AN patients causes them to find it difficult to associate good feelings with food, which is something most find pleasurable.
these high levels also increase anxiety
what does kaye say about serotonin (similar)
disruption of serotonin levels may lead to increased anxiety, which can then trigger the eatingdisorder- cause an overactive stress response, increasing feelings of nervousness or fear. This heightened anxiety may manifest in compulsive behaviors, including obsessive thinking about body image or food.
whats a strength of this approach
empirical evidence increasing external validity
medical treatments
who researched the first point
Frank et al. (2005)
what did they find
used fMRI scans and found that people with anorexia showed different dopamine responses in reward-related areas of the brain (e.g. the striatum), suggesting a blunted sense of reward from food.
what can we conclude from this
real world pratical applicability and can help early diagnosis, tracking treatment etc
highly measurable evidence increases scientific validity
who researched medical treatments
Bailer et al. (2005)
what did he find
abnormal serotonin activity in recovered AN patients, which is associated with high anxiety levels. This has led to the use of SSRIs (Selective Serotonin Reuptake Inhibitors) in some cases to manage anxiety and obsessive thoughts.
what can we conclude
large range of routes to treatments- of patients wants a more straight forward medical treatment helping to guide treatment they can so there are more options than just therapy
whats a weakness
most neural findings are correlational, so we can’t tell if brain differences are a cause or a result of the disorder.
whats an example from a01 of research that supports this limitation
Kaye et al. and others found abnormal neurotransmitter activity, but these studies are often done on individuals who are already malnourished or recovering but malnutrition itself can change brain chemistry
what can be concluded from this
weakens the explanation because it’s unclear whether neural abnormalities lead to anorexia, or are caused by it, limiting its explanatory power
