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Explain the relationship between serotonin and hunger
When we eat, serotonin is released. This stimulates the ventromedial hypothalamus, indicating to the body that we are full. After we eat, the production of serotonin is stopped. The lateral hypothalamus is then stimulated, indicating that we are hungry, causing the cycle to repeat.
What does serotonin do?
Stabilises mood, feelings of well-being and happiness
Explain serotonin in relation to anorexia
Excess serotonin in the ventromedial hypothalamus causes a person to stop eating. This is because, even after the person has finished eating, their serotonin levels remain too high. This means that the lateral hypothalamus is nog stimulated so no more hunger queues are triggered
Over time, serotonin levels can appear low due to malnutrition from not eating (reduced tryptophan intake, this is an amino acid that is converted to serotonin - vital for its production). This could contribute to a persons sense of depression (a common comorbid symptoms of AN). As serotonin increases during episodes of binging, it makes the person feel better. This might explain the binging/purging type of AN
Excess serotonin may also cause increased anxiety in anorexics. Abnormally high levels of serotonin create a sense of perpetual anxiety, as high levels of serotonin are associated with jittery anxious feelings which may link to the patients fear of gaining weight. Therefore, by reducing the intake of calories to starvation level, the result would be a calming or sense of regaining control (due to the reduced levels of serotonin). This can explain why anorexic individuals do not want to eat
What did Barbarich (2002) tell us?
That high levels of serotonin is seen in both anorexia and OCD, demonstrating that they may be both be caused by serotonin dysfunction. This can therefore explain some of the perfectionist and compulsive behaviour seen in anorexics.
Explain dopamine in relation to anorexia
Over activity in dopamine receptors of the basal ganglia is linked to difficulty in associated good feelings with what we normally derive pleasure in, for example, food. Therefore, individuals with AN do not seek or respond to pleasurable activities such as eating
Dopamine over activity seems to increase anxiety in individuals with anorexia, rather than creating the usual response of increased pleasure
Explain epinephrine in relation to anorexia
Decreased levels of epinephrine have been associated with anorexia
Explain norepinephrine in relation to anorexia
Excess norepinephrine in the ventromedial hypothalamus causes a person to stop eating
Two studies supporting neurotransmitters as an explanation of anorexia?
Bailer et al (2007)
Kaye et al (2005)
How is Bailer et al (2007) a strength of the theory?
Supportive research from Bailer et al (2007) found significantly higher serotonin activity in the women recovering from the purging type of anorexia compared to healthy controls. They also found the highest levels of serotonin activity in women who showed the most anxiety, suggesting that persistent disruption of serotonin levels may lead to increased anxiety, which may trigger anorexia. Therefore, the biological explanation can explain why individuals restrict their energy intake and stop eating to try and reduce their serotonin levels and in turn their anxiety.
How is Kaye et al (2005) a strength of the theory?
Supportive research from Kaye et al (2005) compared dopamine activity of 10 women recovering from AN to the activity of 12 healthy women. In the anorexics they found over activity in dopamine receptors in the basal ganglia, and reward centres where dopamine affects the interpretation of harm and pleasure, This suggests that thus over activity may cause individuals with AN to have difficulties associating good feelings with the things that most people find pleasurable, such as food, supporting the biological explanation of anorexia.
Cause and effect - what are the issues of this on the biological explanation? Reference a study
The link between serotonin and anxiety could mean that it is anxiety that triggers anorexia and perhaps AN is just a symptom of anxiety. Whether neurotransmitters are the cause of AN or anxiety the cause of AN cannot be answered by the biological explanation.
Kaye (2011) also reported that in women with anorexia nervosa, increased levels of dopamine activity increased anxiety, whereas in ‘normal’ controls the increased dopamine induced feelings of pleasure. This may suggest why women with AN often experience high levels of anxiety associated with food - something most people would find pleasurable. This research therefore supports the idea that high dopamine levels may explain why individuals with AN are anxious around mealtimes, but it still doesn’t confirm whether ancient is the cause of anorexia, it could be a comorbid disorder and therefore we cannot trust that treating anxiety will definitely treat AN
How can the biological explanation be deemed ‘reductionist’ in terms of drug treatment?
SSRI’s (Selective Serotonin Re-uptake Inhibitors) were developed to treat anxiety and are used to treat the symptoms of anorexia. If anorexics gave low levels of serotonin, causing their illness, the drugs should work to alleviate symptoms. However, they are not an effective treatment for AN, suggesting that anorexia is unlikely to be solely related to neurotransmitters.
Lack of food may also stop the SSRI’s from working, they only become effective once the individual begins eating, so as a treatment, it may not be beneficial until the patient is able to eat more. This suggests that the biological explanation cannot fully explain anorexia, otherwise the drug therapy success rate would be 100% and the symptoms would be immediately alleviated. This theory is reductionist, but in this case it is useful as it allows for development of drug therapy.
If the theory is reductionist, how does this impact treatments for anorexia?
If we are understanding this disorder as being caused by neurobiology alone, it is reductionist. This is good as it allows for the development of drug treatments, but asking means that we lose the experience of the individual and end up treating all patients in the same manner. Having this disorder will impact each individual’s life in a unique way and the biological approach doesn’t account for these effects, meaning that drug treatments can be developed but these won’t be entirely successful on their own.
The theory is reductionist - what factors are not accounted for?
Perhaps other social factors can cause the onset of AN, such as social learning theory which would relate to if an individual has seen their role models on social media sites being complimented for loosing weight, they may be vicariously reinforced to lose weight as well
The biological approach cannot explain the psychological aspects of the disorder (eg- body image). In this way, cognitive explanations might be better at explaining this side of AN and the maladaptive thought process, as patients with AN tend to lack logical thinking and have an unrealistic ideal of body weight, leading to intense fear of being fat which cannot be explained by the biological approach
What is the diathesis-stress model?
It suggests that diathesis (genetic predisposition) and stress (eg- weight gain, bullying) both contribute to the development of eating disorders. This model can explain why an individual may be diagnosed with AN. The model suggests that because of an individual’s neurotransmitters and the biological explanation of AN they had an innate vulnerability to developing AN, however it was not a guarantee that they would develop the disorder, the onset was triggered by stress (eg- teenage years). Therefore, the biological explanation cannot fully explain AN as it is a complex mixture of nature and nurture. In this way, the biological explanation oversimplifies the disorder.