13. Bio explanations for Anorexia

What has been suggested about AN and genetics in the past, what did Scott-Van Zeeland do following this?

• It has been long suggested that there may be a genetic component responsible for the development of anorexia with initial research by Grice et al (2002) being the first to ‘isolate’ specific genes.

• By studying 192 families when one person was diagnosed with anorexia, they looked at others in that family who had also developed AN or a similar disorder.

• Initially they didn’t find anything but when they focused their research more on 37 of these families (those who had diagnoses of restrictive type AN) they found that there appeared to be strong evidence for susceptibility for genes on chromosome 1 as similar markers were found on people in these families.

• Scott-Van Zeeland et al (2013) then took this a step further to research specific gene that could be linked to the development of AN.

What was the aim of Scott-Van Zeeland’s study?

• The aim was to investigate genetic variants associated with the development of anorexia nervosa.

What was the total number of DNA samples used for comparison in this study?

• DNA samples were taken from a group of 261 patients diagnosed with AN.

• And 73 controls without the disorder, all of whom were female.

• Another group of 500 DNA samples from anorexic patients and 500 DNA samples from non-sufferers were taken from the Price foundation repository for further comparison.

• 1,334 = total sample.

How many and which genes were selected for investigation?

• The researchers investigated 152 genes previously suggested to be associated with feeding behaviour, dopamine function, serotonin signalling and other biological mechanisms that could have a relationship with developing AN.

What other measures were used?

• Information was also gathered from the participants originally recruited for this research using data from various psychometric tests, such as Beck’s Depression Inventory, as well as information about lifetime Body Mass Index (BMI).

What were the initial result found in relation to EPHX2?

• The initial sequencing phase of the study suggested that variants in 2 genes (ITPR3 and EPHX2) would be worth further investigation from more in-depth methods.

• The next phase of testing indicated that the most significant variants between the patients with AN and the controls were in the EPHX2 gene, which led to further analysis.

• On further investigation, those Pp with AN, who also had AN associated with the EPHX2 gene variants, showed the highest scores on a measure of depression (Becks Depression Inventory), and lowest BMI scores.

What do the researchers suggest is the relationship between EPHX2 and cholesterol?

• The EPHX2 gene is associated with the body metabolising cholesterol, and other research has previously found that patients with AN often show high levels of cholesterol despite being malnourished.

• This would support the concept of variants in this genes being related to having anorexia.

• The EPHX2 gene is associated in areas of neural tissue related to feeding behaviours and anxiety, both of which are behaviours associated with AN.

• For example, it has been found that there are high levels of expression of the EPHX2 gene in the paraventricular nucleus of the thalamus, which has been associated specifically with food and water intake, and the stress response.

• It has also been found that, in rats, his area of the brain is related to weight gain.

What do the researchers conclude?

• The evidence gathered from this study suggests that variants in the EPHX2 gene may increase the risk of developing anorexia nervosa.

• This gives rise to future research because currently very little is known about the biological causes of AN.

What is a strength of the study in terms of Measures used?

• The advantage of the methods used in this study is that they are very reliable as the researchers were measuring gene variants using highly standardised methods and equipment.

• Psychometric tests (Becks Depression Inventory) and BMI.

• High reliability and replicability.

• Triangulation - validity from more than one source of data collection.

What is a strength of the study in terms of the Sample?

• The total sample was 1,334 - large sample of DNA from AN sufferers and controls to compare genetic information to.

• If we can find consistencies across the large sample we can be confident that we can generalise what we have found to the wider population of AN sufferers.

• The sample sizes used are quite large throughout all stages of the study, so there is a reasonable amount of validity in the conclusions drawn.

What is a weakness of the research in terms of the Sample/Gynocentric research?

• However, all of the patient samples came from females, and although most anorexic patients are females, an increasing number of males are diagnosed.

• Which means there is a lack of population validity in relation to the entire target population.

• It is gynocentric research as it is focused on females but aiming to generalise the results of the gene variant to both male and female AN sufferers.

• Males might have a different expression of that gene.

What is a weakness of the study in terms of Causality?

• A possible problem with research like this is that we are still in a position where very little is actually known about the actions of many different genes and therefore, although a relationship has been seemingly uncovered, the explanation of how this gene is implicated in anorexia is still not understood.

• We cannot establish cause and effect, that the gene variant causes anorexia, it might be that the presence of AN causes the gene variant.

• There is no before and after comparison - can’t confidently say that the EPHX2 gene caused AN.

• But we do have a relationship that we can investigate further.

What is a weakness of the study in terms of Reductionism?

• The research laid out here provides strong evidence of genetic material linked with the development of anorexia.

• This would provide a strongly reductionist explanation for a disorder that has a very complex set of symptoms and features.

• Although some may argue that evidence here is very credible and clearly suggests that genes can be implicated in the development of the illness.

• Others would suggest that simply suggesting genes are to blame, especially in the face of compelling evidence from sociocultural explanations, is taking a very limited view of the disorder.

• However, it doesn’t explain the cognitive processes in the AN individual - beliefs about their weight, body dysmorphia.

How are Treatment implications both a strength and weakness of the study?

• The information gathered in this study has added to the developing body of research helping to understand the origins of AN.

• This could help future treatment development.

• A strength is that if we have identified a particular gene variant involved in AN, we can screen for that variant early on in teenagers and provide early intervention around positive healthy eating.

• Add health education programmes - look at healthy eating, healthy thoughts. (preventative measures).

• It also allows us to develop more effective treatment options.

• However, we need to look at the ethical implications of genetic screening - this raises issues of of social control.

What is a weakness of the study in terms of Nature vs nurture?

• This study/explanation sits heavily on the nature side of the debate as it focuses on the role of the gene variant of EPHX2 on AN.

• But it doesn’t take into account nurture factors such as the sociocultural explanation.

What is the role of Serotonin in AN?

• Research evidence from Bailer et al (2005) found that patients who had recovered from a diagnosis of the binge-purge form of AN showed increased levels of serotonin in the brain.

• This was strongly related to measures of anxiety in the women, showing that both increased serotonin and anxiety symptoms persist even a year after recovery.

• There has been a suggestion that the serotonin rise may increase levels of anxiety, and this increase in anxiety may trigger the binge-purge form of anorexia.

What is the role of Dopamine in AN?

• Research has also associated increased activity in dopamine receptors in patients recovering from AN.

• Kaye et al (2005) documented increased dopamine receptor activity in areas of the basal ganglia, an area of the brain known to be associated with feeding behaviour and learning from experience.

• It is thought that overactivity in this area may interfere with the patients’ ability to seek or respond to pleasurable activities such as eating.

• Interferes with the ability to learn from experience.

• It may also interrupt the ability for patients to react to the negative feedback associated with their health such as the image of their emaciated body or symptoms associated with malnutrition.

• Kaye later (2011) 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 that most people would find pleasurable.

• Therefore they will restrict their diet.

How are the biological explanations useful?

• Much of the recent research into neurotransmitter levels is conducted in highly controlled conditions using high-tech equipment such as brain scans - PET and fMRI.

• Standardised procedures are also used with the brain scans.

• This means that the evidence is very credible, reliable and valid due to its objective nature.

• An example of a control measure taken is that research by Bailer (2005); for example, the patients were studied a year into recovery to be sure that malnutrition was not a confounding variable and poor nutrition has been associated with changes in serotonin activity.

Why are biological explanations problematic?

• A major criticism of research in this area is that the altered levels of neurotransmitters could easily be a result of poor nutrition rather than a cause for it - issues with cause and effect

• For example, a paper by Haleem (2012) suggested that serotonin production was associated with a restrictive diet.

• Tryptophan, an amnio acid that is precursor to serotonin, is only available through diet, so a restricted diet will reduce levels of tryptophan, and consequently is likely to reduce levels of serotonin found in the brain.

• When stored levels of serotonin are reduced, the brain may compensate with up-regulation, which consequently increases the levels of activity.

• This is therefore suggesting that the high level of serotonin activity is actually the result and not the cause of AN.

 

• Another problem is that drugs that are used to treat other disorders associated with high levels of serotonin and dopamine, such as SSRIs and neuroleptics are found to be much less effective in treating AN.

• Which suggests that the cause of the illness is unlikely to be purely related to neurotransmitter levels.

 

What are the evaluation points of the biological explanation in terms of The use of psychological knowledge in society?

• Research into biological factors is developing all the time as new techniques become available.

• The genetic explanation is still very new and research in this area is still quite limited.

• But as new methods develop, the research is becoming more conclusive and will continue to grow.

• An interesting application of this area of research is the way biological research into AN has changed society’s views of the disorder, by considering it as an illness, much as other psychiatric illnesses are beginning to be seen.

• We encourage people to treat sufferers with more compassion.

• It also helps to change the views on treatment of eating disorders by challenging the view that people with AN ‘just need to eat.’

• In the US for example, health insurance companies are now being forced to reconsider their categorisation of AN to allow patients to claim money for treatment.