Here are some example answers to the two longer written Paper 3 questions on Eating Behaviour in the 2019 AQA exams.
One reason is that a volunteer sample has been used and it is possible that the members of the self-help group with an eating disorder who volunteered had a more positive body-image then most people with an eating disorder. This means it would not be appropriate to generalise the findings to all people with eating disorders. This study could be modified by using a random sample of people diagnosed with an eating disorder, as this should produce a less biased and more representative sample, meaning that the findings could be generalised more widely.
Genetic explanations of obesity suggest that it is inherited and runs in families. This is supported by concordance rates from twin studies. For example, Neale and Cordon found a correlation of 0.7 for MZ twins and 0.3 for DZ twins, suggesting that there is a substantial genetic component to obesity. Another finding is that correlations tend to be reduce as twins become older. This could be the effect of non-shared environments as when twins get older they are more likely to live apart and eat different diets and exercise differently. However, separated twin studies have still shown a strong genetic component. For example, Price and Gottesman reported a reared-apart correlation of 0.61 for MZ twins.
One gene that has been linked to obesity is the ‘thrifty gene’. It was suggested by Neel that in our evolutionary past, genes that promoted efficient fat deposition would have been advantageous because they allowed people to survive in times of famine. However, in modern society they are disadvantageous because food is readily available, so they lead to widespread obesity and diabetes. However, there is much criticism of this explanation, one problem being that if it were correct, by now everyone should have inherited this advantageous mutation and therefore we should all be obese, which is not the case. Clearly if there is a genetic component to obedience it is more complex than being a single gene. This is supported by Lock’s study of the genomes of more than 300,000 people, which identified 97 associated with variations in BMI. This means that obesity is a polygenic condition and different genes may influence different aspects of obesity.
Neural explanations for obedience focus on neurotransmitters such as serotonin and dopamine. Obesity is associated with abnormally low levels of serotonin, which can occur due to stress or depression. Normal levels of serotonin regulate feeding behaviour, by inhibiting various sites in the hypothalamus, including the VMH when we are full. However, if serotonin levels become too low, these signals will not be sent and disinhibited eating behaviour will occur. In particular, carbohydrates and energy-dense foods will be craved, leading to obesity. This explanation is supported by research which found that mice genetically engineered to have no functioning 2C (serotonin) receptor developed late-onset obesity. This shows there is a link between obesity and a dysfunctional serotonin system in mice and the same may be true for humans.
Low levels of dopamine have also been associated with obesity. This could be because if levels are low then the person will not feel pleasurable reward in response to eating as dopamine will not activate the reward centres in the brain. Therefore, the person may overeat in an attempt to gain pleasure, leading to addiction to food and obesity. This is supported by Wang et al. who found that obese people had significantly fewer D2 (dopamine) receptors than normal-weight controls in the striatum area of the brain. This has also been linked to genes as Ritchie and Noble found that people who inherited one version of the DRD2 gene had 30 to 40% fewer D2 receptors compared to those with other versions.
However, a problem with the genetic and neural explanations is that they are largely unable to explain the dramatic increase in obesity rates over recent years in Western countries. This is more likely to due to increased availability of high calorie fast foods and people having a more sedentary lifestyle, showing how obesity is a complex phenomenon and that other non-biological factors are also important.
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