Biological explanations for obesity

Biological explanations for obesity
Biological explanations for obesity AO1
Genetic explanations for obesity Obesity runs in the family Genetic explanations often look to family studies for evidence. There are clear family-related patterns to obesity, measured in terms of body mass index (BMI). Caution is obviously needed in interpreting findings because of the difficulty of separating shared genetic and environmental influences in any relatives who live together. Even so, concordance rates for first degree relatives are in the region of 20% to 50%, which indicates a moderate rather than substantial degree of heritability (Chaput et al. 2014) Twin studies have generally suggested a greater genetic component. Cassandra Nan et al. (2012) conducted a meta-analysis of 12 twin studies involving over 8,000 MZ and nearly 10,000 DZ twins. Concordance rates ranged from 61% to 80%, which demonstrates a very substantial genetic component to obesity that remained influential from late childhood through adolescence to adulthood. Polygenic determination Locke et al (2015) studied the genomes of more than 300,000 people, and identified 97 genes associated with verifications in BMI. This finding very clearly demonstrates that the action of genes on obesity is polygenic. That is, genetic inheritance involves multiple genes, their effects interacting with each other. This is made even more complex when you consider there are other ways of measuring obesity (such as waist-to-hip ratio, which focuses on amount of abdominal fat). Different genes may influence different aspects of obesity. So there is no single genetic cause of obesity; many genes are involved, all with relatively small effects. The researchers discovered that these 97 genes account for only 2.7% of BMI variation, a small fraction of the heritability of obesity. Some researchers suspect that the true figure necessary to explain the ,missing heritability’ may be as many as 400 genes.
Neural explanations for anorexia nervosa Serotonin Most research studies of both humans and non-human animals show that obesity is associated with abnormally low levels of serotonin. Normal levels of serotonin regulate feeding behaviour by inhibiting the activity of various sites in the hypothalamus, including the ventro-medial hypothalamus. It is serotonin that signals to the hypothalamus that we have eaten to satiety. Dysfunctions of the serotonin system can occur die to stress or co-morbid disorders such as depression. They must even be genetically inherited. In such cases, levels of serotonin are abnormally low, creating inaccurate satiety signals that are sent to the hypothalamus, disinhibiting eating behaviour. Low serotonin levels lead to cravings for carbohydrates, energy-dense foods including sugars, causing weight gain through too many calories. Dopamine Dopamine has a crucial role in the brains reward and motivation systems. Normal levels of the neurotransmitter stimulate brain areas such as the hypothalamus, hippocampus and amygdala, providing rewarding feelings of pleasure and well-being. Dopamine activity is associated with the pleasure we derive from eating and cues associated with eating (such as smell of food). However, obesity has been linked with a dysfunctional dopamine system in many research studies. Wang et al (2001) found that obese individuals had significantly fewer dopamine D2 receptors than normal weight controls, in a part of the brain called the striatum. Because levels of dopamine are so low in some people, the neurotransmitter cannot perform its usual pleasurable reward function in response to eating; i.e. a person does not feel good after eating. Overrating can therefore be seen as an attempt to activate reward centres in the brain that provide feelings of pleasure, by increasing dopamine levels. This explanation suggests that obesity is the outcome of a food addiction that operates neurochemically in ways similar to other addictions.
Biological explanations for obesity AO3
Limitation of twin studies P: The validity of twin studies on obesity can be questioned as this depends on equal environment assumption. E: For example, to compare concordance rates, we have to assume that MZ and DZ twins are treated with equal degrees of similarity. Only if this is true can we conclude that differences in AN concordance rates are due to genetic factors. E: Views differ, but many psychologists continue to question the equal environments assumption. The argument is that MZ twins are treated more similarly than DZs in many ways – primarily by their parents, but also by friends, teachers etc. and they may even spend more time together and have a closer bond. L: This greater environmental similarity means that heritability estimates are artificially inflated and genetic influences on anorexia may not be as great as twin studies suggest.	Contradictory evidence P: One weakness of the genetic explanation for obesity is that there is contradictory evidence. E: For example, Paracchini et al (2005) carried out a meta-analysis of 25 studies that investigated genes thought to be involved in regulating leptin and leptin receptors. Leptin is an obvious target for speculation about genetic effects, because its activity is known to be central to weight regulation. However, the researchers could find no evidence of a link between these genes and obesity. This suggests that whatever the role of Leptin may be in obesity, it does not appear to have a solely genetic basis. E: This is an important reminder that obesity is a complex phenomenon and that other non-genetic factors are important in its causation and development. L: As a result, these ideas cast doubt over the credibility of the genetic explanations for obesity.	Supporting evidence for serotonin P: One strength for the neural explanation for obesity is that it has supportive evidence in relation to serotonin. E: For example, Ohio et al (2013) highlight the importance in obesity of one serotonin receptor in particular, the 2C receptor. Studies of ‘knockout’ mice genetically engineered to have no functioning 2C receptors show that they develop late-onset obesity. This is further evidence of a link between obesity and a dysfunctional serotonin system. E: This is a strength because low levels of serotonin are associated with obesity, and the fact that these mice who had no functioning of 2C receptors proves this. L: As a result, the explanatory power of the neural explanation for obesity is increased.	Supporting evidence for dopamine P: Another strength for the neural explanation for obesity is that it has supportive evidence in relation to dopamine. E: For example, Ritchie and Noble (2003) conducted PET scan study and found that people who inherited one version of the DRD2 gene had 30%-40% fewer D2 receptors compared to those with other versions E: This finding supports neural explanation because people with low levels of dopamine levels experience less dopamine activated pleasurable reward from eating which makes them more likely to overeat. L: As a result, the credibility of the neural explanation for obesity is strengthened.