Biological explanations for obesity
- Created by: Lishamxrie
- Created on: 20-01-19 15:04
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- Biological explanations for obesity
- Genetic
- Obesity runs in families
- Family related patterns in terms of BMI
- Family and twin studies
- Family studies: BMI concordance rate for obesity in first degree relatives are 20-50%
- Chaput
- Twin studies: MZ concordance rates for obesity are 61-80%
- Nan
- Family studies: BMI concordance rate for obesity in first degree relatives are 20-50%
- Genetic inheritance of obesity is polygenic
- No single gene causes obesity (many genes are involved)
- Locke: found 97 genes associated with variations in BMI but accounted for only 2.7% of BMI variation
- Up to 400 genes involved in heritability of obesity
- Different ways of measuring obesity: waist-hip ratio (different genes may influence different aspects of obesity)
- Obesity runs in families
- Neural
- Neurotransmitters
- Serotonin: regulates eating behaviour by influencing activity of the hypothalamus
- Dopamine: crucial role in brains reward and motivation system involving hypothalamus, hippocampus and amygdala
- Low serotonin levels
- Signals hypothalamus that we have reached satiety
- Dysfunctions of serotonin from stress or co-morbid disorder (depression) may be genetically inherited
- Results in low levels of serotonin, therefore inaccurate signals
- Eating behaviour is disinhibited and leads to carbohydrate cravings, causing weight gain through excess calories
- Low dopamine levels
- Dopamine levels are associated with pleasure from eating and associated cues (e.g. smell of food)
- Wang: found obese people have fewer dopamine D2 receptors in the striatum than normal weight controls
- Low dopamine means this neurotransmitter cannot perform usual pleasurable reward function in response to eating
- Overeating is an attempt to increase dopamine and activity reward centres in the brain, providing pleasure
- Obesity is the outcome of food addiction operating neurochemically like other addictions
- Neurotransmitters
- Evaluation
- Strengths
- Evidence for the role of serotonin
- Ohia: highlighted the importance in obesity of one serotonin receptor in particular
- 2C receptor
- Studies of 'knockout' mice show how those without 2C receptor develop late on-set obesity
- Demonstrates the link between serotonin dysfunction and obesity
- Ohia: highlighted the importance in obesity of one serotonin receptor in particular
- Evidence for the role of dopamine
- there may be a genetic basis to dysfunction of the dopamine reward system
- DRD2 gene codes for the D2 receptor implicated in obesity
- Ritchie and Noble found that people with who inherited one version of the DRD2 gene had 30-40% fewer D2 receptors
- there may be a genetic basis to dysfunction of the dopamine reward system
- Gives rise to treatments
- Biological research is revelling psychological mechanisms as plausible causes of obesity
- Future drug research can provide medicines to correct serotonin and dopamine levels tailored to the individual
- Evidence for the role of serotonin
- Weaknesses
- Twin studies are not conclusive
- Twins may have different environmental stressors and may grow up in different environments
- This suggests that twin studies may over estimate the extent of genetic influences indicating that obesity is not an outcome of genetic factors
- Contradicting the role of genes
- Paracchini conducted a meta analysis of 25 studies investigating genes possible involved in regulating leptin and leptin receptors
- Study found no link between these genes and obesity
- Whatever the role of leptin is in obesity, it does not have a genetic basis
- Untitled
- Paracchini conducted a meta analysis of 25 studies investigating genes possible involved in regulating leptin and leptin receptors
- Twin studies are not conclusive
- Strengths
- Genetic
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