Biological explanations for obesity

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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
      • 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)
    • 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
    • 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
        • 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
        • 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
      • 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


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