Neural and hormonal mechanisms in eating behaviour

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  • Neural and Hormonal mechanisms
    • Neural
      • Hypothalamus
        • controls neural and hormonal mechanisms and maintains homeostasis
        • regulates levels of glucose (energy source) in the blood
          • Glucose strongly influences eating behaviour
          • Neural: glucose sensing neurons in the hypothalamus detect fluctuations in the blood glucose concentration
          • Hormonal: regulates glucose by directing insulin and anti-insulin hormones in the pancreases
      • Dual-centred model: two structures of hypothalamus provide homeostatic control
        • 'on switch' Lateral hypothalamus (LH)
        • 'off switch' Vento-medial hypothalamus (VMH)
      • LH
        • Contains cells to direct glucose levels to liver
        • Activated when glucose levels fall below a certain level (SET POINT)
          • Causes hunger and motivation to eat
        • Neuropeptide Y (NPY) also secreted
          • NPY when injected into rats hypothalamus, causes them to eat excessively and become obese
      • VMH
        • eating leads to a rise of glucose in the bloodstream and liver (glycogen)- detected by cells in the VMH
        • Triggered once levels increase past a certain point- LH activity inhibited and person becomes satiated
        • Damage to the VMH
          • Reeves and Plum: studied a woman who's weight had doubled in 2 years
            • Tumour growing on her VMH causing the normal 'stop eating' function to fail
    • Hormonal
      • Ghrelin
        • appetite stimulant (secreted by the stomach)
        • the longer we go without food, the more ghrelin is released
          • levels detected by the arcuate nucleus in the hypothalamus
            • when levels rise above a certain point, the arcuate nucleus signals the LH to secrete NPY
        • Wren found intravenous ghrelin caused a short term increase in the amount of food eaten
          • levels double before a meal and decrease very quickly afterwards
      • Leptin
        • appetite suppressant (secreted by adipose cells)
        • level increases with fat level and is detected by the VMH
        • level increased past certain point makes the person full and stop eating
        • Licinio
          • studied rare genetic condition (inability to produce leptin) which is associated with severe obesity
          • individuals treated with leptin replacement therapy saw 40% average weight loss and 49% reduction in food intake over 18 months
    • Evaluation
      • Strengths
        • Dual centred model
          • Ranson et al: lesioning in the VMH of rats caused them to overeat
        • model gives rise to potentially useful applications
          • understanding the way the nervous system and hormones interacts can lead to finding cures of obesity and anorexia realistically
      • Weaknesses
        • model is oversimplified
          • CCK is found to be a more powerful hormone suppressant than leptin
        • model ignores social and cultural factors
          • Wood: argues it is outdated
          • Hunger is determined by cultural and social norms of eating at that time of day
        • based on animal research
          • makes generalisation invalid
          • eating behaviour is more complex in humans than it is animals because there are more factors affecting it (e.g. psychological and sociological factors)

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