Biological Explanations to Eating Behaviour

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We eat to survive however when and how much we eat depends on metabolism which is regulated by several biological mechanisms. These mechanisms aim to keep nthe ody in homeostasis. The set point theory argues we have a biologically determined standard aroiund which our body weight is regulated, so if we eat too much or too little our homeostatic mechanisms alter our metabolism accordingly to return to our original weight. However consistent over eating or under eating makes it difficult for these mechanisms to keepup and we enf up having a new weight as our set point. The hypothalamus is the main area involved in regulating our appetite. The lateral hypothalamus produces hunger, the ventromedial hypothalamus trigers sense of feeling full, this is known as ‘satiety’. Evidence for this comes from the fact that damage to the hypothalamus results in drastic changes in food intake. According to the set point theory our weight is controlled by the balance between the two parts of the hypothalamus. Researchers doscovered that damage to the lateral hypothalamus in rats leads to a condition called aphasia ( they did not eat ), whereas stimulation to the lateral hypothalamus leads to eating more. This suggests that the lateral hypothalamus is like the switch for eating and satiety. Damage to the medial hypothalamus caused the rats to overeat, a condiotn known as hyphergia, whereas stimulation of the medial hypothalamus inhibited eating behaviour and led them to eating less. This suggests that the medial hypothalamus is responsible for eating, given its range of glucose receptors. The mdeial hypothalamus has been seen as the satiety centre. However Gold et al argued that lesions to the medial hypothalamus alone are not sufficient to produce changes in satiety. Instead only when lesions included the PVN did satiety behavious change. This suggests that the theory is

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