Neural Mechanisms in Controlling Eating Behaviour

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Outline and evaluate the role of neural mechanisms in controlling eating behaviour (24 marks) Today there is enormous interest in the psychological factors that can affects a person’s eating habits, but some of the clearest research findings have come from research into the brain (neural) mechanisms controlling eating behaviour. One important mechanism to consider is the role of homeostasis in all mammals. Homeostasis is how the body maintains a constant internal environment. Our diet is essential to homeostasis as it provides the nutrients that allow physiological processes to be regulated within narrow limits. The body has evolved two separate systems – one for turning eating ‘on’ and one for turning eating ‘off’. Glucose levels are important in producing feelings of hunger – the less glucose present, the greater the hunger. Our lateral hypothalamus is activated when there is a decline in glucose levels, leading to feelings of hunger. A neurotransmitter found in the hypothalamus, called neuropeptide Y (NPY) is particularly important in turning on eating. Wickens found that if NPY was injected into the hypothalamus of rats, NPY would cause them to immediately begin feeding, even when satiated. This shows how a brain neurotransmitter is capable of controlling eating behaviour by causing an individual to begin feeding. However, there has been doubt on whether the role of NPY is to influence feeding behaviour. Marie et.al genetically manipulated mice so that they did not make NPY and they found that there was no subsequent decrease in their feeding behaviour. Researchers suggest that the hunger stimulated by injection of NPY may actually be an experimental artefact. A NPY flood into the bloodstream could cause behaviours other than the behaviour caused by normal amounts of the neurotransmitter, showing that NPY may not be the key to controlling our eating behaviour. Nonetheless, it has been show in the real world that obese individuals become obese due to the brain producing too much NPY, telling the individual that they are always hungry. Yang et.al also showed that NPY is produced by abdominal fat which leads to a vicious cycle where NPY produced in the brain leads to more eating and the production of more fat cells that leads to a greater NPY production. Such individuals can be treated with drugs that turn NPY production off and thus, decrease their obesity. The other part of our hypothalamus, the ventromedial hypothalamus, is activated when there is a rise in glucose levels, leading to feelings of satiation. Damage to the VMH causes rats to overeat, leading to hyperphagia, while stimulation of the VMH leads to inhibited feeding. However, damage to the nerve fibres passing through the VMH also damages another area of the hypothalamus, the periventricular nucleus. Gold found that damage to the PVN alone causes hyperphagia. This shows that the PVN detects specific foods our body needs, and consequently seems to be responsible for controlling our eating behaviour too, and not only the VMH. There are limitations to the homeostatic explanation – for hunger mechanisms to be adaptive, it must both anticipate and prevent energy deficits, not just to react to them. The explanation that hunger and eating is triggered only when the energy resources fall below their desired level is incompatible. For such a mechanism to be adaptive, it must promote levels of consumption at a higher level than the optimum to act as a buffer when food availability is low. This can be linked to the evolutionary approach that provides a more holistic approach to explaining how individuals control their eating behaviour. Evolutionary theorists suggest that the primary stimulus for hunger and eating is food’s positive-incentive value. People eat because they normally develop a relish for particular tastes that are in nature associated with foods that promote our survival, showing that the control of eating behaviour is related more to our survival based...
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