Discuss neural mechanisms involved in the control of eating behavior. (8marks+16marks)

The first idea of neural mechanisms controlling eating behavior is Homestasis. Homestasis is the tendency of an organism to maintain an internal equilibrium by adjusting physiological process e.g. hungry or thirst balance. The body has evolved two homeostatic mechanisms to regulate food intake, both dependent on glucose levels. When the levels of glucose drop will activates Lateral Hypothalamus(LH), which then leads to feeling of hunger. As a result to individuals consume food. Once the food is eaten the level of glucose will increase again this leads to the activation of Ventromedial Hypothalamus(VMH). This will then leads to satiety, which will make us stop eating.

Another idea is Hypothalamus control our eating. There are 2 parts of hypothalamus in our brains control our eating behavior. When VMH is stimulating it will inhibit us from eating but when it is damaged it will cause us to over eat. Another part is LH when it is stimulated it will leads us to eat but when it is damaged it will prevent us to eat. In LH part there is neurotransmitter called Neuropeptide Y(NPY) this increases our appetites. OB Gene & Leptin is also leads us to decrease appetite. Gherlin hormone is also related to our eating as when we are stressed Gherlin hormone will increase to reduce our stresses but the hormone will also increase our appetite.

Miller carried out the study by using a rat. The rat has had the VMH, which is part of the brain removed. After the surgery the rat kept eating food until it was very fat. This shows that the fat rat over eats. Therefore, this demonstrates that the damage in VMH leads to do not stop eating. There are problems with the explanation of VMH. As Gold claimed that the lesion to VMH alone did not produce overeating but has to damage in Paraventricular Nucleus as well. Wickens carried out the research by injecting NPY to LH part of hypothalamus of rats. The results have shown that the rats still eating even when they are satiated. This shows that the more NPY released, the more we will eat. Therefore, Wickens study can be used to support the role of NPY to our feeding behavior. However, there was a research to refuse this evidence. Mice were genetically manipulated so that they did not make NPY and found no difference in feeding behavior between normal mice and mice without NPY. This demonstrates that NPY does not link to our eating behavior. The studies to the role of hypothalamus in eating behavior used mice to test the theory, which the experiment could be un-ethical to use humans. Therefore, the studies have concerned about ethical issues. Although the studies might be argued to lack generalization to human, the mice brains have similar hypothalamus structure. Moreover, the studies to the role of hypothalamus in eating behavior have real world application. As the NPY has been found out that it is not only being produced in the brain it is also produced in abdominal fat – obese people have more abdominal fat. Hence, obese people will produce more NPY which will make them eat more. Therefore, we can treat people at risk of obesity by giving drugs that turn off NPY.

The Amygdala also play an important role in food selection. We store information about food based on previous experience in Amygdala. Rolls and Rolls carried out the research by removing rats’ amygdala rats show no preference for familiar food and ate familiar and novel food indiscriminately, whereas those rats that have amygdala eat only familiar food. This shows that amygdala has an important role in food selection.

Overall, hunger and eating is not based purely on biological explanations as psychological factors might be factors. Garg carried out the study by giving participants popcorn to eat while watching sad/funny film. The results showed that participants ate 28% more popcorn while watching sad film than funny film. Therefore, it can be concluded that psychological factors also play a role in our eating behavior.