Neural Roles in Eating Behaviour

Outline and evaluate the role of neural mechanisms in controlling eating

(8+16 marks)

Both neural structures and hormones play a role in eating behaviour. Among humans, glucose levels contribute the most important influence in producing feelings of hunger. Hunger increases as glucose levels fall. When blood glucose levels do fall, the stomach releases the hormone ghrelin when it’s empty which activates part of the brain labelled the lateral hypothalamus (LH), resulting in hunger. The LH is the rea of the brain responsible for the starting of eating, causing the individual to search for and consume food. Research has illustrated that blood glucose levels affect hunger. When glucose levels were lowered in rats or in humans, appetite increased; when they were raised, appetite faded away (Smith & Campfield, 1993). This supports this approach since it demonstrates the concept that low glucose levels and the release of ghrelin increase a person’s appetite.

The other evolutionary development for the cessation of eating occurs when blood glucose levels rise. Along with a decrease in the release of ghrelin, the ventromedial hypothalamus (VMH) is activated which leads to the feelings of satiation, which inhibits further feeding. The VMH is also known as the stop switch.

Research has illustrated the crucial roles played by the hypothalamus. Hetherington and Rammington (1942) published a famous study on the control of eating behaviour. They showed that lesioning (i.e. destroying) tiny areas in the VMH in rats, led to an increase in food interest and eating with the animals seemingly unaware that they were over feeding themselves. The rats quickly became obese since they continued to eat even when they were full. This tells us that the VMH is responsible for the recognition of satiety and the stopping of eating. If damaged, it will not receive blood glucose level, or ghrelin signals and so will not stop eating. The opposite happened in Anand and Brobeck’s study with lesions to the LH as this led to the rats unknowingly starving themselves. This supports the concept that a damaged LH will not receive blood glucose signals, and so we will not start feeding.

The VMH is also backed up by a real life genetic disorder that occurs from a spontaneous error in genes on chromosome 15 that occurs at conception. People with Prader-Willi syndrome have a problem in their ventromedial hypothalamus. As a result, they never feel full and have a constant urge to eat that they cannot control. This example is more reliable as evidence since it avoids the constraints of animal studies. When research is performed on rats, you can’t extrapolate the findings to humans as it would be unethical to test this on humans. Rat behaviour is inapplicable to relate to human behaviour, and other factors may too influence the appetite of humans which don’t apply to rats such as media and advertising. Therefore, Prader-Willi syndrome benefits from great inter-rater reliability since consistent estimates of the same phenomenon apply to this genetic disfigurement.