The role of neural mechanisms
The hypothalamus is a gland in the brain responsible for homeostasis. Homeostasis is the way in which our body keeps conditions constant, for example our body temperature, sweat and urine levels. Another condition homeostasis controls is our intake of food and drink, hence why some psychologists believe the hypothalamus controls our eating behaviour.
The Lateral Hypothalamus
In the 1950s researchers found that some rats that had damage to the lateral hypothalamus (LH) stopped eating. They also found that stimulating the LH caused an increase in eating.
Wickens later found that when rats were injected with neuropeptide (NPY) the rats immediately began feeding, even when satiated. This suggests that NPY plays a role in both stimulating the LH and increasing eating.
The Ventromedial Hypothalamus
Research has also found that damage to the ventromedial hypothalamus (VMH) can have the opposite effect, causing rats to overeat. So if the LH is considered the “on switch” for hunger, the VMH could be considered the “off switch”.
The LH and VMH are thought to respond to many different signals from the body. For example, an increase in blood sugar levels from eating is thought to activate the VMH, giving us the feeling of satiety. Conversely, a decrease in blood sugar levels activates the hypothalamus giving us the feeling of hunger. This, and similar reactions, allow our hypothalamus to control the amount we eat and drink so our body is kept in equilibrium.
Research support – There is a wealth of research support for the link between the hypothalamus and eating behaviour. For example, Baylis et al found that rats with lesions in the VMH became obese, whilst control rats without lesions stayed at a normal weight.
Generalisation of research – However an issue with this research is that because of ethical problems nearly all of this research is conducted on animals such as rats. We cannot assume that the rules found in rats can be applied to humans as well, so therefore we can’t be sure this link between the hypothalamus and eating behaviour exists in humans as well.
Gold (1973) – Gold found that although lesions to the VHM and surrounding areas resulted is obesity in a number of different species, lesions restricted to the VHM alone didn’t result in overeating. Indeed it was only when the nearby paraventricular nucleus was also damaged that we saw an decrease in satiety. This suggests that perhaps the VHM does not have such a large role as we first thought in inducing a feeling of satiety.