Discuss neural mechanisms involved in eating behaviour.

(8+16)

AO1 Dual Centre Hypothesis

The dual centre hypothesis suggests that eating behaviour is controlled via a homeostatic system whereby neural mechanisms play a key role. The hypothalamus is the main area of the brain that regulates eating. The lateral hypothalamus (LH) acts as the ‘hunger centre’ and is triggered by falling blood glucose levels and rising ghrelin levels (a hormone released when the stomach is empty). The Ventro-medial hypothalamus (VMH) acts as the satiety centre and is triggered by falling levels of ghrelin, rising levels of CCK (a hormone released when the food is detected in the duodenum) and rising levels of leptin. Neuropeptide Y is thought to be associated with the initiation of eating. Dopamine may be relevant to eating behaviour in that it is commonly associated with the reward pathway in the brain. When dopamine is released in response to eating, it is likely to provide positive feelings for an individual. This is likely to be associated with eating and thus eating becomes a pleasurable experience.

AO2 

Research from Anand and Brobeck supports this theory. They conducted research into the role of hypothalamus in eating behaviour. They found that damage to the LH in rats caused a condition called aphagia. Other researchers also found that stimulation of the LH elicits feeding behaviour. This therefore supports the theory of an on switch in eating behaviour.

However more recent research from Sakurai et al has shown that eating behaviour is controlled by neural circuits that run throughout the brain and not just by the hypothalamus. Although the LH undoubtedly plays a role in controlling eating behaviour it is not as previously thought the brain’s eating centre. The importance of the role of the hypothalamus has been replicated in further studies  where the role of neirochemicals (neuropeptide Y ) has also been supported.   Repeated injections of NPY into the hypothalamus of rats produces obesity in just a few days (Stanley et al., 1986), which demonstrates the impact that this neurotransmitter has in eating behaviour. Lutter (2008) has found supporting evidence for the role of ghrelin as being crucial in boosting appetite. He concluded that extra levels of ghrelin were produced in stressed individuals which caused them to overeat. However, it may be possible that other psychological processes were overlooked in this study (e.g. psychological impact of mood)

There is also empirical research evidence for the role of the VMH. Baylis found that damage to the VMH caused rats to overeat, which lead to the condition hyperaphagia. Similarly stimulation of this area inhibited feeding. Therefore suggesting that the VMH has the role to send signals to stop eating.

IDA 

A great deal of the research done on neural mechanisms has been done using rats which means that it is difficult to generalise. Rats do not have a functioning prefrontal cortex like humans do, and this is what helps humans make judgements so how far can we say the studies using animals supports the role of neural mechanisms in humans. However, Research studies have looked at FMRI of cases of individuals with Prader-willi  (who have a compulsion to eat) syndrome in comparison to controls (when eating) and have found a deactivation  in the hypothalamus of PWS patients. This is a good study as it has been done on humans and uses scientific objective measures (FMRI scans) which means that it is a valid study that shows the importance of the role of the hypothalamus in humans.

IDA 

The neural mechanisms explanations (biological approach) can be seen as an example of Biological determinism: it focuses exclusively on the role of nature and no space left to choice and cultural and social influences. There is substantial and convincing evidence that social, cultural and psychological factors affect our eating behaviours as is evident from psychological explanations of eating disorders. For example research into mood has shown that when we are in a bad mood we are more likely to crave carbohydrates.  This suggests that there are other reasons that govern what we eat and that is not just down to neural control.