Neural mechanisms of eating behaviour

characterised by feelings of hunger which prompts feeding to start. It has been suggested that the hormone Ghrelin is a key component in the feeding process and researchers say that increased ghrelin production may result in feelings of hunger. Cummings et al investigated the changes in blood ghrelin levels overtime between meals in an attempt to determine the effects of ghrelin on hunger. The researchers measured the blood ghrelin levels, of 6 participants who were kept away from daylight, every 5mins until the participants asked for their next meal. Participants were also asked to record their degree of hunger every 30mins. The researchers found that ghrelin levels decreased dramatically after lunch, with the lowest levels being approx 70mins after their meal. Ghrelin levels were at their peaks when the participants asked for their next meal. It was found that in 5 out of the 6 participants, the ghrelin levels were related to hunger.  This evidence supports the theory that the secretion of ghrelin from the stomach may be a key signal for both the feeding centre and satiety centres in the brain, with increased levels stimulating the LH (feeding centre) and decreased levels stimulating the VMH (satiety centre). However there are problems associated with generalising these findings; the research was carried out on only 6 participants- all of which were male. The differences between males and females are being overlooked (beta bias) and although some may argue that the differences don’t apply here, researcher have found evidence that neural pathways associated with pain differ in males and females so there is a possibility that neural pathways associated with eating behaviour may also differ in men and women. Never the less, Cummings et al did try to minimise external variables or cues which may have influenced the behaviour of participants. By removing time cues, the researchers removed any social factors which may have simulated eating behaviour further expanding generalisability of the findings to other cultures. However it could also be argued that this lack of ecological validity doesn’t reflect what would happen in a real life situation. The findings provide correlational data, so we are unable to establish a cause and effect and there may be other factors which influence hunger- this is show by the fact that people who have had their stomachs removed because of cancer are still able to regulate food intake so ghrelin may not be the only hormone involved in the feeding response. One hormone involved in inhibiting feeding behaviour or satiety is leptin. Research has been carried out to test the effects of leptin on mice. It was found that mice lacking the gene that produced leptin overate and became obese hence the name that was given to them- ob mice. Once injected with the hormone, they reduced their meal size. These findings suggest that simply increasing leptin levels in people suffering from obesity would result in decrease in meal size, however researchers are cautious when generalising non human animal findings to the human population as there may be subtle differences in the control of feeding between humans and other animals. This is illustrated further by the fact that people who suffer from obesity often have normal or even higher than average levels of leptin, suggesting that they may be insensitive to the hormone. Another hormone involved in satiety is CCK. Injections of the hormone into human and non human animals found a substantial decrease in meal size, providing evidence for the function of CCK in inhibiting feeding behaviour. Further evidence to support the role of CCK comes from studies showing that animals with a gene mutation eliminating the CCK system over eat and become obese. The role of neural pathways in control of eating behaviour is an aspect of the biological approach, this means that most of the findings from studies are likely to be objective (based on observable phenomenon) and replicable which are two major components central to science. Despite this, the approach is heavily reductionist in that it ignores social and psychological aspects of eating behaviour. For example it fails to explain why we eat even though we are not hungry or in a state of satiety, the reason to this issue is likely to be in the behavioural explanation of eating behaviour e.g. the role of social learning and scheduled feeding. A further criticism of the role of neural mechanisms, in the control of eating and satiation, is that the view is very deterministic and sees behaviour as mostly determined by our brain structure and genetic makeup. This leaves little room for free will, implying that an individual cannot be held responsible for his/her own actions.