According to this theory, Ghrelin is a hormone released from the stomach and as the levels of ghrelin in our body increase, the feelings of hunger increase. This increase if detected by the brain causing us to carry out food seeking behaviours.
CCK is a hormone released from the duodenum in the small intestine and as the levels of CCK increase, the feelings of satiety increase. This increase is also detected by the brain which causes us to stop eating.
Lastly, Leptin is a hormone released from adipocyte cells to maintain our set point. The more fat stored in our body, the more leptin produced in the body that is indicated in the brain.
Concluding this theory, it states that how much you eat is determined by the levels of CCK and Ghrelin detected by the brain and our set point is maintained by the levels of leptin. These hormones regulate our eating behaviour.
Support for the Dual Centre Model comes from research carried out by Hetherington and Ranson (1942) that cut off the Ventromedial Hypothalamus in rats and found that they could no longer sense when they were full so therefore became over-weight. This supports the Dual Centre Model as it provides evidence for the Ventromedial Hypothalamus and its use. However, this study was carried out in lab rats and although it supports the model, it cannot be applied and generalised to a human population as we cannot be sure that same evidence will be found within humans. Also, although the rats became overweight after the removal of the Ventromedial Hypothalamus we cannot be sure that the removal of the VMH was the only cause of the rats becoming overweight. Other factors may be a cause, so in order to fully support this model more research must be carried out in order to provide a clear cause and effect. More research on a human sample must also be carried out in order to provide evidence to support this model.
Another support for the dual centre model comes from research carried out by Anand and Brobeck (1957) who researched damage to the Lateral Hypothalamus in rats and found that the rats could no longer sense when they were hungry resulting in them eating less as according to the Dual Centre Model, damage to the Lateral Hypothalamus results in the body no longer being able to indicate hunger. This supports the Dual Centre Model as it provides evidence of its role however, this study was carried out on rats so therefore this evidence cannot be generalised to a human population as we cannot be sure that humans would have a similar effect. This matters because although it supports the Dual Centre Model, due the results lacking external validity, it cannot be applied to human psychology or medical research, suggesting more research must be carried out in order to provide results that can be applicable.
Support for the role of hormones in eating behaviour comes from research carried out by Smith, Gibbs and Kulkcosy (1982) that carried out research on the role of CCK in both animals and humans. They injected their sample with CCK and found that those who had been injected with CCK had reduced their meal size. This evidence supports the role of CCK in eating behaviour. This study has high internal and external validity by measuring what it intended to measure and providing results that can be generalised to a human population. This evidence has further helped medical research into CCK and eating behaviours as CCK is used in dieting pills to help dieters to feel fuller. This matters because this research can wholly support the role of CCK in eating behaviours.
Another support for the role of hormones in eating behaviour comes from research carried out by Cummings (2006) who found that injections of Ghrelin increase food intake in both animals and humans. Cummings found that ghrelin levels fall immediately after eating and are at its highest peak when people feel hungry. Cummings research 6 patients and found that 5 out of 6 patients requested their evening meal when ghrelin levels were high. This supports the role of ghrelin in eating behaviour as it provides evidence of its affects in both humans and animals. However the results found was correlational therefore a clear cause and effect cannot be established. These results may have also been found due to other factors such as environmental factors that play a role in hunger. Also due to the complications of this study, only 6 participants were used and they were all male. Therefore although the research supports the theory, this evidence cannot be generalised to an entire population and females. This suggests more research must be carried out on the role of Ghrelin to wholly support this theory.
In conclusion, both neural mechanism theories into eating behaviour takes a clear biological approach resulting in the theories being reductionist as these theories over simplify a complicated process. These theories ignore the psychological and social factors involved in influencing eating behaviours, such as cultural influences. This suggests a theory that considers both biological and psychological factors would be more suitable.