3. When we are full the Ventro Medial Nucleus (VMN) of the hypothalamus is activated which inhibits eating and satiety is reached. Blood glucose levels drop again after eating and the Lateral hypothalamus is activated (which initiates feeding) and we become hungry and the process starts again. Damage to the VMH in animals caused overeating (hyperphagia). 4. There are several neurotransmitters in the body which are also involved in eating regulation. Ghrelin is a hormone which is released when the stomach is empty so it triggers eating. The second most important hormone is leptin and this is released from adipocytes, and the more fat a person has the more leptin is released and it acts as a satiety signal so stops food intake. Leptin reduces the release of Neuropeptide Tyrosine (NPY), an amine that influences hunger stimulation: normal leptin levels reduce the production of NPY, in turn reducing hunger and eating.
5. Licinio et al (2004) observed three morbidly obese adults from a Turkish family with a genetic deficiency in leptin to demonstrate that when given leptin supplements, their body weight and eating reduced to a normal level, thus supporting the importance of leptin in controlling eating and satiety. 6. Matochik et al (2005) also studied Effect of Leptin Replacement on Brain Structure in Genetically Leptin-Deficient Adults and showed some sustained structural changes in the cortex with leptin supplements using fMRI scans. After the leptin treatment, there was reduced activity in the insular, parietal and temporal cortices and increased brain activity in the prefrontal cortex. Hence, it would appear that the presence/absence of leptin is not the issue, rather the affect it has on brain structure that has an effect on a persons eating behaviour. 7. Videon and Manning (2003) found that people do not eat simply because they feel hungry, or stop because they feel satiated. Instead, people will evalutate circumstances (e.g. time of day, amount of food eaten that day) and act accordingly. Hence, research based on brain lesions needs to be regarded with caution and it is reductionist in that it does take account of the cognitive aspects of eating.
8. Havel (2000) outlined the action of the hormone leptin on various hypothalamic areas that influence feeding behaviour and energy expenditure. Calories stimulate leptin production; therefore people on low-calorie diets have lower leptin levels, higher NPY levels, and higher levels of hunger. This research also supports the importance of leptin in controlling eating. 9. Havels research (and other research concerning the effect of leptin) has a real-world application. If a low-calorie diet in fact increases hunger levels, thus making it more difficult to remain on the diet and maintain weight loss, then this can be applied to modern dieting programmes i.e. encouraging a low-fat diet rather than a low-calorie one.
10. In a literature review, Araujo et al (2006) concluded that evidence points to the idea that the LH initiates hunger and the VMH initiates satiation. However, in studies using lesioning of the brain, a weakness is that destroying brain tissue is likely to affect far more neurons and neural activity than just those related to eating behaviour. Hence, much of research into the action of the LH and VMH on hunger/satiation is challenged. 11.Bilateral lesions on the amygdala (which selects foods based on past experiences) has also resulted in hyperphagia. A problem with looking at the effect of individual substances (neural mechanisms) upon hunger is that it is unlikely that such substances work in isolation. Further, other factors such as learning and cognitive styles have evidence to support their influence upon eating behaviour; Pike and Rodin (1991) suggested that experiencing attitudes to food in the environment of upbringing significantly affects the development of schemata for eating behaviour. Hence, ignoring the present effect of family dynamics on food preference and eating behaviour renders the neural mechanism explanation as too simplistic.