Homeostasis is the way the body regulates its internal environment and our eating behaviour is an example of the equilibrium created through homeostasis. The way it does this is through the dual centre theory of feeding behaviour; when there is a decrease in blood glucose and an increase in ghrelin they lateral hypothalamus is activated causing hunger and eating to begin. Eating causes an increase in blood glucose levels and a decrease in ghrelin activating the hypothalamus causing satiety. However, for a hunger mechanism to be adaptive it must anticipate and prevent energy deficiencies not just react to them as homeostasis does; therefore homeostasis doesn’t match reality as it would have evolved to be adaptive due to this being advantageous
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It secretes neuropeptide Y (NPY) when it detects decreased blood glucose levels and increased ghrelin in order to start eating; this was shown by Stanley (1986) who found that rats because obese when repeat injected with NPY. Wickens (2000) also found the same when they injected NPY into the hypothalamus of rats as they found the rats began to feed even when they were full. Yang et al (2008) also found that NPY is also released by abdominal fat therefore people with higher levels of NPY will eat more leading to more abdominal fat leading to more NPY production and so on. However, damage to the lateral hypothalamus has also been found to cause thirst. Furthermore, Sakurai (1998) said that the lateral hypothalamus undoubtedly plays an important role but it’s not the eating centre as recent research has shown that neural circuits control eating. The ventromedial hypothalamus is the opposite of the lateral hypothalamus in that it signals to stop eating. Researchers concluded this as stimulation of the area reduces feeding and if it is removed in rats they over eat. Yet, Gold (1973) found that legions restricted to the VMH only didn’t cause hyperphagia and it was only when surrounding areas (such as the paraventricular nucleus) were included was hyperphagia caused suggesting that the VMH doesn’t control satiety alone. Gold’s findings have never been replicated, therefore the reliability can be
It secretes neuropeptide Y (NPY) when it detects decreased blood glucose levels and increased ghrelin in order to start eating; this was shown by Stanley (1986) who found that rats because obese when repeat injected with NPY. Wickens (2000) also found the same when they injected NPY into the hypothalamus of rats as they found the rats began to feed even when they were full. Yang et al (2008) also found that NPY is also released by abdominal fat therefore people with higher levels of NPY will eat more leading to more abdominal fat leading to more NPY production and so on. However, damage to the lateral hypothalamus has also been found to cause thirst. Furthermore, Sakurai (1998) said that the lateral hypothalamus undoubtedly plays an important role but it’s not the eating centre as recent research has shown that neural circuits control eating. The ventromedial hypothalamus is the opposite of the lateral hypothalamus in that it signals to stop eating. Researchers concluded this as stimulation of the area reduces feeding and if it is removed in rats they over eat. Yet, Gold (1973) found that legions restricted to the VMH only didn’t cause hyperphagia and it was only when surrounding areas (such as the paraventricular nucleus) were included was hyperphagia caused suggesting that the VMH doesn’t control satiety alone. Gold’s findings have never been replicated, therefore the reliability can be