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To Eat or Not to Eat - Essay Example

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To Eat or Not To Eat Introduction I am Stephen Thomas, eating disorder counselor and today we will be discussing hunger and satiety. The discussion will dwell much on the physiological factors for hunger and satiety (such as the role of hypothalamus in controlling eating behavior), physiological myths about hunger and satiety (such as blood glucose theory and hypothalamic hunger and satiety centers myth), and the physiological factors that led to hunger and satiety (such as peptides and serotonin)…
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Download file to see previous pages It comprises of both long-term (monthly) and short-term (daily) energy management. The current recognized model is the central feeding system, which consists of two major peripheral systems: a long-term system (that is concerned with the entire body energy balance and the adipose tissue) and a short-term satiety system, which transmits meal-related signals that feed the hypothalamus with information (Mills, 2010). The hypothalamus acts as an integrating relay centre that controls all the eating behavior in all vertebrates. It gets nerve impulses “from other parts of the brain and from a variety of sensory receptors, including chemoreceptors, olfactory and taste receptors, and stretch receptors in the gastrointestinal (GI) tract” (Mills, 2010, p329). The hypothalamus has a hunger centre, which stimulates hunger even when the animal is full, and a satiety centre, which stimulates the animal to stop eating even if it has been under starvation for a number of days. The hunger centre is constantly active but it is usually inhibited by satiety centre (Mills, 2010). Physiological Myths about Hunger and Satiety Some people believe that when the blood glucose levels decrease they will feel hungry; after taking food, the levels will rise and give the individual a feeling of satiety. Attempts to link blood glucose levels to eating have been unsuccessful (Pinel, 2009). An individual can experience an increase in the insulin levels in the bloodstream, and it is countered by a decrease in the levels of blood glucose when he or she desires to eat. Therefore, blood glucose levels do not change in response to the energy reserve levels, but due to the insulin levels (Halverstadt, 2009). The myth of hypothalamic hunger and satiety centers is another physiological myth about hunger and satiety. Experiments done on rats in the 1950s indicated that eating behavior is controlled by two special sections of the hypothalamus; the ventromedial hypothalamus (VMH), which controls satiety and the lateral hypothalamus (LH), which controls feeding. VMH is not the satiety centre because: The primary function of the hypothalamus is to regulate energy metabolism and not to regulate eating. Initial evidence used showed that the VMH-lesioned animals “become obese because they overeat; however, the evidence suggests the converse – that they overeat because they become obese” (Pinel, 2009, p.305). VMH damage is not attributed to the VMH lesions. The ventral noradrenergic bundle passes through the VMH and the huge electrolytic lesions of VMH do not damage it. However, the fibers that emerge from the adjacent hypothalamus paraventricular nuclei are damaged. The paraventricular nuclei produce obesity and hyperphagia that are similar to those generated by VMH lesions. Majority of the evidence that undermine the idea that LH is the feeding center come from the comprehensive analysis of the bilateral LH lesions effects. Initial research focused on adipsia and aphagia generated by the LH lesions. Current research has indicated that LH lesions generate a general lack of sensory input responsiveness (such as food and drink) and various sever ...Download file to see next pagesRead More
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