To Eat or Not to Eat - Essay Example

?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). At the end of the discussion, there will be questions related to obesity and anorexia. These questions are important, since they will assist us in knowing what underlies (myths and truth) anorexia and obesity. Physiological Factors for Hunger and Satiety The physiological system that controls the intake of food through satiety and hunger is very complex and it involves several external and internal factors. 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 motor disturbances. Thus, the notion that LH is the feeding center is just more than a myth (Pinel, 2009). Physiological Factors That Contribute To Hunger and Satiety Peptides are short chains of amino acids that function both as neurotransmitters and as hormones. There is enough evidence that supports the idea that peptides can act as satiety signals. Research shows that when gut peptides (cholecystokinin [CCK]) were injected into hungry rats, the rats ate smaller meals. This resulted in the theory that circulating gut peptides offer the brain the information concerning the nature and quantity of food in the GIT (gastrointestinal tract). The information provided to the brain plays a major role in satiety. A number of gut peptides are considered to bind receptors within the brain, specifically in the hypothalamus. Others, such as somatostatin, glucagon, bombesin, CCK, and alpha-melanocyte-stimulating hormones have been reported to reduce the intake of food. Thus, they have been referred to as satiety peptides, that is, peptides that reduce appetite (Pinel, 2009). Serotonin, a neurotransmitter also plays a major role in satiety. Research conducted in the 1970s on rats showed that serotonin antagonists constantly decreased the rat’s food intake. In humans, agonists of serotonin (such as fluoxetine and dexfenfluramine) minimize body weight, eating, and hunger under various conditions (Pinel, 2009). Response to Questions Response to Lindsey’s Question Though genetics plays a role in the development of obesity, it seems that the environments (e.g., the culture we live in) also play significant role in shaping individual eating habits. There are cultures that believe an individual is supposed to eat three meals each day at regular intervals regardless of whether he/she is hungry or not. This belief is common among many family environments. Others believe that food is supposed to be the focus of social gatherings, as noted by Pinel (2009). The current culture has developed a situation in which people consume unhealthy fatty and processed foods. These foods are acceptable to eat, and they promote weight gain, thus, higher chances of developing problems associated with weight. Cravings for certain foods also make individuals consume more food. Response to Robert’s Question The energy output differs considerably between individuals because of the differences in levels in which they dispel the excess energy consumed. The amount of exercise an individual does also differs and, thus, the differences in weight gain or lose can be explained (Pinel, 2009). Response to Nancy’s Question Positive incentives indicate that a decline in eating in anorexic people is likely to be because of the corresponding decrease in positive-incentive value of the food. In other words, anorexic people show a considerable interest in food. The reason for anorexia may be based on the fast at the start of meals, an individual is in a homeostatic balance, and it is disrupted when there is an abrupt infusion of calories (Pinel, 2009). Response to Tyra’s Question Just like Nancy, Tyra is anorexic, and severe anorexic people do not “experience a massive increase in the positive-incentive value of eating, similar to the increase experienced by other starving individuals” (Pinel, 2009, p.318). Each meal taken by an anorexic person may generate various conditioned taste dislikes that decrease the drive to eat (Pinel, 2009). Conclusion The physiological factors linked with hunger and satiety include peptides and serotonin. Peptides are short amino acids chains that function as neurotransmitters and as hormones. Serotonin is a neurotransmitter. Both serotonin and peptides have an effect on the individual’s satiety levels; in humans, they decrease food intake. There are a number of myths, such as the blood glucose theory and hypothalamic hunger and satiety centers myth that attempt to explain hunger and satiety. However, they have been unsuccessful, since most of their supporting evidence has been proved wrong. For instance, the blood glucose theory has failed to link blood glucose levels to eating. References Halverstadt, W. (2009). To eat or not to eat? Retrieved from http://voices.yahoo.com/too-eat-not-too-eat-4052385.html Mills, D. S. (2010). The encyclopedia of applied animal behavior and welfare. Cambridge, MA: CABI. Pinel, J. P. J. (2009). Biopsychology. Boston, MA: Pearson. Read More