To Eat or Not to Eat

Causes for Eating Disorders

Hello everyone, my name is Clark Graham and I will be the eating disorder counselor for this evening. Those here today are probably wondering, “why is obesity a growing epidemic?” and “why do people become anorexic?” To better understand these issues, I will explain some of the myths and physiological factors that influence hunger and satiety, the feeling of no longer being hungry. Following this explanation, I will be more than happy to answer questions.

Physiological Findings on Hunger and Satiety

In past years, a set-point theory was created with the idea that after eating a meal our energy level would gradually decrease until it reached a certain point, alerting us to consume food for more energy, and when our energy level was brought back to the set-point we would no longer feel hungry (Pinel, 2007). This idea seems feasible, but in reality it is too simplistic to credit the many processes that occur within the body when utilizing and storing the energy taken from digested food. Many assume that the body has run out of energy due to this theory, when in fact it is simply a conditioned response to prepare for the internal stress caused by bodily processes used to distribute the foods energy content (Pinel, 2007). Having regular meal time’s programs the body to get hungry and be prepared so the processes can begin before the food enters the mouth to reduce the amount of activity required once the food is digested, thereby reducing stress. The set-point theory also influenced researchers to develop simplistic ideas as to the body’s use of blood glucose and insulin, which work against one another to maintain a healthy balance. The glucostatic theory presented “the idea … that we become hungry when our blood glucose levels drop significantly below their set point and that we become [full] when eating returns our blood glucose levels to their set point” (Pinel, 2007, p. 306). This theory claims that eating is the factor crucial to restoring blood glucose levels back to the set point. According to Pinel (2007), blood glucose levels drop just before a meal in preparation to begin eating and if for some reason the meal is not able to be consumed, blood glucose levels will return to the previous levels. I wonder how glucostatic theory accounts for the glucose levels returning to normal without eating, since it accounted for becoming satiated by eating to return blood glucose levels to normal. It was once believed that there were two regions of the hypothalamus that controlled motivations for eating: the ventromedial hypothalamus (VMH) that regulated satiety and the lateral hypothalamus (LH) that controlled feeding; we know now that this is not true.

To clarify before we look at why this is not true, it is important to note that lesions refer to areas of damage to certain parts of the brain. Evidence suggests that “bilateral VMH lesions increase blood insulin levels, which increases lipogenesis (the production of body fat) and decreases lipolysis (the breakdown of body fat to utilizable forms of energy)” (Pinel, 2007, p. 314). This evidence reveals one of the causes of obesity due to a increase in the production of body fat along with a decrease in the breakdown of body fat to utilizable forms of energy leave the body feeling as though it has not acquired any energy from the food; therefore inducing the urge to keep eating to gain energy. According to Pinel (2007), lesions on the LH impair many motor functions and the sensitiveness to sensory input, such as the sense of taste. The role of satiety within the gastrointestinal tract was once theorized to be the feeling of distention within the stomach, but studies have shown that this is not the case. The gastrointestinal tract has been found to contain receptors that release chemical messengers, called peptides, into the bloodstream that communicate the quantity and nutritional value of food to the brain to help regulate satiety (Pinel, 2007). Finally, serotonin is a neurotransmitter that has been linked to mood regulation and now we know it plays a role in satiety as well. “In humans, serotonin agonists (e.g., fenfluramine, dexfenfluramine, fluoxetine) have been shown to reduce hunger, eating, and body weight under a variety of conditions” (Pinel, 2007, p. 305).

Lindsey’s Question:

“My parents were both obese, is that why I am?”

Well Lindsey, genetics is a factor that can contribute to obesity, but it is not the only factor. A major factor contributing to obesity is the poor eating habits formed by our society. “For example, in [our] culture, it is commonly believed that one should eat three meals per day at regular times, whether [you] are hungry or not; that food should be the focus of most social gatherings; that meals should be served in courses of progressively increasing palatability; and that salt, sweets (e.g., sugar), and fats (e.g., butter) should be added to foods to improve their flavor, thereby increasing their consumption” (Pinel, 2007, p. 323). Another contributing factor includes an eating behavior that we all inherited from our hunter-gatherer ancestors. When we had to hunt and gather our food there were times when food was not readily available, such as when the winter season made it difficult to find an abundance of wild game or flourishing vegetation. “As a result, the fittest individuals were those who preferred high-calorie foods, ate to capacity when food was available, stored as many excess calories as possible in the form of body fat, and used their stores of calories as efficiently as possible” (Pinel, 2007, p. 323). At the beginning of our session I explained that past theories claimed we become hungry due to an energy deficit that must be replenished by eating, but the eating behaviors of our ancestors is also a supporting fact that hunger is not our body’s way of saying it needs more food for energy; if this was the case, our ancestors would have found it difficult to survive. Take all of these factors together and we have a serious health-related situation that is quickly getting out of hand.

Robert’s Question:

“My girlfriend and I eat together all of the time, so we eat the same food and amounts of food, but she never gains weight like I do. Why is that?

There are “two kinds of individual differences [that] play a role in obesity: those that lead to the differences in energy input and … in energy output” (Pinel, 2007, p. 324). Since you both take in the same amounts of food, a possible reason for your weight gain may have to do with how efficiently your body uses that energy. There could possibly be an imbalance in the production of insulin and glucose that may be causing your body to use your energy less efficiently than your girlfriend. It is rare but another possibility could be due to an inefficient production of leptin, “a critical hormone that normally inhibits fat production” (Pinel, 2007, p. 325). The other possibility is that your girlfriends daily activities provide more exercise used to consume the extra energy she stores.

Nancy’s Question:

“My mom says that I became anorexic because I’ve been reading too many Cosmo magazines and want to look like those girls. Maybe I did, but I really just don’t crave food. What do you think it is?”

“Evidence suggests that people – primarily adolescent females – begin dieting in response to great pressure from a cultural emphasis on slenderness, and those who are highly controlled, rigid, and obsessive overcome the attraction of food” (Pinel, 2007, p. 327). In our society we have so many food choices that most of us no longer seek food for nutritional value, rather we choose based on how good a particular food tastes, referred to as a foods positive incentive value (Pinel, 2007). Along with a culture that emphasizes slenderness and taste over nutrients, it is easy for us to forget the true value of food, thereby reducing food cravings.

Tyra’s Question:

“I don’t eat because every time I do, I just feel sick! Do you know why this is?”

Well Tyra, if you have ever induced vomiting after eating a large meal, it could have conditioned a response to dislike certain meals that could have easily become a generalized response to dislike all foods. We all develop a disfavor of food following a meal, which is why many find it difficult to eat the same food for two weeks straight; it begins to lose its appeal and I have even gagged when I repeatedly ate the same foods for a workout diet. The cause of your sickness is likely due to eating “meals, which produce … extremely noxious effects on starving humans” (Pinel, 2007, p. 328). This is evidence that small amounts of food given at irregular intervals throughout the day helps mediate the sick feeling (Pinel, 2007).

If there are no more questions we will go ahead and conclude our meeting for today.

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

References

Pinel, J. P. J. (2007). Basics of biopsychology. Boston, MA: Allyn and Bacon.

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