Sample Obesity And Eating Disorders Research Paper. Browse other research paper examples and check the list of research paper topics for more inspiration. If you need a religion research paper written according to all the academic standards, you can always turn to our experienced writers for help. This is how your paper can get an A! Feel free to contact our research paper writing service for professional assistance. We offer high-quality assignments for reasonable rates.
This research paper covers obesity and the eating disorders of anorexia nervosa and bulimia nervosa. People diagnosed as obese, anorexic, or bulimic eat too much or too little. As a result, they may weigh too much or too little, with consequent adverse effects on their health. Even considering each eating disorder separately, there are substantial individual differences with respect to etiology and the relative success of different types of treatment.
Academic Writing, Editing, Proofreading, And Problem Solving Services
Get 10% OFF with 24START discount code
1. Anorexia Nervosa
People with anorexia nervosa eat less food than is necessary to sustain a healthy weight. To be diagnosed as anorexic someone must have a maximum body-mass index (BMI) of 17.5 kg/m2(BMI measures someone’s mass per meter of height, and is calculated as weight in kilograms divided by the square of height in meters). Along with this loss of weight, females must stop menstruating to be classiﬁed as anorexic. Anorexics may occasionally go on feeding binges and then compensate for the calories ingested using such means as self-induced vomiting, laxatives, or excessive exercise. Anorexia nervosa usually occurs in females ranging in age from their teens to their 30s. The overall prevalence of the condition has been estimated at between ﬁve and ten anorexics per 1000 late-adolescent and early-adult females (American Psychiatric Association 1994).
Using the word anorexia for this disorder is misleading because, contrary to its meaning—which is lack of appetite—anorexics are completely obsessed with food and food consumption. They carefully calculate just how many calories they can and do consume. They think and dream about food constantly (Bruch 1978). Many have a different perception of their body size compared with the impression that other people have of them. Anorexics tend to see themselves as being heavier than they really are (Garﬁnkel and Garner 1982).
1.1 Possible Explanations And Causes
A great many explanations for the cause of anorexia nervosa have been proposed. These explanations include, ﬁrst, the current fashion image of thinness, which encourages young women to feel that they must be very thin in order to be attractive (Garﬁnkel and Garner 1982). In addition, anorexia nervosa may be a way to gain attention, an attempt at individuality, a denial of sexuality (in addition to not menstruating, girls who are severely underweight lack secondary sexual characteristics), or an attempt to resolve various problems associated with overdemanding parents (Bruch 1973). In addition, the neurotransmitter systems of anorexics tend to exhibit a variety of abnormalities, although it is not clear if these abnormalities are a cause or an effect of the condition (Kaye 1995). Several of the behavioral characteristics of anorexia nervosa—dawdling over food, obsession with food, and hyperactivity—have also been observed in humans and nonhumans who have been deprived of food either in the laboratory or under natural conditions (Logue 1991).
It appears that no one cause will suffice to explain all cases of anorexia nervosa; in fact, it is likely that no one cause will suffice to explain any single case. There are many paths to this very complex disorder.
Treatments for anorexia nervosa can be divided into two groups: short-term treatments designed primarily to induce an immediate weight gain in the patient, sometimes without her consent; and long-term treatments designed primarily to maintain or prolong a weight gain (Van Buskirk 1977). An example of a short-term treatment is nurturance, one or more different techniques that attempt to improve the patient’s nutrition. Nurturance may take the form of bed rest accompanied by a high-calorie diet, or of force feeding the patient through a tube inserted down her throat (Garﬁnkel and Garner 1982). Other examples of short-term treatments are behavior therapy, in which engaging in activities known to be pleasant for the anorexic is made contingent on eating (Van Buskirk 1977), and drug therapy, in which speciﬁc types of medication are used to enhance appetite or mood (Walsh 1995). Each of these types of short-term therapy can be useful for obtaining an initial weight gain. However, given that there are potential medical problems associated with using any drug, use of drugs should be approached with caution.
Examples of long-term treatments are individual psychotherapy, family psychotherapy, and self-help groups. Within each of these types of treatment are many different approaches. Unfortunately there have been few controlled studies on the long-term effects of different treatments of anorexia nervosa, therefore we do not have a clear picture as to which treatments are successful in the long term for which types of patients.
Anorexia nervosa is a very serious disorder with an average mortality rate of 5 percent. However, most treated patients improve (Steinhausen 1995). We know that the overall treatment package used for patients, usually consisting of some form of nurturance plus psychotherapy, seems to have fairly good results.
2. Bulimia Nervosa
People suffering from bulimia nervosa repeatedly eat, in a short period of time, a very large amount of food (known as binge eating). In addition, bulimics frequently rid themselves of the excessive calories that they have consumed using self-induced vomiting, laxatives, starvation, or vigorous exercise. Bulimics are usually within normal weight ranges, and are, as with anorexia nervosa, mostly young women. The prevalence of bulimia nervosa has been estimated as between 1 and 3 bulimics per 100 adolescent and young-adult females.
Similar to anorexics, bulimics appear to have a distorted view of their own weight, and are obsessed with controlling their food intake. However, unlike anorexics, they repeatedly slip and consume huge amounts of food. Once the binge starts, it seems uncontrollable. Then the bulimic usually attempts to compensate for the effects of the excessive food consumption (American Psychiatric Association 1994).
Repeated binging and purging can have devastating physiological effects. Some of the less serious effects include sore throat and swollen glands caused by repeated vomiting; the vomitus being acidic, it eats away at the enamel of the teeth, making bulimics prone to tooth decay. More serious is that both the vomiting and the use of laxatives can cause dehydration and cardiac arrhythmias (Mitchell 1995). In addition, possibly due to their repeated cycles of binging and purging, bulimics have a signiﬁcantly lower metabolic rate than do nonbulimics, making it relatively easy for bulimics to gain weight (Energy expenditure 1989; Gwirtsman et al. 1989).
2.1 Possible Explanations And Causes
Many of the possible explanations and causes that have been proposed for anorexia nervosa have also been proposed for bulimia nervosa. However, one possible cause appears to be unique to bulimia; many bulimics are depressed. In addition, bulimics tend to come from families with a history of mood disorders. Many mood disorders appear to have a genetic component, and it has been suggested that a single, genetically based chemical disorder may be at least partly responsible for both depression and bulimia (Strober 1995).
As with anorexia nervosa, various types of psychotherapy have been used in treating bulimia. In addition, consistent with the hypothesis that the causes of bulimia nervosa and depression are in some way physiologically related, several researchers have reported improvement in the eating behavior of bulimics after administration of antidepressants. However, these ﬁndings are by no means uniform. Furthermore, some researchers feel it is necessary to combine psychotherapy with antidepressants to ensure both the cessation of unhealthy eating behavior and an increase in healthy eating behavior (Walsh 1995).
There are many deﬁnitions of obesity. A common one is based on the BMI: people with BMIs in excess of 30 kg/m2 are considered to be obese, and people with BMIs between 25 and 30 kg/m2are considered to be overweight. However, the BMI deﬁnitions of obesity and overweight are not perfect. The BMI does not distinguish between lean body mass, such as muscle and bone, and stored fat. Some researchers believe that the limits for overweight and obesity should be adjusted upwards as people age (Bray 1987).
Obesity is an increasing problem in the United States; approximately one-third of United States adults are obese. In general in the United States, more women than men are obese and obesity increases with age (Williamson 1995). Increasing obesity among children is a particular problem in the United States (Kennedy and Goldberg 1995). It has recently been estimated that the direct costs of health care related to obesity constitute 5.7 per cent of the total health-care costs in the United States. Medical conditions associated with obesity include high cholesterol, high blood pressure, and diabetes (Rossner 1998)
3.1 Possible Explanations And Causes
Contrary to popular belief, there are few consistent differences in the eating behavior of obese and nonobese people. Many people who are obese eat no more calories or no more sweet or fatty foods than do people who are not obese. Therefore particular aspects of eating behavior are, on average, not useful in explaining obesity (Logue 1991).
In contrast, there is no question that genes play a role in obesity; the biological children of obese parents also tend to be obese, and weight tends to be more similar between identical twins (who have identical genes) than between fraternal twins who on average share half of their genes; Gurney 1936). However, it is important to note that there are also signiﬁcant correlations between the weights of adoptive mothers and their children; the environment also plays an important role (Foch and McClearn 1980).
One way in which genes may inﬂuence obesity is through the number of adipose (fat storage) cells that someone has. When these cells are not full, there is more hunger, and the number of adipose cells that someone has is inﬂuenced by heredity. In addition, if someone gains weight, the number of adipose cells can increase, but their number can never decrease (Bjorntorp 1987, Sjostrom 1980).
Much research has focused on energy expenditure as a factor contributing to obesity. Research has shown that individuals with identical body weights may have different metabolic rates; the lower the metabolic rate, the greater the person’s tendency to become obese (Geissler 1988, Ravussin et al. 1988). Various factors can inﬂuence metabolic rate. For example, low levels of food consumption, such as occur with dieting, can decrease metabolic rate, and this decrease may last even after food consumption increases (Elliot et al. 1989). In contrast, exercise can increase metabolic rate, and the increase may last even after the exercise has stopped (Brownell 1995). Therefore lack of exercise and (paradoxically) dieting may contribute to obesity.
Many other factors have been demonstrated to contribute to eating large amounts of food. Such factors include easy access to highly palatable food, stress-induced eating, relatively great physiological responsiveness to food stimuli in the environment, and a learning history such that food comes to satisfy needs other than nutritional (Logue 1991). Nevertheless, it is important to remember that eating large amounts of food by itself does not necessarily result in obesity.
There are very few treatments that have been reliably shown to decrease obesity for an extended period of time. Drugs such as amphetamines, diets, and behavior therapy can all result in a weight loss, but such losses are usually temporary. This is not surprising given what we know about adipose cells and metabolic rate, as described above.
One treatment that has long-term success is gastric bypass surgery, in which the lower part of the stomach is bypassed by ﬁrst disconnecting it from the top part, and by then connecting the top part of the stomach directly to the intestine. Bypass surgery is extremely successful in decreasing obesity. Five years after the operation, patients have only about 40–50 percent of the excess weight that they had before the operation (Kral 1995). Patients also appear to be better adjusted and happier after surgery; their weight loss enables them to engage in many activities that were previously difficult or impossible, plus they feel more attractive. However, there can be some potentially dangerous side effects from this operation, with vomiting being the most common (Bray and Gray 1988). In addition, major surgery of any kind always involves risk. Therefore bypass surgery is not recommended for anyone unless they are severely overweight and have been unable to lose weight by other, less drastic, means.
The other treatment that has been shown to have signiﬁcant long-term success in terms of weight loss is exercise. Exercise uses calories and under certain conditions can elevate metabolic rate for several hours following the exercise, thus burning additional calories (Brownell 1995). Further, exercise has more beneﬁts than simply burning calories: cardiovascular ﬁtness, increased muscle tone and bone strength, and improved mood (Dubbert and Martin 1988, Folkins and Sime 1981). Thus exercise has much to recommend it as a means of weight control.
It is extremely unfortunate that in a country such as the United States, where so many of life’s problems have been solved or ameliorated by industrialization, other problems, such as obesity, anorexia nervosa, and bulimia nervosa have been enhanced. Our industrialized environment with its easy access to food, laborsaving devices, and fashion industry has aided and abetted situations in which people eat too much or too little. As long as our environment contains these elements, treating these disorders will remain extremely difficult. Nevertheless, scientists are making some progress in determining the best methods for treating obesity, anorexia nervosa, and bulimia nervosa.
- American Psychiatric Association 1994 Diagnostic and Statistical Manual of Mental Disorders, 4th edn. American Psychiatric Association, Washington, DC
- Bjorntorp P 1987 Fat cell distribution and metabolism. In: Wurtman R J, Wurtman J J (eds.) Human Obesity. New York Academy of Sciences, New York
- Bray G A 1987 Overweight is risking fate: Deﬁnition, classiﬁcation, prevalence, and risks. In: Wurtman R J, Wurtman J J (eds.) Human Obesity. New York Academy of Sciences, New York
- Bray G A, Gray D S 1988 Obesity. Part II—Treatment. Western Journal of Medicine 149: 555–71
- Brownell K D 1995 Exercise in the treatment of obesity. In: Brownell K D, Fairburn C G (eds.) Eating Disorders and Obesity: A Comprehensive Handbook. Guilford, New York
- Bruch H 1973 Eating Disorders. Basic Books, New York
- Bruch H 1978 The Golden Cage. Harvard University Press, Cambridge, MA
- Dubbert P M, Martin J E 1988 Exercise. In: Blechman E A, Brownell K D (eds.) Handbook of Behavioral Medicine for Women. Pergamon, New York
- Elliot D L, Goldberg L, Kuehl K S, Bennett W M 1989 Sustained depression of the resting metabolic rate after massive weight loss. American Journal of Clinical Nutrition 49: 93–6
- Energy expenditure and the control of body weight 1989 Nutrition Reviews 47: 249–52
- Foch T T, McClearn G E 1980 Genetics, body weight, and obesity. In: Stunkard A J (ed.) Obesity. Saunders, Philadelphia, PA
- Folkins C H, Sime W E 1981 Physical ﬁtness training and mental health. American Psychologist 36: 373–89
- Garﬁnkel P E, Garner D M 1982 Anorexia Nervosa. Brunner Mazel, New York
- Geissler C 1988 Genetic differences in metabolic rate. In: Birch G G, Lindley M G (eds.) Low-calorie Products. Elsevier, New York
- Gurney R 1936 The hereditary factor in obesity. Archives of Internal Medicine 57: 557–61
- Gwirtsman H E, Kaye W H, Obarzanek E, George D T, Jimerson D C, Ebert M H 1989 Decreased caloric intake in normal-weight patients with bulimia: Comparison with female volunteers. American Journal of Clinical Nutrition 49: 86–92
- Kaye W H 1995 Neurotransmitters and anorexia nervosa. In: Brownell K D, Fairburn C G (eds.) Eating Disorders and Obesity: A Comprehensive Handbook. Guilford, New York
- Kennedy E, Goldberg J 1995 What are American children eating? Implications for public policy. Nutrition Reviews 53: 111–26
- Kral J G 1995 Surgical interventions for obesity. In: Brownell K D, Fairburn C G (eds.) Eating Disorders and Obesity: A Comprehensive Handbook. Guildford, New York
- Logue A W 1991 The Psychology of Eating and Drinking: An Introduction. Freeman, New York
- Mitchell J E Medical complications of bulimia nervosa. In: Brownell K D, Fairburn C G (eds.) Eating Disorders and Obesity: A Comprehensive Handbook. Guilford, New York
- Ravussin E, Lillioja S, Knowler W C, Christin L, Freymond D, Abbott W G H, Boyce V, Howard B V, Bogardus C 1988 Reduced rate of energy expenditure as a risk factor for body-weight gain. New England Journal of Medicine 318: 467–472
- Rossner S 1998 Why prevention of obesity has become necessary—A foreword. Appetite 31: 407–36
- Sjostrom 1980 Fat cells and body weight. In: Stunkard A J (ed.) Symposium on Obesity: Basic Mechanisms and Treatment. Saunders, Philadelphia, PA
- Steinhausen H-C 1995 The course and outcome of anorexia nervosa. In: Brownell K D, Fairburn C G (eds.) Eating Disorders and Obesity: A Comprehensive Handbook. Guilford, New York
- Strober M 1995 Family-genetic perspective on anorexia nervosa and bulimia nervosa. In: Brownell K D, Fairburn C G (eds.) Eating Disorders and Obesity: A Comprehensive Handbook. Guilford, New York
- Van Buskirk S S 1977 A two-phase perspective on the treatment of anorexia nervosa. Psychology Bulletin 84: 529–38
- Walsh B T 1995 Pharmacotherapy of eating disorders. In: Brownell K D, Fairburn C G (eds.) Eating Disorders and Obesity: A Comprehensive Handbook. Guilford, New York
- Williamson D F 1995 Prevalence and demographics of obesity. In: Brownell K D, Fairburn C G (eds.) Eating Disorders and Obesity: A Comprehensive Handbook. Guilford, New York