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OBESITY AND ESOPHAGEAL CANCER byValentino John Bianco IIIBA, Mercyhurst College, 2005DO, Midwestern University, 2012Submitted to the Graduate Faculty ofGraduate School of Public Health in partial fulfillment of the requirements for the degree of Master of Public Health University of Pittsburgh2014UNIVERSITY OF PITTSBURGHGRADUATE SCHOOL OF PUBLIC HEALTHThis essay is submittedbyValentino BiancoonAugust 6, 2014and approved byEssay Advisor:David Finegold, MD ______________________________Multidisciplinary MPH Program DirectorHuman GeneticsGraduate School of Public Health University of PittsburghEssay Reader:Arjun Pennathur, MD______________________________Assistant Professor of Cardiothoracic surgery Department of Cardiothoracic Surgery University of Pittsburgh Medical CenterCopyright ? by Valentino J. Bianco2014David N. Finegold, MDOBESITY AND ESOPHAGEAL CANCERValentino Bianco, MPH University of Pittsburgh, 2014ABSTRACTThe widespread prevalence of obesity is one of the most pressing matters of international public health importance in the present day. In the United States the amount of people either obese or overweight has reached epidemic proportions. There is growing empirical evidence that suggests that obesity is responsible for nearly one-quarter of all cancers. Numerous studies have supported the correlation between obesity and/or increased BMI and esophageal disease. The incidence of esophageal adenocarcinoma (EAC) has rapidly increased in the United States over the past thirty years and there is a strong association between body mass index (BMI) and esophageal adenocarcinoma. There is currently an urgent need for the implementation of preventive public health measures to quell the growing obesity crisis and reduce the incidence of esophageal cancer.TABLE OF CONTENTSINTRODUCTION ............................................................................................................1THE OBESITY EPIDEMIC.................................................................................2OBESITY AND CANCER……………………………………………………....3Cancer prevalence………………………………………………………..4Biological mechanisms…………………………………………………...5ESOPHAGEAL CANCER………………………………………………………………6RISK FACTORS FOR ESOPHAGEAL ADENOCARCINOMA……………8GERD and Obesity……………………………………………………....8Obesity / BMI / Barrett’s Esophagus………………………………....10Intra-gastric Pressure…………………………………………………..11OBESITY AND ESOPHAGEAL ADENOCARCINOMA……………..…...12PREVENTION…………………………………………………………………………15CONCLUSION…………………………………………………………………………18BIBLIOGRAPHY………………………………………………………………………………19 INTRODUCTIONThe widespread prevalence of obesity is one of the most pressing international public health crises in the present day. In the United States the amount of people either obese or overweight has reached epidemic proportions at approximately 65% of the population.1 The rapid rise in obesity has resulted in serious concern from medical professionals for the detrimental health consequences.2 There has been evidence showing an association between obesity and a number of cancers including esophageal, colon, thyroid, renal, liver, prostate, breast, and endometrial neoplasm; among others.3 The incidence of esophageal adenocarcinoma (EAC) has rapidly increased in the United States over the past thirty years. Among white men and women, EAC has increased by >450% and >300%, respectively.4 Rapid rise in the incidence of EAC has increased in parallel with the obesity epidemic in the United States. A strong linear relationship between increased BMI and esophageal adenocarcinoma has been identified.5 Surgical removal of the esophagus (esophagectomy) is currently the standard of care for early stage esophageal cancer. However, there is a high morbidity and mortality associated with esophagectomy, including mortality rates as high as 23% in low volume hospitals.6 Obesity is a largely modifiable risk factor for EAC, which may be significantly reduced with the diligent implication of lifestyle changes. Therefore, it is crucial for public health professionals, physicians, oncologists, and surgeons to join efforts in the promotion of healthy living and preventive medicine to reduce the current obesity epidemic and its numerous adverse consequences.1.1 THE OBESITY EPIDEMICIt comes as no surprise that obesity is currently considered one of the most frequently recognized public health issues affecting American’s.7 It has been reported that obesity has doubled in children and adults and tripled in adolescents in the past two decades. Obesity has had an immense impact on population mortality and health care costs in the United States, with an annual death toll of 400,000 deaths and cost of $117 billion.7There is an ongoing effort to identify the causal factors which are associated with the rise in obesity. The factors affecting lifestyle habits that may predispose to being overweight are multiple, but commonly cited contributors include calorie-rich foods, increased meal portion sizes, excessive television use, and a lifestyle which is generally sedentary in nature. Currently, health care providers along with the public health community have had little success at convincing overweight individuals to lose weight.7 If the difficulty in curbing the obesity epidemic remains, the future health state of the general population will likely remain in substandard condition. A recent study by Duke University estimated that there will be a 33% increase in the prevalence of obesity and a 130% increase in the prevalence of severe obesity over the next two decades.8Obesity has long been associated with numerous health conditions. The “all cause” risk of death from obesity related diseases including cardiovascular disease and cancer, along with other diseases, increases throughout the range from moderate to severely overweight individuals for all age groups in both males and females.9 The associated risk between increased BMI and mortality is more prominent in Caucasians as compared to the Black population .9 The overall prevalence of cardiovascular disease remains high and increases among those who are overweight or obese.10 The cardiovascular health consequences of obesity include congestive heart disease, arrhythmias, stroke, coronary artery disease and sudden cardiac death.11 From 2007-2010, cardiovascular risk factors were substantially higher in obese individuals compared to those of a normal weight.10 Fifty percent of obese adults had dyslipidemia, 36% had hypertension, and 18% had diabetes. The presence of cardiovascular risk factors was even higher in the morbidly obese subset. Type II diabetes is also commonly associated with obesity. Mortality due to diabetes is expected to increase by 50% in the next decade.12 The projected rise in mortality is due in part to both increased prevalence of childhood obesity and ‘metabolic syndrome’, a syndrome commonly associated with obesity. There is currently “urgent need” for novel approaches to address type II diabetes and obesity.12 All of these adverse effects of obesity are of serious health concern and there is a growing need to address the importance of practicing daily prevention targeted at reducing excess body weight.1.2OBESITY AND CANCERThe impact of heightened body weight and obesity goes far beyond the known health risks of cardiovascular disease and diabetes and has been said to account for 20 percent of all cases of cancer.3 Some estimates of the current patterns of obesity in the United States have indicated that 14 percent of all cancer deaths in men and 20 percent of all cancer deaths in women can be attributed to being overweight or obese.13 1.2.1Cancer prevalenceObesity and increased BMI are strongly associated with a number of different types of cancer. A recent systematic review and meta-analysis reviewed 221 datasets (141 articles) including a total of 282,137 incident cancer cases.14 Results were categorized based upon cancer in men and women. In men, there was a strong association between a 5 kg/m2 increase in BMI and cancer incidence including esophageal adenocarcinoma, renal, thyroid, and colon cancers (p <0.0001). In women, a 5 kg/m2 increase in BMI was strongly associated with esophageal adenocarcinoma, endometrial, and renal cancers (p <0.0001). Gallbladder cancer was also associated (p <0.04) with increasing BMI. The associated risk of renal cell cancer, although previously considered to be a stronger association in the female gender, indicates equal risk in both men and women.15 An analysis of 8 cohort and 3 case control studies including a total of 3288 cases confirmed an association between increased BMI and gallbladder cancer.16 The risk of developing gallbladder cancer is 15% higher in overweight individuals and 66% higher in those who are obese as compared to those of a normal weight. There has been shown to be a greater association between obesity and gallbladder cancer in women, compared to men.16 There is currently evidence accumulating that shows that the risk of developing pancreatic cancer is increased in the obese population and in those with a high BMI.17 A number of factors potentially contribute to the development of pancreatic cancer but obesity is one of the few risk factors that is considered to be modifiable via lifestyle changes. Further, obesity is a risk factor for diabetes which, in turn, increases the risk for pancreatic cancer. Therefore, preventative medicine may play an important role in lessening the potential development of pancreatic cancer by intervening and preventing obesity in populations. The importance of implementing preventative medicine to thwart obesity-related cancer will serve an increasingly important role in present and future healthcare efforts.1.2.2Biological mechanismsIn order to gain an understanding of the potential biological mechanisms responsible for obesity-related cancer, it is necessary to separate obesity into its component parts: adipose tissue, which is composed of adipocytes. The adipocyte is a cell with the inherent capability to store excess energy in lipid form, which can be efficiently utilized during times of metabolic demand. The ability to respond to metabolic needs has given the adipocyte the potential to drastically increase in size over a relatively short period of time; a transformation that typically requires a phenotypic change in other cells in the body.18 In response to signals from both central and peripheral organs, adipocytes are capable of secreting numerous adipocyte specific proteins, known as adipokines. Adipose tissue plays a prominent role by integrating signals from organs and responding through the secretion of proteins. Adipocytes have effects throughout the body and play a large role in maintaining metabolic homeostasis. Therefore, when adipose tissue is dysregulated the result can be far-reaching, negative consequences to the normal system (Rajala 2003).18 Adipocytes have been the target for recent interest in obesities role in tumor initiation, growth, and metastasis.19 Two primary reasons for emerging interest in the link between adipose tissue and cancer have been proposed: 1) the current epidemiological studies that have demonstrated associations between cancer and obesity; 2) the tumor microenvironment of breast cancer and malignancies that have metastasized to the abdomen is largely composed of adipocytes which promote tumor growth.19 There are similarities between the microenvironment composed of numerous adipocytes in tumors and the function of adipocytes in the pathology of type II diabetes; both of which have similar histological features including the presence of macrophages and inflammatory cells known to secrete inflammatory cytokines.19 Proposed biological mechanisms for the cancer risk associated with obesity include but are not limited to chronic hyperinsulinaemia, growth hormone and insulin-like growth factor 1(IGFI), endogenous sex steroids, and non-alcoholic fatty liver disease.20 Tumorigenic effects of increased insulin levels may be a result of insulin receptors located within the (pre)neoplastic target cells. Insulin’s ability to alter endogenous hormone levels and chronic hyperinsulinemia may also be viable explanations for the association between obesity, insulin levels, and cancer. Epidemiological evidence supports the association between increased serum levels of IGF1 and heightened cancer risk. The bioavailability and synthesis of endogenous sex hormones is directly influenced by adipose tissue. Estrogens, progesterone, and androgens are all influenced by adiposity through numerous mechanisms. Breast, endometrial, and prostate cancer have been associated with the alternations in endogenous sex steroids as a result of adiposity.20 Therefore, the evidence suggests that there are a several potential biological etiologies that may account for the obesity/cancer association.2.0ESOPHAGEAL CANCEREsophageal cancer is currently one of the most aggressive malignancies known to medicine. The global impact of this pernicious upper GI cancer is presently affecting over 450,000 people worldwide.21 Depending on the histology and stage at the time of diagnosis, esophageal cancer has an invariably poor prognosis with 5 year survival rates ranging from 15-25%.21 The incidence of esophageal adenocarcinoma is rapidly rising and without significant medical intervention the international medical community will have to face a rising mortality rate. Esophageal cancer can present differently depending on what cellular type the patient has. Squamous cell carcinoma and adenocarcinoma are the two main histological types of esophageal cancer. Squamous cell carcinoma is the predominant type worldwide, but adenocarcinoma has become more prevalent in certain nations and is currently of higher incidence than squamous cell in the United States and other western countries. The major risk factors for esophageal cancer include tobacco, alcohol, and obesity.22 However, risk factors do vary depending on what specific histological type the cancer is. Tobacco use and alcohol consumption are often considered major risk factors for squamous cell cancer. Gastroesophageal reflux disease (GERD) and obesity are risk factors for esophageal adenocarcinoma. These two histologies present differently during symptomatology and diagnosis. Squamous cell carcinoma is most often found in the proximal to mid esophagus and adenocarcinoma is typically found in the distal esophagus (GEJ). Further, there is also a histological difference with respect to race. Black males are more likely to get squamous cell carcinoma and white males are more frequently diagnosed with adenocarcinoma.The gastroesophageal junction (GEJ) is a crucial anatomical point in the understanding of one of the primary initiating pathological events of adenocarcinoma of the esophagus. Incompetence of the GEJ can predispose one to gastroesophageal reflux disease (GERD). GERD is a condition where gastric contents flow in a retrograde fashion back up into the esophagus. The substance that is refluxed into the esophagus from the stomach is composed of highly acidic content due to the elevated concentration of hydrochloric acid (HCL) which is present in gastric secretions. Although HCL is advantageous for the breakdown of food in the stomach, it causes potentially harmful cellular changes in the esophagus. The lining of the esophagus is placed under considerable cellular stress from high concentrations of acid. The acidic environment in the distant esophagus forces an adaptive change on a cellular/histological level. This condition, also known as Barrett Esophagus (Barrett’s), is a shift in histological morphology from the normal stratified squamous cell lining of the esophagus to metaplastic columnar epithelium.23 This histological metamorphosis helps the distal esophagus survive the newly acidic environment by changing morphology to mimic the cellular lining of the stomach. Simple columnar and goblet cells are better equipped to thrive in a highly acidic environment. The potential for malignancy increases when the metaplastic cells become dysplastic. This cellular dysplasia often serves as a precursor to the malignant cells of esophageal adenocarcinoma. The histopathological change of Barrett’s esophagus is manifested by a reddish colored mucosal lining in the distal esophagus that transitions into the normal healthy stratified columnar cells of the esophagus. 2.1 RISK FACTORS FOR ESOPHAGEAL ADENOCARCINOMA2.1.1 GERD and ObesityGastroesophageal reflux disease (GERD) is a common disease affecting between 10% - 20% of the adult population in the United States.24 The complications (Barrett esophagus, erosive esophagitis, and esophageal adenocarcinoma) related to GERD are becoming more prevalent in both the United States and Western Europe.24 The prevalence of GERD is rising and one of the major factors that could be contributing is the concurrent rise in the prevalence of obesity.25 Known factors that play a role in pathophysiology of GERD include visceral adipose tissue, central obesity, esophageal motor disorders, increased intra-abdominal pressure, and variations in the frequency of lower esophageal sphincter relaxation .25Numerous studies have supported the correlation between obesity and/or increased BMI and esophageal disease. A recent meta-analysis analyzed the results of 9 studies that examined the association between BMI and GERD symptoms.24 Six of the 9 studies found statistically significant associations. Six of 7 studies indicated that there was a significant association between BMI and both erosive gastritis and esophageal adenocarcinoma. There was a “dose-response” relationship noted in 8 studies where-by increased BMI translated to heightened risk for esophageal cancer. Similar findings were reported in a study which examined a morbidly obese population to define the relationship between GERD and BMI.26 A total cohort of 30 morbidly obese patients who initially presented for bariatric surgery were assessed to identify both objective findings and symptoms as evidence of GERD. Patients underwent esophageal function testing including manometry (n=30) and pH monitoring (n=28). A statistically significant (p <0.01) correlation was found between an increase in patient weight and an increase in esophageal acid exposure. Both an increase in the number of reflux episodes and amount of acid exposure were correlated with increasing BMI (p < 0.05). Furthermore, there was significantly increased lower esophageal pressure in patients with normal esophageal acid exposure (p <0.05).In an analysis of a multiphasic cohort assessing abdominal obesity of patients from members of the Kaiser Permanente health plan, it was found that there was an independent association between reflux symptoms and abdominal diameter in white subjects; however, this association was not present for either blacks or Asians.27 There was an association between gastro-esophageal (GERD) symptoms and BMI; this association was more pronounced in white subjects. The presence of abdominal obesity occurred more commonly in men. It was concluded that obesity may be responsible for a disproportional increase in GERD symptoms in white males.27 2.1.2 Obesity / BMI / Barrett’s EsophagusThe use of anthropomorphic measurements, often used to estimate the BMI and body fat of an individual, are a convenient way to objectively quantify body weight variations in patient populations. A case-control study was performed consisting of 193 cases with newly diagnosed specialized intestinal metaplasia on ≥ 1 of 4 biopsies.28 Anthropometric measurements were taken for all patients and an analysis was performed to measure associated risk between BMI, central obesity, smoking, and Barrett’s esophagus (BE). Waist-to-hip (WHR) and waist-to-thigh (WTR) were used as measurements for obesity. After potential confounders (age, race, gender, education, smoking, alcohol) were taken into account, it was found that central adiposity was strongly associated with risk factors for BE. Interestingly, when GERD symptoms were controlled for, the strength of the association between WHR and BE did not diminish. This may suggest that a “substantial proportion” of the association between obesity, BE, and esophageal adenocarcinoma is due to factors other than GERD.28 Some risk factors (i.e. abdominal obesity) may be independent from general BMI measurements. A case control study was performed consisting of 320 cases of Barrett’s esophagus, 316 patients with GERD and 317 controls which assessed the relationship between BMI, abdominal obesity and Barrett’s Esophagus.29 There was an association between larger abdominal circumference and Barrett’s, independent of BMI. Furthermore, there was an association between the severity of GERD symptoms and abdominal circumference; per 10 cm circumference. Waist circumference, but not BMI, was independently associated with the risk of Barrett’s.29 This supports the hypothesis that abdominal obesity is a contributing factor for GERD.2.1.3Intra-gastric PressureIn addition to anthropomorphic measurements, biomechanical changes in the stomach and esophagus including frequency of lower esophageal sphincter relaxation and intra-gastric pressure have been utilized as ways to identify associations between obesity and GERD. Transient [postprandial] lower esophageal sphincter relaxation (TLOSR) was assessed in three different groups of patients; obese patients (BMI >30), overweight patients (BMI 25-30), and patients who were normal weight (BMI ≥20 <25).30 It was found that during the 2hr post-prandial (after eating) period obese and overweight patients had a significantly higher rate of transient lower esophageal sphincter relaxations (p < .001). Furthermore, the proportion of patients who had TLOSR and acid reflux was significantly associated with both the obese and overweight groups as compared to the normal weight group (p <.001). There was a strong correlation between anthropomorphic (BMI, waist circumference) measurements and the rate of TLOSRs. It was concluded that abnormal post-prandial TLOSR may be an initiating event in the pathogenesis of GERD. In addition to esophageal sphincter relaxation, variations in intragatric pressure have been shown to influence cancer risk. There has been shown to be a weak positive correlation between both waist circumference (r = 0.11, p = 0.06) and BMI (r = 0.11, p = 0.05) with intragastric pressure. 31 Approximately a 10% increase in intragastric pressure for each unit increase in BMI has been demonstrated.31 2.2OBESITY AND ESOPHAGEAL ADENOCARCINOMAA direct correlation between increased BMI and esophageal adenocarcinoma has been established.5 A recent consortium analysis of pooled individual data has provided convincing results that show a linear association between increasing BMI and both EAC and esophagogastric junction adenocarcinoma.5 Cancer risk was significantly higher than predicted in an additive model for obese individuals with a history of GERD; suggesting a synergistic relationship between GERD and BMI.5An association between esophageal adenocarcinoma or gastric cardia adenocarcinoma and body mass index (BMI) has been identified.32 A homogenous positive association was shown between increased BMI and esophageal adenocarcinoma using cancer location and BMI category (Overweight, Obese). As BMI increases, the strength of association with the development of esophageal adenocarcinoma increases and there is a trend indicating a stronger association in men compared to women.32 It has been demonstrated that the association between increased BMI and incidence of gastric cardia adenocarcinoma is not as pronounced as that for BMI and esophageal adenocarcinoma. 32When assessing obesity as a potential risk factor for esophageal cancer it is important to take into consideration anthropometric variations and fat distribution in the study cohort. A nested case-control study consisting of 206,974 patients using the Kaiser Permanente multiphasic health checkup cohort indicates the importance of anthropometric measurements.33 All members of the cohort were given extensive questionnaires and detailed examinations which included anthropometric and BMI measurements. During the follow-up time period there were 144 cases of esophageal squamous cell carcinoma, 105 cardia adenocarcinomas, and 101 esophageal adenocarcinomas. There was a strong association between increasing abdominal diameter and heightened risk of esophageal adenocarcinoma. However, there was no association between abdominal diameter and the risk of gastric cardia adenocarcinoma or squamous cell carcinoma. It is important to note that the association between increasing abdominal diameter and EAC was independent of BMI. Therefore, since males more commonly experience abdominal obesity, the increasing obesity epidemic may disproportionately increase the risk of developing esophageal adenocarcinoma in men, as compared to women. This evidence suggests the importance of modifying abdominal obesity in the population by taking the necessary steps for weight reduction. Not all findings are consistent with the heightened cancer risk being associated with specific anthropometric findings. A multivariate analysis was performed testing for associations between anthropometric measures and BMI as risk factors for esophageal adenocarcinoma (EAC) and squamous cell carcinoma (ESCC) among 346,554 participants in the European Prospective Investigation into Cancer and Nutrition (EPIC).34 Over a follow-up time of 8.9 years, 88 cases of EAC and 110 cases of ESCC were identified. There was a positive association between EAC and BMI, waist-to-hip ratio (WHR) and waist circumference. However, BMI and waist circumference were inversely associated with ESCC. Body fat distribution was not predictive of EAC risk beyond obesity in a general sense.34 After “mutually” adjusting for BMI WHR, and waist circumference anthropometric measurements were no longer significantly associated with EAC risk. Therefore, it appears that general adiposity may be a more relevant factor than specific fat distribution measurements in determining EAC risk.34It is important to consider other possible risk factor that may confound the association between obesity and esophageal adenocarcinoma. Multiple potential risk factors were assessed in a study that was part of the European Prospective Investigation of Cancer-Norfolk (EPIC-Norfolk) that took place between 1993 and 1997 consisted of 24,068 patients ages 39-79.35 The primary aim of this study was to define whether or not there was a correlation between alcohol, BMI, and smoking with the development of BE and EAC. There was no associated risk between either smoking or alcohol consumption and the development of BE. For patients with EAC, although there was an association with all BMIs, there was only statistical significance for the highest category (>35 kg/m2). A case control study was performed between 2002 and 2005 which included patients with esophageal adenocarcinoma (EAC ; n = 364), gastroesophageal junction adenocarcinoma (GEJAC; n = 425), and a control group ( n = 1,580).36 An attempt was made to quantify the three major risk factors associated with EAC and GEJAC; smoking, BMI, and gastroesophageal reflux (GER). It was found that a combination of BMI, smoking, and GER together accounted for 76% of EAC cases and 69% of GEJAC cases. Analyzed individually, increased BMI (>30) and frequent acid reflux (≥1/week) were the factors primarily accountable for EAC risk (23% and 36%, respectively). The greatest proportion of GEJAC was associated with smoking (43%) and frequent symptoms of acid reflux (28%). For the combination of all cases, symptoms of acid reflux accounted for the greatest (49%) population attributable fraction. Three risk factors accounted for cancer risk in more than 2/3 of the population being studied in this article. Smoking cessation and maintaining a healthy BMI can largely prevent the development of esophageal cancer. Since the majority of esophageal cancer risk comes from modifiable risk factors, there is a strong potential to significantly limit disease in the population through taking preventive public health measures.PREVENTIONPrevention and health protection measures are grossly neglected on a nation scale, accounting for less than 5% of the United States’ health services spending .37 There is an increasing need for preventive medicine to play a major role in the public health effort to reduce the national incidence of obesity. Public health officials, as well as thoracic surgeons, should be encouraged that some of the major etiological factors for esophageal adenocarcinoma (EAC) including increased BMI and obesity, are largely modifiable risk factors. Numerous preventive measures have been taken to reduce the incidence of EAC including endoscopic surveillance, screening, and chemoprevention.21 Endoscopic screening is often recommended for patients who have symptoms of chronic gastroesophageal reflux disease in an effort to identify Barrett’s esophagus.38 Ongoing endoscopic surveillance with tissue biopsies is performed for those with Barrett’s esophagus in order to monitor the patients for potential progression to malignancy.38 A single strategy for endoscopic screening and surveillance is not currently universally accepted as the standard of care. There is a patient-centered trial underway with the primary aim of assessing the comparative effectiveness of varying endoscopic strategies and surveillance vs. no surveillance for patients with Barrett’s esophagus. 39 In addition to preventive endoscopic measures, clinicians are investigating other potential strategies for esophageal cancer including chemoprevention. A study assessing riboflavine, retinol, and zinc was unable to show conclusive evidence of effective prevention.40 Interestingly, a recent trial for esophageal and colon cancer prevention indicated that freeze-dried berries and berry components may be effective at inhibiting phases of tumor development including initiation and promotion/progression . 41 It stands to reason, since there is a strong association between increasing BMI and EAC, that preventing obesity would aid in reducing the incidence of esophageal malignancy. The International Agency for Research on Cancer (IARC) has deemed that there is “sufficient” evidence linking excess body weight to increased risk for a number of malignancies including esophageal adenocarcinoma.42 Furthermore, excess body weight and physical inactivity contribute to heightened cancer risk.43 In order to properly assess the necessary preventive measures for obesity it is important to realize the continual influence and pressure placed on individual lifestyle choices based on societal trends. A common “misconception” is that the choices people make regarding what they eat are conscious decisions.44 A poignant example of marketing influence that governs unconscious or “spur-of-the-moment” food purchasing decisions is the placement of candy at the cash register.44 The easily accessible sugary/salty/fatty food is strategically placed to influence purchasing power and only adds to the difficulty of avoiding unnecessary calories. The restaurant industry can also be targeted as a potential area for improving obesity prevention. Failure to provide the nutritional content on menus and increased portion sizes for food prepared outside of homes, have likely contributed to the current obesity crisis.45,46 Portion sizes have continued to grow since the 1970s and continued to rise in parallel to increasing body weight.45 A survey assessing consumer perception of the relative nutritional value of restaurant meals indicated that participants drastically misjudged the fat and caloric content of menu items, with actual levels being approximately twice consumer estimates.46 Subsequent experiments indicated that providing the nutritional content of foods significantly influenced what customer’s purchased.46 Therefore, public health efforts should focus on reducing portion sizes, promotion of consuming smaller meals, and providing nutritional content on restaurant menus.45,46The national public health initiative would benefit from improvements in both academic research and clinical settings. There is currently a need for greater emphasis on the management of overweight patients for new primary care physicians.47 Physicians in training should have more time dedicated to developing a solid background of the pathophysiological mechanisms involved with obesity. 47 Both the University of Michigan and UCSF have included pre-clinical curriculum dedicated to enhancing the medical students understanding of nutrition and obesity.47 Furthermore, large improvements in funding for public health research for effective interventions and cost effectiveness are needed.37 Indicating some progress, a $30 million dollar Health Protection Research Initiative plan that will focus on cost-effectiveness in wellness programs was recently announced by the CDC.37 Future studies of this nature will serve to benefit the effort by the public health community and enhance the efficiency with which patients receive preventive healthcare.4.0CONCLUSIONTraditionally, the success of medical therapy is judged by the immediate result of treatment. Obesity is an elusive disease in that it develops over a long period of time and is influenced by multiple factors. Therefore, there is no well-established treatment for obesity that will yield quick results. It is crucial to implement preventive measures immediately in an attempt to change the growing obesity epidemic. Lifestyle changes including physical exercise, good nutrition, and altering daily habits play important roles in fighting increased body weight. In order to gain lasting results at treating obesity, the medical community as a whole must push for a paradigm shift in healthcare which places large emphasis on preventive medicine. The current obesity crisis in the United States has numerous serious consequences including cardiovascular disease, type II diabetes, and several cancers. Evidence is beginning to accumulate which shows a strong link between obesity and esophageal adenocarcinoma. 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