Table 1.

Obesity* and the Risk of Esophageal Adenocarcinoma

Vial, M., Grande, L. & Pera, M. Epidemiology of adenocarcinoma of the esophagus, gastric cardia, and upper gastric third. Recent Results Cancer Res. 182, 1-17 (2010).
Lagergren, J. & Lagergren, P Oesophageal cancer. BMJ 341, c6280 (2010).
Sharma, P Clinical practice. Barrett's esophagus. N. Engl. J. Med. 361, 2548-2556 (2009).
Badreddine, R. J. & Wang, K. K. Barrett esophagus: an update. Nat. Rev. Gastroenterol. Hepatol. 7, 369-378 (2010).
Kahrilas, P. J. Clinical practice. Gastroesophageal reflux disease. N. Engl. J. Med. 359, 1700-1707 (2008).
WHO. Obesity: Preventing and Managing the Global Epidemic. Report of a WHO Consultation (Stationery Office Books, London, 2000).
Jaffrin, M. Y. Body composition determination by bioimpedance: an update. Curr. Opin. Clin. Nutr. Metab. Care 12, 482-486 (2009).
Andreoli, A., Scalzo, G., Masala, S., Tarantino, U. & Guglielmi, G. Body composition assessment by dual-energy X-ray absorptiometry (DXA). Radiol. Med. 114, 286-300 (2009).
Brown, L. M. et al. Adenocarcinoma of the esophagus: role of obesity and diet. J. Natl Cancer Inst. 87, 104-109 (1995).
Vaughan, T. L., Davis, S., Kristal, A. & Thomas, D. B. Obesity, alcohol, and tobacco as risk factors for cancers of the esophagus and gastric cardia: adenocarcinoma versus squamous cell carcinoma. Cancer Epidemiol. Biomarkers Prev. 4, 85-92 (1995).
Chow, W. H. et al. Body mass index and risk of adenocarcinomas of the esophagus and gastric cardia. J. Natl Cancer Inst. 90, 150-155 (1998).
Whiteman, D. C. et al. Combined effects of obesity, acid reflux and smoking on the risk of adenocarcinomas of the oesophagus. Gut 57, 173-180 (2008).
Lindblad, M., Rodríguez, L. A. & Lagergren, J. Body mass, tobacco and alcohol and risk of esophageal, gastric cardia, and gastric non-cardia adenocarcinoma among men and women in a nested case-control study. Cancer Causes Control 16, 285-294 (2005).
Engeland, A., Tretli, S. & Bj0rge, T. Height and body mass index in relation to esophageal cancer; 23-year follow-up of two million Norwegian men and women. Cancer Causes Control 15, 837-843 (2004).
Merry, A. H., Schouten, L. J., Goldbohm, R. A. & van den Brandt, P. A. Body mass index, height and risk of adenocarcinoma of the oesophagus and gastric cardia: a prospective cohort study. Gut 56, 1503-1511 (2007).
Abnet, C. C. et al. A prospective study of BMI and risk of oesophageal and gastric adenocarcinoma. Eur. J. Cancer 44, 465-471 (2008).
Löfdahl, H. E., Lu, Y. & Lagergren, J. Sex-specific risk factor profile in oesophageal adenocarcinoma. Br. J. Cancer 99, 1506-1510 (2008) .
Chak, A. et al. Assessment of familiality, obesity, and other risk factors for early age of cancer diagnosis in adenocarcinomas of the esophagus and gastroesophageal junction. Am. J. Gastroenterol. 104, 1913-1921 (2009).
Calle, E. E., Rodriguez, C., Walker-Thurmond, K. & Thun, M. J. Overweight, obesity, and mortality from cancer in a prospectively studied cohort of, U. S. adults. N. Engl. J. Med. 348, 1625-1638 (2003).
Renehan, A. G., Tyson, M., Egger, M., Heller, R. F. & Zwahlen, M. Body-mass index and incidence of cancer: a systematic review and meta-analysis of prospective observational studies. Lancet 371, 569-578 (2008).
Lagergren, J., Bergstrom, R. & Nyrén, O. Association between body mass and adenocarcinoma of the esophagus and gastric cardia. Ann. Intern. Med. 130, 883-890 (1999).
Samanic, C., Chow, W. H., Gridley, G., Jarvholm, B. & Fraumeni, J. F. Jr Relation of body mass index to cancer risk in 362,552 Swedish men. Cancer Causes Control 17, 901-909 (2006).
Nordenstedt, H. & El-Serag, H. The influence of age, sex, and race on the incidence of esophageal cancer in the United States (19922006). Scand. J. Gastroenterol. doi:10.3109/00365521.2011.551890.
Lagergren, J. & Mattsson, F. No further increase in the incidence of esophageal adenocarcinoma in Sweden. Int. J. Cancer doi:10.1002/ ijc.25701.
Lagergren, J., Bergström, R., Lindgren, A. & Nyrén, O. Symptomatic gastroesophageal reflux as a risk factor for esophageal adenocarcinoma. N. Engl. J. Med. 340, 825-831 (1999).
MacInnis, R. J., English, D. R., Hopper, J. L. & Giles, G. G. Body size and composition and the risk of gastric and oesophageal adenocarcinoma. Int. J. Cancer 118, 2628-2631 (2006).
Steffen, A. et al. Anthropometry and esophageal cancer risk in the European prospective investigation into cancer and nutrition. Cancer Epidemiol. Biomarkers Prev. 18, 2079-2089 (2009) .
Corley, D. A., Kubo, A. & Zhao, W. Abdominal obesity and the risk of esophageal and gastric cardia carcinomas. Cancer Epidemiol. Biomarkers Prev. 17, 352-358 (2008).
Beddy, P et al. Association of visceral adiposity with oesophageal and junctional adenocarcinomas. Br. J. Surg. 97, 1028-1034 (2010) .
Lagergren, J., Ye, W., Bergström, R. & Nyrén, O. Utility of endoscopic screening for upper gastrointestinal adenocarcinoma. JAMA 284, 961-962 (2000).
Ortiz, V. et al. Value of heartburn for diagnosing gastroesophageal reflux disease in severely obese patients. Obesity (Silver Spring) 14, 696-700 (2006).
Küper, M. A. et al. Dysfunction of the lower esophageal sphincter and dysmotility of the tubular esophagus in morbidly obese patients. Obes. Surg. 19, 1143-1149 (2009).
McElholm, A. R. et al. A population-based study of IGF axis polymorphisms and the esophageal inflammation, metaplasia, adenocarcinoma sequence. Gastroenterology 139, 204-212 (2010).
MacDonald, K., Porter, G. A., Guernsey, D. L., Zhao, R. & Casson, A. G. A polymorphic variant of the insulin-like growth factor type I receptor gene modifies risk of obesity for esophageal adenocarcinoma. Cancer Epidemiol. 33, 37-40 (2009) .
Ogunwobi, O. O. & Beales, I. L. Leptin stimulates the proliferation of human oesophageal adenocarcinoma cells via HB-EGF and Tgfa mediated transactivation of the epidermal growth factor receptor. Br. J. Biomed. Sci. 65, 121-127 (2008).
Brochu-Gaudreau, K. et al. Adiponectin action from head to toe. Endocrine 37, 11-32 (2010).
Howard, J. M. et al. Associations between leptin and adiponectin receptor upregulation, visceral obesity and tumour stage in oesophageal and junctional adenocarcinoma. Br. J. Surg. 97, 1020-1027 (2010).
Doecke, J. D. et al. Single nucleotide polymorphisms in obesity-related genes and the risk of esophageal cancers. Cancer Epidemiol. Biomarkers Prev. 17, 1007-1012 (2008).
Stein, D. J., El-Serag, H. B., Kuczynski, J., Kramer, J. R. & Sampliner, R. E. The association of body mass index with Barrett's oesophagus. Aliment. Pharmacol. Ther. 22, 1005-1010 (2005).
Smith, K. J. et al. Interactions among smoking, obesity, and symptoms of acid reflux in Barrett's esophagus. Cancer Epidemiol. Biomarkers Prev. 14, 2481-2486 (2005).
Healy, L. A., Ryan, A. M., Pidgeon, G., Ravi, N. & Reynolds, J. V. Lack of differential pattern in central adiposity and metabolic syndrome in Barrett's esophagus and gastroesophageal reflux disease. Dis. Esophagus 23, 386-391 (2010) .
Gerson, L. B. et al. Does body mass index differ between patients with Barrett's oesophagus and patients with chronic gastro-oesophageal reflux disease? Aliment. Pharmacol. Ther. 25, 1079-1086 (2007).
Corley, D. A. et al. Abdominal obesity and body mass index as risk factors for Barrett's esophagus. Gastroenterology 133, 34-41 (2007) .
Smith, K. J. et al. Current and past smoking significantly increase risk for Barrett's esophagus. Clin. Gastroenterol. Hepatol. 7, 840-848 (2009).
Edelstein, Z. R., Farrow, D. C., Bronner, M. P., Rosen, S. N. & Vaughan, T. L. Central adiposity and risk of Barrett's esophagus. Gastroenterology 133, 403-411 (2007).
Caygill, C. P. et al. Lifestyle factors and Barrett's esophagus. Am. J. Gastroenterol. 97, 1328-1331 (2002).
El-Serag, H. B., Kvapil, P., Hacken-Bitar, J. & Kramer, J. R. Abdominal obesity and the risk of Barrett's esophagus. Am. J. Gastroenterol. 100, 2151-2156 (2005).
Akiyama, T. et al. Visceral obesity and the risk of Barrett's esophagus in Japanese patients with non-alcoholic fatty liver disease. BMC Gastroenterol. 9, 56 (2009).
Rubenstein, J. H. et al. A pilot study of the association of low plasma adiponectin and Barrett's esophagus. Am. J. Gastroenterol. 103, 1358-1364 (2008).
Sowers, J. R. Endocrine functions of adipose tissue: focus on adiponectin. Clin. Cornerstone 9, 32-38 (2008).
Rubenstein, J. H. et al. Association of adiponectin multimers with Barrett's oesophagus. Gut 58, 1583-1589 (2009).
Ryan, A. M. et al. Barrett esophagus: prevalence of central adiposity, metabolic syndrome, and a proinflammatory state. Ann. Surg. 247, 909-915 (2008) .
Kendall, B. J. et al. Leptin and the risk of Barrett's oesophagus. Gut 57, 448-454 (2008).
Lagergren, J., Bergström, R. & Nyrén, O. No relation between body mass and gastro-oesophageal reflux symptoms in a Swedish population based study. Gut 47, 26-29 (2000).
Nilsson, M., Johnsen, R., Ye, W., Hveem, K. & Lagergren, J. Obesity and estrogen as risk factors for gastroesophageal reflux symptoms. JAMA 290, 66-72 (2003).
Jacobson, B. C., Somers, S. C., Fuchs, C. S., Kelly, C. P. & Camargo, C. A. Jr. Body-mass index and symptoms of gastroesophageal reflux in women. N. Engl. J. Med. 354, 2340-2348 (2006).
Murray, L. et al. Relationship between body mass and gastro-oesophageal reflux symptoms: the Bristol Helicobacter Project. Int. J. Epidemiol. 32, 645-650 (2003).
Nandurkar, S. et al. Relationship between body mass index, diet, exercise and gastro-oesophageal reflux symptoms in a community. Aliment. Pharmacol. Ther. 20, 497-505 (2004).
Hampel, H., Abraham, N. S. & El-Serag, H. B. Meta-analysis: obesity and the risk for gastroesophageal reflux disease and its complications. Ann. Intern. Med. 143, 199-211 (2005).
Corley, D. A. & Kubo, A. Body mass index and gastroesophageal reflux disease: a systematic review and meta-analysis. Am. J. Gastroenterol. 101, 2619-2628 (2006).
Solhpour, A. et al. Gastro-esophageal reflux symptoms and body mass index: no relation among the Iranian population. Indian J. Gastroenterol. 27, 153-155 (2008).
Corley, D. A., Kubo, A. & Zhao, W. Abdominal obesity, ethnicity and gastro-oesophageal reflux symptoms. Gut 56, 756-762 (2007).
Gunji, T. et al. Risk factors for erosive esophagitis: a cross-sectional study of a large number of Japanese males. J. Gastroenterol. doi:10.1007/s00535-010-0359-0355.
Zheng, Z. et al. Effects of estrogen with and without progestin and obesity on symptomatic gastroesophageal reflux. Gastroenterology 135, 72-81 (2008).
Chung, S. J. et al. Metabolic syndrome and visceral obesity as risk factors for reflux oesophagitis: a cross-sectional case-control study of 7078 Koreans undergoing health check-ups. Gut 57, 1360-1365 (2008).
Nam, S. Y. et al. Abdominal visceral adipose tissue volume is associated with increased risk of erosive esophagitis in men and women. Gastroenterology 139, 1902-1911 (2010).
de Vries, D. R., van Herwaarden, M. A., Smout, A. J. & Samsom, M. Gastroesophageal pressure gradients in gastroesophageal reflux disease: relations with hiatal hernia, body mass index, and esophageal acid exposure. Am. J. Gastroenterol. 103, 1349-1354 (2008).
Crowell, M. D. et al. Obesity is associated with increased 48-h esophageal acid exposure in patients with symptomatic gastroesophageal reflux. Am. J. Gastroenterol. 104, 553-559 (2009).
Ayazi, S. et al. Obesity and gastroesophageal reflux: quantifying the association between body mass index, esophageal acid exposure, and lower esophageal sphincter status in a large series of patients with reflux symptoms. J. Gastrointest. Surg. 13, 1440-1447 (2009).
Menon, S. & Trudgill, N. Risk factors in the aetiology of hiatus hernia: a meta-analysis. Eur. J. Gastroenterol. Hepatol. 23, 133-138 (2011).
Nilsson, M., Lundegårdh, G., Carling, L., Ye, W. & Lagergren, J. Body mass and reflux oesophagitis: an oestrogen-dependent association? Scand. J. Gastroenterol. 37, 626-630 (2002).
Nordenstedt, H. et al. Postmenopausal hormone therapy as a risk factor for gastroesophageal reflux symptoms among female twins. Gastroenterology 134, 921-928 (2008).
De Groot, N. L. et al. Systematic review: the effects of conservative and surgical treatment for obesity on gastro-oesophageal reflux disease. Aliment. Pharmacol. Ther. 30, 1091-1102 (2009).
Flegal, K. M., Carroll, M. D., Ogden, C. L. & Curtin, L. R. Prevalence and trends in obesity among US adults, 1999-2008. JAMA 303, 235-241 (2010).

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Author(s)

Jesper Lagergren, MD, PhD

Professor; Senior Consultant of Upper Gastrointestinal Surgery, Karolinska Institute, Stockholm, Sweden; King's College, London, United Kingdom

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Disclosure: Jesper Lagergren, MD, PhD, has disclosed no relevant financial relationships.

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Natalie Wood

Chief Editor, Nature Reviews Gastroenterology & Hepatology

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Charles P. Vega, MD

Associate Professor; Residency Director, Department of Family Medicine, University of California, Irvine

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Disclosure: Nafeez Zawahir, MD, has disclosed no relevant financial relationships.

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CME

Influence of Obesity on the Risk for Esophageal Disorders

Authors: Jesper Lagergren, MD, PhD
CME Released: 6/6/2011
THIS ACTIVITY HAS EXPIRED FOR CREDIT
Valid for credit through: 6/6/2012

Start Activity

Target Audience and Goal Statement

This activity is intended for primary care physicians, gastroenterologists, and other physicians who care for patients at risk for esophageal disorders.

The goal of this activity is to evaluate the relationship between obesity and esophageal disorders.

Upon completion of this activity, participants will be able to:

Evaluate the interaction between body mass index and GERD
Distinguish the type of adiposity most associated with esophageal disorders
Identify molecular mechanisms in obesity that may promote esophageal adenocarcinoma
Analyze the relationship between body mass index and esophageal adenocarcinoma

Disclosures

Author(s)

Jesper Lagergren, MD, PhD

Professor; Senior Consultant of Upper Gastrointestinal Surgery, Karolinska Institute, Stockholm, Sweden; King's College, London, United Kingdom

Disclosures

Disclosure: Jesper Lagergren, MD, PhD, has disclosed no relevant financial relationships.

Editor(s)

Natalie Wood

Chief Editor, Nature Reviews Gastroenterology & Hepatology

Disclosures

Disclosure: Natalie Wood has disclosed no relevant financial relationships.

CME Author(s)

Charles P. Vega, MD

Associate Professor; Residency Director, Department of Family Medicine, University of California, Irvine

Disclosures

Disclosure: Charles P. Vega, MD, has disclosed no relevant financial relationships.

CME Reviewer(s)

Nafeez Zawahir, MD

CME Clinical Director, Medscape, LLC

Disclosures

Disclosure: Nafeez Zawahir, MD, has disclosed no relevant financial relationships.

Sarah Fleischman

CME Program Manager, Medscape, LLC

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Disclosure: Sarah Fleischman has disclosed no relevant financial relationships.

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Obesity and GERD

The relationship between obesity and GERD was still uncertain in the early 2000s because of too sparse data. The need for well-designed epidemiological studies to address this clinically relevant relationship was highlighted in a study that questioned the association.^[54] As GERD is typically a chronic or recurrent condition it is difficult to conduct studies of newly diagnosed patients with GERD. Thus, most of the findings are based on cross-sectional studies, which makes it more difficult to establish a causal link between obesity and GERD.

Association Between BMI and GERD

In 2003, a nested, population-based, case-control study from Norway (which included 3,113 individuals with GERD and 39,872 individuals without GERD) found a positive association between increasing BMI and GERD in both sexes, but the association was more robust in women.^[55] Compared with those who had a normal BMI (<25), the risk of GERD was increased among men (OR 3.3; 95% CI 2.4-4.7) and women (OR 6.3; 95% CI 4.98.0) who were severely obese (BMI >35). Any increase in BMI was associated with an increase in the risk of GERD, even among individuals whose BMI was within the normal range.^[55] A cohort study from the USA, which comprised 10,545 women, confirmed the finding that any increase in BMI in individuals of normal weight was associated with an increased risk of GERD, and even moderate weight gain among persons of normal weight might cause or exacerbate GERD.^[56] A positive association between BMI and GERD has also been reported by other studies from the UK and USA.^[57,58] Meta-analyses have concluded that individuals with BMI >30 have an approximately twofold increased risk of GERD compared with individuals who have a normal BMI. A similar association has also been reported for erosive esophagitis, which is a complication that can occur in patients with chronic GERD.^[59,60]

The association between BMI and GERD seems to be stronger in the white population than in individuals of other ethnicities.^[61-63] This observation might help to explain the high incidence rates of esophageal adenocarcinoma reported in industrialized countries.

Effect of Body Fat Distribution

A cross-sectional study of 80,110 US individuals revealed that waist circumference (rather than BMI) was associated with GERD in the white population, while no such association was found for the black or Asian populations. The association between waist circumference and GERD was similar between sexes.^[62] In a large US study that comprised 27,347 women, researchers identified a positive relationship between waist circumference and the risk of GERD.^[64] Moreover, the results of a South Korean study that included 7,078 patients who had undergone upper endoscopy during health check-ups showed that occurrence of the metabolic syndrome was associated with an increased risk of GERD, and abdominal obesity (especially intra-abdominal obesity) was an important risk factor for this condition.^[65] Finally, analysis of a cohort of 5,329 Korean individuals showed a correlation between intra-abdominal adipose tissue volume, but not BMI or waist circumference, and erosive esophagitis.^[66]

Mechanisms

The mechanisms underlying the association between obesity and GERD are only partly understood. Obesity-related changes in gastroesophageal anatomy and physiology (such as an increased prevalence of esophageal motor disorders, a diminished lower esophageal sphincter pressure, development of hiatal hernia, and increased intragastric pressure) might contribute to an explanation for this association. In a Dutch study of 149 patients with GERD, de Vries et al. found that BMI predicted intragastric pressure, inspiratory gastroesophageal pressure gradient and expiratory intraesophageal pressure.^[67] Similarly, in a US study, the analysis of esophageal pH in patients with GERD (n = 157) demonstrated that obese individuals had a fivefold increase in risk of abnormal total acid exposure (which provides a more objective assessment of reflux) compared with those of normal weight (OR 5.0; 95% CI 2.9-13.0).^[68] In another US study Ayazi and colleagues quantified the association between BMI, esophageal acid exposure, and the status of the lower esophageal sphincter in 1,659 patients with GERD. The investigators showed a positive correlation between increasing BMI and esophageal acid exposure. Additionally, they found that a mechanically defective lower esophageal sphincter was over-represented in patients who were obese compared with those of normal weight (OR 2.1; 95% CI 1.6-2.8).^[69] A meta-analysis of four studies found an association between BMI >25 and hiatal hernia, an anatomical condition that promotes the reflux of gastric contents and is thus associated with GERD (OR 1.9; 95% CI 1.1-3.4).^[70]

The association between obesity and GERD might also be mediated by increased estrogen exposure in individuals who are obese. The results of a preliminary case-control study from Sweden (including 179 cases and 179 controls), in which there was a strong association between increasing BMI and the risk of esophagitis in women (but not in men), indicated that estrogen might be involved in this association.^[71] Nilsson et al.^[55] found that the association between BMI and GERD was stronger in premenopausal women (n = 592) than in those who were postmenopausal (n = 847). In addition, the use of postmenopausal hormone therapy increased the strength of the association, adding evidence to the hypothesis that estrogens might have a role in the etiology of GERD, particularly in individuals who are obese.^[55] The results of a twin study from Sweden (which comprised 4,365 twins with GERD and 17,321 without)^[72] and those from a large US trial of 10,739 postmenopausal women who underwent hysterectomy and 16,608 women who did not provide further support for this hypothesis.^[64] The first study showed that hormone replacement therapy with estrogen was an independent risk factor for reflux symptoms (OR 1.32; 95% CI 1.18-1.47), a finding that was supported by the latter study.^[64]

Weight Loss

The literature regarding the potential beneficial effect of weight loss on alleviating the symptoms of GERD is limited, heterogeneous and partly contradictory. Nevertheless, a systematic review of the available literature, published in 2009, concluded that weight loss resulting from dietary or lifestyle interventions or after surgical intervention can reduce the symptoms of GERD.^[73] On the basis of available data, weight loss through changes in dietary and lifestyle habits should be recommended to individuals with GERD, but bariatric surgery should not be used for the treatment of this condition.

Weight Loss

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Page 5 of 7

Conclusions

CME Information

References

Table 1.

CME

Influence of Obesity on the Risk for Esophageal Disorders

Target Audience and Goal Statement

Disclosures

Author(s)

Jesper Lagergren, MD, PhD

Editor(s)

Natalie Wood

CME Author(s)

Charles P. Vega, MD

CME Reviewer(s)

Nafeez Zawahir, MD

Sarah Fleischman

Accreditation Statements

For Physicians

Instructions for Participation and Credit

Influence of Obesity on the Risk for Esophageal Disorders: Obesity and GERD

Obesity and GERD

Association Between BMI and GERD

Effect of Body Fat Distribution

Mechanisms

Weight Loss

Weight Loss

Table of Contents

Table 1.

References

Faculty and Disclosures

Author(s)

Jesper Lagergren, MD, PhD

Editor(s)

Natalie Wood

CME Author(s)

Charles P. Vega, MD

CME Reviewer(s)

Nafeez Zawahir, MD

Sarah Fleischman

CME

Influence of Obesity on the Risk for Esophageal Disorders

Target Audience and Goal Statement

Disclosures

Author(s)

Jesper Lagergren, MD, PhD

Editor(s)

Natalie Wood

CME Author(s)

Charles P. Vega, MD

CME Reviewer(s)

Nafeez Zawahir, MD

Sarah Fleischman

Accreditation Statements

For Physicians

Instructions for Participation and Credit

Influence of Obesity on the Risk for Esophageal Disorders: Obesity and GERD

Obesity and GERD

Association Between BMI and GERD

Effect of Body Fat Distribution

Mechanisms

Weight Loss

Weight Loss

Table of Contents