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Ann Thorac Surg 2009;87:655-662. doi:10.1016/j.athoracsur.2008.08.003
© 2009 The Society of Thoracic Surgeons
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Review

Exploring the Association Between Elevated Body Mass Index and Barrett's Esophagus: A Systematic Review and Meta-Analysis

Paresh Kamat, MD, MPHa,c, Sijin Wen, PhDb, Jeffrey Morris, PhDb, Sharmila Anandasabapathy, MDa,*

a Division of Gastroenterology, The Mount Sinai Medical Center, New York, New York
b Department of Biostatistics, The University of Texas, MD Anderson Cancer Center, Houston, Texas
c Department of Internal Medicine, St. Lukes Roosevelt Hospital Center, New York, New York

* Address correspondence to Dr Anandasabapathy, Division of Gastroenterology, The Mount Sinai Medical Center, Box 1069, One Gustave Levy Place, New York, NY 10029 (Email: sharmila.anandasabapathy{at}mountsinainyuhealth.org).


   Abstract
Top
 Abstract
Introduction
 Methods
 Statistical Analysis
 Results
 Comment
 References
 
We performed a systematic review and meta-analysis to study the association between elevated body mass index (BMI) and Barrett's esophagus (BE). Cross-sectional, case-control and cohort studies published through February 2008 that met strict inclusion and exclusion criteria were included. Summary estimates were calculated for the association between BE and being either overweight (BMI ≥ 25 kg/m2) or obese (BMI ≥ 30 kg/m2), or both. Based on 11 studies included in this analysis, there was a statistically significant relationship between increasing BMI and BE. Further studies are needed to evaluate if the presence of reflux attenuates the strength of this relationship, and if a particular pattern of obesity is more strongly associated with BE.


   Introduction
Top
 Abstract
 Introduction
Methods
 Statistical Analysis
 Results
 Comment
 References
 
In the last 3 decades we have witnessed a dramatic increase in the incidence of esophageal adenocarcinoma (EAC). Indeed, incidence rates for EAC have risen by 300% to 500% in the past 30 years [1–5], a trend which has prompted great interest in Barrett's esophagus (BE), its predominant precursor. Barrett's esophagus is characterized by the replacement of the normal squamous epithelium of the esophagus by a specialized metaplastic columnar epithelium. Although Barrett's esophagus is fairly prevalent in the American population, the vast majority of individuals affected never progress to cancer.

Risk factors that lead to BE have been poorly understood. Gastroesophageal reflux disease (GERD) has been identified as a risk factor for BE [6–8]. However, several studies have found that not all patients with EAC, in previously undiagnosed BE, had GERD symptoms [9–11]. The identification of risk factors associated with BE is vital, as this offers opportunities for the early detection and surveillance of at-risk populations. Several studies have found an association between obesity and GERD, erosive esophagitis and EAC [12–20]. Given these associations, it would seem logical that increasing body mass index (BMI) is associated with BE. During the past 5 years there has been a proliferation of articles that have attempted to evaluate this association. Nevertheless, the results of these various studies have been conflicting, and only a few have found a strong relationship between obesity and BE.

We evaluated the relationship between BMI and BE by performing a systematic review and statistical synthesis of all available literature published through February 2008. Most of the studies included in this review have been published during the past 2 years. By pooling data from appropriate studies, significant information can be obtained, which individual studies may lack the power to evaluate, including the influence of other factors (eg, age, gender) and the presence of confounders. By performing a meta-analysis of the 11 studies that met our strict selection criteria, we hoped to better characterize and quantify the association between increased BMI and BE.


   Methods
Top
 Abstract
 Introduction
 Methods
Statistical Analysis
 Results
 Comment
 References
 
Search Strategy
Two investigators independently performed a systematic search of all existing literature published through February 2008. Studies were included if they either evaluated the association between BMI and BE or compared BMI in a Barrett's esophagus and comparison population. Both English and non-English language publications were evaluated. Medical subject headings (MeSH) or keywords for separate searches using MEDLINE, Web of Science Database and Cumulative Index to Nursing & Allied Health Literature using the following strategy of terms: obesity or body mass index or overweight or body weight or risk factors or risk assessment searched with Barrett's; Barrett; or Barretts esophagus; or Barrett ulcer or columnar lined esophagus. A similar search was done using the word "oesophagus" a common British spelling for esophagus. We then manually searched for bibliographies of retrieved articles to insure thoroughness (Fig 1). Only the 633 potential articles identified after the preliminary search were reviewed in further details.


Figure 1
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  		Fig 1. Flow diagram. (BE = Barrett's esophagus; BMI = body mass index.)

 
Study Selection Criteria
The following were chosen as the inclusion criteria:
1 Cross-sectional, case-control, or cohort studies that permitted assessment of a causal relationship between BMI and BE.
2 Studies with documented and clearly-defined BMI in kg/m2 in all participants.
3 Studies that presented or had sufficient information to allow for calculation of risk estimates.
4 Studies with histologic confirmation of BE seen on upper endoscopy.

The inclusion criteria were not otherwise restricted by study size, publication type, or language of publication.

The following were chosen as the exclusion criteria:

1 Studies not limited to humans
2 Case-reports, case-series or studies that lacked a comparison group
3 BE diagnosed on endoscopic appearance alone without histologic confirmation or studies that did not include all subtypes (ie, segment lengths) of BE.

Data Abstraction
Data abstracted included information on source of the study population, study design (case-control, cohort, or cross-sectional), years of study, primary aim of study, exposure definitions (BMI definitions of normal, overweight, or obese, or mean BMI with standard deviation), exposure measurement method (self-reported vs measured BMI), outcome definitions (diagnosis of BE with histologic confirmation), total number of subjects in the case (BE), and comparison group, case and control criteria, demographics of case group, measure(s) of relative risk (ie, odds ratios) (OR) or risk ratios (with and without adjustment for potential confounders) and potential confounders used for adjustment.

Exposure Definition
We defined BMI categories using the World Health Organization classification for normal (18.5 kg/m2 – 24.9 kg/m2), overweight (25 kg/m2 – 29.9 kg/m2), and obese (≥30 kg/m2). The majority of articles we reviewed used a similar classification, although some studies used a slightly different classification [21–26]. For those studies, we selected a BMI category that closely approximated each classification (ie, normal if BMI < 25 kg/m2, overweight if BMI 25 kg/m2 – 30 kg/m2, and obese if BMI > 30 kg/m2. In addition, for the pooled analysis we created a category that included both overweight and obese (BMI ≥ 25 kg/m2), and there was also a category for normal and overweight (BMI ≤ 30 kg/m2).

Outcome Definition
An outcome was defined as BE, which was diagnosed on endoscopy and confirmed on histopathology. We did not include studies that excluded particular segment lengths of Barrett's esophagus or that only used endoscopic criteria for Barrett's esogphagus without histologic confirmation.


   Statistical Analysis
Top
 Abstract
 Introduction
 Methods
 Statistical Analysis
Results
 Comment
 References
 
We abstracted or calculated risk estimates (ie, odds ratios) for cross-sectional and case-control studies for the association between BMI and BE. For studies that did not report them but presented sufficient information to calculate them, unadjusted-odds ratios were determined [21–24, 26–29, 30].

The studies were organized into three sets for determination of summary estimates: Set I consisted of 7 studies [22, 26, 28–32] that compared individuals with a normal BMI to those who were overweight (BMI 25 to 29.9) or obese (BMI ≥ 30). Set II consisted of nine studies [21–23, 26, 28–32] that compared subjects who were obese (BMI ≥ 30) with those who were not obese (BMI < 30). Set III consisted of eight studies [21, 22, 26, 28–32] that compared subjects with a normal BMI (< 25) to those in the overweight plus obese group (BMI ≥ 25). Summary estimates were calculated for all three sets by pooling the unadjusted-odds ratios for the inclusive studies. Two studies [26, 27] used subjects with GERD as the comparison group, and for these studies a separate analysis was performed.

Summary odds ratios were calculated using a fixed effect model (Mantel-Haenszel method) and a random effects model (DerSimonian-Laird's method). We examined for potential heterogeneity among studies as follows. First, the Woolf's test (Woolf, 1955) was used to assess homogeneity of odds ratios for all studies with heterogeneity considered present if p < 0.05. Second, to exclude an excessive influence of any single study, we evaluated whether exclusion of any single study substantially altered the magnitude or heterogeneity of the summary estimate. We also evaluated heterogeneity by comparing results between the fixed effects model and a random effects model, with heterogeneity considered present if there was a greater than 20% difference in the summary estimates between the two models. Finally, we performed visual inspection of forest plots in which 95% confidence intervals for odds ratios for each study were represented by horizontal lines and the point estimate by a square. The height of each square is inversely proportional to the standard error of the estimate. The summary odds ratio is represented by a diamond with horizontal limits at the 95% confidence interval and the width is inversely proportional to its standard error.

The presence of publication bias was assessed by using the log rank correlation test (Kendall's correlation) by calculating a correlation coefficient between the effect estimates and their variances (surrogate for sample size) with p < 0.05 considered significant. We also evaluated unusual patterns by assessing funnel plots of odds ratios versus their standard errors. Statistical analyses were carried out using S-Plus, version 2000 (Insightful Corp, Seattle, WA) and R, version 2.2.0 (GNU General Public License, 2005, Free Software Foundation, Inc).


   Results
Top
 Abstract
 Introduction
 Methods
 Statistical Analysis
 Results
Comment
 References
 
An initial electronic and manual search identified a total of 633 potential published articles (Fig 1). After an initial review of titles and abstracts, 62 publications appeared to meet the initial inclusion criteria. The remaining studies that were excluded were comprised of review articles, case series that lacked a comparison group, and studies that did not report on the subject of interest. On further detailed review of these 62 studies, we excluded an additional 51 articles of which 27 did not provide information on BMI, 11 did not have an appropriate comparison group (ie, control subjects without BE), 5 did not have histopathologic confirmation of BE, 3 excluded patients with short-segment Barrett's esophagus studies, and 5 did not have sufficient or obtainable information to calculate risk estimates. Ultimately, 11 articles were included in the final review (ie, 3 cross-sectional, 1 cohort, and 7 case-control studies).

Table 1 summarizes the characteristics of the 11 studies included in our review. Six studies were conducted for the primary purpose of evaluating the relationship between BMI and BE [22, 26–28, 30, 31], whereas three were done to study a variety of risk factors for BE, including BMI [23, 29, 32]. In all the studies included, data had been collected from 1990 onward. Seven studies were conducted in the United States, one in Canada, two in Sweden, and one in Australia. Four studies were population-based, five studies were hospital based (three of which were conducted among a predominantly male veteran population), whereas two studies compared hospital-based cases to population controls.


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  		Table 1 Study Characteristics
 
Tables 2 and 3 Go summarize the risk estimates, crude odds ratios (reported or calculated), adjusted-odds ratios and the factors adjusted for in the 11 studies in which risk estimates were either reported in the original study or where sufficient information was available to calculate them. Nine studies provided sufficient information for calculating crude risk estimates and the 95% confidence interval (CI) [21–24, 26–30]. Among these, five studies [22, 26, 28, 30, 31] found a statistically significant association between obesity (BMI ≥ 30) and BE, whereas two studies [22, 28] found a statistically significant association between being overweight (BMI ≥ 25 to 29.9) and BE. Adjustment for age and race by Stein and colleagues [28], and for age and gender by Veugelers and colleagues [29], increased the strength of association between BE and BMI. In contrast, adjustment for additional factors, such as frequency of acid reflux symptoms, smoking, and nonsteroidal anti-inflammatory drug (NSAID) use in the study by Smith and colleagues decreased the strength of association [32]. Interestingly, Edelstein and colleagues [30] found that association between BMI and risk of BE was lost when BMI was modeled simultaneously with waist-to-hip ratio.


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  		Table 2 Adjusted-Odds Ratio (Relative Risk)
 

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  		Table 3 Unadjusted-Odds Ratio (Relative Risk)
 
As mentioned previously, the studies were grouped into three sets to calculate summary estimates for the relationship between obesity (BMI ≥ 30) and BE, and being "overweight" (BMI ≥ 25.0 to 29.9) and BE. Set I compared individuals with a normal BMI to those who were overweight or obese [22, 26, 28–32]. The pooled unadjusted-odds ratios for BE in subjects who were overweight or obese were 1.33 (95% CI 1.07 to 1.64; p = 0.01) and 1.70 (95% CI 1.36 to 2.12; p < 0.001), respectively. Set II included studies that compared subjects with obesity (BMI ≥ 30) to normal and overweight combined (BMI < 30) [21–23, 26, 28–32]. The pooled unadjusted-odds ratio for risk of BE in subjects with obesity was 1.35 (95% CI 1.15 to 1.59; p < 0.001). Set III was comprised of studies that compared subjects who were overweight plus obese (BMI ≥ 25) with those who had a normal weight (BMI < 25) [21, 22, 26, 28–32]. The pooled unadjusted odds ratio for risk of Barrett's in subjects who are overweight or obese was 1.49 (95% CI 1.24 to 1.80; p < 0.001). Thus, results of the overall meta-analysis suggest an association between BE and an elevated BMI. The results of this meta-analysis are illustrated in Figures 2A and 2B.


Figure 2
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  		Fig 2. (A) Unadjusted-odds ratios for association of Barrett's esophagus in nine studies that compared subjects who were obese (BMI ≥ 30 kg/m2) with those who were not obese (BMI <30 kg/m2). (B) Unadjusted-odds ratios for association of Barrett's esophagus in eight studies that compared subjects who were either overweight or obese (BMI ≥ 25 kg/m2) with those who were not overweight (BMI <25 kg/m2). The 95% confidence interval (CI) for odds ratios for each study is represented by the horizontal lines and the point estimate is represented by a square. The size of the square corresponds to the weight of the study in the meta-analysis. The 95% confidence interval for summary estimates is represented by a diamond. (BE = Barrett's esophagus; BMI = body mass index.)

 
Two studies compared subjects with BE to controls with known GERD. Using a chronic GERD population, Gerson and colleagues [27] compared subjects with an increased BMI (ie, overweight or obese) with those who had a normal BMI. In a large, population-based study, Corley and colleagues [26] evaluated the risk of elevated BMI in subjects with BE in comparison with those who had GERD, as well as population-based controls. Using GERD controls, the unadjusted, pooled, odds ratios for these two studies for risk of Barrett's esophagus in overweight and obese subjects was 1.16 (95% CI 0.87 to 1.56; p = 0.38) and 1.19 (95% CI 0.87 to 1.63; p = 0.302), respectively.

Heterogeneity and Publication Bias
To evaluate heterogeneity, we initially performed visual inspection of forest plots to explore the odds ratios for all studies. The odds ratios in Figure 2A (BMI < 25 vs ≥ 25) show better homogeneity than those in Figure 2B (BMI < 30 vs ≥ 30). In addition, we evaluated heterogeneity of odds ratios for all studies based on Woolf's test, and the comparison between the fixed effects model and a random effects model. The pooled odds ratio for risk of BE in subjects with obesity was 1.35 (95% CI 1.15 to 1.59) from the fixed effect model and 1.41 (95% CI 1.11 to 1.79) from the random effects model; therefore, there was less than a 20% difference in the summary estimates between the two models, although the p value is 0.06 from the Woolf's test. Similarly, the pooled unadjusted-odds ratio for risk of BE in subjects who are overweight or obese was 1.49 (95% CI 1.24 to 1.80) from the fixed effect model and 1.49 (95% CI 1.12 to 1.99) from the random effects model. Again, there was less than a 20% difference in the summary estimates between the two models and the p value is 0.08 from Woolf's test. In summary, the combined summary estimates obtained by pooling the odds ratio for the association between increased BMI and BE were not statistically significant for heterogeneity.

Finally, the log rank correlation test (Kendall's correlation), along with visual inspection of funnel plots, did not demonstrate any publication bias. For example, the p value from Kendall's rank test was 0.286 for overweight subjects (ie, BMI < 25 vs ≥ 25) and 0.111 for obese subjects (ie, BMI < 30 vs ≥ 30).


   Comment
Top
 Abstract
 Introduction
 Methods
 Statistical Analysis
 Results
 Comment
References
 
A systematic review and meta-analysis of the literature was performed examining the association between elevated BMI (ie, overweight defined as BMI 25 to 29.9 kg/m2, or obese defined as BMI ≥ 30 kg/m2) and BE. Unlike other nonmodifiable risk factors such as age, race, and gender, and partially modifiable risk factors, such as GERD, BMI is potentially modifiable. Thus, identifying a relationship between obesity and BE might have significant implications for both counseling and cancer prevention. Researchers have thereby been increasingly drawn to study this association for the past few years. This is evidenced by the fact that nearly all of the studies included in our analysis were published within the last 3 years. Based on the results of eight studies that compared subjects with BE to population or hospital-based controls, there is a statistically significant association between BE and elevated BMI. This is in contrast to findings in a prior meta-analysis by Cook and colleagues [33] that did not find a statistically significant association between increasing adiposity and BE. It is important to note, however, that the Cook meta-analysis did not include several key studies that were included in our review and that had been published after 2006. In addition, the inclusion and exclusion criteria used in our study differed somewhat from that used by Cook and colleagues [33]. Most notably, we did not include articles in which BE was diagnosed without pathologic confirmation.

Several mechanisms have been postulated by which obesity might increase the risk of BE and EAC, some of which may not be related to the development of GERD as suggested in a report by Lagergren and colleagues [18], in which as many of 40% of patients with EAC did not report antecedent reflux symptoms. Elevated levels of serum pro-inflammatory cytokines (adipocytokines), including interleukin-6 and tumor necrosis factor—{alpha} associated with visceral fat has been shown to be over-expressed in persons with BE [34–36]. Various biological mediators including leptins, insulin, and insulin-like growth factors, which are intricately associated with obesity, have been shown to stimulate cell proliferation and inhibit apoptosis [37–41]. It is possible that similar mechanisms may underlie the development of esophageal neoplasia.

In total, we performed three separate analyses to evaluate the relationship between Barrett's and being obese and overweight. All three were statistically significant, although the magnitude of this effect was not great (odds ratio, 1.35 and 1.49 for BMI ≥ 30 kg/m2 and BMI ≥ 25 kg/m2, respectively). Interestingly, our detailed evaluation of the individual studies failed to show a consistent association between BE and elevated BMI in the majority of studies. Although most studies noted a trend toward an association between being overweight and obesity, and BE, few of these risk estimates reached statistical significance. Nevertheless, the strength of such data pooling is that associations may become evident that individual studies lack the power to identify. The results of our heterogeneity test were not statistically significant, thus, supporting the decision to pool odds ratios.

One of the major strengths of the review is that strict criteria were used for defining our outcome of interest. Indeed, all of the studies included used histopathology to confirm the diagnosis of BE. This virtually eliminates the possibility of including false positive BE cases. Two independent reviewers used stringent search criteria to eliminate bias inherent to the selection process and extended the search criteria to also include literature published in languages other than English. Moreover, we evaluated the association between BE and elevated BMI (sets I, II, and III) in three separate analyses, all of which showed a positive association.

There are several limitations to this review. Most of the studies were hospital-based, conducted either in tertiary care referral centers or in Veterans Affair medical centers on participants that underwent endoscopy for various indications. An inherent selection bias may be present in that individuals referred for endoscopy may be experiencing more severe gastrointestinal symptoms, such as heartburn, regurgitation, or dyspepsia. The incorporation of some subjects with reflux symptoms into the control group of certain studies may decrease the strength of the association between BE and BMI. In addition, only observational studies were included. Because all of the included studies are either case-control or cross-sectional studies, a temporal association between the risk factor (BMI) and outcome of interest (BE) can not be determined. Secondly, the exposure definitions (ie, normal, obese or overweight) differed slightly among the studies. However, we addressed this by creating more comparable and consistent classifications, although small differences may remain. Finally, all odds ratios used in our meta-analysis were unadjusted and the effect of confounding factors (including smoking, alcohol consumption, diet, and so forth) on risk estimates could not be assessed.

Obesity has been shown to be associated with GERD. Thus, BMI in subjects undergoing endoscopy for various upper gastrointestinal symptoms may be relatively higher than in an asymptomatic population. Because the population controls did not undergo endoscopy to exclude BE, there is a potential for incorporation of some Barrett's esophagus patients in the control groups of certain studies. According to a recent report by Ronkainen and colleagues [23], the percentage of Barrett's esophagus subjects in such a control population would be approximately 1% to 2%. Although this could affect risk estimates, the magnitude of error would be marginal. Interestingly, one study that used both endoscopic controls and population controls, found no difference in risk estimates [24].

We identified two studies that used subjects with known GERD as controls. In a separate analysis of these studies, there was no significant difference in BMI between subjects with BE and those with GERD. Given the limited study number, it is difficult to make significant generalizations from these results. Indeed, in the study by Corley and colleagues [26], there was no association between Barrett's esophagus and BMI. There was, however, an association between Barrett's esophagus and abdominal circumference, an association which was only partially attenuated by adjusting for reflux symptoms. Thus, the role of GERD in the strength of the association between BMI and BE warrants further evaluation.

Thus, based on our extensive review and synthesis of the literature, there appears to be a statistically significant association between elevated BMI and BE. Given the prevalence of obesity and increasing incidence rates for EAC, there is a clear need for further studies examining this important association, and the role of symptomatic reflux in this association. Unlike other risk factors, obesity is potentially modifiable, and there may be opportunities for behavioral or medical intervention in high-risk subjects, or both. To better risk stratify, it will also be important to determine whether a particular pattern of obesity plays a role. Several studies have found abdominal obesity to be an independent risk factor for BE [26, 30]. In addition, Vaughan and colleagues [42] have demonstrated an increased risk for cell cycle (aneuploidy) and genetic abnormalities (chromosome 17p loss) in Barrett's esophagus subjects with increased waist to hip ratio. Along these lines, it will also be important to determine whether weight loss decreases progression to adenocarcinoma in subjects with known BE. Clearly many questions remain and further studies are needed to evaluate the relationship between Barrett's esophagus and obesity.


   References
Top
 Abstract
 Introduction
 Methods
 Statistical Analysis
 Results
 Comment
 References
 

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