Elsevier

Cancer Epidemiology

Volume 38, Issue 3, June 2014, Pages 266-272
Cancer Epidemiology

Total body fat and the risk of Barrett's oesophagus – A bioelectrical impedance study

https://doi.org/10.1016/j.canep.2014.03.006Get rights and content

Abstract

Background

Body mass index is associated with the risk of Barrett's oesophagus (BO). It is uncertain whether this is related to total body fat or other factors that correlate with body mass index. We aimed to quantify the association between total body fat (measured by bioelectrical impedance) and risk of BO and examine if this association was modified by gastro-oesophageal reflux (GOR) and abdominal obesity.

Methods

In 2007–2009, we surveyed 235 cases (69% Males, Mean age 62.1 years) and 244 age and sex matched population controls from a population based case–control study of BO. We conducted structured interviews, standard anthropometry and bioimpedance analysis of total body fat. Odds ratios (OR) and 95% confidence intervals (CI) were estimated using multivariable logistic regression analysis.

Results

There was a significantly increased risk of BO among those in the highest tertile of total body fat weight (OR 2.01; 95%CI 1.26–3.21) and total body fat percentage (OR 1.86; 95%CI 1.10–3.15). These risks were largely attenuated after adjustment for GOR and waist circumference. There was a significantly increased risk of BO among those in the highest tertile of waist circumference (OR 2.21; 95%CI 1.39–3.51) and this was minimally attenuated after adjustment for total body fat and moderately attenuated after adjustment for GOR.

Conclusions

Total body fat is associated with an increased risk of BO but this appears to be mediated via both abdominal obesity and GOR. These findings provide evidence that abdominal obesity is more important than total body fat in the development of BO.

Introduction

Obesity is defined as the accumulation of excessive body fat that may impair health [1]. Body mass index (BMI) has long been used as a surrogate measure for total body fat, but recent studies have shown that BMI correlates only modestly with total body fat, particularly with increasing age, increasing muscle mass and at the extremes of BMI [2], [3]. Direct measurement of total body fat has previously been difficult and expensive requiring whole body plesmography or dual-energy X-ray absorptiometry. Bioimpedance analysis (BIA) is a simple, cheap, highly reproducible bedside technique that accurately measures total body fat [4], [5], [6].

Obesity has been associated with a number of cancers, including oesophageal adenocarcinoma (OA) [7], [8], [9]. Barrett's oesophagus (BO) is a metaplastic change in the distal oesophagus and is the precursor of OA [10], [11], [12]. There is conflicting evidence as to whether obesity is associated with an increased risk of BO. A meta-analysis has shown the risk of BO increases monotonically with BMI (OR 1.02 per kg/m2; 95%CI 1.01–1.04), most likely mediated through gastro-oesophageal reflux (GOR) [13]. Moderate heterogeneity was found in the included studies. A subsequent cohort study has shown that in females, a high BMI ≥30 kg/m2 was associated with an increased risk of BO (OR 1.52; 95%CI 1.02–2.28) and this risk persisted after adjustment for GOR symptoms [14]. In contrast, a recent study, predominantly in males, found no association between a high BMI and risk of BO but did find an association between abdominal obesity and risk of BO [15].

The heterogeneity of the previously reported studies may be related in part to the limitations of BMI in accurately reflecting total body fat among different populations. A recent clinic based case–control study of 70 predominately male BO cases has suggested that total body fat mass, measured by BIA, is not associated with an increased risk of BO [16]. Given the modifiable nature of obesity as a risk factor, an understanding of the association between obesity, abdominal obesity and BO is important in developing preventive strategies for both BO and OA.

In this study we sought to determine whether there is an association between total body fat measured by BIA and risk of BO, and if present, is this association modified by adjusting for GOR symptoms and abdominal obesity.

Section snippets

Methods

This study was nested within the Study of Digestive Health (SDH), a population-based case–control study of BO conducted between 2003 and 2006 and previously described [17]. Cases were people aged 18–79 years newly diagnosed with BO defined as the presence of intestinal metaplasia (columnar epithelium with goblet cells) in a biopsy taken from the oesophagus by upper gastrointestinal endoscopy, regardless of the extent of involved mucosa. Control participants from the same geographic region were

Results

Characteristics of the 235 cases (163 males, 72 females) and 244 control participants (163 males, 81 females) are presented in Table 1. BO cases reported higher prevalences of cigarette smoking (current smoker: 14% BO cases, 9% controls; p < 0.0001) and GOR symptoms (more than weekly: 78% BO cases, 31% controls; p < 0.0001) than population controls. This strong association with GOR symptoms was found in both males (p < 0.0001) and females (p < 0.0001). We observed no differences in the prevalence of

Discussion

We have measured total body fat in a large series of patients with BO and population controls using a well-characterized instrument. We found that people in the highest tertile of total body fat (whether measured in terms of absolute weight or percentage) had statistically significant 2-fold increases in the risk of BO. This association between total body fat and BO was abolished after adjusting for waist circumference, whereas the strong association between waist circumference and risk of BO

Competing interests

The authors have no competing interests.

Author contributions

Guarantor of the article – BJK. BJK, GAM, JBP and DCW designed and obtained funding for this study and DCW for the SDH study. SO managed the research nursing staff. BJK performed the statistical analysis and wrote the first draft of the manuscript. DCW provided overall supervision. All authors read and approved the final version of the manuscript.

Funding

This study was funded by grants by the Queensland Cancer Fund (Grant 442962) and, Queensland Government Smart State Fund. The SDH was funded by the National Cancer Institute (Grant RO1 CA 001833). DCW is supported by a Future Fellowship from the Australia Research Council. The funding bodies played no role in the design or conduct of the study; the collection, management, analysis, or interpretation of the data; or preparation, review, or approval of the manuscript.

Acknowledgements

The authors thank Sullivan and Nicolaides Pathology, Queensland Medical Laboratories and the Queensland Health Pathology Service for identifying participants for this study. They are also grateful to Peter Schultz, Lauren Aoude, Loralie Parsonson, Stephen Walsh, Mitchell Stark and John Cardinal for technical support.

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    Study of Digestive Health Investigators are listed in Appendix A.

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