© The Author 2006. Published by Oxford University Press.
CORRESPONDENCE |
RESPONSE: Re: Carbonated Soft Drink Consumption and Risk of Esophageal Adenocarcinoma
Affiliation of authors: Yale University School of Medicine and Yale Cancer Center, New Haven, CT (STM, HAR, RD); National Cancer Institute, Division of Cancer Epidemiology and Genetics, Bethesda, MD (WHC, JFF); University of North Carolina, School of Public Health, Chapel Hill, NC (MDG); Fred Hutchinson Cancer Research Center and University of Washington School of Public Health and Community Medicine, Seattle, WA (TLV)
Correspondence to: Susan T. Mayne, PhD, Yale University School of Medicine, Department of Epidemiology and Public Health, 60 College Street, New Haven, CT 06520-8034 (e-mail: Susan.Mayne{at}yale.edu).
We appreciate the opportunity to address comments by Gallus et al. and by Mallath regarding our recent publication on carbonated soft drink (CSD) consumption and lack of increased esophageal adenocarcinoma risk. Gallus et al. analyzed data from a case–control study in Italy and reported a statistically non-significant inverse association between CSD consumption and risk of esophageal cancer. This was a study of esophageal squamous cell carcinoma rather than adenocarcinoma. Although these findings do not inform a possible link between CSDs and esophageal adenocarcinoma, the replication of our results for squamous cell carcinoma in a different population is reassuring.
Citing data from the Continuing Survey of Food Intakes by Individuals showing greater consumption of CSDs in younger and higher-income subjects, Mallath suggests that case–control differences in age and income might account for the lower consumption of CSDs by case patients than control subjects. We examined variables that could be associated with CSD consumption and, as shown in Table 1 of our manuscript, younger age and higher income were both related to higher CSD consumption among control subjects. Consequently, all of the risk estimates were adjusted for age, income, and education and several other potential confounders (shown in Table 2 of the manuscript). That the determinants of CSD consumption parallel those in the Continuing Survey of Food Intakes by Individuals suggests that the population control subjects in our study are representative of the general population.
Mallath also indicates that we had no data on duration of CSD consumption. We noted this potential limitation in our publication: "intake of CSDs 3–5 years prior to diagnosis might not reflect intake in the distant past." For this to explain our findings, however, case patients who reported consuming fewer CSDs 3–5 years before diagnosis would have had to consume substantially more CSDs in the distant past than control subjects. This seems unlikely unless case patients changed consumption habits to avoid exacerbation of reflux. However, the inverse association between CSD consumption and esophageal adenocarcinoma risk was found to persist among persons without reflux symptoms.
Mallath concludes that CSD may be a new risk factor for gastroesophageal reflux disease, which is consistent with our finding that control subjects who consumed more CSDs reported more frequent reflux symptoms than those who consumed less. An alternative explanation, however, is that CSDs may affect perception of reflux. Recent studies have shown that a majority of reflux episodes are asymptomatic (1), with symptomatic episodes associated with pure gas reflux, acid exposure in the 75 minutes before the reflux episode, and greater refluxate acidity (pH <4), all of which may be related to CSD consumption. Because the determinants of self-reported reflux may simply reflect reflux perception, a causal relationship with esophageal adenocarcinoma risk cannot be assumed without supporting clinical and epidemiologic data.
REFERENCES
(1) Bredenoord AJ, Weusten BLAM, Curvers WL, Timmer R, Smout AJPM. Determinants of perception of heartburn and regurgitation. Gut 2006;55:313–18.
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J Natl Cancer Inst 2006 98: 644-645.
J Natl Cancer Inst 2006 98: 645-646.
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