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Dietary glycaemic index, glycaemic load and risk of reflux oesophagitis, Barrett's oesophagus and oesophageal adenocarcinoma

Published online by Cambridge University Press:  13 January 2009

H. G. Mulholland
Affiliation:
Cancer Epidemiology & Prevention Research Group, Queens University Belfast, Belfast BT12 6BJ, UK
M. M. Cantwell
Affiliation:
Cancer Epidemiology & Prevention Research Group, Queens University Belfast, Belfast BT12 6BJ, UK
L. A. Anderson
Affiliation:
Cancer Epidemiology & Prevention Research Group, Queens University Belfast, Belfast BT12 6BJ, UK
B. T. Johnston
Affiliation:
Belfast Health & Social Care Trust, Belfast BT8 8BH, UK
R. G. P. Watson
Affiliation:
Belfast Health & Social Care Trust, Belfast BT8 8BH, UK
S. J. Murphy
Affiliation:
Daisy Hill Hospital, Belfast BT35 8DR, UK
H. R. Ferguson
Affiliation:
Craigavon Area Hospital, Belfast BT63 5QQ, UK
J. McGuigan
Affiliation:
Belfast Health & Social Care Trust, Belfast BT8 8BH, UK
J. V. Reynolds
Affiliation:
St James's Hospital, Dublin, Republic of Ireland
H. Comber
Affiliation:
National Cancer Registry, Cork, Republic of Ireland
L. J. Murray
Affiliation:
Cancer Epidemiology & Prevention Research Group, Queens University Belfast, Belfast BT12 6BJ, UK
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Abstract

Type
Abstract
Copyright
Copyright © The Authors 2009

Incidence rates of reflux oesophagitis (RO), Barrett's oesophagus (BO) and oesophageal adenocarcinoma (OAC) appear to be rising in Western communities, particularly among men(Reference Bosetti, Levi, Ferlay, Garavello, Lucchini, Bertuccio, Negri and La Vecchia1Reference Lassen, Hallas and de Muckadell3). The majority of OAC cases develop as a result of progression from BO, which is often preceded by RO. It is important to identify potentially-modifiable risk factors, such as dietary habits, that may affect the risk of developing RO, BO and OAC. Studies of other cancer sites have suggested a possible association between dietary glycaemic index (GI) and glycaemic load (GL) and cancer risk(Reference Gnagnarella, Gandini, La Vecchia and Maisonneuve4) but this relationship has yet to be explored for OAC.

In an all-Ireland case–control study information was collected from patients with OAC (n 224), long-segment BO (n 220), RO (n 219) and healthy population-based controls (n 256) on lifestyle factors and dietary intake using a 101-item FFQ between March 2002 and July 2005. Multiple logistic regression analysis was applied to examine the association between dietary GI, GL or total carbohydrate intake and disease risk, comparing the highest v. lowest tertiles of intake and also using continuous variables. Regression models adjusted for confounding variables including age, gender, energy intake, smoking, education, occupation, alcohol, medication use and gastro-oesophageal reflux symptoms. The analyses were also conducted based on stratification by BMI and waist:hip ratio categories.

There were no significant associations between total carbohydrate, GI or GL intake and RO or BO. OAC risk was significantly reduced for each 50 g/d increase in total carbohydrate intake (OR 0.46 (95% CI 0.33, 0.63)), which remained across all BMI and waist:hip ratio categories. However, a significant increased risk of OAC was detected for each 10 unit increment in GI intake (OR 1.36 (95% CI 1.01, 1.82)), which was further increased among overweight individuals with a high waist:hip ratio (OR 1.86 (95% CI 1.20, 2.90)). No significant associations were observed between GL and OAC risk.

These findings indicate that a high GI intake is positively associated with the risk of OAC, particularly among centrally-overweight individuals, and may have contributed to the rising incidence rates. However, total carbohydrate intake was inversely associated with OAC risk. These findings suggest that individuals should eat a diet that is high in carbohydrate content and choose low-GI carbohydrates where possible to reduce their risk of developing OAC.

References

1.Bosetti, C, Levi, F, Ferlay, J, Garavello, W, Lucchini, F, Bertuccio, P, Negri, E & La Vecchia, C (2008) Int J Cancer 122, 11181129.CrossRefGoogle Scholar
2.Fitzgerald, RC (2004) Aliment Pharmacol Ther 20, Suppl. 8, S45S49.CrossRefGoogle Scholar
3.Lassen, A, Hallas, J & de Muckadell, OB (2006) Am J Gastroenterol 101, 11931199.CrossRefGoogle Scholar
4.Gnagnarella, P, Gandini, S, La Vecchia, C & Maisonneuve, P (2008) Am J Clin Nutr 87, 17931801.Google Scholar

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