Several prospective studies have suggested that physical activity may decrease the risk for symptomatic gallbladder disease. None of these studies were able to include subjects with asymptomatic gallstones in their case group.
This investigation examined the relationship between physical activity levels and the development of gallbladder disease determined by ultrasonography in a population-based cohort of 3143 men and women, 45-74 yr of age, from 13 American Indian communities. Participants were examined at baseline (1989-1992), at which time physical activity levels, age, body mass index, waist circumference, smoking status, and diabetes status were determined. Gallbladder disease status was assessed in the entire cohort at follow-up (1993-1995) by ultrasonography.
Individuals who reported at baseline that they had gallbladder surgery or that a physician had told them that they had gallbladder disease were removed from the analyses. Out of the 2130 remaining, 650 individuals (403 women and 247 men) were found to have gallbladder disease according to ultrasound or reported surgery by the follow-up clinic visit. After adjusting for potential confounders including body mass index, increased activity levels were inversely related to gallbladder disease status. These findings were maintained when the data were stratified by sex, but they were only significant in individuals without diabetes (not in those with diabetes).
Physical activity seems to be significantly and inversely related to the development of gallbladder disease as assessed by ultrasonography in a population at high risk for gallbladder disease. These findings add to the evidence supporting a causal link between physical activity levels and a decreased risk of gallbladder disease, and they provide yet another reason to encourage the achievement and maintenance of a physically active lifestyle.
1Department of Epidemiology, Graduate School of Public Health, University of Pittsburgh, Pittsburgh, PA; 2School of Health and Rehabilitation Sciences, University of Pittsburgh, Pittsburgh, PA; 3MedStar Research Institute, Phoenix, AZ and Hyattsville, MD; 4National Institute of Diabetes and Digestive and Kidney Diseases, Bethesda, MD; 5University of Pittsburgh Medical Center, Pittsburgh, PA; and 6Family Medicine, University of Michigan, and VA Medical Center, Ann Arbor, MI
Address for correspondence: Andrea Kriska, Ph.D., Department of Epidemiology, GSPH, University of Pittsburgh, 130 DeSoto Street, Pittsburgh, PA 15261; E-mail: email@example.com.
Submitted for publication October 2006.
Accepted for publication June 2007.