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REVIEW

Contributions of Obesity and Weight Loss to Gallstone Disease

right arrow James E. Everhart

15 November 1993 | Volume 119 Issue 10 | Pages 1029-1035

Objective: To examine the relation of obesity and weight loss to the formation of gallstones according to pertinent clinical and research issues.



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Figure 1. Risk for developing gallstones according to percentage of weight loss. Patients were evaluated with gallbladder ultrasonography before and after a 16-week, very low calorie diet (520 kcal, 1 g of fat per day).

 
Data Sources and Extraction: Original reports obtained through a MEDLINE search from 1966 to 1992 on gallstones plus obesity or reducing diets, supplemented by a manual search of bibliographies, a Current Contents title search from 1991 to 1992 on gallstones and gallbladder, and expert opinion. Only studies of humans were cited.

Data Synthesis: For women, but less so for men, obesity is a strong risk factor for gallstones, and this risk is increased during weight loss. Between 10% and 25% of obese men and women may develop gallstones within a few months of beginning a very low calorie diet, and perhaps one third of these will develop symptoms of gallstones. Persons with the highest body mass index before weight loss and those who lose weight most rapidly appear to be at the greatest risk for gallstones. Treatment with ursodeoxycholic acid (ursodiol) during weight loss dieting is the only proven prevention for the formation of gallstones. Issues to be resolved include how different diets affect the risk for developing gallstones, the identification of other risk factors for gallstone formation during weight loss, the effect of weight loss among people with preexisting gallstones, and the optimum means of preventing gallstones during weight loss.

Conclusions: During weight loss, particularly among the obese, an increased risk exists for symptomatic gallstone formation. This acute risk offers the opportunity to investigate the cause of gallstones and possibly to prevent them.

Author and Article Information
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From the National Institute of Diabetes and Digestive and Kidney Diseases, Bethesda, Maryland.
Requests for Reprints: James Everhart, MD, MPH, 5333 Westbard Avenue, Room 3A-10, Westwood Building, Bethesda, MD 20892.
Acknowledgments: The author thanks Willis Foster of the National Institute of Diabetes and Digestive and Kidney Diseases for his literature search on this topic and members of the National Task Force on Prevention and Treatment of Obesity for their guidance and comments on the manuscript. Data for Figure 1 were graciously provided by Dr. Huiying Yang of the Division of Medical Genetics, Cedars-Sinai Medical Center, Los Angeles, California.

 

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