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  Vol. 160 No. 7, April 10, 2000 TABLE OF CONTENTS
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Serum Ascorbic Acid and Gallbladder Disease Prevalence Among US Adults

The Third National Health and Nutrition Examination Survey (NHANES III)

Joel A. Simon, MD, MPH; Esther S. Hudes, PhD, MPH

Arch Intern Med. 2000;160:931-936.

Background  Ascorbic acid–deficient guinea pigs frequently develop gallstones, and ascorbic acid status may also affect the risk of gallbladder disease in humans. To examine the relationship of ascorbic acid, an antioxidant nutrient involved in cholesterol catabolism, to gallbladder disease, we analyzed data collected from a probability sample of US adults.

Methods  Analyses of data from 7042 women and 6088 men enrolled in the Third National Health and Nutrition Examination Survey, 1988-1994, were performed. Multiple logistic regression models stratified by sex were examined, controlling for the effects of age, race, diet, body mass index, and other potential confounders.

Results  A total of 761 women (11%) and 235 men (4%) reported a history of clinical gallbladder disease (symptomatic gallstones or cholecystectomy). Of the 9650 participants without a history of clinical gallbladder disease or abdominal pain consistent with gallbladder disease, and with valid abdominal ultrasonography, 408 (8%) of 4863 women and 274 (6%) of 4787 men had asymptomatic gallstones. Serum ascorbic acid level was inversely related to prevalence of clinical and asymptomatic gallbladder disease among women, but not among men. Among women, each SD (27 µmol/L) increase in serum ascorbic acid level was independently associated with a 13% lower prevalence of clinical gallbladder disease (P=.006) and asymptomatic gallstones (P=.048).

Conclusion  Ascorbic acid, which affects the catabolism of cholesterol to bile acids and, in turn, the development of gallbladder disease in experimental animals, may affect the risk of gallbladder disease among women.


From the General Internal Medicine Section, Medical Service, Veterans Affairs Medical Center, San Francisco, Calif, and University of California, San Francisco (Dr Simon); and Department of Epidemiology and Biostatistics, University of California, San Francisco (Drs Simon and Hudes).



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