gallstones
Gut 2005;54:823-828 doi:10.1136/gut.2003.031435
Hepatobiliary disease
Dietary carbohydrates and glycaemic load and the incidence of symptomatic gall stone disease in men
C-J Tsai1,
M F Leitzmann2,
W C Willett3,
E L Giovannucci3
+ Author Affiliations
1Division of Digestive Diseases and Nutrition, University of Kentucky Medical Center, Lexington, Kentucky, USA, and Channing Laboratory, Department of Medicine, Harvard Medical School and Brigham and Women’s Hospital, Boston, Massachusetts, USA
2Channing Laboratory, Department of Medicine, Harvard Medical School and Brigham and Women’s Hospital, Boston, Massachusetts, USA, and Division of Cancer Epidemiology and Genetics, National Cancer Institute, NIH, DHHS, Bethesda, Maryland, USA
3Channing Laboratory, Department of Medicine, Harvard Medical School and Brigham and Women’s Hospital, Boston, Massachusetts, USA, and Departments of Nutrition and Epidemiology, Harvard School of Public Health, Boston, Massachusetts, USA
Correspondence to:
Dr C-J Tsai
Division of Digestive Diseases and Nutrition, University of Kentucky Medical Center, 800 Rose St, Lexington, Kentucky 40536-0298, USA; hpcjt@channing.harvard.edu
Accepted 8 November 2004
Revised 29 October 2004
Abstract
Background: Diets with a high glycaemic response exacerbate the metabolic consequences of the insulin resistance syndrome. Their effects on the incidence of gall stone disease are not clear, particularly in men.
Methods: Dietary information was collected as part of the Health Professionals Follow up Study starting in 1986 using a semiquantitative food frequency questionnaire with follow up until 1998. On biennial questionnaires participants reported new symptomatic gall stone disease, diagnosed by radiology, and whether they had undergone cholecystectomy.
Results: During 12 years of follow up, we documented 1810 new cases of symptomatic gall stones. After adjusting for age and other known or suspected risk factors in multivariate models, the relative risk (RR) for the highest compared with the lowest quintile of carbohydrate intake was 1.59 (95% confidence interval (CI) 1.25, 2.02; p for trend = 0.002). The RR for the highest compared with the lowest quintile of dietary glycaemic load was 1.50 (95% CI 1.20, 1.88; p for trend = 0.0008), and 1.18 for dietary glycaemic index (95% CI 1.01, 1.39; p for trend = 0.04). Independent positive associations were also seen for intakes of starch, sucrose, and fructose.
Conclusions: Our findings suggest that a high intake of carbohydrate, glycaemic load, and glycaemic index increases the risk of symptomatic gall stone disease in men. These results add to the concern that low fat high carbohydrate diets may not be an optimal dietary recommendation.
Hepatobiliary disease
Dietary carbohydrates and glycaemic load and the incidence of symptomatic gall stone disease in men
C-J Tsai1,
M F Leitzmann2,
W C Willett3,
E L Giovannucci3
+ Author Affiliations
1Division of Digestive Diseases and Nutrition, University of Kentucky Medical Center, Lexington, Kentucky, USA, and Channing Laboratory, Department of Medicine, Harvard Medical School and Brigham and Women’s Hospital, Boston, Massachusetts, USA
2Channing Laboratory, Department of Medicine, Harvard Medical School and Brigham and Women’s Hospital, Boston, Massachusetts, USA, and Division of Cancer Epidemiology and Genetics, National Cancer Institute, NIH, DHHS, Bethesda, Maryland, USA
3Channing Laboratory, Department of Medicine, Harvard Medical School and Brigham and Women’s Hospital, Boston, Massachusetts, USA, and Departments of Nutrition and Epidemiology, Harvard School of Public Health, Boston, Massachusetts, USA
Correspondence to:
Dr C-J Tsai
Division of Digestive Diseases and Nutrition, University of Kentucky Medical Center, 800 Rose St, Lexington, Kentucky 40536-0298, USA; hpcjt@channing.harvard.edu
Accepted 8 November 2004
Revised 29 October 2004
Abstract
Background: Diets with a high glycaemic response exacerbate the metabolic consequences of the insulin resistance syndrome. Their effects on the incidence of gall stone disease are not clear, particularly in men.
Methods: Dietary information was collected as part of the Health Professionals Follow up Study starting in 1986 using a semiquantitative food frequency questionnaire with follow up until 1998. On biennial questionnaires participants reported new symptomatic gall stone disease, diagnosed by radiology, and whether they had undergone cholecystectomy.
Results: During 12 years of follow up, we documented 1810 new cases of symptomatic gall stones. After adjusting for age and other known or suspected risk factors in multivariate models, the relative risk (RR) for the highest compared with the lowest quintile of carbohydrate intake was 1.59 (95% confidence interval (CI) 1.25, 2.02; p for trend = 0.002). The RR for the highest compared with the lowest quintile of dietary glycaemic load was 1.50 (95% CI 1.20, 1.88; p for trend = 0.0008), and 1.18 for dietary glycaemic index (95% CI 1.01, 1.39; p for trend = 0.04). Independent positive associations were also seen for intakes of starch, sucrose, and fructose.
Conclusions: Our findings suggest that a high intake of carbohydrate, glycaemic load, and glycaemic index increases the risk of symptomatic gall stone disease in men. These results add to the concern that low fat high carbohydrate diets may not be an optimal dietary recommendation.
posted by vanwash at 10:32 AM
3 Comments:
The liver produces bile, which is composed of bile acids, cholesterol, and a few other substances. This bile travels from the liver to the gall bladder—a little sack tucked beneath the liver—through a small tube called the hepatic duct. The gall bladder stores the bile and waits for a fatty meal to enter the small intestine. When the fatty meal arrives, the gall bladder squeezes the bile out through the bile duct (another small tube) that joins with the hepatic duct to form the common duct and empties into the upper end of the small intestine. So when the fatty meal arrives, the gall bladder douses it with the bile it has been storing for just this occasion. The bile then mixes with the fat and breaks it down for absorption as described above.
If very few fatty meals come down the tract—for example, if the owner of the GI tract is following the Ornish or other low-fat diet—the bile sits around in the gall bladder, unsquirted. The liver continues to make bile, but slows down a little in its production. The cholesterol component of the bile tends to become more concentrated with time and can ultimately become supersaturated and precipitate as a small cholesterol gallstone (cholesterol accounts for 80-90% of gallstones). If the stone stays in the gall bladder, it typically doesn’t pose a problem. The problem arises when the stone makes its way into and occludes the bile duct, or, even worse, if it travels further and blocks the common duct. In either case, terrible, colicky pain ensues ending up with a trip to the surgeon.
If one eats fatty foods often, then the gall bladder constantly empties itself and generally stays free from gall stones. If a one doesn’t eat much fat because one is following a low-fat diet or one is on one of the modified fasting programs (Optifast, Medifast, etc.), then one’s gall bladder doesn’t empty and the bile sits around supersaturating. Then if one blows it out, so to speak, on a big steak dinner, or a giant cheeseburger, or any kind of fatty meal, the gall bladder squeezes this sludgy gunk that may contain a few small stones into the bile duct, and, bingo!, one has a serious problem all of a sudden. One of the big problems people have with the fasting programs and with low-fat diets is a high incidence of gall bladder disease. We did a large maintenance study a few years ago in our clinic for the weight-loss drug Orlistat (now Xenical) during which we had to put patients on a low-fat weight-loss diet for six months, then they were randomized onto on of a number of doses of Orlistat or placebo. Before they started the six month low-fat diet, the subjects all underwent a gall bladder ultrasound looking for stones. Anyone found with stones couldn’t participate in the study. Those without stones started the diet and had another ultrasound at the end of the six months on the low-fat diet, but before starting the medication. I can’t remember how exactly many patients developed gall stones during that six month period without going back through the data, which is stored 1000 miles away right now, but I do remember that it was a considerable number, something like 10-20% it seems.
On Orlistat-According to researchers, unabsorbed bile acids and fatty acids react with calcium forming "soaps" in the intestinal lumen that limit the amount of free calcium binding with oxalate. Hence, more oxalate is available to be absorbed and eventually excreted with urine
The increased intraluminal free fatty acids complex with intraluminal calcium ions, competitively inhibiting the precipitation of oxalate with calcium. The increase in soluble uncomplexed oxalate facilitates oxalate absorption.
Further absorption can occur in the colon which has increased permeability to oxalate in the presence of excess bile salts and free fatty acids
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