The role of gallbladder emptying in gallstone formation during diet-induced rapid weight loss

Gebhard, Roger L.; Prigge, William F.; Ansel, Howard J.; Schlasner, Linda A.; Ketover, Scott R.; Sande, Deborah; Holtmeier, Karen; Peterson, Francis J.

doi:10.1002/hep.510240313

Cited by 91 publications

(38 citation statements)

References 30 publications

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“…Thus, the risk for gallstones is substantially increased in these patients [106] that might be further increased by higher levels of DCA by impaired intestinal motility [107, 108]. For the prevention of gallstone development by gallbladder dysmotility, CCK injections have been recommended in patients receiving long‐term TPN [109], and small fat containing meals during weight reducing diets [110]. Recent study in mice showed that fibroblast growth factor 15 (FGF‐15; human homologue, FGF‐19), a hormone made by the distal small intestine in response to bile acids suppressing Cyp7a1 in the liver [111] as a counter player of CCK also controls gallbladder filling [112].…”

Section: Gallbladder Hypomotilitymentioning

confidence: 99%

Gallstone disease

Marschall

Einarsson

2007

Journal of Internal Medicine

171

130

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Gallstone disease is one of the most prevalent gastrointestinal diseases with a substantial burden to health care systems that is supposed to increase in ageing populations at risk. Aetiology and pathogenesis of cholesterol gallstones still are not well defined, and strategies for prevention and efficient nonsurgical therapies are missing. This review summarizes current concepts on the pathogenesis of cholesterol gallstones with focus on the uptake and secretion of biliary lipids and special emphasis on recent studies into the genetic background.Keywords: gastroenterology, hepatology.Gallstones are a common clinical finding in the Western populations. Ultrasound studies indicate mean prevalence rates of 10-15% in adult European, and of 3-5% in African and Asian populations [1]. In the US, the prevalence rates range from 5% for nonHispanic black men to 27% for Mexican-American women [2]. In American Indians, gallstone disease is epidemic and found in 73% of adult female Pima Indians [3], and in 30% of male and 64% of female in other American Indians [4].More than 80% of gallstone carriers are unaware of their gallbladder disease [5,6], but about 1-2% per year of patients develop complications and need surgery [7]. In the US, gallstone disease has the most common inpatient diagnosis among gastrointestinal and liver diseases [8] and stands for $5.8 billion direct costs, exceeded only by gastroesophageal reflux disease [9]. Risk factorsFemale gender, fecundity, and a family history for gallstone disease are strongly associated with the formation of cholesterol gallstones [10] (Table 1). Obesity [11,12] as well also other factors contributing to the metabolic syndrome [13] such as dyslipidemia (in particular hyperlipoproteinemia type IV [14-16] with hypertriglyceridemia and low HDL cholesterol), hyperinsulinemia-insulinresistence [17,18] or overt type 2 diabetes are risk factors for the development of gallstones, itself supposed to be a complication of the metabolic syndrome [19]. Oestrogen-treatment enhances the risk, both in women when used for anticonception or hormone-replacement [20] and in men with prostatic cancer [21,22]. Among specific dietary factors, short-time high cholesterol [23] as well as high-carbohydrate diets were associated with increased risk for gallstones [24,25], and in highly prevalent areas, the intake of legume [26], while unsaturated fats [27], coffee [28], and moderate consumption of alcohol [24,29] seem to reduce the risk. Also physical activity was found to decrease the risk for symptomatic gallstone disease, both for men and women [30,31], and independent of weight reduction. On the other hand, rapid active weight loss [32,33] and weight cycling [34,35] strongly increase the risk for the development of gallstones. Thus, weight reductions should not exceed 1.5 kg per week [36]. Fibrates, used for the treatment of dyslipidemia, interfere with cholesterol and bile acid synthesis and increase cholesterol secretion into bile [37,38]. However, in contrast to the prototype Clofibrate, during ...

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Section: Gallbladder Hypomotilitymentioning

confidence: 99%

Gallstone disease

Marschall

Einarsson

2007

Journal of Internal Medicine

171

130

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“…Rapid weight loss and weight cycling alter the ratio of cholesterol to bile salts in the gallbladder. This results from increased cholesterol mobilisation from peripheral tissue, coupled with increased hepatic synthesis of cholesterol [84,85,86]. Additionally, gallbladder motility is impaired, which leads to bile stasis and the formation of biliary sludge.…”

Section: Lifestyle Factorsmentioning

confidence: 99%

Gallstones: Environment, Lifestyle and Genes

Stokes

Krawczyk

Lammert³

2011

Dig Dis

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Gallstone disease represents one of the most common and costly gastroenterological disorders. In Germany, 0.25% of the population undergo cholecystectomy per year, and cholelithiasis incurs annual medical expenses of more than USD 6.5 billion in the United States. The paradigm of environmental risk factors for gallstones has lately been challenged by genetic studies in experimental models and humans. The analysis of more than 40,000 Swedish twin pairs with gallstones demonstrated that genetic factors account for 25% of the phenotypic variance. Since then, studies employing genome-wide association analysis, case-control cohorts and analysis of sib-pairs in families with gallstones have expanded our knowledge of ‘gallstone genes’. Indeed, gallstone disease phenotypes are likely to result from the complex interaction of genetic factors, chronic overnutrition with carbohydrates, depletion of dietary fibre and other not fully defined environmental factors including physical inactivity and infections. This hypothesis is supported by the profound increases of cholesterol gallstone prevalence rates in Native Americans, post-war European countries and current urban centres in East Asia, all of which were associated with ‘westernized’ nutrition. Herein, we summarise the spectrum of environmental and genetic risk factors which should pave the way to ‘personalised’ strategies for the prevention and therapy of gallstones.

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“…10, 11, 12, 13, 14 Later studies included VLCDs containing higher fat content (12–30 g per day), 21, 22, 23, 24 two of which were randomized controlled trials. 21, 22 None developed systematic gallstones in the high-fat group in either of the studies, suggesting that an adequate fat intake reduces gallstone formation. The fat content of the VLCD in our study was 7–9 g per day, consistent with the 7 g per day recommendation given by the European SCOOP-report on VLCD use.…”

Section: Discussionmentioning

confidence: 99%

Risk of symptomatic gallstones and cholecystectomy after a very-low-calorie diet or low-calorie diet in a commercial weight loss program: 1-year matched cohort study

et al. 2013

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Background:Concern exists regarding gallstones as an adverse event of very-low-calorie diets (VLCDs; <800 kcal per day).Objective:To assess the risk of symptomatic gallstones requiring hospital care and/or cholecystectomy in a commercial weight loss program using VLCD or low-calorie diet (LCD).Design:A 1-year matched cohort study of consecutively enrolled adults in a commercial weight loss program conducted at 28 Swedish centers between 2006 and 2009. A 3-month weight loss phase of VLCD (500 kcal per day) or LCD (1200–1500 kcal per day) was followed by a 9-month weight maintenance phase. Matching (1:1) was performed by age, sex, body mass index, waist circumference and gallstone history (n=3320:3320). Gallstone and cholecystectomy data were retrieved from the Swedish National Patient Register.Results:One-year weight loss was greater in the VLCD than in the LCD group (−11.1 versus −8.1 kg; adjusted difference, −2.8 kg, 95% CI −3.1 to −2.4; P<0.001). During 6361 person–years, 48 and 14 gallstones requiring hospital care occurred in the VLCD and LCD groups, respectively, (152 versus 44/10 000 person–years; hazard ratio, 3.4, 95% CI 1.8–6.3; P<0.001; number-needed-to-harm, 92, 95% CI 63–168; P<0.001). Of the 62 gallstone events, 38 (61%) resulted in cholecystectomy (29 versus 9; hazard ratio, 3.2, 95% CI 1.5–6.8; P=0.003; number-needed-to-harm, 151, 95% CI 94–377; P<0.001). Adjusting for 3-month weight loss attenuated the hazard ratios, but the risk remained higher with VLCD than LCD for gallstones (2.5, 95% CI 1.3–5.1; P=0.009) and became borderline for cholecystectomy (2.2, 95% CI 0.9–5.2; P=0.08).Conclusion:The risk of symptomatic gallstones requiring hospitalization or cholecystectomy, albeit low, was 3-fold greater with VLCD than LCD during the 1-year commercial weight loss program.

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The role of gallbladder emptying in gallstone formation during diet-induced rapid weight loss

Cited by 91 publications

References 30 publications

Gallstone disease

Gallstone disease

Gallstones: Environment, Lifestyle and Genes

Risk of symptomatic gallstones and cholecystectomy after a very-low-calorie diet or low-calorie diet in a commercial weight loss program: 1-year matched cohort study

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