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Gallstones are round or oval, smooth or faceted lumps of solid matter found in the gallbladder (the sac under the liver where bile is stored and concentrated). Gallstones may be without symptoms or may be associated with periods of intense pain in the abdomen that radiates to the upper back. Symptoms begin only when a gallstone gets stuck in the duct leading from the gallbladder to the intestine. An ultrasound exam provides definitive diagnosis of gallstones.
Gallstones arise when there is an imbalance among the bile components. Bile is composed of: bile salts; bilirubin; cholesterol, phospholipids, and fatty acids; water; electrolytes; and other substances. The most common stones are mixed, containing cholesterol and its derivatives along with varying amounts of bile salts, bile pigments, and inorganic salts of calcium. The required step in mixed stone formation is elevations of cholesterol within the gallbladder. The solubility of bile is based on the relative concentrations of cholesterol, bile acids, phosphatidylcholine (lecithin) and water. Since free cholesterol is water-insoluble, it must be incorporated into a lecithin-bile salt mixture. Either an increase in cholesterol secretion or a decrease in bile acid or lecithin secretion will result in the bile becoming supersaturated with cholesterol. Once the bile is supersaturated with cholesterol, it sets the stage for any particulate matter to begin attracting the cholesterol and initiate stone formation.
A low fiber diet is one of the main causes of gallstones. Such a diet, high in refined carbohydrates and fat and low in fiber, leads to a reduction in the synthesis of bile acids by the liver and a lower bile acid concentration in the gallbladder. Thereby, significantly reducing the solubility of the bile. A high intake of refined sugar is also a risk factor for gallstones.
The frequency of gallstones is two to four times greater in women than in men. Women are predisposed to gallstones because of either increased cholesterol synthesis or suppression of bile acids by estrogens. Pregnancy, use of oral contraceptives, or other causes of elevated estrogen levels greatly increase the incidence of gallstones. Obesity is also associated with a significant increased risk for gallstones.
For prevention and treatment of gallstones, increase intake of vegetables, fruits, and dietary fiber, especially the gel-forming or mucilaginous fibers as found in flaxseed, oat bran, guar gum, and pectin; reduce consumption of saturated fats, cholesterol, sugar, and animal proteins; avoid all fried foods; and drink at least 6 eight-ounce glasses of water each day to maintain the proper water content of the bile.
A vegetarian diet has been shown to be protective against gallstone formation. While this simply may be a result of the increased fiber content of the vegetarian diet, other factors may be equally important. Animal proteins, such as casein from dairy products, have been shown to increase the formation of gallstones in animals while vegetable proteins, such as soy, have been shown to be preventive against gallstone formation.
Achieving ideal body weight is an important goal in the treatment and prevention of gallstones. Obesity causes an increased secretion of cholesterol in the bile as a result of increased cholesterol synthesis. It is important to recognize that during active weight reduction, bile cholesterol saturation initially increases. The secretion of all bile components is reduced during weight loss, but the secretion of bile acids decreases more than that of cholesterol. Therefore, it is a good idea for people on weight-loss programs to support liver function with high-fiber foods and plenty of liquids. Consumption of 6-to-8 glasses of liquids is necessary each day to maintain the water content of bile. Pure water or fresh fruit and vegetable juices are the preferred ways to meet your body;s water requirements. Once the weight is stabilized, bile acid output returns to normal levels while the cholesterol output remains low. The net effect of weight loss is a significant reduction in cholesterol saturation.