The majority of gallstone patients remain asymptomatic; however, interest toward the gallstone disease is continuing because of the high worldwide prevalence and management costs and the development of gallstone symptoms and complications. For cholesterol gallstone disease, moreover, a strong link exists between this disease and highly prevalent metabolic disorders such as obesity, dyslipidemia, type 2 diabetes, hyperinsulinemia, hypertriglyceridemia and the metabolic syndrome. Information on the natural history as well as the diagnostic, surgical (mainly laparoscopic cholecystectomy) and medical tools available to facilitate adequate management of cholelithiasis and its complications are, therefore, crucial to prevent the negative outcomes of gallstone disease. Moreover, some risk factors for gallstone disease are modifiable and some preventive strategies have become necessary to reduce the onset and the severity of complications.
Cholesterol gallstone disease is a major health problem in Westernized countries and depends on a complex interplay between genetic factors, lifestyle and diet, acting on specific pathogenic mechanisms. Overweigh, obesity, dyslipidemia, insulin resistance and altered cholesterol homeostasis have been linked to increased gallstone occurrence, and several studies point to a number of specific nutrients as risk- or protective factors with respect to gallstone formation in humans, motivating a rising interest in the identification of common and modifiable dietetic factors that put the patients at risk of gallstones or that are able to prevent gallstone formation and growth. In particular, dietary models characterized by increased energy intake with highly refined sugars and sweet foods, high fructose intake, low fiber contents, high fat, consumption of fast food and low vitamin C intake increase the risk of gallstone formation. On the other hand, high intake of monounsaturated fats and fiber, olive oil and fish (ω-3 fatty acids) consumption, vegetable protein intake, fruit, coffee, moderate alcohol consumption and vitamin C supplementation exert a protective role. The effect of some confounding factors (e.g., physical activity) cannot be ruled out, but general recommendations about the multiple beneficial effects of diet on cholesterol gallstones must be kept in mind, in particular in groups at high risk of gallstone formation.
Several beneficial effects of physical activity are anticipated on metabolic disorders linking liver steatosis, gallstone disease, gut motility, enterohepatic circulation of signalling bile acids in relation to intestinal microbiota and inflammatory changes.
Irritable bowel syndrome (IBS) is a chronic functional disorder of the gastrointestinal tract and is one of the most commonly diagnosed gastrointestinal diseases. The impact of IBS on the general population is large due to its high prevalence, suboptimal medical treatments and significant economic burden. The pathophysiology of IBS is complex and treatments are often symptom-specific. The most common therapeutic approaches for IBS include education and reassurance, lifestyles (especially nutrition-based interventions), peripherally acting medications (which typically target motility), centrally acting medications (which target visceral hypersensitivity and pain) and psychological interventions (which aim to reduce the effects of stress or symptom-specific anxiety). A beneficial dietary approach might include the following measures: a diet low in fermentable oligo-,di- and monosaccharides and polyols (FODMAPs), limitation or exclusion of gas-producing foods and/or lactose and gluten and fiber supplementation in selected cases. New therapeutic agents, namely nutraceutics, are also an interesting option in the management of IBS patients. This paper will focus on available dietary interventions for IBS and will review the evidence for nutrition-based therapies.
Realsil administration effectively contrasts hepatocyte fat deposition, NO derivatives formation, and mitochondrial alterations, allowing the liver to maintain a better glutathione and thioredoxin antioxidant activity.
The precipitation of classical parallelogram-shaped cholesterol monohydrate crystals from supersaturated gallbladder bile is the fi rst irreversible physical-chemical event during the early stage of cholesterol gallstone formation ( 1 ). It is well known that estrogen has a critical role in the pathogenesis of cholesterol cholelithiasis because gallstone prevalence is markedly higher in women than in men at all ages in every population studied ( 2 ). Many clinical studies have found that the use of oral contraceptives and conjugated estrogens in premenopausal and postmenopausal women signifi cantly increases the prevalence of gallstones ( 3-5 ). Because elevated estrogen levels have a linear and positive relationship with the duration of gestation, the risk of gallstone formation becomes higher in the third trimester of pregnancy ( 6 ). Increasing parity is a risk factor for gallstones, especially in younger women. Similar lithogenic effects are also found in men with prostatic cancer during estrogen therapy ( 7,8 ). These epidemiological and clinical studies have clearly demonstrated that high susceptibility to gallstone formation in women compared with men is related to differences in how the liver metabolizes cholesterol in response to estrogen ( 9 ).We have found that the classical estrogen receptor ␣ (ER ␣ ), but not ER  , in the liver plays a critical role in the pathogenesis of 17  -estradiol (E 2 )-induced gallstones in female mice ( 10 ). Despite these observations, the metabolic abnormalities underlying the lithogenic effect of E 2 on gallstone formation is not fully understood because the targeted deletion of the Er ␣ gene cannot completely protect against gallstone formation in ovariectomized (OVX) female mice treated with high doses of E 2 ( 11 ). Moreover, the discovery of the G protein-coupled receptor 30 (GPR30), a novel estrogen receptor, has led to a new question of whether it is involved in the lithogenic effect of
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