what's the best protocol for a fatty liver ?
many stones liver is clogged
i have read alot about liver flush with oil and epson salt is there anything else ?
did this once many stones came out.
opcorn:
i think i got this from the Epstein barr virus many years ago and stil getting worse
What makes you believe you have a "fatty liver?" By "liver stones," do you mean bile duct or gall stones? Currently, the only accepted treatment for NAFLD is lifestyle modifications. These include weight loss by a combination of decreased caloric intake and increased physical activity. There is sparse research for supplements (Milk Thistle) in fatty liver disease.
Nonalcoholic fatty liver disease (NAFLD) represents a spectrum of conditions characterized by mainly hepatic steatosis and occurs in those who do not consume alcohol in amounts generally considered to be harmful to the liver. NAFLD is an increasingly recognized cause of liver-related morbidity and mortality. Currently, the only accepted way to diagnose NAFLD is by a careful medical history combined with liver biopsy. Most individuals with NAFLD have been diagnosed after abnormal liver function tests and/or ultrasound or computed tomography scans indicated a fatty liver. It is possible to have NAFLD, especially the chronic, progressive form, in the setting of apparently normal liver function tests and a minimal fatty liver. It also is important to note that NAFLD is not obligatorily associated with obesity, metabolic syndrome, or type 2 diabetes. Individuals without these conditions can, and do, develop NAFLD, and certainly not all individuals who are obese or have metabolic syndrome or type 2 diabetes develop progressive NAFLD.
The following are some resources to begin a search.
Mehta SR.
Advances in the treatment of nonalcoholic fatty liver disease. Therapeutic Advances in Endocrinology and Metabolism.
Advances in the treatment of nonalcoholic fatty liver disease — Therapeutic Advances in Endocrinology and Metabolism
Nonalcoholic fatty liver disease (NAFLD) is the most common cause of chronic liver disease in the Western world, and its prevalence is predicted to rise in the future in parallel with rising levels of obesity and type 2 diabetes mellitus. It is commonly associated with insulin resistance. Many patients have coexisting obesity, hypertension, dyslipidaemia or hyperglycaemia, and are at increased risk of developing cardiovascular disease. Although patients with simple steatosis have a good prognosis, a significant percentage will develop nonalcoholic steatohepatitis which may progress to cirrhosis, end-stage liver failure and hepatocellular carcinoma. Despite promising results from several pilot studies and small to medium randomized controlled trials, there is currently no pharmacological agent that is licensed for the treatment of NAFLD. At present the mainstay of treatment for all patients is lifestyle modification using a combination of diet, exercise and behavioural therapy. With recent advances in the understanding of the pathogenesis of NAFLD, the goal of treatment has shifted from simply trying to clear fat from the liver and prevent progressive liver damage to addressing and treating the metabolic risk factors for the condition. To reduce liver-related and cardiovascular morbidity and mortality, all patients with NAFLD should be invited to enrol in adequately powered, randomized controlled studies testing novel therapies, many of which are targeted at reducing insulin resistance or preventing progressive liver disease. Coexisting obesity, hypertension, dyslipidaemia or hyperglycaemia should be treated aggressively. Orlistat, bariatric surgery, angiotensin receptor blockers, statins, fibrates, metformin and thiazolidinediones should all be considered, but treatments should be carefully tailored to meet the specific requirements of each patient. The efficacy and safety of any new treatment, as well as its cost-effectiveness, will need to be carefully evaluated before it can be advocated for widespread clinical use.
Erickson SK.
Nonalcoholic fatty liver disease. J Lipid Res 2009;50(Supplement):S412-6. http://www.jlr.org/cgi/content/full/50/Supplement/S412
Nonalcoholic fatty liver disease (NAFLD) is the most common liver disease in the United States and, indeed, worldwide. It has become a global public health issue. In the United States, the prevalence in the general population is estimated at [~]20%, while that in the morbidly obese population at [~]75-92% and in the pediatric population at [~]13-14%. The progressive form of NAFLD, nonalcoholic steatohepatitis, is estimated at [~]3-5%, with [~]3-5% of these having progressed to cirrhosis. Thus, the numbers of individuals at risk for end-stage liver disease and development of primary liver cancer is large. NAFLD is an independent risk factor for cardiovascular disease, leads to increased all-cause mortality, and to increased liver-related mortality. This review focuses on recent advances in our understanding of the NAFLD disease spectrum, including etiology, diagnosis, treatment, and genetic and environmental risk factors and suggests future directions for research in this important area.
Stefan N, Kantartzis K, Haring H-U.
Causes and Metabolic Consequences of Fatty Liver. Endocr Rev 2008;29(7):939-60.
Causes and Metabolic Consequences of Fatty Liver -- Stefan et al. 29 (7): 939 -- Endocrine Reviews
Type 2 diabetes and cardiovascular disease represent a serious threat to the health of the population worldwide. Although overall adiposity and particularly visceral adiposity are established risk factors for these diseases, in the recent years fatty liver emerged as an additional and independent factor. However, the pathophysiology of fat accumulation in the liver and the cross-talk of fatty liver with other tissues involved in metabolism in humans are not fully understood. Here we discuss the mechanisms involved in the pathogenesis of hepatic fat accumulation, particularly the roles of body fat distribution, nutrition, exercise, genetics, and gene-environment interaction. Furthermore, the effects of fatty liver on glucose and lipid metabolism, specifically via induction of subclinical inflammation and secretion of humoral factors, are highlighted. Finally, new aspects regarding the dissociation of fatty liver and insulin resistance are addressed.
