Fatty Liver Homeopathic Cure

Fatty Liver Remedy

The fatty liver remedy is a program that uses natural ways to treat diseases related to fatty liver. The creator of this program goes by the name of Layla Jeffrey and has for the better part of her life majored in the field of nutrition. This program is very secure and safe to use all the recommended methods in the guide because they have undergone testing and results have proven that they give 100% positive results. This program is worth trying as it involves zero-risk. Within 60 days after joining the program, a total money refund is guaranteed to any user who feels unsatisfied with the program. The program is a life changer as it will help you in the elimination of toxic elements in your body, help improve the level of efficiency of your liver. Also, help you save on the cost as you will use natural treatment methods and the program will free bonuses to help boost your health in a big way. Following all the benefits associated with this program, I highly recommend the fatty liver remedy program to everyone as it will enhance your healthy living permanently. More here...

Fatty Liver Remedy Summary


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All of the information that the author discovered has been compiled into a downloadable book so that purchasers of Fatty Liver Remedy can begin putting the methods it teaches to use as soon as possible.

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Fatty Liver Solution

Fatty Liver Solution is a newly updated book that provides people with an effective treatment for liver damage, and a list of healthy foods to restore their liver function quickly. The book is created by Duncan Capicchiano, a medical researcher with over 10 years of experience in healing hepatic diseases naturally. The Fatty Liver Solution is the achievement of Duncan Capicchianos practial experience when treating his fatty liver patients. Through this guide, the creator brings to readers specific information about symptoms, root causes of fatty liver disease, and solutions to face with this obstinate disease. This treatment does not involve prescription drugs, or any harsh diet. More here...

Fatty Liver Solution Summary

Contents: Ebook
Author: Duncan Capicchiano
Official Website: www.thefattyliversolution.com
Price: $47.00

Acute Fatty Liver of Pregnancy

Acute fatty liver of pregnancy (AFLP) was first described in 1934 and is a rare, idiopathic, potentially fatal disease presenting in the third trimester of pregnancy. Incidence ranges from 1 of 7,000 to 1 of 16,000 deliveries and it constitutions 16 to 43 of severe liver disease seen during pregnancy. In its most severe form, it is manifest by fulminant hepatic failure. Seen worldwide, there appears to be no ethnic or geographic variation. FIGURE 120-1. Acute fatty liver of pregnancy. The zone 3 cen-trilobular hepatocytes are swollen with microvesicular fat globules. Sinusoidal compression can be seen but signs of hepatic necrosis and inflammation are often subtle. Hepatic necrosis is a minor feature. Courtesy of Carolyn A Riely, MD. FIGURE 120-1. Acute fatty liver of pregnancy. The zone 3 cen-trilobular hepatocytes are swollen with microvesicular fat globules. Sinusoidal compression can be seen but signs of hepatic necrosis and inflammation are often subtle. Hepatic necrosis is a...

Brent A Neuschwander TetriMD

Disorders of the liver characterized by fat accumulation in the absence of excessive alcohol consumption are collectively known as nonalcoholic fatty liver disease (NAFLD). Although the presence of excess amounts of fat as triglyceride in hepatocytes may not always be directly harmful, it is typically associated with progressive liver disease. In fact, in some people, NAFLD is capable of causing cirrhosis and leading to death or liver transplantation. The necroinflam-matory changes associated with progressive liver disease are generally identified pathologically as steatohepatitis, and the pattern of injury and constellation of findings most commonly associated with more severe liver disease is called nonalcoholic steatohepatitis (NASH). Insulin resistance (IR) is commonly found in patients with NAFLD and has been implicated as a causative factor in the development of NASH and the associated necroin-flammatory changes (Marchesini et al, 2003). This recent finding has bolstered the...

Interpretation of Abnormal Liver Enzymes

Chronic viral infections, such as hepatitis B (HB) or HC, and fatty liver disease are the most common causes of persistently elevated enzymes. Again, enzymes rarely rise above 300 U L in these settings. HC is the most common chronic hepatotropic infection in Western countries, is asymptomatic, and ALT can range from normal to 10-fold above normal values. HB affects 400 million worldwide and can also present with a spectrum of aminotransferase abnormalities ranging from normal levels to the thousands (U L). Nonalcoholic fatty liver disease is increasingly recognized even in those without the classic risk factors of obesity and diabetes mellitus. Steatosis may develop from medication use, including corticosteroids, amiodarone, and tamoxifen. There is more evidence lately that steatosis may not cause significant enzyme elevations. The typical pattern of enzyme elevation is AST ALT ratio of less than one, with numbers sometimes as high as fivefold the upper limit of normal. Unfortunately,...

Problemsspecial considerations

The differential diagnoses at initial presentation include pre-eclampsia, acute viral hepatitis, drug-induced hepatitis, cholestasis of pregnancy and biliary tract disease. Pruritus is uncommon in acute fatty liver and is highly suggestive of cholestasis. Clinical examination the mother is usually, but not invariably, jaundiced. Although she may complain of abdominal pain it is unusual to find marked Laboratory findings serum alanine and aspartate transaminases levels are increased, but not as high as in viral hepatitis. Bilirubin is increased. Platelet counts fall, and there may be giant platelet formation. Prothrombin time is prolonged, and the more severe the liver damage the more deranged the coagulation profile becomes. There are reduced levels of antithrombin III, and DIC with low fibrinogen levels and increased fibrin degradation products occurs in severe disease. Haemoconcentration may occur secondary to hypovolaemia. There is frequently an increased white cell count and...

Acute renal failure related to pregnancy

Septic abortion and massive haemorrhage (traditionally caused by placental abruption, although any cause of hypovolaemia may be followed by renal failure). Other important causes include pyelonephritis, drug reactions (especially non-steroid anti-inflammatory drugs NSAIDs ), acute fatty liver and incompatible blood transfusion. In most cases, ARF is caused by acute tubular necrosis, although cortical necrosis has been seen after abruption and pre-eclampsia. Problems are those of ARF generally, especially related to fluid balance and the apparently increased susceptibility of pregnant women to developing pulmonary oedema.

Supplemental Reading

Abdelmalek MF, Angulo P, Jorgensen RA, et al. Betaine, a promising new agent for patients with nonalcoholic steatohepatitis results of a pilot study. Am J Gastroenterol 2001 96 2711-7. Angulo P, Lindor KD. Treatment of nonalcoholic fatty liver present and emerging therapies. Semin Liver Dis 2001 21 81-8. Marchesini G, Bugianesi E, Forlani G, et al. Nonalcoholic fatty liver, steatohepatitis, and the metabolic syndrome. Hepatology 2003 37 917-23.

Metabolic Miscellaneous Etiologies

Included in this group are FHF secondary to Wilson's disease (see Chapter 124, Management of Wilson's Disease ), autoimmune hepatitis, Reye's syndrome, and pregnancy-related ALF from acute fatty liver of pregnancy, hemolysis, abnormal liver enzymes and low platelets(HELLP) syndrome, or hepatic rupture (see Chapter 133, Biliary Strictures and Neoplasms ). FHF may be the first clinical manifestation of Wilson's disease. Indeed, Wilson's disease should be considered in any young patient with unexplained FHF, particularly when

Nutritional Management

Nutritional support is less effective in patients with enterocolitis associated with systemic infections. The metabolic rate is elevated, and metabolic derangements promote protein wasting irrespective of intake. Alterations in lipid metabolism often result in the development of fatty liver when nutritional support is attempted. In one study, TPN resulted in weight gain, but the increase was due entirely to an increase in body fat content. Although nutritional support might help prevent progressive protein depletion, the key to successful therapy is proper diagnosis and treatment of the specific disease complication.

Liver Disease and Total Parenteral Nutrition

NAFLD and cholestasis are common complications of total parenteral nutrition (TPN) use in adults (Buchman, 2002). Since the advent of TPN four decades ago, it has been difficult to establish the etiology of these disorders with certainty. Patients receiving TPN often have multiple coexisting medical problems, potential hepatotoxic medication use, or altered bowel anatomy. Nonetheless, both choline and essential fatty acids are necessary for lecithin synthesis, a step that must occur in the liver to allow fat transport out of the liver. This essential metabolic step provides one rationale for ensuring that patients receiving The approaches to NAFLD and cholestasis during TPN administration include ensuring that patients are not receiving too many calories, reducing small bowel overgrowth with antibiotics, or reducing the toxicity of bile with ursodeoxycholic acid. There is a separate chapter on enteral and parenteral nutrition (Chapter 54).

Pericystectomy for Hydatid Liver Cyst

Patients with hydatid cysts in the liver used to present a therapeutic challenge. Although surgical techniques have improved, considerable controversy still exists regarding the most effective operative technique. The main principle of the surgery is to eradicate the parasite and prevent intraoperative spillage of cyst contents avoiding peritoneal spread. Pericystectomy provides a radical treatment removing the whole cyst en bloc including the adventitia without resection of healthy liver tissue.

Neurolymphomatosis of fowls virus

Nevirapine A non-competitive nucleoside inhibitor of reverse transcriptase that interacts with tyrosine residues on the enzyme. In clinical trials against HIV, resistant mutants rapidly developed, but it was effective when used in combination with AZT. Recommended as a single dose to prevent perinatal transmission of HIV. Has caused severe liver damage and other adverse events in some healthcare workers taking high doses prophylactically. Synonyms BI-RG-587 Viramune.

Stem cells of the adult liver

Polygonal Cells Liver

A number of different cell types can be activated to repair or regenerate the liver depending on the nature and extent of injury or tissue deficit (15). In an otherwise healthy liver, the replacement of hepatocytes (and tissue mass) lost to surgical resection or toxic injury is achieved through the proliferation of differentiated, normally quiescent hepatocytes contained in the residual (viable) tissue (Fig. 1). However, certain forms of liver injury impair the capacity of the remaining differentiated hepatocytes to proliferate in response to liver tissue deficit. When this occurs, a reserve or facultative stem cell compartment is activated to proliferate and replace the lost hepato-cytes. Evidence suggests that there are at least two distinct cell populations that can be activated to generate new hepatocytes or cholangiocytes (Fig. 1). Rodent livers contain a population of normally quiescent (facultative), undifferentiated stem cells that reside in or around the biliary ductules of...

Intrahepatic Cholestasis of Pregnancy

Liver disease in pregnancy. Clin Perspectives Gastroenterol 2001 4 351(17). AFLP acute fatty liver of pregnancy ALT alanine aminotransferase AST aspartate aminotransferase HELLP hemolysis, elevated liver enzymes, and low platelets syndrome ICPH intrahepatic cholestasis of pregnancy PT prothrombin time. Adapted from Larson AM. Liver disease in pregnancy. Clin Perspectives Gastroenterol 2001 4 351(17). AFLP acute fatty liver of pregnancy ALT alanine aminotransferase AST aspartate aminotransferase HELLP hemolysis, elevated liver enzymes, and low platelets syndrome ICPH intrahepatic cholestasis of pregnancy PT prothrombin time.

Feed Related Disorders in Aquaculture

Lipoid liver disease, a significant problem in farmed fish, is usually linked to rancidity (auto-oxidation) of fats in fish feeds (Roald et al., 1981 Saraiva et al., 1986). Clinical and pathological correlates include reduced haematocrit, an abundance of ceroid laden macrophages in visceral organs, and an enlarged pale, friable liver due to macrovesicular lipidosis. Oxidant damage occurs when free radical production overwhelms the free radical scavenging enzyme system of the animal (Winston, 1991). Systemically, free radicals damage cellular membranes. Damage to red blood cells leads to anaemia (Moccia et al., 1984) and ceroidosis results from breakdown products of dead cells. So called 'acute-on-chronic' episodes can occur, during which large portions of tissue, often the fatty liver, undergo an acute oxidation stress and necrosis. Oxidant stress can also promote other diseases. Manifestations of 'pancreas disease', a condition of farmed Atlantic salmon early in their first sea water...

Breaking T and B Cell Tolerance

Experiments with transgenic or non- transgenic mice have shown that, in principle, tolerant T and B cells can be reactivated by infectious agents. Infections are capable of restoring in silenced T cells the capacity to produce cytokines (Rocken et al. 1992 Racke et al. 1994). This phenomenon was extended to the situation of transplantation induced tolerance (Ehl et al. 1998). Similarly, reactivity and immunoglobulin production by B cells that were silenced either by exogenous or transgenic endogenous antigens can be restored with mitogens, including bacteria derived lipopolisacchrides (Louis et al. 1973 Goodnow et al. 1991). Even though these experiments have shown that infectious agents can abolish solid T and B cell tolerance there are little data showing that this reactivation of tolerant T and B cells can also lead to autoimmune disease. One first example suggesting such a situation is given by double transgenic mice that bear a TCR recognizing a transgenic self-antigen expressed...

Alcoholic Liver Disease Role Of Free Radicals

A substantial body of evidence exists to support the contention that ROS generated during ethanol metabolism may be involved in the pathogenesis of alcoholic liver disease (ALD). Decades ago, it was already emphasized by Lieber that the induction of cytochrome P450 is a critical event with respect to the development of ALD 85 , If free radical production and lipid peroxidation play a role in the development of ALD, depletion of dietary antioxidants such as vitamin E or an increase in oxidants such as non-heme iron in the liver, should enhance the ethanol induced liver damage. Indeed, a diet deficient in vitamin E has been shown to reduce hepatic vitamin E stores, increase lipid peroxidation and increase serum transaminase activities after alcohol feeding in rats 86 , Furthermore, iron supplementation in the diet increases ethanol-induced serum transaminase activities, lipid peroxidation and fibrosis 41 , In addition, a significant correlation between hepatic lipid peroxidation,...

Blood to liver

In bone marrow transplant models, unmanipulated bone marrow cells were transplanted into lethally irradiated hosts. Following engraftment, the animals were given 2-acetylaminofluorene, which blocks hepatocyte proliferation, and liver damage was induced using carbon tetrachloride. Two weeks following injury, donor contribution to the organ was determined. Between 0.1 and 0.15 of the hepatocytes were donor derived, and approx 0.1 of oval cells were donor derived (Fig. 2). Fig. 2. Hepatic reconstitution of bone marrow derived cells. Brown Norway L21-negative liver was transplanted into a Lewis animal (L21 positive). At 75 d posttransplantation, liver damage was induced with carbon tetrachloride. The liver was harvested 15 d later and stained for L21. (Photomicrograph courtesy Bryon Petersen.) (See color plate 2 in the insert following p. 82.) Fig. 2. Hepatic reconstitution of bone marrow derived cells. Brown Norway L21-negative liver was transplanted into a Lewis animal (L21 positive)....

Weight Loss

Weight loss, with or without exercise, has been investigated as a therapy for fatty liver disease in several studies (Angulo and Lindor, 2001). Although weight loss is encouraged in overweight patients to prevent its many known complications, the data justifying its recommendation for liver disease remains unconvincing. Several difficulties with the interpretation of earlier studies have been suggested. The duration of weight loss in previous clinical trials was often relatively short and effective means of sustaining weight loss have been elusive. Adjuncts to weight reduction, such as the luminal lipase inhibitor orlistat, are now being investigated in clinical trials of NASH. One provocative observation is that early studies of weight loss as a treatment of NAFLD were associated with improved steatosis but possibly worsened fibrosis and inflammation. Because the histological characteristics of NAFLD as it improves during effective intervention are unknown, biopsy scoring systems...

Insulin Resistance

One large trial in patients with diabetes comparing a pharmacological approach (metformin) with aggressive changes in lifestyle found that increasing physical activity may improve insulin sensitivity more than the drug would (Knowler et al, 2002). Because IR may be the most common predisposing factor for the development of NAFLD, these findings in the diabetic and prediabetic populations may be equally relevant to people with fatty liver.

Liver Enzymes

The aminotransferases are generally reflective of parenchymal liver injury, such as that seen with viral hepatitis, medication or toxin-induced injury, autoimmune hepatitis, and several infiltrative disorders, such as hemochromatosis, Wilson's disease, a-1-antitrypsin deficiency, and fatty liver disease. Of course, in some of these conditions, alkaline phosphatase and GGT can be elevated to some extent as well, but bilirubin is not elevated unless there is obstruction to bile flow or significant liver dysfunction or injury. fatty liver disease,

Figure 1016

Most pregnant women with acute renal failure have acute tubular necrosis secondary to either hemodynamic factors, toxins, or serious infection. Occasionally, glomerulonephritis or obstructive nephropathy may be seen. Acute cortical necrosis may complicate severe obstetric hemorrhage. Acute renal failure may be a complication of the rare syndrome of acute fatty liver of pregnancy, a disorder that occurs late in gestation characterized by jaundice and severe hepatic dysfunction. This syndrome has features that overlap with the hemolysis, elevated liver enzymes, and low platelet count (HELLP) syndrome variant of preeclampsia as well as microangiopathic syndromes (eg, hemolytic uremic syndrome and thrombotic thrombocytopenic purpura).


Pre-eclampsia encompasses HELLP (haemolysis, elevated liver enzymes and low platelets) syndrome, eclampsia and possibly acute fatty liver of pregnancy. Although the disease is progressive, a mother may be asymptomatic until she presents with an eclamptic fit, and although pre-eclampsia is a disease of pregnancy, terminated only by delivery, pre-eclampsia, HELLP syndrome and eclampsia may all present only after delivery.

Medications for IR

One approach to IR is to improve insulin sensitivity pharmacologically. A class of drugs called thiazolidinediones (TZDs), has been developed as a novel treatment of type 2 diabetes and these drugs act by improving peripheral insulin sensitivity. Two such agents, rosiglitazone and pioglitazone, are indicated and available for diabetes treatment. Both drugs are being studied in clinical trials for NAFLD, and the early results are now becoming available. Improvements in NASH and NAFLD are seen with both drugs, but perhaps at the cost of important side effects. Drugs in this class cause adipocyte differentiation which may have been the cause of weight gain observed in the study subjects. Interestingly, studies in subjects with diabetes suggest that the weight gained is peripheral rather than central, and central adiposity is most associated with NAFLD and cardiovascular risk factors. Weight gain is nonetheless disheartening in these patients who are often battling obesity anyway. In...

Vitamin E

Oxidant stress is commonly invoked as a mechanism that ties together the accumulation of fat in the liver with the hepatocellular injury of NASH. Vitamin E is readily available and a biologically effective antioxidant. For these reasons, vitamin E is commonly used as a potentially beneficial therapy for NASH. Unfortunately, the data linking oxidant stress as a cause of the necroinflammation in humans has been scant, and data supporting the use of vitamin E has not been impressive. In children, vitamin E usually causes enzyme normalization and perhaps histological improvement (Lavine, 2000). In adults, an antioxidant approach to therapy has been more disappointing, either due to a true lack of effectiveness or failure of specific antioxidants to effectively block oxidant stress where it can cause damage. Nonetheless, vitamin E is commonly recommended to patients with NAFLD because in typically recommended doses (400 to 800 IU daily), little if any harm is thought to occur and the...


Treating, and caring for, the elderly is a complex endeavor. Older people are usually suffering from several simultaneous disorders that, because of the patient's age, cannot be treated with the drugs or therapies that are routine for younger individuals. Drug therapies assume a clearance time (physiological deactivation of the drug), made possible by a healthy liver that may not exist in an older patient. Drugs that are safely used to treat depression or cardiovascular disease in young patients can have devastating effects on the elderly. Accurate medical histories are often difficult to obtain from elderly patients, either because of poor memory or because of psychological compensation by which the patient ignores and minimizes danger signs and symptoms. Growing old is often a time of loss lost physical abilities, lost friends, the patient's spouse may have passed away, and the family home may have been given up for a room in a nursing home or hospital ward. All these elements...

Other diseases

Porphyria cutanea tarda usually occurs in men, with a genetic predisposition, who have liver damage as a result of an excessive intake of alcohol. There is impaired porphyria metabolism leading to skin fragility and photosensitivity, with blisters and erosions, photosensitivity on the face and the dorsal surface of the hands.

Liver Disease in CF

As with the pancreas, the CFTR protein is localized to the apical membrane of bile duct cells, and the biliary fluid is more viscous and less alkaline than normal due to this defect of cholangiocyte transport. The small ducts become obstructed, and the reaction to this obstruction is proliferation of small ducts, cholangitis, and fibrosis. The liver damage, therefore, affects the hepatocyte late in the process, and patients may present with cirrhosis and portal hypertension, with relatively preserved overall hepatic function. Efforts to correlate a specific CF mutation with liver disease have been unsuccessful. Although cirrhosis seems to occur more commonly in those with the more severe mutations, these patients may have mild to moderate lung disease, and are candidates for liver transplant. Monitoring for liver disease should be part of routine care for all patients. Biochemical testing of transaminases, y-glutamyl transpeptidase (GGT), and alkaline phosphatase on an annual basis is...


The mechanisms of hepatotoxicity explained above can result in combined hepatic or cholestatic liver disease. For example, the canalicular secretion of toxic metabolites causes bile duct injury and inflammation and induces immune responses to haptenized duct cells. Because the same toxic metabolites can also injure hepatocytes, mixed patterns of liver injury may occur (cholestatic hepatitis). Some drugs (eg, rifampicin and cyclosporin A) may also cause cholestasis without producing appreciable liver damage by inhibiting bile salt excretory proteins. Reduced function of the bile salt transporters causes bile acids and other factors that are normally excreted in the bile to accumulate in liver and serum and can lead to pruritus.


Gene transfer of 2 x 1010 particles of this vector in immunocompetent C57BL 6J mice resulted in tissue-specific and stable gene expression for longer than 1 year. Transcription of the human al-antitrypsin RNA in the liver of transduced animals was initiated from the liver-specific promoter, but not from the macrophage-specific promoter. Gene transfer with increasing vector doses resulted in high and stable al-antitrypsin levels in serum. Significantly, with increasing vector doses, serum levels of al-antitrypsin were obtained that would be considered supraphysiological in humans. Even these very high vector doses were not accompanied by liver toxicity. Mice that received the same dose of a first-generation vector carrying the human al-antitrypsin cDNA under the control of the murine phosphogylcerate kinase (PGK) promoter experienced liver damage as documented by histological abnormalities and elevated liver enzymes detected in the serum of transduced mice 50 . Gene transfer of this...

Hypolipidemic Agents

The relationship between hypercholesterolemia and NASH is uncertain. Most circulating cholesterol is made by the liver and secreted in lipoproteins. Drugs that specifically impair hepatic cholesterol synthesis, the 3-hydroxy-3-methyl-glutaryl-coenzyme A (HMG-CoA) reductase inhibitors, or statins, can increase liver enzymes independent of known preexisting liver disease. A commonly encountered clinical problem is whether to use this class of drugs in patients with known NASH or NAFLD. Because there is no evidence that statins increase the damage to the liver caused by NASH, most experts in liver disease allow the use of statins in patients with elevated aminotransferase due to NAFLD when these drugs are clinically indicated, as long as the liver enzymes are monitored regularly and the drug is changed if its use clearly causes a further increase above the pretreatment baseline. Rationalizing the use of statins as therapeutic agents for NAFLD is problematic based on the known property of...

Systemic treatment

Cosyntex Failing Control Psoriasis

Methotrexate inhibits folic acid synthesis during the S phase of mitosis and diminishes epidermal turnover in the lesions of psoriasis. Because it is hepatotoxic liver function has to be assessed initially and at regular intervals during treatment. The dosage must be monitored, and when a total of 1-5 g is reached a liver biopsy is indicated to exclude significant liver damage.

Liver Biopsy

Percutaneous liver biopsy is one of the most widely used procedures in hepatology today. Although there are some limitations to the procedure and histologic analysis, there is still no reliable noninvasive alternative. The primary purpose of a biopsy is to confirm the suspected diagnosis, and to quantify the extent of hepatic damage that has occurred. In addition to these indications, occasionally a systemic disease diagnosis is made through liver biopsy. For example, tuberculosis and sarcoidosis are occasionally first diagnosed through histologic assessment and culture of the liver tissue. Likewise, the diagnosis of amyloidosis is often made by liver biopsy. It is still the only definitive way to diagnosis hemochromatosis and fatty liver disease. Medication-induced hepatotoxicity can only be confirmed through liver biopsy, though it may be suspected based on history and enzyme abnormalities.


Pilot studies of betaine have shown some promise for this agent. Perhaps one of the most controversial aspects of its use in clinical medicine is the proper pronunciation of its name. In clinical practice, bee-tane is commonly used, whereas chemists tend to use its original pronunciation of beta-een. Common use of the former may dictate its pronunciation by clinicians by affirmation. Betaine, or dimethyl glycine, is an alternative source for methyl groups, and as such can replace essential functions of methionine and choline in the synthesis of lecithin, an essential fatty acid for elimination of fat from the liver. It could also serve as an antioxidant by increasing the synthetic capacity for intracellular glutathione. Although the mechanisms of its actions in NAFLD remain to be fully worked out, betaine could be promising for the patients with NASH. Unfortunately, the doses used in the successful clinical trial were quite large and compliance was a problem for some patients.

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