Natural Solution for Liver Cirrhosis

Liver Tracker

This new program is designed to help you live with your liver disease, and make it easier to live with liver problems. If you join Liver Tracker, you have the ability to get a supportive community that helps you cope with your liver problems in an environment that will help with your liver issues. If you non-alcoholic liver disease, liver cirrhosis, Hepatitis A and B, or alcoholic fatty liver disease, you will be a fit for this community AND we can offer you the help that you need! You will also get healthy recipes that are created by dietitians; you never again have to wonder if it is safe to eat what you are eating! You will get progress tracking to check and see if you are meeting your health goals, and the direct help of a health team. You do not have to go through this alone; let us help you!

Liver Tracker Summary


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Contents: Ebook

My Liver Tracker Review

Highly Recommended

Of all books related to the topic, I love reading this e-book because of its well-planned flow of content. Even a beginner like me can easily gain huge amount of knowledge in a short period.

All the modules inside this e-book are very detailed and explanatory, there is nothing as comprehensive as this guide.

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The Liver Cirrhosis Bible & Ezra Protocol

The Liver Cirrhosis Bible & Ezra Protocol is a 183 page downloadable eBook, that is jam packed cover to cover with all the answers that you'll ever need about this thing that torments you. Learn the dramatic truth about the Extracellular Matrix in liver cirrhosis sufferers and how going public with this breakthrough ruined the life of one doctor. A substance that's in your kitchen right now lowers the risk of cirrhosis by a shocking 80%. It is literally unbelievable that this information confirmed in 6 large scale double blind studies is not made available to the sufferers. Who and why prevented the information being widely available. I was so mad when I learned this. What shocking discovery about liver cirrhosis triggers has been made in a double blind study in Russia. What shocking discovery about liver cirrhosis triggers has been made in a double blind study in Russia. Malfunction of one small organ in our abdomen (not the liver) is where so many answers lay. Find out which organ and how to amend the damage within weeks. Learn about the one deadly mistake that over 90% liver cirrhosis sufferers makes every day. This mistake alone can rob them of their healing. How an American doctor stirred the water by saving the lives of hepatitis patients with such heavy liver damage that the other doctors practically pronounced dead. The maverick doctor has been curing terminal liver damage using a simple, cheap natural acid. The same acid is one of the corner stones of the Ezra protocol. A problem in the lymphatic sacks of the liver cirrhosis sufferer causes a congestion and can leave you with 30 billion dead cells trapped in your body every day. There is only one substance known to man that can dissolve this clutter. Find out which today and put it to use. Why every attempt to reverse liver cirrhosis, fatty liver and loose weight fails miserably every time. The truth will shock you. The answers lay in your liver and your adrenal gland. It was a common belief that reversing failing cirrhotic liver cells is practically impossible until a study at the University of Londons School of Pharmacy changed everything. Every liver cirrhosis sufferer is in grave danger of extremely active Reactive Oxygen Species. How to shift the process within 36 hours. The dishes you cook prevent you from resolving your health issues. If you fail to learn this, you will continue with the deadly practices forever. The most deadly man made chemical is lurking from your supermarket shelves and literally scavenging your liver. Learn the truth that has been kept from you. precise practical rules to avoid the terrible chemical mentioned above. 4 personal care products make it impossible to shift the chemical imbalances in your body. Once you get rid of these offenders, your body's self healing ability will skyrocket. You'll feel it right away. I promise. Continue reading...

The Liver Cirrhosis Bible & Ezra Protocol Summary

Contents: 183 Page EBook
Author: Debra Elkin
Official Website:
Price: $47.00

The Liver Cirrhosis Freedom Cookbook

Without these information you almost no chance of planning a comprehensive dietary strategy without spending months on it. This is how The Liver Cirrhosis Freedom Cookbook will change your life: You will never eat a meal that aggravates your liver condition again. And you very likely did it today. You will gently soothe your endocrine system and shift the ravaging chemical imbalance that is eating away your organs. Boost the secretion of self-healing chemicals that will repair your organs before it's too late. Enjoy delicious meals while knowing every second that you are healing your body with every bite. You won't have to think about where to start in your healing, you will have all the work done for you. When you wake up in the morning you'll feel light and positive, knowing that healing chemicals in your body are doing their work every second. You won't have to spend endless hours in front of your computer or buy nutrition books to know what is completely safe for you. Never again buy another book about diet and health, because you have it all right here and written just for your condition, not general and vague, but laser precise and understandable. Start your healing today, without any procrastination. Once again, feel that health and energy you so desperately pursu Continue reading...

The Liver Cirrhosis Freedom Cookbook Summary

Contents: EBook
Author: Debra Elkin
Official Website:
Price: $29.00

Fatty Liver Hepatitis And Cirrhosis

Chronic alcohol consumption can cause the deposition of excess triglycerol in the liver leading to a condition known as 'fatty liver'. This damage can lead to hepatitis and, if severe enough, to cirrhosis. The damage is thought to be due to the high concentrations of ethanal within the cell and if severe enough will result in cell death. Cell damage and death trigger an inflammatory response, i.e. infiltration of lymphocytes and activation of an immune response. If this is not treated it will lead to the formation of fibrous tissue and a severe reduction in the functioning of the liver.

Inhibition of Myofibroblast Differentiation and Hyperplasia by HGF

Another important role of HGF toward myofibroblasts is inhibition of the cellular proliferation and differentiation that is induced by fibrogenic cytokines (11,72,86,115). Platelet-derived growth factor (PDGF) is a major mitogen for myofibroblasts. Overexpression of PDGF in the normal kidney leads to lesions mimicking mesangial proliferative glomerulonephritis (MPGN) (81), whereas anti-PDGF antibody treatment suppresses myofibroblast overgrowth in an experimental model of MPGN (117). Of interest, PDGF-mediated proliferation of MCs in culture is inhibited by HGF via inac-tivation of ERK-42 44 (86). Similarly, HGF inhibited the PDGF-mediated proliferation of mesangium-derived myofibroblasts in association with early de-phosphorylation of ERK in a rat model of Thy-1 nephritis (i.e., MPGN). As a result, glomerular fibrosis was attenuated in HGF-treated rats (86). This effect was also reproduced in the case of experimental hepatic cirrhosis (115) and in the atherosclerosis of pulmonary...

Insulinsensitising agents and cardiac failure see also Chapter

To metformin use have come under scrutiny. The historical concern regarding biguanides and lactic acidosis was based largely upon data from phenformin therapy. Mechanistically, the two drugs have differing effects on lactic acid metabolism, while plasma metformin levels do not correlate with lactate levels. In large observational studies, it is very hard to separate the effects of metformin from the effects of acute illness that may have precipitated lactic acidosis, such as renal failure, cardiac failure and liver failure. Despite this, data from Brown and colleagues are certainly reassuring in that in 41 000 patient-years of therapy with metformin, they found no increase in the incidence of lactic acidosis compared to the period prior to its availability (Brown etal., 1998). A subsequent meta-analysis suggested the incidence of lactic acidosis to be 9.9 per 100 000 patient-years in those not taking metformin and 8.1 per 100000 patient-years for those receiving metformin (Salpeter...

Nonalcoholic Steatohepatosis

Non-alcoholic fatty liver disease, has recently become increasingly recognized and may progress to end-stage liver disease. It is histologically indistinguishable from the liver damage that is secondary to alcohol abuse, but occurs in people with no history of alcohol excess. Non-alcoholic fatty liver disease has a wide spectrum of liver damage ranging from simple steatosis to steatohepatitis, advanced fibrosis and cirrhosis. The combination of steatosis, infiltration by mononuclear or polymorphonuclear cells (or both), and hepatocyte ballooning and spotty necrosis is known as nonalcoholic steatohepatitis (NASH). Non-alcoholic fatty liver disease is the most common cause of abnormal liver blood results among adults in the USA. It is particularly common in those with combined diabetes and obesity in a group of severely obese patients with diabetes, 100 were found to have mild steatosis, 50 had NASH and 19 had cirrhosis. Insulin resistance seems to be the most reproducible causative...

Microorganisms Strongly Associated With Infections In Patients With Diabetes

Patients with diabetes sem to be at a disproportionately high risk for infections with certain micro-organisms. The prevalence of diabetes was reported to be 27.5 in one study of nonpreganant adults with group B streptococcal bacteremia (69). Several series report an incidence of underlying diabetes of up to 30-60 in patients with a variety of Klebsiella infections such as bacteremia, liver abscess, thyroid abscess, and endophthalmitis (70-73). Among enteric pathogens, Campylobacter and Salmonella enteritidis have been reported with increased frequency in patients with diabetes (74,75). There is a strong association of diabetes with chronic hepatitis C virus (HCV) (76). Additionally, patients with HCV-related cirrhosis have an increased incidence of diabetes compared to patients with cirrhosis resulting from other causes (77,78). Although an increased incidence of staphylococcal infections has been noted in diabetic patients, a careful recent review did not confirm this association...

Antifibrotic Mechanisms Common To Parenchymal Organs

Thus far, we have discussed how HGF prevents or improves renal fibrosis in DN and other CRDs. We have also accumulated evidence that HGF is anti-fibrotic in other chronic nonrenal diseases, such as liver cirrhosis (66,105), pulmonary fibrosis (67,103), cardiomyopathy (108), and scleroderma (109), thus suggesting common mechanisms of fibrosis and its counteraction. Hyperplasia of interstitial myofibroblasts is the common denominator in multiple tissues, and the degree of myofibroblast hyperplasia reflects the severity and course of fibrosis in diseases including the kidney (110), liver (111), and lung (112). To understand the extensive actions of HGF, we will further discuss the role of HGF in myofibroblastosis, the common pathology in multiple disease states.

Complications Of Preeclampsia

Preeclampsia may cause both acute complications to the mother and neonate, as well as long-term complications for the mother. Usually maternal and perinatal outcomes are more favorable in women with mild preeclampsia that develops after 36 weeks of gestation (116-118). Women who develop preeclampsia prior to 33 weeks who have preexisting medical conditions or who live in developing countries have increased maternal and neonatal morbidity and mortality. Immediate complications for the mother include placental abruption, disseminated intravascular coagulation (DIC) HELLP syndrome, acute renal failure, eclampsia, liver failure, and extremely rarely stroke and death. Complications for the neonate include preterm delivery, fetal growth restriction, and rarely hypoxia, neurologic injury, and perinatal death (Table 6). Liver failure or hemorrhage

Secondary haemochromatosis

Chronic anaemia such as aplastic anaemia, sickle cell anaemia, and thalassaemia cause iron overload mostly because of frequent blood transfusions. Each 250 ml transfused red cells adds about 250 mg elemental iron to the body. Frequent transfusions may promote diabetes mellitus and cardiac failure when iron concentrations exceed 268 ymol g dry weight liver (15 mg g). The endorgan manifestations of iron overload, such as cirrhosis, cardiac failure, hepatocellular carcinoma, diabetes mellitus and hypopituitarism resemble the manifestations in hereditary haemochromatosis patients.

The Metabolic Syndrome Diabetes and Steatosis and Incidence of Hepatocellular Carcinoma

The incidence of hepatocellular carcinoma (HCC) is increasing, but the temporal changes of risk factors remain unclear. A significant proportion of HCC develops in crypto-genic cirrhosis, and may present the most worrisome complication of non-alcoholic It is likely that the association of HCC with obesity and diabetes represents the progression of underlying non-alcoholic fatty liver disease to cirrhosis. The mechanisms most likely involve replicative senescence of steatotic mature hepatocytes and compensatory hyperplasia of progenitor cells as a reaction to chronic injury due to ongoing non-alcoholic steatohepatitis 55 and inflammation 56 .

Why do Obesity TDM and Nafld Cluster The Liver as the Metabolic Sensor of Lipotoxicity

While obese patients with the MS and T2DM are more prone to fatty liver and develop more severe disease (NASH), the reasons are unclear and most other aspects of the disease in T2DM remain poorly understood. It is tempting to speculate that the liver is like a metabolic sensor with the degree of steatosis being a reflection of the ability of the body to cope with a lipotoxic environment. There is an increasing awareness that insulin resistance, lipotoxicity, and T2DM are major risk factors for fatty liver disease, necroinflammation, and fibrosis. Still the information available on the natural history of the disease with paired biopsies is limited to a handful of small studies (281-284). In these studies, involving from 22 to 103 patients with an average follow-up ranging from 3.2 (283) to 13.8 years (284), fibrosis progressed over time in 32-41 of patients with NAFLD (281-284). However, disease remained stable in 34-50 of patients and even improved in a minority. This has brought...

Nutrients That Can Help

In the 1970s and 1980s Berkson used large doses of alpha-lipoic acid to treat Amanita mushroom poisoning, which often precipitates liver failure and death. Alpha-lipoic acid boosts the liver's production of glu-tathione, which aids the breakdown of Amanita toxins and promotes the synthesis of new liver cells. Similarly, selenium is needed for the liver to make several glutathione peroxidase compounds, all potent antioxidants. The herb milk thistle has been used for thousands of years as a liver tonic, and its silymarin extract is now recognized as a powerful antioxidant.

The aGlucosidase Inhibitors

Acarbose is contraindicated in patients with cirrhosis, whereas miglitol is not con-traindicated in patients with liver disease. a-Glucosidase inhibitors are not indicated in patients with severe renal insufficiency or in patients with inflammatory bowel disease or pre-existing bowel obstruction.

When is renal transplantation desirable in persons with DM

According to American official sources, diabetic nephrosclerosis is the primary cause of end stage renal disease treated with transplantation (37 percent), followed by hypertensive nephrosclerosis (27 percent). Patients with severe heart failure, uraemic encephalopathy, active hepatitis, malignancy or bone marrow depression are unsuitable for transplantation, as are elderly persons. Chronic hepatitis is not a contraindication (as long as there is no active disease or cirrhosis) and neither is tuberculosis (if proper treatment is given).

Peroxisome Proliferator Activated Receptory Key Regulator of Adipogenesis and Insulin Sensitivity

PPAR-y was first identified as a part of a transcriptional complex essential for the differentiation of adipocytes, a cell type in which PPAR-y is highly expressed and critically involved (6). Homozygous PPAR-y-deficient animals die at about day 10 in utero as a result of various abnormalities including cardiac malformations and absent white fat (7-9). PPAR-y is also involved in lipid metabolism, with target genes such as human menopausal gonadotropin coenzyme A synthetase and apolipoprotein (apo)-A-I (10,11). Chemical screening and subsequent studies led to the serendipitous discovery that thiazolidinediones (TZDs) were insulin sensitizers that lower glucose by binding to PPAR-y. Used clinically as antidiabetic agents, the TZD class includes pioglitazone (Actos) and rosiglitazone (formerly BRL49653, now Avandia) (12,13). Troglitazone (ReZulin) was withdrawn from the market because of idiosyncratic liver failure. Naturally occurring PPAR-y ligands have been proposed, although with...

Rosiglitazone And Pioglitazone

They usually take a few days to work, so you should not expect glucose levels to fall for at least a week or two. The medicine does depend on having enough insulin to be effective. In addition to their glucose-lowering effect, thiazolidinediones lower triglycerides and free fatty acid levels and raise total cholesterol, LDL cholesterol, and HDL cholesterol. Pioglitazone, when compared to rosiglitazone, is more effective in lowering triglycerides and raising HDL cholesterol. It also does not raise LDL cholesterol as much as rosiglitazone does. Since lipid abnormalities are associated with heart disease, it has been proposed that the lipid changes seen with these drugs (especially pioglitazone) might be beneficial. In small research studies these drugs have been shown to prevent the reblockage of coronary arteries after they have been opened with a procedure called coronary angioplasty. These medicines also seem to help fatty liver, an important abnormality found in many people with...


Even ultrasonography can be practically difficult and is unlikely to be diagnostic. At the very least children should be screened for autoimmune hepatitis and Wilson's disease as these are potentially treatable conditions. The natural history of this condition is not known. On the whole it is felt to be a benign condition although a small number of adults with NASH go on to develop cirrhosis necessitating liver transplantation (James and Day, 1998 Shiva Kumar and Malet, 2000). Results of exercise interventions in adults with NASH have been promising but there are no paediatric data available at the current time (Ueno et al., 1997). Insulin sensitizers such as metformin have been used with some benefit but their use in clinical paediatric practice is also to be defined (Marchesini et al., 2001).


The living things are both large and small from worms we can see, to microscopic bacteria, viruses and fungi. The non living things are pollutants in our air, food, dental metal and body products. Taking in a lot of pollutants hampers the body's ability to kill and get rid of the invaders. And so, gradually, as we get older or sicker, the body's invaders get the upper hand and take over. Don't be discouraged if you have lupus, cerebral palsy, cirrhosis, or any complex-sounding disease. Every disease is an example of the same process.

Other Medications

Many people with diabetes take oral medications along with insulin or alone to better manage their condition. These medications come in various categories, based on type, and each works differently. They can have side effects, including upset stomach, low blood glucose, weight gain, liver failure, headache, and fluid retention. They must be taken as prescribed and under a doctor's care. Studies have shown that diabetes and its complications might be prevented by these oral medications. This is especially true when the person taking them also eats a healthy diet and gets adequate regular exercise.

Side Effects

Rarely, people taking metformin can develop a serious medical condition called lactic acidosis, which can lead to death and so requires immediate hospitalization. The symptoms of lactic acidosis include nausea, vomiting, abdominal pain, rapid breathing, and feeling very unwell. People with liver failure, kidney failure, or severe heart failure are at a higher risk for lactic acidosis and therefore should not take this medicine.

Choice of Patients

Given the fact that incretins (both GIP and GLP-1) are eliminated via the kidneys and that patients with impaired renal function have elevated circulating concentrations of GIP and GLP-1, treatment with usual doses of DPP-4 inhibitors might lead to further elevations in incretin plasma levels, potentially causing adverse events. Therefore, lower doses of DPP-4 inhibitors may be appropriate in such patients. Like in the case of renal functional impairment, not much is known on the use of DPP-4 inhibitors in patients with type 2 diabetes and associated diseases leading to severe organ failure (liver cirrhosis, heart failure, pulmonary disorders, etc.).

Natural History

Overall, patients with diabetes mellitus compared to the general population, have a greater relative risk of death from cirrhosis (2.5-fold) than cardiovascular disease (1.3-fold) (1). Death from chronic liver disease or hepatoma is the fourth most common cause of death among diabetics, accounting for approximately 1 in 20 deaths (1). The relative risk of death from cirrhosis increases as the severity of diabetes increases with those requiring oral hypoglycemic medications having a 4.9-fold increased risk and those on insulin having a 6.8-fold increased risk compared to those treated with diet alone (1). The prognosis of patients with diabetes mellitus and concomitant NAFLD is not well defined. No population-based studies exist, however one study from a tertiary referral centre found cirrhosis developed in 25 of diabetics with NAFLD and liver related death occurred in 18 (41). Although there was no control group, it would be reasonable to predict that the incidence of cirrhosis and...

Clinical Features

Patients with NAFLD are generally asymptomatic although may have abdominal discomfort and hepatomegaly. Clinical examination may reveal signs of portal hypertension such as splenomegaly or ascites if cirrhosis is present. Children may have acanthosis nigricans reflecting underlying insulin resistance. Liver enzymes may be normal in up to 78 of patients including those with cirrhosis, and thus are insensitive for both the detection of NAFLD and the exclusion of advanced liver disease (3). When present, liver enzyme elevations are generally modest and restricted to alanine aminotransaminase (ALT) and aspartate aminotransaminase (AST). Elevations of ALT and AST greater than five times the upper limit of normal are uncommon and should prompt investigation for an alternative cause. A ratio of AST ALT 1 may signify advanced fibrosis (36). Iron studies are also frequently elevated with elevated ferritin observed in 20 to 50 of patients and raised transferrin saturation in 5 to 10 of cases...


NAC is used in every hospital emergency room in the nation to treat overdoses of acetaminophen (Tylenol). Acetaminophen depletes liver levels of glutathione and, in large amounts, can rapidly lead to liver failure. NAC quickly rebuilds normal glutathione levels in the liver, which then helps the organ break down and detoxify the drug. The same glutathione-enhancing effect of NAC has also been found to increase the life expectancy of people with AIDS, which depletes glutathione levels.


The histological changes of NAFLD are similar to that produced by alcohol (31). Thus the diagnosis of NAFLD cannot be made by histological means alone and requires the clinical exclusion of excessive alcohol intake. The histological hallmark of NAFLD is hepatocellular triglyceride accumulation, which is predominantly macrovescicular, although may be mixed with microvescicular fat, which implies defective mitochondrial FFA oxidation. Steatohepatitis requires the presence of lobular inflammation, which is usually a mixed mononuclear neutrophilic infiltrate and is frequently associated with hepatocyte ballooning and less commonly Mallory's hyaline (32). Hepatocellular ballooning, disarray and fibrosis are typically predominant in zone three of the hepatic lobule. Fibrosis is typically pericellular and perisinusoidal giving a chickenwire appearance. Eventually, fibrotic septae form between the hepatic vein and portal tract and nodules may form heralding the onset of cirrhosis....

Finding help

Alcohol abuse has numerous physical and mental consequences, including cirrhosis of the liver (when the liver loses its ability to function properly and you die of hemorrhage or liver failure) and degeneration of the brain (when you lose coordination and develop severe emotional instability). Alcohol also is a home wrecker.