Fatty Liver Diet Plan

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. Continue reading...

Fatty Liver Remedy Summary


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Author: Layla Jeffrey
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Highly Recommended

This is one of the best ebooks I have read on this field. The writing style was simple and engaging. Content included was worth reading spending my precious time.

As a whole, this manual contains everything you need to know about this subject. I would recommend it as a guide for beginners as well as experts and everyone in between.

Fatty Liver Fix

The liver has a miraculous way to heal itself. However, like every other organ of your body, if it is over-burdened, it will give away its normal functions and pose a grave threat to your life. One of the many conditions or diseases resulting from over-burden is the Fatty Liver Disease. This disease is characterized by fat invading your liver until most if not all of its vital functions are stressed. You could experience a never-ending fat spree despite eating less along with other symptoms such as sugar rush, paling, low energy, and many more. However, rest assured as Fatty Liver Fix contains all the ways in which you can help your liver get rid of extra layers of fat clogging its veins and invading it inside out. This guide can teach you techniques that do not involve starvation, has nothing to do with diets and can relieve you of unrealistic exercises. All you have to do is follow the steps stated therein for a healthier lifestyle leading you on the road to a healthy liver. Besides this, you could also learn other techniques that are vital to detoxification of your body. You also get three bonuses with it. Continue reading...

Fatty Liver Fix Summary

Contents: Ebooks
Official Website: healthhackspublishing.com
Price: $27.00

Doublecontrolled Conditionally Replicating Adenoviruses

After the systemic administration of adenoviral vectors, most of the virus ends up in the liver. When adenoviral replication is not strictly restricted to certain cell types or tissues, severe liver damage might occur due to adenoviral replication and consequential lysis of the liver cells. Because of this importance to restrict adenoviral replication, solutions have to be found for the observed aspecific replication of CRAds. One solution is a double-controlled conditionally replicating adenovirus (dcCRAd). 8 In a dcCRAd not one but two replication essential genes are controlled by two tumor-specific promoters. For example, both the adenoviral E1A and E1B genes have been placed under the control of two different tumor-specific promoters. Also, studies have already been conducted with both the E1A and the E4 gene under control of two different tumor-specific promoters.1-9-1 E1A, E1B, and E4 are all examples of adenoviral genes that are essential for replication of the adenovirus. The...

Apoptosis In Vertebrates Development

Mice lacking another pro-apoptotic Bcl-2 member, Bak, develop normally and do not show any obvious abnormality. However, mice deficient both in Bak and in Bax exhibit interdigital webs, imperforate viginal and accumulated neurons in the central nervous system (75). The vast majority of the double knockout mice die perinatally due to the developmental defects. The survived mutant mice are still sensitive to anti-Fas-induced liver damage. Interestingly, embryonic fibroblasts (EFs) from the double-mutant mice are resistant to many apoptotic stimuli including ones causing endo-plasmic reticulum (ER) stress, which is strengthened by the fact that cytochrome c release by the truncated Bid is abrogated in the double-mutant EFs. Because neither Bak nor Bax is reported to be associated with ER, this data may suggests that ER stress causes mitochondorial dysfunction leading to apoptosis.

Clinical Features and Pathology

Except for MVMi, natural infections of rodents are clinically inapparent. Experimental infections of rodents may produce (1) an acute lethal disease in newborn animals, (2) an osteolytic syndrome, (3) cerebellar ataxia or (4) hemorrhagic encephalitis. Successive passaging of H-l or RV in newborn hamsters can increase the pathogenicity in newborn animals to close to 100 mortality. After 4-10 days, infected animals suddenly become sluggish, gasp for breath and die. Necropsy often reveals hemorrhage of the gut and congestion of the liver. In contrast, no liver damage is observed with the RT strain, but intestines often contain a sanguineous exudate.

Treatment of the Failing Heart

Treatment of heart failure is directed to correction of the two major problems associated with failure venous congestion and reduced cardiac output. Systemic venous congestion can cause renal and liver damage as well as discomfort. The threat of pulmonary edema from pulmonary congestion has already been discussed. Diuretics and reduced salt intake can reduce the accumulated blood volume and venous congestion even though these treatments may actually lower the filling pressure of the heart and thus the stroke volume. One of the oldest cardiac drugs is digitalis, which increases the contractility of the heart by causing the muscle cells to accumulate SR calcium (see Chapter 11). Increasing contractility with digitalis increases the cardiac output and lowers the venous pressure. Digitalis in the absence of a diuretic will often cause a brisk diuresis, as the kidney detects the rising cardiac output. Although digitalis and other cardiac stimulants can improve the exercise tolerance in...

Pathology and Histopathology

Hepatocytes are the primary target of HCV. Therefore, the histological alterations of chronic hepatitis C are hepatocellular injury, portal and parenchymal inflammation, and necrosis. The injury of the hepatocyte is thought to be induced primarily by the immune reaction rather than by viral cytopathogenicity. Liver damage is typically spotty and focal with accompanying chronic inflammatory cells, macrophages, and, eventually, variable degrees of fibrosis. The progression rate of hepatic fibrosis is the major determinant for the outcome of chronic hepatitis C in terms of developing cirrhosis and hepatocellular carcinoma. Unfortunately, there are only a few histologi-cal markers that are more often associated with hepatitis C than with other causes of hepatitis, such as steatosis. Although the liver is the primary target, persistent HCV infection is often associated with extrahepatic symptoms, such as renal complications, lymphoma, and diabetes. A high proportion of patients with...

Clinical And Pathologic Characterization

Of muscle butyrylcarnitine in the controls. The mutant mice develop severe fatty liver with fasting, as well as excessive fat in the liver without fasting as compared to normal controls. Immunoprecipitation studies later showed that there was no detectable SCAD antigen produced in multiple tissues.8 Clinically, these mutants have remained consistently normal.3 We have challenged them with fasting,3 medium-chain triglyceride loading,3 as well as, sodium butyrate loading, sodium benzoate and salicylate loading in an attempt to overload the glycine conjugation pathway. We have also fed them a high fat diet (40 fat) composed of butter fat with a relatively high short-chain fatty acid content. Even after consuming this diet for over a month, these mice showed no clinical signs of disease with fasting. Pathological characteristics include predominately fatty liver and kidney3,9 ultrastructural studies demonstrated swollen, disorganized mitochondria in hepatocytes from fasted mutants with...

Transgenic Correction Studies In Vivo The Potential For Gene Therapy

We have explored the potential therapeutic effects of liver specific expression of a short-chain acyl-CoA dehydrogenase (SCAD) transgene in the SCAD deficient mouse model.24 Transgenic mice were produced with a rat albumin promoter enhancer controlling a mouse SCAD minigene (ALB-SCAD) on both the SCAD normal genetic background (C57BL 6J x SJL J-F1) and an SCAD deficient background. In three transgenic lines produced on the SCAD deficient background, recombinant SCAD activity and antigen in liver mitochondria increased up to 7-fold of normal control values. All three lines showed a markedly reduced organic aciduria and fatty liver, which are sensitive indicators of the metabolic abnormality seen in this disease found in children. We found no detrimental effects of high liver SCAD expression in transgenic mice on either background. These studies provide important basic and practical therapeutic information for the potential gene therapy of nuclear-encoded mitochondrial enzyme...

Studies of gene therapy for breast and ovarian cancer

Nielsen et al. (1998a) demonstrated a reduced number of tumour metastases in a murine model of metastatic breast cancer after the intravenous administration of recombinant-adenovirus-expressing p53. This approach, however, resulted in significant liver damage that was thought to be due to the adenoviral vector. New conditionally replicative adenoviral vectors with E1 and E4 gene deletions are much less hepatotoxic and may be useful for p53 transduction in the future.

Products of the maillard reaction

Premelanoidins have been shown to inhibit growth, cause liver damage, and interrupt reproduction in laboratory animals. Maillard products of fructose-glycine and fructose-arginine increase the mutagenicity of 3-amino-1,4-dimethyl 5H-pyridol-(4,3-b)indole. Antimutagenic effects seem to correlate well with antioxidant effects. However, mutagenicity of benzo(a)pyrene is moderately inhibited by such products. Some products of the Maillard reaction have been shown to induce allergic reactions.

Management of the polycystic ovary syndrome

Trans Vaginal Scan And Polycystic Ovarys

100 mg) do not appear to confer additional benefit 21 , but are sometimes prescribed for the first 10 days of each 21-day cycle for women who are particularly resistant to treatment with Dianette alone. The effect on acne and seborrhoea is usually evident within a couple of months. Cyproterone acetate can rarely cause liver damage and liver function should be checked regularly (after 6 months and then annually). Once symptom control has been obtained it is advisable to switch to a combined oral contraceptive pill containing a lower dose of ethinyl oestradiol, because of concerns about increased risk of thromboembolism with Dianette.

Viruses that Promote Apoptosis DNA viruses

Flavivirus The hepatitis C virus (HCV) core protein activates the FAS-mediated cell death pathway, by upregulating FAS. It can be prevented by inhibiting the CPP32 cysteine protease, but not ICE. Thus, the CPP32 protease is involved in the apoptosis effector pathway of HCV and may contribute to HCV immune-mediated liver damage. It has also been reported that HCV core protein can overcome some types of apoptotic death and thus contribute to transformation. Dengue (DEN) virus induces apoptosis late in the virus life cycle. This may be a key element in the pathophysiology of hepatic failure associated with DEN hemorrhagic fever shock syndrome. Another major target cell type of DEN type 1

Role of Complement in Ethanol Induced Liver Injury

Alcoholic liver disease (ALD) develops in approximately 20 of all alcoholics with a higher prevalence in females (Lieber 1994). The development of fibrosis and cirrhosis is a complex process involving both parenchymal and non-parenchymal cells resident in the liver, as well as the recruitment of other cell types to the liver in response to damage and inflammation (Gressner and Bachem 1995). The progression of the alcohol-induced liver injury follows a pattern characteristic to all types of liver fibrosis, regardless of the causative agent. This progression is marked by the appearance of fatty liver, hepatocyte necrosis and apoptosis, inflammation, regenerating nodules, fibrosis and cirrhosis (Martinez-Hernandez and Amenta 1993). Fibrosis is thought to be initiated in response to hepatocellular damage, with inflammatory processes contributing to the progression of the disease (Gressner and Bachem 1995). Interestingly, many of the events involved in the development of fibrosis are...

Effects on Particular Organs or Organ Systems

Hepatic (pertaining to the liver) damage can occur in a number of ways. Fatty liver is an accumulation of lipid globules inside the liver cells and is caused by several Carbon tetrachloride may act in several ways. Besides forming radicals, it can also be converted to phosgene. It also has an indirect effect. It causes a large release of the hormone epinephrine by sympathetic nerves. As with other hormones, epinephrine is quickly broken down after performing its function. This takes place in the liver, and the high levels caused by carbon tetrachloride can result in liver damage. Liver damage can be detected clinically by several functional tests, such as the rate at which it clears certain injected dyes or bilirubin, a chemical produced normally by the breakdown of heme from red blood cells. More sensitive than the liver function tests are tests for certain enzymes. Often when the excretory capability of the liver is impaired, the effects are visible as jaundice, the yellowing of the...

TABLE 123 Phenolic Substances

Tannins have evolved to be less desirable foods for herbivores, and they may protect the plant against microbial and fungal attack. There are two subgroups of tannins the condensed and hydrolyzable compounds (Figure 12.7). Hydrolyzable tannins include gallic, digallic, and ellagic acid esters of glucose or quinic acid. Tannic acid is an example of a hydrolyzable tannin. Condensed tannins are fla-vonoids. They tend to polymerize at positions where carbon bonds link the monomers. Tannins such as gallic acid can tie up metals. Tannins are found in tropical fruits such as mangoes, dates, persimmons, and in tea, coffee, grapes, wine, and cocoa. Black tea contains oxidized tannins. Tannins have been reported to cause liver injury (necrosis and fatty liver). Tannins bind proteins or cause precipitation of proteins, inhibiting digestive enzymes. They also reduce the bioavailability of iron. In the Far East, betel nuts are often chewed after dinner, and because they contain 26 tannins, are...

Some Common Zoonotic Viruses Around the World

Yellow fever (YF), first recognized clinically in the Neotropics in the sixteenth century, periodically ravaged human populations in the Americas, Europe and Africa until as recently as the beginning of the twentieth century. Infection causes hemorrhagic disease with severe liver damage and death in up to half of the most acute cases. Presently, the virus is maintained enzootically in Africa and the tropical Americas in primates and arboreal mosquitoes. Humans or primates transport the virus from its sylvan cycle in forested areas to rural or urban areas, where other vector mosquitoes transmit it. YF may be a public health time bomb there has been an alarming increase in human cases in West Africa in recent years, and, for the first time in history, in Kenya in 1992-1993. Although the number of 'jungle' YF cases in the American tropics has not increased as dramatically, re-establishment of the major urban vector, Aedes aegypti, and the recent appearance and spread of a potential YF...

The Role Of Complement In Liver Regeneration

C3 and C5 are cleaved into their effector fragments following activation of the complement system. Further analysis of liver regeneration after PHx and CCl4 injection in complement-deficient mice has demonstrated the importance of these effector molecules, especially the anaphylatoxins C3a and C5a. Defects in cytokine signaling and transcription factor activation have already been noted when mice were treated with a C5aR antagonist. These mice also display impaired liver regeneration and increased liver injury and mortality after PHx108. Reconstitution of C5-'- mice with murine C5 restores cell division and greatly diminishes injury to near-wild-type levels following injection of CCl4109. C5a has been shown to be the main effector for this improvement in recovery, as it can be accomplished through reconstitution with only the C5a component of C5, while blockage of the C5aR with antagonist impairs regeneration in a manner similar to that seen in C5-'- mice. C3a has also been shown to...

Clinical Features of Infection

In humans, influenza is characterized by the sudden onset of an acute respiratory illness with headaches, chills and nonproductive cough, followed by high fever, muscle aches, generalized weakness and loss of appetite. The fever declines by the third day and is usually gone by the sixth day, but cough and weakness can persist for an additional 2 weeks. More severe illness can develop if primary influenza pneumonia or secondary bacterial pneumonia occurs. People over 65 years of age and those with health problems, such as heart conditions, emphysema, asthma or acquired immune deficiency syndrome (AIDS), and children and adults receiving cancer chemotherapy are at increased risk for complications from influenza and should receive yearly vaccination. At least 10000 excess deaths (over expected) have been documented in each of 19 different US epidemics in the period 1957-1986 in three epidemics there were 40 000 excess deaths. Approximately 80-90 of the excess deaths attributed to...

Assessment of the mother

Positive Predictive Value Screen Test

Platelets are consumed due to the endothelial activation. A falling count, particularly to less than 100 x 109 l may indicate a need to consider delivery. Counts above 50 are likely to support haemostasis. An increasing haematocrit or haemoglobin indicates hypovolaemia, which is characteristic of severe disease. If labour is anticipated then clotting abnormalities should be checked as pre-eclampsia can cause disseminated intravascular coagulation. This is important if regional anaesthesia is used, which is preferable to general anaesthesia. Renal tubular function can be assessed by measuring uric acid, which is a marker of disease severity, although normal levels can occur in severe disease. Acute fatty liver can result in spuriously high levels of uric acid (along with high white cell count, and low glucose). Urea and creatinine are associated with late renal involvement and generally not useful as indicators of disease severity. Liver transaminases should be measured to indicate...

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...

Regulation Of The Jakstat Pathway Suppressors of Cytokine Signaling

Since SOCS-1 acts to inhibit cytokine signaling, mice lacking this protein would be expected to exhibit inappropriate or prolonged responses to cytokine stimulation. The phenotype of the SOCS-1 - - mice does not immediately indicate dysregulated responses to any particular cytokine. However, aspects of the disease seen in these mice, for instance, the specific depletion of B cells, suggest inappropriate signaling in response to an inhibitory cytokine. Indeed, overexpression of IFN-y in vivo has been seen to cause very similar defects, including liver damage and B-cell loss (71,72). Alternatively, it has been proposed that SOCS-1 (SSI-1) functions to inhibit expression of the pro-apoptotic molecule Bax (70). Loss of this regulation in SOCS-1- - mice has been suggested to lead to increased apoptosis possibly accounting for the depletion of lymphocytes (70). Further examination of the SOCS-1- - mice should help define which cytokine signal transduction pathways require regulation by...

Hydrocarbons Solvents Pahs And Similar Compounds

Aldehydes tend to be more irritating than they are CNS depressants. One unique toxicity of the aldehydes, especially formaldehyde, is sensitization. That is, it can increase a person's response to other chemicals. Formaldehyde is a common industrial chemical used in plastics and resins. The LD50 in humans for formalin (37 to 50 formaldehyde solution) is about 45 g, although deaths have been reported at as low as 30 g. Ingestion can produce headaches, GI tract corrosion, pulmonary edema, fatty liver, kidney necrosis, unconsciousness, and vascular collapse. Formaldehyde has been associated with muta-genicity and carcinogenicity in laboratory tests, but a steep dose-response relationship, the lack of epidemiological evidence for carcinogenicity in humans, plus the following facts, suggest the presence of a carcinogenicity threshold. Formaldehyde is a metabolic by-product, normally present at several ppm in tissues. Thus, it appears that carcinogeni-city is associated with exposures high...

What went wrong

Surrogate outcomes have a smaller sample size than conventional morbidity mortality studies, so the available information regarding intervention safety is compromised. There are few good surrogate markers of drug safety. Increases in liver function tests predict liver damage or failure and QT prolongation on the electrocardiogram is associated with higher risks of serious ventricular arrhythmias and sudden cardiac death.


Immune thrombocytopaenic purpura (ITP) Heparin-induced thrombocytopaenia (HIT) Post-transfusion purpura (PTP) Acute fatty Liver of pregnancy Pre-eclampsia (PET) HELLP syndrome Thrombotic thrombocytopaenic purpura (TTP) Haemolytic uraemic syndrome (HUS) Disseminated intravascular coagulation (DIC) Drug induced thrombocytopenia Systemic lupus erythematosis (SLE) antiphospholipid

Liver disorders

Acute fatty liver of pregnancy (AFLP) is a serious but rare liver condition arising in pregnancy which can be very non-specific at time of presentation. It is associated with nausea, vomiting, abdominal pain and jaundice. Diagnosis is normally confirmed by a moderately elevated aspartate amino transferase (AST), and no direct evidence of pre-eclampsia. The diagnosis may be supported by imaging suggestive of fatty change. Manifestations of liver failure include coagulopathy, haemodynamic instability and hypoglycaemia. Hypoglycaemia is a common feature, especially in labour, and may be profound and requires immediate correction. Serial assessment of blood clotting is also important. Delivery must be achieved prior Liver dysfunction in pregnancy can also be caused by incidental viral or autoimmune hepatitis. Where it is unexplained, serology for acute hepatitis must be sent and medical help requested. It is often difficult to determine whether liver dysfunction is due to a pregnancy...

Eruptive Xanthoma

Chylomicron remnants return to the liver via apolipoprotein E receptors for metabolic breakdown. VLDL particles originate within the liver, contain relatively more cholesterol than triglyceride, yet perform a similar function, delivering triglycerides to the peripheral tissues and returning to the liver for breakdown. These lipids are usually markedly elevated in the serum as a directly inherited consequence of faulty lipid metabolism such as lipoprotein lipase or apolipoprotein C-II deficiency or as an indirect mechanism following heavy ethanol consumption (3). As the liver is critical to the metabolism of lipoproteins, ethanol and various medications including miconazole and retinoic acid that are similarly metabolized within or are affected by the status of the liver may result in lipid abnormalities (4,5). Similarly, serious endocrinologic disturbances, such as hypo-thyroidism or diabetes mellitus, or intrinsic liver disorders, such as the condition of fatty...


The BALB cByJ mice are direct descendents of the BALB cBy strain maintained originally by Donald Bailey at the Jackson Laboratory through a subline removed from his research colony in 1975 and put in the Jackson Laboratory production colony 2 these became the BALB cByJ subline, now known to have SCAD deficiency. In later studies based on PCR analysis of the BALB cByJ-fld mutants,6 it was determined that the Acads mutation occurred sometime between 1981 and 1982. This study also established that the mutation for fatty liver dystrophy (fld) was not the same as SCAD deficiency, although fatty liver is found in both. Having been separated since 1935,7 BALB cByJ are more distantly related to the other common BALB cJ mouse strain also available from the production colony of the Jackson Laboratory. BALB cJ mice have a very aggressive, hyperactive behavior as compared to the relatively reserved BALB cByJ mice. We initially speculated that the BALB cByJ mice were mentally retarded as a result...

Whats in a Name

In addition to its myeloablative effects, HDC is extremely toxic to other tissues with dividing cells, such as the gastrointestinal tract, the skin, and the hair follicles. Acute toxicities include cramping and dysfunction in the gastrointestinal tract, mouth sores, nausea, diarrhea, rashes, and fatigue. Total hair loss is very common but varies with the type of chemotherapy used. Severe organ toxicity is less common but can be fatal. The lungs are particularly sensitive to some drugs (e.g., vincristine in the Solid Tumor Autologous Marrow Program I regimen), and life-threatening interstitial pneumonitis can occur, resulting in fluid accumulation and reduced blood oxygen. Other severe adverse effects may include liver damage and inflammation of the bladder. Cardiac events occur more often with HDC. For these reasons, patients who underwent HDC ABMT were usually hospitalized for several weeks and sometimes for months if complications occurred. During hospitalization, patients were at...


Breathing air with very high levels of cadmium severely damages the lungs and can cause death. Breathing lower levels for years leads to a build-up of cadmium in the kidneys, which can cause kidney disease. Long-term oral exposure to cadmium leads to nephrotoxicity. Renal effects always occur before or with other effects. Other effects that may occur after breathing cadmium for a long time are lung damage and fragile bones. Workers who inhale cadmium for a long time may have an increased chance of getting lung cancer. There is no proof about mice or hamsters getting lung cancer on breathing cadmium. However, some rats that breathe cadmium develop lung cancer. In humans, breathing cadmium can affect the ability to have children or can harm unborn babies. Female rats and mice that breathe high levels of cadmium have fewer litters and the pups may have more birth defects than usual. Breathing cadmium causes liver damage and changes in the immune systems of rats and mice. Eating food or...


High dose, although there have been two cases of kidney problems and one case of liver damage reported. A longer-duration study with a larger number of subjects is needed to find out if chromium supplements are beneficial for people with diabetes. An important question is whether the supplement adds much for patients who already may be on several drugs for their diabetes.


The two concerns about aflatoxins are their acute toxicity and ability to produce cancer. The LD50 of aflatoxin is 0.5 mg kg of the body weight, and death occurs within 72 h. Death is due to liver damage and hemorrhaging in the intestinal tract and peritoneal cavity. As animals mature, they become more resistant. Compared with a substance such as lead whose toxicity is about 500 mg kg of body weight, aflatoxin is extremely toxic. Consumption of aflatoxin at sublethal concentration for several days to several weeks results in moderate to severe liver damage. Several forms of hepatic damage include biliary hyperplasia or excessive growth of cells in the bile duct region of the liver. Also prevalent are accumulation of fat and changes in appearance of the liver from purple-red to yellow-red.

Hepatitis B

Hepatitis B, or serum hepatitis, is spread mainly through contaminated blood, often from unsterilized needles shared by drug users or used for tattoos or ear or body piercing. The virus can also be transmitted sexually. Over 100,000 people are infected yearly in the United States, but this number is decreasing due to the recent introduction of a vaccine. In addition to the initial disease, which is more severe than hepatitis A (more liver damage and fatality rate of 10 ), those infected are at higher risk of liver cancer.

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