Foods you can eat with Fatty Liver Disease
In young chicks, biotin deficiency is associated with the fatal fatty liver and kidney syndrome. Apparently healthy chicks 3 to 5 weeks old become lethargic, then sink onto the sternum and become motionless, dying within 6 to 10hours of the onset of the condition. Postmortem examination shows enlarged liver and kidneys, with extensive fatty infiltration, but none of the classical skin and feather signs of biotin deficiency. The syndrome can be induced with only a moderate degree of biotin deficiency if the birds are maintained on a high-carbohydrate, low-fat and low-protein diet a mild stress, such as short-term fasting, will then induce the syndrome in up to 20 of the birds. Supplementing the diet with biotin prevents the problem. Gluconeogenesis is severely impaired in birds suffering from the fatty liver and kidney syndrome the administration of biotin rapidly restores gluconeogenesis to normal, by activating apopyruvate carboxylase. The affected animals also have impaired glucose...
Lipoprotein (VLDL) of which lecithin is a required component. In choline deficiency, the diminished ability of liver cells to synthesize new lecithin molecules results in the intracellular accumulation of TG. Treating malnourished patients with high-calorie total parenteral nutrition (TPN) solutions that contain little or no choline will deplete choline stores and cause fatty liver and hepatic dysfunction that can be reversed by treatment with phosphatidylcholine.
Antihyperlipidaemic Ginsenoside Rb1 has been shown to lower triglyceride and cholesterol levels via cAMP-production in the rat liver (Park et al 2002b). P. ginseng extract (6 g day) for 8 weeks resulted in a reduction in serum total cholesterol, triglyceride, LDL and plasma malondialdehyde levels and an increase in HDL (Kim & Park 2003) in eight males. Ginseng has also been reported to decrease hepatic cholesterol and triglyceride levels in rats, indicating a potential use of ginseng in the treatment of fatty liver (Yamamoto et al 1983).
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,...
Small areas of liver tissue may be supplied by another venous system, the third inflow which comprises aberrant veins that enter the liver directly, independently of the portal venous system. Such veins communicate with intrahepatic portal branches to various degrees and lead to focally decreased portal perfusion. However, little overall change in the hepatic arterial perfusion is seen. Because this hemodynamic state is persistent, focal metabolic changes are occasionally observed, typically as sparing in the fatty liver or as accumulations of fat 20 .
The differential diagnosis of confluent fibrosis in cirrhotic patients includes non-neoplastic processes such as segmental fatty liver or hepatic infarction and neoplastic processes such as infil-trative sclerosing HCC. Although irregular fatty infiltration may appear with variable shape and dis-
Focal Fatty Liver Fatty liver infiltration is a common, metabolic complication of a variety of toxic, ischemic and infectious insults to the liver, such as obesity, diabetes mellitus, alcoholic liver disease, malnutrition, and chemotherapy. Other causes include hy-peralimentation, inherited metabolic disturbance, inflammatory bowel disease, severe hepatitis, endogenous and exogenous steroid use, and pregnancy 1 . Generally, fat is deposited in response to different metabolic changes, such as increased hepatic synthesis of fatty acids (ethanol), decreased hepatic oxidation or utilization of fatty acids (carbon tetrachloride, tetracycline), impaired release of hepatic lipoproteins (steroids), or excessive mobilization of fatty acids from adipose tissue (alcohol, steroids). The prevalence of focal fatty infiltration of the liver increases significantly with advancing age whereas it is uncommon in infants and young children, it is present in roughly 10 of the adult population 23 . There...
Ethionamide (Trade name Trecator-SC) An antibacterial drug used to treat tuberculosis, usually in conjunction with other drugs. It is administered by mouth or as a suppository. Patients with liver damage should not use this drug. pyrazinamide An antimycobacterial drug prescribed in combination drug therapy to treat hospitalized patients with tuberculosis who don't respond to other drugs. Patients with severe liver damage should not use this drug. diarrhea are fairly common side effects. Others include more severe gastrointestinal disturbances, kidney and liver damage, inflammatory lesions in the anal-genital area, hemolytic anemia, and rash. Patients may also be susceptible to infection with tetracycline-resistant organisms.
The reasons for the elevations in medical problems are not fully understood, but point to binge eating behavior itself. Some research has found that BED is associated with increased risk of metabolic abnormalities, which may be attributed to the pattern of eating observed in BED. For example, eating large amounts of food in a discrete period of time (BED Diagnostic Criterion A1 in DSM-5) (American Psychiatric Association 2012) is associated with exaggerated insulin secretion, increased fasting glucose levels, decreased glucose tolerance, and elevated serum lipids (Jenkins et al. 1992 Taylor et al. 1999). Eating rapidly (Criterion B1) is associated with elevated serum lipids, higher waist-hip circumference ratio, and fatty liver in obese individuals (Kral et al. 2001). Irregular meal patterns, which are frequently observed in BED (Masheb and Grilo 2006 Masheb et al. 2011) and are described more below, are associated with the metabolic syndrome in the general population (Sierra-Johnson...
Think I am a good candidate for gastric bypass surgery What do I need to do to obtain insurance coverage for this
Ship with your primary care doctor, he or she will know about your weight loss attempts and will be treating you for any of your obesity-related illnesses or conditions (elevated cholesterol and triglycerides, gallstones, pancreatitis, abdominal hernia, fatty liver, diabetes or prediabetes, polycystic ovary syndrome, high blood pressure, heart disease, pulmonary hypertension, stroke, blood clots in the legs and lungs, sleep apnea, arthritis, gout, lower back pain, infertility, urinary incontinence, or cataracts).
Of particular interest is the remarkable effect of kolaviron on AFB1-induced liver damage. We demonstrated the chemopreventive effect of kolaviron against the hepatic oxidative damage induced by aflatoxin in rats (Farombi et al., 2005) by mechanisms involving induction of phase 2 antioxidant enzymes capable of detoxifying toxic aflatoxin metabolites.
Fat accumulation in the liver is an almost universal response to excessive alcohol consumption. It occurs in the majority of heavy drinkers. How and why fat accumulates in liver cells is complicated and not completely understood but we know for sure that it happens. If you examine a piece of biopsied liver tissue from an alcoholic under the microscope, you see that many liver cells are loaded with big bubbles consisting of fat, almost totally occupying the cell. In most cases, this fatty change does not matter too much as far as the patient s health is concerned. It is an almost invariable response to too much alcohol consumption and an early warning. The person who has nothing worse than an alcoholic fatty liver may not feel sick at all, and only if a biopsy is done can the fatty liver be diagnosed. The doctor may feel an enlarged liver by palpation, which may be a bit tender. The laboratory test may show a slight elevation in the blood of some liver enzymes,...
Hepatocellular carcinoma (HCC) is the most common primary hepatic malignancy and one of the most prevalent visceral malignances worldwide 21 . HCC usually occurs in the setting of cirrhosis with a known cause, such as chronic viral hepatitis or alcoholism. Regarding alcoholism as a cause of cirrhosis, it is thought that alcoholism promotes hepatic malignancies indirectly via its immuno-suppressive effects. These effects facilitate the development of hepatitis B virus (HBV) and hepatitis C virus (HCV) infections. Furthermore, alcoholic cirrhosis is triggered by the well-known oxidative effects that deplete the anti-oxidative defense system 35 . Whereas in Asia HCC occurs almost exclusively in patients with chronic liver damage from hepatitis, in North America many patients develop HCC without cirrhosis or known risk factors 74 . In these latter patients it is possible that steroid hormones may play a role in carcinogene-
Nigella sativa L. has not shown the specific inhibitory activity against tyrosinase (Mukherjee et al., 2001). The oil has microbial activity and has been investigated as antimicrobial (Minakshi and Banerjee, 1999), antiococeptive (Abdel-Fattah et al., 2000) and carminative (El-Dakhakhny, 2000). Nigella oils have played a significant role for altering the liver damage induced by Schistosoma mansoni infection in mice and helped in improving the immunological host system and to some extent with its antioxidant effect (Mahmoud et al., 2002). Recent studies had revealed that extract of Nigella sativa L. has a strong immunomodulatory and interferon-like activity (Medenica et al., 2000). It inhibits cancer and endothelial cell progression, and decreases the production of the angiogenic protein fibroblastic growth factor made by tumour cells.
Surgical resection of hepatic tumors should be performed if the lesion is surrounded by healthy liver tissue in order to leave a resection safety margin of 1 cm. Tumor locations near larger blood vessels or bile duct structures may make it difficult to achieve this safety margin. Therefore, cryotherapy of the resection edge with a specially designed flattened cryo-probe can be performed as a therapeutic adjunct to achieve tumor-free resection margins 41-43 . On post-operative MR imaging the resulting cryonecrosis is characterized by a flattened elliptical area (Fig. 13) with identical peripheral imaging features as endohepatic cryotherapy. Criteria for detection of residual tumor should be applied analogously.
Both the oil extract and the defatted fraction of S. maxima lowered total lipids and triacylglycerols in livers of rats with carbon tetrachloride (CCl4)-induced fatty liver indicating the presence of bioactive principles in both fractions. The authors attributed the hepatoprotective effects of spirulina to More recently, S. maxima has been shown to prevent fatty liver formation in male and female mice with alloxan-induced diabetes. The administration of S. maxima to these animals reduced the levels of thiobarbi-turic acid-reactive substances in serum and liver as well as triglyceride and LDL and VLDL levels (40). Spirulina has also been shown to prevent liver fibrosis (41) and arrest the progress of chronic hepatitis into hepatocirrhosis (42).
Hepatoprotection may also be mediated by radical-scavenging properties of G. lucidum. It has been hypothesized that CCl4 and alcohol toxicity is associated with increased oxidative stress and free-radical-associated injury. Lin et al. (176) reported that hot-water extracts of G. lucidum showed significant radical-scavenging activity against both superoxide and hydroxyl radicals however, the extracts were not further characterized. Interestingly, in a similar animal study of CCl4-induced liver damage (142), oral administration of the medium in which G. lucidum mycelia were grown (but not the mycelium alone) had marked benefical effects, as assessed by lower 96 hr postinjury serum AST and ALT activities. No decrease was seen in the actual damage caused, as 24-hr transaminase activites were not different from levels in control animals, implying that the mycelium-medium may have promoted Polysaccharides extracted from G. lucidum were found by Park et al. (180) to have antifibrotic...
In most cases, metabolic diseases affecting the liver ultimately lead to cirrhosis. Typically, the imaging findings in these cases are similar to those in adults in whom liver cirrhosis arises for other reasons. In other cases, however, the findings may be more subtle. Frequently hepatomegaly or fatty liver is the main finding during the early stages of disease.
There are several advantages to infusing parent-eral nutrition in a cyclic manner over 12-16 h during the hours of sleep. First, it permits the patient to pursue a normal lifestyle during the day hours. Second, it minimizes the risks of fatty liver and hepatomegaly that are associated with long-term continuous calorie and protein infusions.
Bannister DW (1976a) The biochemistry of fatty liver and kidney syndrome. Biotinmediated restoration of hepatic gluconeogenesis in vitro and its relationship to pyruvate carboxylase activity. Biochemical Journal 156, 167-73. Bannister DW (1976b) Hepatic gluconeogenesis in chicks effect of biotin on gluconeogenesis in biotin-deficiency and fatty liver and kidney syndrome. Comparative Biochemistry and Physiology B 53, 575-9.
Consequence of severe liver damage that occurs in many patients with chronic liver diseases, such as persistent infection with hepatitis C and B viruses, as well as alcoholic liver disease and bile duct obstruction (12). Liver stellate cells are regarded as the primary target cells for inflammatory stimuli (13). It has been shown that activation of hepatic stellate cells in injured livers leads to their proliferation and transformation into myofibroblast-like cells. The transformed cells synthesize large quantities of the major components of the ECM, including collagen types I, III, and IV, fibronectin, laminin, and proteoglycans, leading to fibrosis.
Although the causes and clinical manifestations of CLD may vary, it is often accompanied by liver damage. The obstruction or absence of bile ducts leads to accumulation of bile acids in hepatocytes, which results in liver damage. Because the enterohepatic circulation of bile acids is interrupted, the resulting absence of bile acids in the intestinal lumen leads to impaired micelliza-tion and therefore to strongly reduced absorption of fats and fat-soluble nutrients. Another feature of CLD is the high serum bile acid level, which can cause secondary tissue injury. In biliary atresia, it is often attempted to correct the enterohepatic circulation of bile acids by performing a Kasai portoenterostomy. During this procedure the liver is directly connected to the proximal small intestine to optimize bile flow into the intestine as much as possible. However, Kasai portoenteros-tomy is frequently only a transient solution, due to the presence of intrahep-atic bile duct damage and ongoing...
Numerous studies suggest that curcumin lowers serum cholesterol levels (78-84). Soudamini et al. investigated the effect of oral administration of curcumin on serum cholesterol levels and on lipid peroxidation in the liver, lung, kidney, and brain of mice treated with carbon tetrachloride, paraquat, and cyclophosphamide (81). Oral administration of curcumin significantly lowered the increased peroxidation of lipids in these tissues produced by these chemicals. Administration of curcumin also significantly lowered the serum and tissue cholesterol levels in these animals, indicating that the use of curcumin helps in conditions associated with peroxide-induced injury such as liver damage and arterial diseases. Soni and Kuttan examined the effect of curcumin administration in reducing the serum levels of cholesterol and lipid peroxides in 10 healthy human volunteers receiving 500 mg of curcumin per day for 7 days (82). A significant decrease in the level of serum lipid peroxides (33 ), an...
ALT is also called SGPT (serum glutamic pyruvic transaminase). When doctors talk about liver functions, they are usually referring to tests on blood samples that measure liver damage. If the chemotherapy is proving to be toxic to your childs liver, the damaged liver cells release an enzyme called ALT into the blood serum. ALT levels can go up in the hundreds or even thousands in some children on chemotherapy. Each institution and protocol has different points at which they decrease dosages or stop chemotherapy to allow the childs liver to recover. If you notice a change in your childs ALT, ask for an explanation and plan of action. (For example Johns ALT is now 450. What is your plan to reduce or stop the chemotherapy to allow his liver to recover )
Alcoholic liver disease The term 'alcoholic liver disease' refers to a spectrum of types of hepatic injury associated with continuous alcohol ingestion, ranging from alcoholic fatty liver to alcoholic stea-tohepatitis, fibrosis, and cirrhosis. Nutritional disturbances in alcoholics are an important cause of morbidity and mortality all classes of nutrients are affected. Anorexia leads to decreased food intake and subsequent protein-calorie malnutrition. Maldigestion and malabsorption can occur secondary to chronic alcohol injury to small intestinal mucosa. Alcohol consumption is often associated with chronic pancreatic insufficiency, which results in steatorrhea and decreased absorption of dietary protein, fat, and fat-soluble vitamins. Chronic alcohol ingestion also results in impaired hepatic amino acid uptake and protein synthesis. A variety of international associations have made nutritional recommendations for patients with various types of alcoholic liver disease. The primary...
Obesity-related illnesses and conditions include elevated cholesterol and triglycerides, gallstones, pancreatitis, abdominal hernia, fatty liver, diabetes and prediabetes, polycystic ovary syndrome, high blood pressure, heart disease, pulmonary hypertension, stroke, blood clots in the legs and lungs, sleep apnea, arthritis, gout, lower back pain, infertility, urinary incontinence, and cataracts. If you have one of these conditions gastric surgery can be considered when the BMI is 35 or higher. In many cases gastric bypass surgery can dramatically improve obesity-related conditions. I have had many patients who after gastric bypass surgery were able to give up their blood pressure, diabetes, and cholesterol lowering medications. Many young women who have been unable to become pregnant conceive and go on to have healthy babies (more on this later).
At intake in excess of 1 g of niacin per day, there is evidence of toxicity, with changes in liver function tests, carbohydrate tolerance, and uric acid metabolism that are reversible on withdrawal of niacin (Parsons, 1961a, 1961b). Baggenstoss and coworkers (1967) reported changes in liver ultrastructure in patients receiving high doses of niacin, including dilatation of the endoplasmic reticulum with formation of vesicles and sacs, and a diminution in the parallel arrays of rough endoplasmic reticulum, with fewer ribosomes on the outer surface. There was also elongation of the mitochondria, withbud-like projections and crystalloid inclusions. The mechanism of niacin hepatotox-icity is not known. Sustained release preparations are associated with more severe liver damage than crystalline preparations, presumably because they permit more prolonged maintenance of high concentrations of the vitamin, whereas after an acute high dose there is normally considerable excretion of unchanged...
Alcoholic liver disease is among the top ten causes of mortality in the US with somewhat higher mortality rates in western European countries where wine is considered a dietary staple, and is a leading cause of death in Russia. Among the three stages of alcoholic liver disease, fatty liver is related to the acute effects of alcohol on hepatic lipid metabolism and is completely reversible. By contrast, alcoholic hepatitis usually occurs after a decade or more of chronic drinking, is associated with inflammation of the liver and necrosis of liver cells, and carries about a 40 mortality risk for each hospitalization. Alcoholic cirrhosis represents irreversible scarring of the liver with loss of liver cells, and may be associated with alcoholic hepatitis. The scarring process greatly alters the circulation of blood through the liver and is associated with increased blood pressure in the portal (visceral) circulation and shunting of blood flow away from the liver and through other organs...
How can I rationalize surgically changing my insides and risking significant complications even death just to lose
An article in the Journal of the American Medical Association (January 8, 2003) reported that marked obesity in a man aged twenty to thirty could reduce his life expectancy by up to thirteen years. An extremely obese woman in this same age range might expect to lose up to eight years compared to her normal-weight friends. These are not small numbers. People who are overweight are more likely to develop obesity-related illnesses such as heart disease, pulmonary hypertension, stroke, diabetes, sleep apnea, and arthritis. And obese people are much more likely than lean people to develop blood clots in the legs and lungs, gallstones, pancreatitis, abdominal hernia, fatty liver, polycystic ovary syndrome, high blood pressure, arthritis, gout, lower back pain, infertility, urinary incontinence, and cataracts.
Choline, methionine, methyltetrahydrofolate (methyl-THF), and vitamins B6 and B12 are closely interconnected at the transmethylation metabolic pathways that form methionine from homocys-teine. Perturbing the metabolism of one of these pathways results in compensatory changes in the others. For example, as noted above, choline can be synthesized de novo using methyl groups derived from methionine (via S-adenosylmethio-nine). Methionine can be formed from homocys-teine using methyl groups from methyl-THF, or using methyl groups from betaine that are derived from choline. Similarly, methyl-THF can be formed from one-carbon units derived from serine or from the methyl groups of choline via dimethylglycine. When animals and humans are deprived of choline, they use more methyl-THF to remethylate homocysteine in the liver and increase dietary folate requirements. Conversely, when they are deprived of folate, they use more methyl groups from choline, increasing the dietary requirement for...
Dangerous side effects include decreasing blood counts, decreasing platelet counts, confusion, and liver damage (see Table 6). These effects can happen at any time in the course of taking an H2 blocker or PPI. In these cases, immediately stop taking the medication and discuss the side effects with your doctor.
Several reports concerning the role of Sho-saiko-to with respect to the prevention and treatment of experimental liver damage induced in rats by D-galactosamine (36), carbon tetrachloride (37), dimethylnitrosamine (DMN) (38), and pig serum (PS) (38) have appeared. Although the mechanism by which Sho-saiko-to prevents hepatic fibrosis is not at present clear, it has been reported that the preadministration of this herbal medicine protects the liver plasma membrane and HSCs against injury (31). Moreover, Sho-saiko-to was reported to prevent the development of hepatic fibrosis by the inhibition of HSC activation in a different animal model, the choline-deficient rat (39). We confirmed the preventive and therapeutic effects of Sho-saiko-to on rat experimental hepatic fibrosis induced by DMN and PS (7). The rats were fed a basic diet that contained Sho-saiko-to for 2 weeks prior to the induction of hepatic fibrosis, or during the last 2 weeks of treatment. Sho-saiko-to suppressed the...
Now imagine that the animal receives an injury that slices away a small section of its liver. The injured area soon becomes inflamed and steeped in growth factors. These factors, produced by immune cells, released from the blood, or derived from other sources, cause various types of cells to proliferate. For example, blood vessel cells proliferate to replace those damaged in the injury, and liver cells are also stimulated to proliferate by these growth factors. In addition, the reduced cell-to-cell contact at the edge of the healthy liver tissue signals that new liver cells are needed. In response to the growth factors and signals from reduced cell-to-cell contact, stem cells or other poorly differentiated cells in the liver enter the cell cycle and proliferate. The entire repair process and all the cell proliferation that goes on in it is wondrously orchestrated so that once tissue repair is complete, no new tissue is produced.
Flushing (burning and itching of face, arms and chest) and stomach irritation arc the main side effects of moderately high supplemental niacin intake (more than 35 mg d). Liver damage that may culminate in irreversible liver failure is a risk associated with long-term use of very high doses (3000 and more mg dl as a cholesterol-lowering drug. Such high doses must never be used without close monitoring of liver function. High intakes of nicotinic acid may interfere with the effects of sulfinpyrazone (Anturane).
Of alcohol that would be expected after moderate drinking. The metabolism of alcohol by ADH causes a redox change that promotes lipid synthesis in the liver as well as reduced gluconeogenesis and increased lactate production. Thus, even moderate drinking can cause fatty liver with elevated serum triglyceride levels and, in the absence of dietary carbohydrate, may result in low blood glucose levels that impair concentration and even consciousness. The second liver enzyme, CYP2E1, is part of the cytochrome P450 family, and metabolizes alcohol at levels to be expected after heavy drinking. During metabolism of high levels of alcohol, CYP2E1 utilizes adenosine triphosphate (ATP) energy units and thus 'wastes' stored calories, with resultant potential for weight loss. Another form of this enzyme, gastric CYP2E1, exists in the stomach and, as the first of the three alcohol-metabolizing enzymes to encounter alcohol, accounts for about 30 of all alcohol metabolism in men, but only 10 in...
Many developed functional foods seem to have benefits for human health. For example, calcium-fortified orange juice provides approximately the same amount of calcium as milk. With more than half of all children under the age of five and nearly 85 percent of females age twelve to nineteen not meeting the Dietary Reference Intake (DRI) for calcium, calcium-fortified orange juice may contribute significantly to calcium intake. On the other hand, a positive impact on health is more difficult to establish for other developed functional foods. These include prepared foods spiked with herbal preparations, which may contain little of the herbal ingredients listed on the label, or insufficient quantities of these ingredients to produce the claimed effect. Additionally, some herbal ingredients can be harmful, such as kava, which has been associated with liver damage, and belladonna, which is toxic.
Alcohol dehydrogenase converts ethanol to acet-aldehyde and hydrogen. Hydrogen is a form of fuel that can be burned (oxidized). Normally, the liver burns fat to produce the energy required for its own functioning but, when alcohol is present, its hydrogen displaces fat as the preferred fuel. When the liver stops burning fat and instead burns the hydrogen from the ethanol, however, fat accumulates, and a fatty liver develops, which is the first stage of alcoholic liver disease (Lieber, 1992a). Once a fatty liver has developed, fat accumulation does not increase indefinitely, even though alcohol consumption may be continued (Salaspuro et al., 1981). Fat deposition is offset, at least in part, by lipoprotein secretion, resulting in hyperlipemia elevated amounts of fat in blood. Hyperlipemia of a moderate degree is commonly associated with early stages of alcoholic liver injury, but it wanes with the progression of liver disease (Lieber & Pignon, 1989). In some individuals, marked...
Fatty liver while the 9c,11t isomer had little or no effect (Clement et al., 2002 Degrace et al., 2003). While adipose tissue mass was shown to decrease after feeding CLA for 6 days, plasma levels of leptin and adiponectin decreased after 2 days of feeding, and hyperinsulinaemia developed on day 6 (Poirier et al., 2005). CLA was shown to alter the capacity of pancreatic islets to secrete insulin and the increase in insulin secretion was correlated to an increase in beta cell mass and number, leading to liver steatosis (Poirier et al., 2005). Degrace et al. (2003) demonstrated using C57BL 6J mice that the steatosis was not due to an alteration of the liver lipoprotein production. A three-fold decrease in plasma triacylglycerol and induction of mRNA expression of low-density lipoprotein receptors suggest an increase in the lipoprotein clearance at the level of liver. Further work also indicated that the steatosis was not due to impaired fatty acid oxidation as in fact in the liver,...
In many animals, dietary deprivation of choline leads to liver dysfunction and growth retardation, and some patients maintained on choline-free total parenteral nutrition develop liver damage that resolves when choline is provided, suggesting that endogenous synthesis may be inadequate to meet requirements (Zeisel, 2000). There is inadequate information to permit the setting of reference intakes, but the Acceptable Intake for adults is 550 mg (for men) or 425 mg (for women) per day (Institute of Medicine, 1998). In experimental animals choline deficiency is exacerbated by deficiency of methionine, folic acid, or vitamin B12, which impairs the capacity for de novo synthesis.
The liver is commonly seen as the literal oil filter of the body-but it does so much more. Reserves of blood are stored in the liver along with fat soluble vitamins including A, D, E, and K. Your liver creates bile necessary for proper metabolism of fat. Kupfer cells are active in a healthy liver seeking and destroying unhealthy invaders including cancer cells and parasites. Toxins (modern-day arrows) from the air, water, and processed foods and drinks stress the liver.
As a part of my patient coaching workshops I encourage the following daily protocol. You should eat half of an apple daily. The Apple has malic acid to help thin bile for better digestion as well as fiber and pectin for bulk and healing. Wash and eat the peel along with the seeds. Beets and their fiber, especially grated raw, organic, act as an intestinal wall cleanser. Pickled and canned beets should be your last choice. Carrots have Vitamin A for skin, eye, and liver health. Raw, organic carrot slices or a handful of baby carrots go a long way in promoting basic body function.
Echium plants produce alkaloids as a chemical defense mechanism. The specific echium alkaloids are called pyrrolizidine alkaloids (PAs). PAs are hepatotoxic, and cause liver damage (Cheeke, 1988). In Australia, echium poisoning has been reported in sheep, cattle, horses, swine, and poultry (Cheeke, 1988). For humans, it is suggested that PA levels in herbal products of proven health benefit should be 1 mg per day for oral and 100 mg per day for external use, for a period of no more than 6 weeks in a year (Edgar et al., 2002). The use of PA-containing herbal products in pregnant and lactating women is prohibited. Culvenor et al. (1981) reported 0.950 mg of PA per g of honey from E. plantagineum hence, caution should be exercised in using honey from an area where bees largely rely on echium pollens and nectars to produce honey. With respect to ESO itself, the alkaloids are removed during extraction, and the PA content of echium seeds does not limit their use for the supply of n-3 oil.
A key anti-inflammatory cytokine in the liver that assists regeneration and downregulation of TNF (Arteel et al 2003, Casini et al 1989, Song et al 2004). Research using animal models demonstrate that SAMe is a natural growth regulator in hepatocytes and is anti-apoptotic in healthy liver cells, but pro-apoptotic in hepatic carcinoma cells (Lu & Mato 2005).
Protection against paracetamol-induced liver damage has been demonstrated in animal models using gomisin A (Yamada et al 1993). Gomisin A inhibited not only the elevation of serum aminotransferase activity and hepatic lipoperoxide content, but also the appearance of histological changes such as degeneration and necrosis of hepatocytes. In 2003, protection against paracetamol-induced liver damage and d-galactosamine-induced liver damage was confirmed for a fractionated extract of 5. chinensis in an experimental model (Nakagiri et al 2003). Liver regeneration Two animal studies have demonstrated that oral administration of gomisin A, a lignan isolated from 5. chinensis, accelerates liver regeneration after partial hepatectomy and hastens recovery of liver function (Kubo et al 1992, Takeda et al 1987). The mechanism for these effects is not fully elucidated however, gomisin A increases ornithine decarboxylase activity, which is important during the early stages of regeneration and...
Hepatoprotective Curcumin prevents carbon tetrachloride-induced liver injury both in vivo and in vitro (Deshpande et al 1998, Kang et al 2002), reverses aflatoxin-induced liver damage in experimental animals (Soni et al 1992) and effectively suppresses the hepatic microvascular inflammatory response to lipopolysaccharides in vivo (Lukita-Atmadja et al 2002). An ethanol soluble fraction of turmeric was shown to contain three antioxidant compounds, curcumin, demethoxycurcumin and bisdemethoxycurcumin, which exert similar hepatoprotective activity to silybin and silychristin in vitro (Song et al 2001).
Today, the most high-risk group for development of pellagra signs and symptoms in Western society is chronic alcoholics, whose diets are often poor, and in addition are subject to liver damage from alcohol abuse and its cellular toxicity. Certain forms of psychosis, including depression and schizophrenia, are associated with abnormalities of the tryptophan metabolism pathways, including those involved in the formation of 5-hydroxytryptamine (serotonin)
SNPs (single nucleotide polymorphisms) in humans may exist and, if so, would influence dietary requirements for choline. In mice in which this gene is knocked out, the dietary requirement for choline is increased and they get fatty liver when eating a normal choline diet. Estrogen induces greater activity of PEMT perhaps explaining why premenopausal women require less choline in their diets. In addition to formation of choline, this enzyme has an essential role in lipoprotein secretion from the liver.
Early pharmacological studies have demonstrated the ability of Sch B and other lignans in protecting against liver damage induced by a variety of chemicals, such as acetaminophen, carbon tetrachloride (CCl4), thiacetamide, and immunlogical toxins, in rodents (11-18). Recent studies in our laboratory have also shown that Sch B pretreatment (0.5-4 mmol kg day x 3 days) protected against CCl4 and tumor necrosis factor-a-induced hepatotoxicity in a dose-dependent manner in mice (19,20). Preliminary structure-activity relationship study, using Sch B and its lignan analogs, namely, schisandrin A (Sch A, Fig. 1b), schisandrin C (Sch C, Fig. 1c), and a synthetic intermediate of Sch C, dimethyl diphenyl bicarboxylate (DDB, Fig. 1d), indicated that the methylenedioxy group as well as the cyclooctadiene ring structure of Sch B are important structural determinants in its hepatoprotective action (21,22). Petreating mice with Sch B at a daily dose of 0.125-0.5 mmol kg or
Cirrhosis is a well-established risk factor for gallstones particularly in the more advanced stages.54,55 The overall prevalence is much higher than the general population at 25 to 30 .56 Increasing Child-Pugh score and obesity are more likely associated with gallstones. Most stones in cirrhosis are of the black pigment type.57 The biologic mechanism likely relates to altered pigment secretion, abnormal gallbladder motility, or increased estrogen levels.1 The threat of these stones becoming symptomatic seems higher in women, those more advanced in age, and patients with viral hepatitis compared with alcohol-related cirrhosis.58 Gallstone disease is also associated with hepatitis C virus (even when not yet cirrhotic)59 and nonalcoholic fatty liver disease, the connection being the metabolic syndrome and obesity.60
Results of studies on alcoholic subjects without evidence of heart disease suggest that a subclinical disease state may exist. In this situation, recognition of the possibility of disease exists, but no methodology has been developed to detect one in the clinic. In one study, those with at least a ten-year history of heavy alcohol consumption were compared to controls. These patients had biopsy-proven fatty liver disease (a common sequel to chronic alcohol use) without prior history of heart disease. The response of the heart s main pumping chamber the left ventricle to storehouses was assessed. Alcoholic hearts were found to have abnormally high internal pressures and could not appropriately compensate by increasing forward blood flow. An index of heart contractions in response to the stimulus was correspondingly low in the alcoholics compared to control. Doppler echocardiography, an ultrasound technique for assessing heart function, has also demonstrated an...
A major diagnostic category that has received increasing attention in research and clinical practice is substance abuse in contrast to dependence. This category permits the classification of mal-adaptive patterns of alcohol or drug use that do not meet criteria for dependence. The diagnosis of abuse is designed primarily for persons who have recently begun to experience ALCOHOL or drug problems, and for chronic users whose substance-related consequences develop in the absence of marked dependence symptoms. Examples of situations in which this category would be appropriate include (1) a pregnant woman who keeps drinking alcohol even though her physician has told her that it could be responsible for FETAL damage (2) a college student whose weekend binges result in missed classes, poor grades, and alcohol-related traffic ACCIDENTS (3) a middle-aged beer drinker regularly consuming a six-pack each day who develops high blood pressure and fatty liver in the absence of alcohol-dependence...
COMPLICATIONS This section has articles on some aspects of the physical and psychological complications of substance abuse. It contains an overview of Medical and Behavioral Toxicity and individual articles on the following Cardiovascular System Cognition Dermatological Endocrine and Reproductive Systems Immunologic Liver (Alcohol) Liver Damage (Other Drugs) Mental Disorders Neurological Nutritional and those Due to Route of Administration. Each article is extensively cross-referenced and will refer the reader to other articles throughout the Encyclopedia that will either expand or simplify concepts introduced here, and to articles on the many other behavioral and nonmedical complications that arise as a result of alcohol and drug use.
Liver Damage (Other Drugs) The liver is the largest organ of the human body, normally weighing about 3.3 pounds (1.5 kg). It occupies the right upper quadrant of the abdominal cavity just below the diaphragm. As befitting its anatomical prominence, its function is essential to maintain life. If we surgically removed the entire liver from any animal (including humans), it will fall into a coma shortly and die. The absence of a certain critical mass of functioning liver tissue is incompatible with life. While the human liver has a remarkable resilience and regenerative capacity after injury or illness, this is true only up to a certain point.
Alcohol has direct toxic effects on neurons and, in association with other medical consequences of alcohol abuse, such as liver damage and inadequate nutrition, can result in significant and lasting cognitive deficits. There is no clear indication of the level of consumption that might put one at risk for such consequences, but safe drinking guidelines of no more than twelve to fourteen drinks per week probably represent a minimum level. Although there are no precise data on the incidence of neurological or cognitive impairment in alcohol abusers, it is estimated that 50 to 70 percent of individuals seeking treatment may present with some form of neurocognitive impairment. Most of these report
Liver damage may develop into hepatitis or cirrhosis, a chronic inflammatory disease of the liver. Excessive alcohol use also affects the cardiovascular and nervous systems. Oral effects shown in alcoholics include bleeding gums and easy bruising. Individuals who drink excessively usually have poor oral hygiene habits.
Comfrey has come into disrepute in recent years because it contains pyrrolizidine alkaloids. This is a large group of chemicals, some of which are toxic to the liver and can cause hepatic veno-occlusive disease. Poisoning has been reported in people eating other plants with high levels of these alkaloids, and there are a few reported cases of liver damage that appear to be based on the use of comfrey root.
Cereals see also niacytin. niacin toxicity High doses of nicotinic acid have been used to treat hypercholesterolaemia they can cause an acute flushing reaction, with vasodilatation and severe itching (nicotinamide does not have this effect, but is not useful for treatment of hyper-cholesterolaemia). Intakes of niacin above 500mg day (the reference intake is 17 mg day) can cause liver damage over a period of months the risk is greater with sustained release preparations of niacin.
Accumulation of fat within hepatocytes is commonly found in diabetic or obese patients or in patients who have been exposed to ethanol or other chemical toxins. In addition, in patients with advanced malignant neoplasms, fatty changes of the liver may be present due to poor nutrition and the hepatotoxic effects of chemotherapy. In most cases, fatty liver is associated with elevated levels of hepatic transaminases 48,74 . from the case of lipoma of the liver, out-of-phase images are more sensitive for the detection of fatty liver than fat suppressed images. The intensity on out-of-phase images is determined from the absolute value of water intensity minus the fat intensity. Thus, whereas most tissues (including fat) appear similar on in-phase and out-of-phase images, fatty liver will be noticeably darker. if, for example, in a given case of focal fatty infiltration, fat accounts for 10 of the lesion's SI and water accounts for 90 on in-phase images, fat suppression, assuming that the...
The sixth study was a two-year, unblinded, uncontrolled, pilot study on 10 patients with inoperable pancreatic cancer.216 This study by Nicholas Gonzalez, M.D., and Linda Isaacs, M.D., was a continuation of work originally started by Dr. John Beard and others in the early 1900s and later carried on by William Kelly, a dentist from Texas.229,230231 Dr. Gonzalez became interested in the effects of proteolytic enzymes and other modalities after reviewing the work of Dr. Kelly. In this study, patients were treated with an intensive program of diet, oral supplementation of nutrients and enzymes, and routines such as coffee enemas (for the purpose of liver detoxification). The proteolytic enzymes are the proposed anticancer element in the program, while the other components are considered supportive in nature. The daily dose of pancreas enzymes (derived from pigs) was 25 to 40 grams, which was spread out over multiple doses throughout the day and night. Although the exact protocol has not...
Physical examination and laboratory evaluation are unreliable.69 Fever is generally present but other physical findings cannot be relied on, particularly physical examination of the abdomen.12 Leukocytosis and jaundice are commonplace, but nonspecific in the setting of critical illness. The differential diagnosis of jaundice in the critically ill patient is complex and context-sensitive, including intrahepatic cholestasis from sepsis or drug toxicity and fatty liver'' induced by TPN, in addition to AAC.68 Jaundice caused by AAC may be caused most often by sepsis-related cholestasis, or rarely by extrinsic compression of the common duct by the phlegmon (Mirizzi-type syndrome).70 Other biochemical assays of hepatic enzymes are of little help. The diagnosis of AAC often rests on radiologic studies (Box 2).
Urobilinogen indicates the presence of bilirubin in the urine. This occurs only in the setting of liver damage or disease that results in an elevated bilirubin level in the blood. This may occur in children with hemolytic anemia because all the broken-down blood cells are metabolized into bilirubin. Another cause of a positive test for urobilinogen is the NSAID etodolac. When etodolac is excreted in the urine, it will react with the test strip and give a false positive test for urobilinogen.
This comparison of a normal liver to a fibrotic liver demonstrates the mechanism through which cirrhosis develops. During fibrosis, stellate cells in the liver lose vitamin A and secrete scar tissue. This scar tissue interferes with the normal exchange of nutrients into and out of the sinusoid which is essential to maintaining a healthy liver. Activation of the Kupffer cells (specialized cells in the liver that destroy bacteria and worn-out blood cells) by alcohol may be responsible for starting this chain of events, which ultimately inhibits the normal functioning of the liver.
All of the scare stories exaggerated the dangers of solvent inhalation, saying that it certainly led to brain, heart, and liver damage, destruction of the bone marrow, blindness, and death. There is medical evidence of harm from exposure to organic solvents, but most of it concerns factory workers who breathe the fumes all day long over months and years or rare individuals who drink the liquids. Young people who sniff solvents occasionally are not likely to develop serious medical problems.
Unlike disulfiram, carbimide does not have the potential side effect of liver damage. Carbimide, however, exerts antithyroid activity, which can be clinically significant in patients with preexisting hypothyroid disease. According to a 1999 Canadian monograph, other side effects of calcium carbimide include fatigue, skin rashes, ringing in the ears, mild depression, a need to urinate frequently, and impotence. The clinical significance of transient white blood cell increases remains unclear.
The adipose fat cell is not only a passive storage site but an endocrinologically active secretor of many substances like leptin, adiponectin, and cyto-kines, which participate in an inflammatory response and may mediate a host of adverse consequences, including insulin resistance and diabetes. Obesity is related to an increased risk of developing type 2 insulin-resistance diabetes mellitus, hyper-lipidemia, heart disease, obstructive sleep apnea, asthma and other respiratory problems, back pain and orthopedic problems, fatty liver (nonalcoholic steato-hepatitis or NASH), gallstones, and depression. The increasing incidence of type 2 diabetes in obese adolescents is already being noticed, with estimates of 200 000 diabetics under age 20 years in the US predicted to rise to a lifetime risk of developing diabetes of 33-39 for those born in the year 2000.
Ketones are the toxic elements in essential oils and these molecules can penetrate the blood-brain barrier causing damage to the nervous system and irreversible liver damage. The ketone most widely found in oils is thujone, a component in mugwort, sage, thuja, wormwood, and yarrow oils. Although sage oil has a high content of the ketone, it appears to have low toxicity and can be used by adults with caution. The toxic effects of ketones depend on how it is administered inhalation being the safest, followed by skin contact, vaginal, rectal, and oral ingestion.
Of liver damage and increases the rate of synthesis of ribosomal ribonucleic acids. Centapicrin is an ultrabitter (bitterness value ca. 4,000,000) secoiridoid glycoside from the century plant (Centaurea erythraea). The circuminoids are responsible for the yellow pigment and cholagogic properties of turmeric (Curcuma domestica). Hypericin, a flavonoid from St. John's wort (Hypericum per-foratum), is a monoamine oxidase inhibitor. Emetine and cephaeline are the active ingredients of syrup of ipecac, powerful emetics from ipecacuanha (Ceph-aelis ipecacuanha). The isoflavones genistein and daidzein are found in high concentrations in soybeans (Glycine max) as well as several other legumes. Both genistein and daidzein have been found to have anticancer activity.
Overfeeding usually results from overestimation of caloric needs. Overestimation occurs when actual body weight is used, such as in critically ill patients with significant fluid overload and in obese patients. Indirect calorimetry can be used to quantify energy requirements. Estimated dry weight should be obtained from preinjury records or family members. Adjusted lean body weight can also be calculated. Clinically, increased oxygen consumption, increased carbon dioxide production, fatty liver, suppression of leukocyte function, and increased infectious risks have been documented with overfeeding.
Chronic alcoholic patients are often iron deficient because of increased frequency of gastrointestinal bleeding, typically due to alcoholic gastritis or eso-phageal tears from frequent retching and vomiting, or from rupture of esophageal varices in patients with cirrhosis and portal hypertension. The major consequence of iron deficiency is anemia, which may be compounded by the concurrent effects of folate and pyridoxine deficiencies. Conversely, increased exposure to iron, e.g., from cooking in iron pots, increases the likelihood and severity of alcoholic liver disease, since the presence of iron in the liver promotes oxidative liver damage during the metabolism of alcohol.
The hepatoprotective properties of rosemary extract are attributed to its antioxidant properties and improving detoxification systems dependent on glutathione S-transferase (Sotelo-Felix et al 2002). Rosemary extract has been shown to reduce thioacetamide-induced cirrhosis (Galisteo et al 2000) and azathioprine-induced toxicity in rats (Amin & Hamza 2005), as well as partially prevent carbon tetrachloride induced liver damage in both rats (Sotelo-Felix et al 2002) and mice (Fahim et al 1999, Sotelo-Felix etal 2002).
The liver not only processes nutrients but must detoxify all the harmful substances the villi were unable to prevent from being absorbed into the bloodstream. Other situations that can tax the liver considerably include overeating and eating foods that are refined. Refined foods are missing the nutrients they need to be properly metabolized. If the liver can no longer filter and cleanse the blood, or properly metabolize nutrients, or take care of its own health, it is because liver cells are damaged or begin to die. Liver damage is not easily detected by conventional testing and its condition may not be known until dysfunction becomes apparent through illness. Symptoms may range from headache, diarrhea, constipation, food sensitivities, flatulence, sleeplessness, and aching joints to cirrhosis and hepatitis.
This illustration shows a healthy liver above, and a diseased liver below. Liver disease in alcoholics progresses from an enlargement of the liver to cirrhosis, which is characterized by liver scarring and is usually fatal unless alcohol consumption ceases. Custom Medical Stock Photo, Inc. Reproduced by permission. This illustration shows a healthy liver above, and a diseased liver below. Liver disease in alcoholics progresses from an enlargement of the liver to cirrhosis, which is characterized by liver scarring and is usually fatal unless alcohol consumption ceases. Custom Medical Stock Photo, Inc. Reproduced by permission. In conclusion, knowing the effects of alcohol on the body and the consequences of alcohol abuse and misuse is very important. When consumed in large amounts or irresponsibly, alcohol can cause extensive damage to health and well-being, including liver damage, poor nutritional status, birth defects, and death. Therefore, if alcohol is consumed, it should be done...
More than 30 percent of men and more than 40 percent of women take a daily multivitamin mineral supplement. Doses of about 100 percent of the Daily Value (DV) of most nutrients are common in these supplements. Although nutrition experts agree that the average American does not need supplements, there is little harm in taking them. Problems can arise, however, when individual nutrients are taken. Megadoses of certain minerals and relatively low supplemental doses of certain fat-soluble vitamins can lead to toxicity. For example, a surplus of vitamin A can lead to cheilitis (cracking and inflammation of the lips), dryness of the nasal mucosa and eyes, hair loss, and, eventually, liver damage. Megadoses of vitamin D can lead to the calcification of soft tissues, such as the lungs, heart, and kidneys.
As in the adult population, there are both diffuse and focal forms of fatty liver infiltration. Approximately 30-40 of cases occur focally, either as solitary areas (10 of cases) or as multiple areas with a more widespread distribution (20-30 of cases). Most cases of fatty liver infiltration are of the diffuse type with a segmental, lobar, or irregular distribution. More details on imaging of fatty liver are given in Chapter 5, Hepatic Pseudole-sions .
Hepatic disease Abnormalities in hepatic function are commonly reported in obese people. Fatty liver, due to increased concentrations of fatty acids, digly-cerides, and triglycerides in hepatocytes, is reported in obese people. The frequency of fatty liver has been reported to be as high as 94 in very obese subjects. A small number of very obese subjects will develop micronodular cirrhosis. Abnormal liver enzymes on laboratory screening are very common in obese people and do not require further evaluation unless they are markedly elevated. Weight loss results in disappearance of the excess fat and normalization of the liver function tests.
Hepatobiliary complications, including steatosis and cholestasis, are associated with PN patients due to the lack of enteral stimulation and limited gastrointestinal motility. Cholestasis is universal in patients receiving PN for more than 6 weeks without enteral feedings. Transition to enteral or oral feedings will help prevent the potential development of gallstones associated with cholestasis. In adults, hepatic steatosis, or fatty liver, is generally
Tumours, wherever they present, are classified as benign or malignant. In the pancreas most tumours are malignant and most commonly affect the exocrine portion of the pancreas. Over 90 of malignant tumours are adenocarcinomas. Pancreatic cancer most often develops in persons aged between 60 and 80. Potential risk factors for the development of a pancreatic tumour include chronic pancreatitis, smoking and a high fat diet. Of pancreatic carcinomas, over 60 occur in the head of the pancreas, 15-25 in the body and 5 in the tail (Russell 2000). Symptoms are most common in tumours of the head of pancreas and typically result in dull abdominal pain, weight loss and obstructive jaundice. Obstruction and or metastasis may also cause signs and symptom of liver damage (dark urine and light stools). ERCP is the most efficient test for detection of pancreatic cancer. The prognosis for pancreatic cancer is very poor median survival time is only 2-3 months following diagnosis (Russell 2000)....
Children with persistent or recurrent liver enzyme abnormalities should be taken off methotrexate. Failure to do so could result in long-term liver damage. However, this is rarely necessary. Occasional mild abnormalities in the white blood cell count or liver enzymes may be the result of viral infections or other unrelated problems. These situations are best dealt with by withholding the methotrexate until the problem corrects itself, then restarting the methotrexate while monitoring carefully to make sure the problem does not return. Everyone must remember that individuals using methotrexate must not drink alcoholic beverages, as the use of alcohol greatly increases the risk of liver damage. If your child drinks alcohol, make sure the doctor knows. If you can't trust the child to stop drinking, don't let him or her take methotrexate.
Continuing research on NRTIs and other treatments was and remains vital. For one thing, the toxic side effects of these drugs on healthy cells are undeniable. To a certain extent, the drug interferes with the normal cellular processes in healthy tissue as well, which leads to tissue damage. For example, even in the earliest trials, patients suffered significant reductions in their red and white blood cell counts from damage to bone marrow. In fact, so severe are side effects like nausea, anemia, diarrhea, liver damage, nerve damage, and bone marrow damage that many patients between 40 percent and 80 percent of AZT users are forced to discontinue treatment.
Chronic drinking also causes damage to a number of major organs. Permanent alterations in brain function have already been discussed. By far, one of the most important causes of death in alcoholics (other than by accidents) is liver damage. The liver is the organ that metabolizes ingested and body toxins it is essential for natural detoxification. Alcohol damage to the liver ranges from acute fatty liver to hepatitis, necrosis, and cirrhosis. Single doses of ethanol can deposit droplets of lipids, or fat, in the liver cells (called hepatocytes). With an accumulation of such lipid, the liver's ability to metabolize other body toxins is reduced. Even a weekend drinking binge can produce measurable increases in liver fat. It was found that liver fats doubled after only two days of drinking blood eth-anol levels ranged between twenty and eighty mg dl, suggesting that one need not be drunk in order to experience liver damage. Alcohol-induced hepatitis is an inflammatory condition of the...
In addition, the side effects of protease inhibitors could be just as debilitating to patients as those of NRTIs. Nausea, abdominal pain, vomiting, and diarrhea are common kidney toxicity, liver damage, pancreas problems, and headache can also be severe, sometimes even life threatening.
There are many drugs in medicinal use that can have direct liver toxicity. Peculiarly, most of the psychoactive drugs that people tend to abuse are not known to be particularly harmful to the liver. Occasional liver damage has been reported with Solvent sniffing and Cocaine use, but this is not a common problem. Narcotics (opioids), anti-anxiety, and other sedative drugs (such as BARBITURATES), Marijuana, and Hallucinogens do not usually cause liver injury. Acetaminophen itself does not have any psycho-active (mind-altering) properties thus people do not abuse it for such reasons. Many marketed acetaminophen preparations, however, are combined with Codeine (a Narcotic). People seeking narcotic highs from such preparations might ingest them in large enough quantities to subject themselves to potentially severe liver injury. It is the codeine they are after, but it is the bystander acetaminophen that may kill them. There is an antidote against acetaminophen poisoning (called...
|Fatty Liver Solution||www.thefattyliversolution.com|
|Fatty Liver Diet Guide|
Official Download Page Fatty Liver Remedy
Fatty Liver Remedy is not for free and currently there is no free download offered by the author.