~Liver Cirrhosis, continued

~Liver Cirrhosis, continued
The Benefit of Natural Therapies
  • B Vitamins and Metabolic Functioning
  • The Synergistic Effects of Vitamins C and E
  • Essential Trace Minerals
  • Protecting and Improving Liver Function
  • Improving Cellular Metabolism
  • Amino Acids that Support Liver Health
  • Herbal Extracts
Due to the small number of conventional drug therapies presently used to treat cirrhosis, alternative therapies must be considered. Note that the vast majority of natural or alternative treatments act by having an antioxidant or anti-inflammatory effect. As with almost all disease processes, research has demonstrated that good antioxidant levels are necessary for optimum health and to protect us from the physical assaults of trauma and disease. Some of the therapies listed in this section also act by having an effect on the immune system (an immune modulating effect).

Because the liver can often continue to perform essential functions in spite of serious damage, it is important to eat foods and take proper nutrients to retain its regeneration and detoxification abilities.

B Vitamins and Metabolic Functioning
  • Vitamin B Complex
  • Folic Acid
  • Choline
Vitamin B Complex

Vitamin B complex is a group of vitamins (B1, thiamine; B2, riboflavin; B3, niacin; B5, pantothenic acid; B6, pyridoxine; folic acid; betaine; inositol; and B12, cyanocobalamin) that differ from each other in structure and the effect they have on the human body. The B vitamins (thiamine, riboflavin, niacin, pantothenic acid, pyridoxine) play a vital role in numerous metabolic functions including enzyme activities. These enzyme activities have many roles and are involved in the metabolism of carbohydrates and fats, functioning of the nervous and digestive systems, production of red blood cells, and having a synergistic effect with each other (Clayman 1989). The B vitamins are found in large quantities in the human liver. Dietary sources of vitamin B are wheat germ, bran, whole grain cereals and bread, brown rice, pasta, fish, lean meats, beans, nuts, bananas, green leafy vegetables, and eggs (Clayman 1989). Heat and overcooking destroys the B vitamins (Glanze 1996).

Folic Acid

Folic acid (vitamin B4) is an important member of the B complex family, known for reducing harmful levels of homocysteine (a sulfur-containing amino acid) known to be a major culprit in heart disease. At normal levels, homocysteine plays a vital role in the biosynthesis of cysteine, which assists glutathione in the liver to detoxify carcinogens and other toxins, but without adequate methylation, which is provided by folic acid and other B vitamins, biochemical reactions generated from beneficial byproducts of homocysteine cannot occur.

Decreases in folate (folic acid) are also associated with increased levels of lipoperoxidases, that is, an indicator of increased oxidative stress. Therefore, folic acid is potentially beneficial in the early stages of cirrhosis or for the ongoing oxidative damage seen in the cirrhotic process. In humans with viral hepatitis, treatment with folic acid improved liver chemistry measurements in the recovery period following the illness. This improvement was thought to be due to an effect on nucleotide (genetic building block) synthesis (Zviarynski et al. 1999). In an experiment using rats, the occurrence of decreased folate and elevated homocysteine documented the strong association of decreased folate with increased oxidative stress and liver peroxidation (Huang et al. 2001).

Dietary sources of folic acid are green, leafy vegetables such as broccoli and spinach; mushrooms; liver; nuts; dried beans and peas; egg yolk; and whole-wheat breads and cereals (Clayman 1989; Glanze 1996). A varied diet that includes fruits and vegetables will usually provide sufficient folic acid, but mild to moderate deficiencies are not uncommon. More severe deficiencies result from certain blood disorders, malabsorption disorders, alcohol dependence, and certain drugs (oral contraceptives, anticonvulsants, antimalarials, analgesics, corticosteroids, and sulfonamides) (Clayman 1989).


Choline is another of the B complex vitamins, essential for the use of fats in the body. It is a precursor to acetylcholine, a nerve signal carrier in the brain. Choline also stops fats from being deposited in the liver and help move fats into the cells. Deficiency of choline can lead to cirrhosis with associated conditions such as bleeding; kidney damage hypertension (high blood pressure); cholesterolemia (high blood levels of cholesterol); and atherosclerosis (occulsive deposits in blood vessels) (Glanze 1996). Sources of dietary choline are liver, wheat germ, legumes, brewer's yeast, and egg yolk.

The Synergistic Effects of Vitamins C and E

Vitamins C and E

Vitamins C and E used in combination have been demonstrated to improve liver function in chronic liver disease patients. Both vitamins C and E act as antioxidants. Vitamin C is a potent antioxidant that is found naturally in many fruits and vegetables. Researchers have found inadequate levels of vitamin C in patients with degenerative diseases. According to Garg et al. (2000), vitamin C has protective effects against liver oxidative damage, particularly when used in combination with vitamin E. Garg et al. (2000) found that supplementation in rats lowered plasma and liver lipid peroxidation, normalized plasma vitamin C levels, and raised vitamin E above normal levels, suggesting that the improved levels of lipid peroxidation products in the plasma and liver with vitamin C and E supplementation and the activities of antioxidant enzymes in the liver indicated that vitamins C and E reduced lipid peroxidation by quenching free radicals.

Sources of dietary vitamin C are fresh fruits and vegetables. Particularly good sources are citrus fruits, tomatoes, green leafy vegetables, potatoes, green peppers, strawberries, and cantaloupe. Vitamin E is found in vegetable oils, nuts, meats, green leafy vegetables, whole grain cereals, wheat germ, and egg yolk (Clayman 1989).

Essential Trace Minerals
  • Selenium
  • Zinc
  • CoQ10

Selenium is a trace element that acts by several mechanisms, including detoxifying liver enzymes, exerting anti-inflammatory effects, and providing antioxidant defense. Selenium is found in minute amounts in foods (Glanze 1996), with the richest sources being from meats, fish, whole grains, and dairy products. The selenium content of vegetables is dependent on the soil in which they are grown (Clayman 1989). Using selenium-deficient rats, experiments have shown that selenium deficiency causes oxidative stress (Ueda et al. 2000). The presence of selenium helps induce and maintain the glutathione antioxidant system.

Epidemiological studies in China have also shown that selenium provides protection against both hepatitis B and C and liver cancer. In a 4-year trial on 130,471 Chinese individuals, those who were given selenium-spiked table salt showed a 35.1% reduction in primary liver cancer, compared with the group given salt without selenium added. A clinical study of 226 hepatitis B-positive people showed that one 200-mcg tablet daily of selenium reduced the incidence of primary liver cancer to zero. Upon cessation of selenium supplementation, primary liver cancer incidences began to rise, indicating that viral hepatitis patients should take selenium on a continuous basis (Yu et al. 1997).


Zinc is used in numerous drugs and preparations that are protective: zinc oxide in skin ointments; zinc stearate in acne and eczema preparations; and zinc permanganate to treat bladder inflammation. Zinc deficiency features weakness, decreased taste and appetite, lengthy wound healing, and risk of infection. Zinc levels that are low have also been related to the progression of cirrhosis to hepatic encephalopathy (Romero-Gomez et al. 2001). An earlier study in rats (Okegbile et al. 1998) demonstrated that the amount of dietary zinc dramatically affected the ability of the rats' livers to synthesize cellular components (nucleic acid building blocks) and maintain normal alkaline phosphatase (indicated by a blood test of liver function, which is related to cholestasis or accumulation of bile acids). Cholestasis has been shown to play a role in facilitating the development of cirrhosis.) Dietary sources of zinc are meats, eggs, liver, seafood, vegetables with pods, nuts, peanut butter, and whole-grain cereals (Glanze 1996). Zinc supplementation can vary from 25-90 mg daily.

Multifaceted Effects of CoQ10

Coenzyme Q10 (CoQ10) is an excellent antioxidant that is protective for a liver that has been damaged by ischemia (reduced blood flow). CoQ10 is also an important component of healthy metabolism. It protects the mitochondria and cell membrane from oxidative damage and helps generate ATP, the energy source for cells. CoQ10 is absorbed by the lymphatic system and distributed throughout the body. Japanese researchers studied the effects of the toxic drug hydrazine on liver cells. They administered hydrazine to rats to study the effect of free radicals on liver cells (hepatocytes). One group of rats was given hydrazine only; a second group of rats was given CoQ10 in addition to the hydrazine. Hepatocyte cell mitochondria from the hydrazine-only group were found to be extremely enlarged, a state often preceding cell death from oxidative stress. The mitochondria of rats given CoQ10 along with hydrazine were nearly normal, showing only slight enlargement.

Note: Cachexia is a condition of general poor health and dietary state associated with wasting diseases. Hydrazine sulfate is an anticachexia drug. Hydrazine sulfate is also used to reverse the metabolic processes of debilitation and weight loss in some cancer patients (NCI 2001). Other researchers have reported that hydrazine sulfate also acts to stabilize or cause some types of tumors to regress in some patients, but this benefit has been contested (Green 1997). Therefore, drugs containing hydrazine may be required in a treatment plan even when the liver is weakened or at risk.

In other studies in rats, liver ischemia (poor blood supply) was induced surgically to investigate the effects of CoQ10 on oxidative stress (Yamamura et al. 1980; Genova et al. 1999). In the study by Genova et al. (1999), lipid peroxidation occurred as a result of ischemia. However, when the rats were pretreated with CoQ10 for 14 days, the liver peroxidation parameters were normalized. The CoQ10-treated rats were also more resistant than nontreated rats to oxidative stress by free radicals. According to Genova et al. (1999), their preliminary study suggests that pretreatment with CoQ10 can have a beneficial effect against oxidative damage during surgical liver transplantation. Ito et al. (1999) induced hepatic ischemia by clamping the liver artery, portal vein, and bile duct. After 15 minutes, the levels of glutathione rapidly decreased. When reperfusion was started, the glutathione levels promptly increased for about an hour before they began to decline. When Ito et al. administered CoQ10 to the rats prior to ischemia, the reduction of glutathione levels induced by ischemia/reperfusion was protected.

Our bodies can produce some of the CoQ10 that we need. The rest is synthesized from our diet. The best dietary sources of CoQ10 are fresh sardines and mackerel; heart and liver of beef, pork, and lamb; meat from beef and pork; and eggs. Vegetable sources of CoQ10 are spinach, broccoli, peanuts, wheat germ, and whole grains. Meat sources of CoQ10 are higher than vegetable and grain sources. It is important to remember that foods must be fresh and unprocessed (no milling, canning, freezing, preserving, etc.) and grown in unpolluted areas to be considered as viable sources (Bliznakov 1987).

Protecting and Improving Liver Function
  • N-Acetyl-Cysteine
  • S-Adenosyl Methionine
  • Polyenylphosphatidylcholine
  • Alpha-Lipoic Acid
N-Acetyl-Cysteine (NAC)

N-acetyl-cysteine (NAC) is a substance that acts as an antioxidant or free-radical scavenger. Most scientific articles related to liver protection with NAC emphasize this effect. NAC is frequently used in medical settings to treat liver toxicity associated with ingesting Tylenol (also poisonous mushrooms). In this situation, NAC is given orally or intravenously. In liver transplantation, NAC reduces liver injury associated with reperfusion (resumption of blood flow after transplant) (Taut et al. 2001; Weinbroum et al. 2001). NAC also has been found to improve liver blood flow and liver function in patients who have extremely critical infections such as septic shock (Rank et al 2000).

In ingestion of methanol (a very toxic form of alcohol different from the ethanol in alcoholic drinks), NAC partially prevented liver damage from methanol (Dobrzynska et al. 2000). Another study also showed that NAC slowed liver damage caused by methanol (Dobrzynska et al. 2000). In another experiment that used cocaine as a pro-oxidant, NAC was found to exert a protective effect by acting as a precursor for glutathione, a vitally important antioxidant and free-radical scavenger (Zaragoza et al. 2000). The best dietary sources of NAC are meat, fish, poultry, eggs, and dairy products (Young et al. 1994).

S-Adenosyl Methionine (SAMe)

SAMe is a methylation agent (a methyl group donor) and is necessary for the synthesis of glutathione, necessary for liver health. Medical studies have shown that SAMe has beneficial antioxidant effects on the liver and other tissues, particularly in protecting and restoring liver cell function destroyed by the hepatitis C virus. When mice were given paracetamol (a hepatotoxic substance), SAMe was found to be as effective as N-acetyl-cysteine (NAC) in preventing liver damage. Additionally, SAMe has a positive effect on the fluidity of the cell membrane, as demonstrated in red blood cells from patients with cirrhosis (Turchetti et al. 2000). However, in a major review that was limited to alcoholic liver disease and cirrhosis (Rambaldi et al. 2001), researchers concluded that there were no significant effects of SAMe on mortality, liver-related mortality, liver transplantation, or liver complications in patients with alcoholic liver disease. This review concluded that SAMe should not be used routinely in alcoholic liver disease.

In critical care medicine, it is occasionally necessary to provide total nutrition via special IV solutions to patients who are unable to eat for a prolonged period of time (i.e., several months). This process is called total parenteral nutrition (TPN). Various complications are associated with the parenteral method of providing calories and nutrients, including liver cholestasis (interruption or blockage of the bile ducts). When studying extremely ill pediatric surgical patients, Amii et al. (1999) stated, "SAMe is the most promising treatment of total parenteral nutrition-associated cholestasis." In another study on hepatic cholestasis and oxidative stress in rats, Lopez et al. (2000) concluded, "the results confirmed the function of SAMe as an antioxidant and hepatoprotector."

SAMe is found naturally in every cell of the body. It is synthesized from a combination of the amino acid L-methionine, folic acid, vitamin B12, and trimethylglycine, provided all these ingredients are present and performing (Anon. 2002).

Polyenylphosphatidylcholine (PC)

PC is one of the most important substances for liver protection and health and is a primary constituent of the cell membrane. As such, PC is necessary for integrity of liver cells. In studies in rats, PC has prolonged the survival of rat liver cells in culture by stabilizing the cell membrane (Miyazak et al. 1991). Liver cells that have been damaged by alcohol or cirrhosis are unable to meet the ongoing demands of the liver for phospholipid synthesis. Adding phospholipids such as PC via oral intake played an important role in regeneration of damaged liver cells (Horejsova et al. 1994). In an early study, Neuberger (1983) stated: "It has been shown that orally administered polyunsaturated PC can be incorporated into the liver cell membrane."

Other studies have shown the antifibrotic effect of PC. Not only does PC inhibit the development of hepatic fibrosis, it actually accelerates the regression of existing fibrosis (Ma et al. 1996). Part of this effect is probably due to PC promoting the breakdown of collagen (Lieber 1999), but it may also be due to an inhibitory effect on the stellate cell (Poniachik et al. 1999). In experimental studies, PC was also found to protect against alcoholic cirrhosis in baboons and against carbon tetrachloride-induced cirrhosis in rats (Aleynik et al. 1997). In another study (Navder et al. 1997), PC was shown to prevent earlier changes induced in the alcoholic liver before cirrhosis even develops.

When liver cells are damaged, apoptosis (programmed cell death) is activated. If apoptosis can be decreased, more liver cells (hepatocytes) can be preserved and actually still function. PC decreases apoptosis, but alcohol consumption increases the rate of apoptosis in liver cells (Mi et al. 2000). The positive effect of PC on hepatocyte apoptosis is probably via an antioxidant mechanism. As a result, the antioxidative hepatoprotective mechanism of PC is one of the most studied mechanisms. Numerous medical articles have noted the antioxidant properties of PC and other related phospholipid compounds and how toxic metabolites associated with liver injury are decreased when they are used (Navder et al. 1999).

The best dietary sources of phosphatidylcholine are beef steak, liver, organ meats, egg yolks, spinach, soybeans, cauliflower, germ, peanuts, and brewer's yeast. Smaller amounts are found in oranges, apples, potatoes, lettuce, and whole-wheat bread (Canty et al. 1994).

Alpha-Lipoic Acid (ALA)

Alpha-lipoic acid is an antioxidant that has been shown to decrease the amount of hepatic fibrosis associated with liver injury. Both of these mechanisms suggest it has promise for cirrhosis. Alpha-lipoic acid is considered to be the universal antioxidant by Dr. Lester Packer, who has studied the effects of ALA extensively (Constantinescu et al. 1994; Packer 1994, 1997; Podda et al. 1994). Because alpha-lipoic acid is fat-soluble, it can penetrate the cell membrane to exert therapeutic action. It has been shown to effectively scavenge harmful free radicals, chelate toxic heavy metals, and help to prevent mutated gene expression (Biewenga et al. 1997). Another of its most beneficial functions is to enhance the effects of other essential antioxidants including glutathione, which is vital to the health of the liver (Lykkesfeld et al. 1998; Khanna et al. 1999).

The effects of ALA have been studied in rats and mice. In studies in rats, when the rat liver was insulted with a chemical agent, dietary alpha-lipoic acid encouraged healing (Arend et al. 2000). Alpha-lipoic acid also demonstrated promise in the treatment of sepsis (a life-threatening systemic infection) (Liang et al. 2000) in septic mice. In septic mice, alpha-lipoic acid improved carbohydrate metabolism in liver cells by its effect on nitric oxide pathways.

The body can make some of its own lipoic acid, but most must be obtained from dietary sources, either from food or supplements. Dietary sources of alpha-lipoic acid include yeast, liver, and spinach, potatoes, and carrots. Unfortunately, the best sources of dietary alpha-lipoic acid are red meats, which also contain high levels of saturated fats, and it would require huge amounts of spinach to consume the amount of alpha-lipoic acid conveniently obtained from the supplementation of 1 capsule.

Improving Cellular Metabolism


Acetyl-L-carnitine has been shown to convert some hepatic parameters to more youthful levels. Acetyl-L-carnitine is the biologically active form of the amino acid L-carnitine that has been shown to protect cells throughout the body from age-related degeneration. By facilitating the youthful transport of fatty acids into the cell mitochondria, acetyl-L-carnitine facilitates conversion of dietary fats to energy and muscle. Acetyl-L-carnitine has also been shown to regenerate nerves (Fernandez et al. 1997); provide protection against glutamate and ammonia-induced toxicity to the brain (Rao et al. 1999); and to reverse the effects of heart aging in animals (Paradies et al. 1999).

In an aging mouse model, two studies (Hagen et al. 1998a, b) illustrated the ability of acetyl-L-carnitine to increase cellular respiration. The first study at the University of California (Berkeley) examined liver parenchymal cells in old mice after feeding them a 1.5% solution of acetyl-L-carnitine for 1 month (Hagen et al. 1998a). The results showed that acetyl-L-carnitine supplementation significantly reversed the age-associated decline of mitochondrial membrane function. In the second study, also at Berkeley, researchers again confirmed the ability of acetyl-L-carnitine to reverse age-related mitochondrial decay (Hagan et al. 1998b). In another study, also conducted with old rats, acetyl-L-carnitine improved liver metabolism and slowed age-related decline in metabolism and biosynthetic function (Mollica et al. 2001).

Primary dietary sources of L-carnitine are meats (especially beef and lamb) and dairy products. The liver and kidneys can also synthesize L-carnitine from the amino acids lysine and methionine (Plawecki 2001).

Amino Acids that Support Liver Health
  • Taurine
  • L-Arginine
  • L-Glutamine
  • Branched-Chain Amino Acids

Taurine is a conditionally essential amino acid produced from cysteine by the body. It is abundantly found in the body, particularly the central nervous system where it is thought to have a regulating influence. Taurine is a crystallized acid that comes from bile, which is produced by the liver. Sources of dietary taurine are cow's milk, meats, seafood, and poultry. Plants have virtually no taurine. Taurine can be deficient in our daily diet and can also be insufficiently produced by the body in certain disease states. Taurine exerts a protective effect against liver cirrhosis, working by a mechanism that decreases oxidative stress (Balkan et al. 2001).


L-arginine is an essential amino acid. L-arginine is also a key building block for repair of damaged tissue. Numerous studies have documented enhanced wound healing in response to L-arginine supplements. Dietary sources of L-arginine are high-protein foods (meats, eggs, nuts and nut products), seeds, brown rice, whole-wheat grains, oatmeal, raisins, and legumes. Persons with diabetes (or borderline diabetics), persons who do not have complete bone growth (children and teenagers), pregnant women, persons who have a latent herpes virus, or persons with psychoses should consult their physician before taking L-arginine. Antioxidants should always be taken with L-arginine.


L-glutamine is a nonessential amino acid that has benefits for the liver and intestines, particularly for those who use NSAIDs (nonsteroidal anti-inflammatory drugs). L-glutamine may also be useful in neutralizing the effects of alcohol and strengthening the immune system. Sources of dietary L-glutamine are plant (e.g., nuts and nut products, seeds, and brown rice) and animal protein (e.g., meats and eggs).

Branched-Chain Amino Acids

BCAAs are leucine, isoleucine, and valine. They are considered to be essential amino acids because humans cannot survive unless these amino acids are present in the diet. BCAAs are needed for the maintenance of muscle tissue and appear to preserve muscle stores of glycogen (stored form of carbohydrates that can be converted into energy). Dietary sources of BCAAs are dairy products and red meat. Whey protein and egg protein supplements are other sources. Most diets provide the daily requirement of BCAAs for healthy people. However, in cases of physical stress, we have increased energy requirements, in particular in persons with cirrhosis.

Studies on alcoholic cirrhosis patients have shown benefits from supplementing valine, leucine, and isoleucine. These branched-chain amino acids can enhance protein synthesis in liver and muscle cells, help restore liver function, and prevent chronic encephalopathy (Shimazu 1990; Chalasani et al. 1996). In studies, BCAAs have also been shown to have therapeutic value in adults with cirrhosis of the liver. According to the researchers, BCAAs seem to be the preferred substrate to meet this requirement (Kato et al. 1998).

Herbal Extracts
  • Silymarin
  • Green Tea
  • Artichoke

Silymarin (also known as milk thistle or Silybum marinum) is a member of the aster family (Asteraceae) that has been used as a medicinal plant since ancient times and is widely used in traditional European medicine. The active extract of milk thistle is silymarin (Bosisio et al. 1992), a mixture of flavolignans, including silydianin, silychristine, and silibinin, with silibinin being the most biologically active. Although the mechanisms are not yet fully understood, silymarin has proven to be one of the most potent liver-protecting substances known. Its main routes of protection appear to be the prevention of free-radical damage, stabilization of plasma membranes, and stimulation of new liver cell production.

According to several early studies, silymarin acts as an antioxidant and free-radical scavenger that is many times more potent than vitamin E (Hikino et al. 1984) and has also been shown to inhibit lipid peroxidation and to prevent glutathione depletion induced by alcohol and other liver toxins, even increasing total glutathione levels in the liver by 35% over controls (Valenzuela et al. 1989). However, perhaps the most interesting effect from the early studies of silymarin was its ability to stimulate protein synthesis, resulting in production of new liver cells to replace older, damaged ones (Sonnenbichler et al. 1986).

Studies also demonstrate the benefits of silymarin for protection from numerous toxic chemicals such as carbon tetrachloride, ethanol, poisonous mushrooms (Desplaces et al. 1975); alcohol and chronic alcoholic hepatitis (Salmi et al. 1982); cirrhosis (Ferenci et al. 1989); acute and chronic hepatitis (Berenguer et al. 1977); and hypercholesterolemia (high cholesterol) (Krecman et al. 1998).

Most medical studies cover the use of silymarin in the early forms of liver degeneration, which occur prior to the development of cirrhosis. However, ongoing research indicates that the development of cirrhosis is a continuum, beginning with damaged liver cells and progressing on to an intermediate stage such as fatty liver before actual development of cirrhosis. Therefore, the potential for obtaining protective benefits from silymarin is worth consideration.

Green Tea

Green tea has been in widespread, common use in China for thousands of years. In the last several decades, green tea has also been widely used in the treatment of hepatic disease in Europe. Green tea has active ingredients called catechin polyphenols. Catechins in green tea have potential therapeutic significance because of their potent antioxidants, which have an ability to neutralize free radicals and act as free-radical scavengers. Green tea has been shown to have antiviral activity and immune-stimulating properties (Kaul et al. 1985); protective benefits from hepatotoxicity caused by carbon tetrachloride, ethanol, and 2-nitropropane (a common industrial solvent also found in tobacco smoke) (Lewis et al. 1979); promise for treatment of many types of hepatic disease, particularly acute and chronic viral hepatitis; and fibrosis (overgrowth of collagen) (Pontz et al.1982).

Additionally, green tea has hepatoprotective qualities that include killing dangerous intestinal bacterial strains (Clostridium and Escherichia coli) and promoting the growth of friendly bacteria in the intestine; inhibiting several viruses, including viral hepatitis; and lowering excessive iron levels in the liver that would interfere with ribavirin and interferon treatment for hepatitis C.

For most people, drinking green tea daily seems to be a most practical, readily available means for providing protective liver benefits and preventing chronic toxicity induced by oxidative stress from environmental chemicals. The dose used for hepatic diseases in clinical studies has typically been 1 gram of green tea three times daily.


Artichoke (Cynara scolymus) is an herb with antioxidant properties that are similar to silymarin. Artichoke is used in Eastern parts of the world for its hepatoprotective qualities. Like silymarin, it is a member of the aster family (Asteraceae). It is native to the Mediterranean, where it has been in common use for more than 2000 years. Also similar to silymarin, artichoke extract has demonstrated strong antioxidant potential and a hepatoprotective effect, protecting the liver from the damaging effects of toxins, such as carbon tetrachloride and other environmental chemicals (Adzet et al. 1987; Gebhardt 1995). Artichoke extract is also able to stimulate regeneration of damaged liver tissue (Maros et al. 1966). The usefulness of artichoke to prevent or reduce buildup of fat in the liver from chronic alcohol consumption is noteworthy (Samochowiec et al. 1971; Wojciki 1978).

Experimental studies of hepatoprotective mechanisms have only been conducted in animals because the procedure involves exposure to toxins. The basic research method in this type of investigation is to administer the test substance, in this case artichoke leaf extract, to the animal prior to or simultaneously with, administration of a toxic substance and observe the results. Gebhardt (1995) demonstrated hepatoprotective effects against carbon tetrachloride-induced toxicity on liver cells from rats. When studying rat liver cells exposed to t-BHP (tertiary butylhydroperoxide), they found that artichoke leaf extract significantly prevented damage.

Living with Cirrhosis

There is no cure for cirrhosis at this time. However, physicians attempt to delay its progress, minimize liver cell damage, and reduce the complications of the disease through the use of drugs and dietary and lifestyle recommendations.

Once cirrhosis has been diagnosed, sodium and fluids should be restricted and all alcohol consumption must cease. Antiemetics, diuretics, and supplemental vitamins are often prescribed. Because of the potential of bleeding, persons with cirrhosis should avoid straining at the bowel and use stool softeners as directed by a qualified medical caregiver. Violent sneezing, coughing, and nose blowing should also be avoided. Untreated cirrhosis can be fatal. Patients should avoid exposure to infections. They should eat small but frequent meals of nutritious foods. They should also carefully follow caregiver instructions from a medical professional.

More than half of all liver disease could be prevented if only we simply acted on knowledge we already have! Avoiding or limiting the use of alcoholic beverages is an excellent place to start because it is well documented that alcohol destroys liver cells. Man-made chemicals also pose an extreme threat to the liver. Always follow recommended standard safety precautions for handling man-made chemicals. All ingested, inhaled, and absorbed chemicals and toxins must be processed by the liver.

If you have cirrhosis, stay one step ahead of the disease by watching for the appearance of additional symptoms of cir

The statements made here have not been evaluated by the FDA. The foregoing statements are based upon sound and reliable studies, and are meant for informational purposes. Consult with your medical practitioner to determine the underlying cause of your symptoms. Please always check your purchase for possible allergins and correct dosage on the bottle before use.

While we work to ensure that product information is correct, on occasion manufacturers may alter their ingredient lists. Actual product packaging and materials may contain more and/or different information than that shown on our Web site. We recommend that you do not solely rely on the information presented and that you always read labels, warnings, and directions before using or consuming a product. For additional information about a product, please contact the manufacturer. Content on this site is for reference purposes and is not intended to substitute for advice given by a physician, pharmacist, or other licensed health-care professional. You should not use this information as self-diagnosis or for treating a health problem or disease. Contact your health-care provider immediately if you suspect that you have a medical problem. Information and statements regarding dietary supplements have not been evaluated by the Food and Drug Administration and are not intended to diagnose, treat, cure, or prevent any disease or health condition. Life Extension Institute assumes no liability for inaccuracies or misstatements about products.