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Cirrhosis and Liver Disease 

Nutritional And Supplemental Support

Because they are often metabolized in the liver, nutritional supplements (like conventional pharmaceuticals) should be used with caution by people with liver diseases. It is important that people with liver disease work in close cooperation with a knowledgeable and qualified physician to design a program of nutritional support.

Nevertheless, there have been numerous nutritional approaches studied that can help slow the inflammation associated with advancing liver disease and support healthy liver function. For more detailed information, please see the Chronic Inflammation protocol. It is also critical that alcohol be strictly avoided.

The following nutrients have been shown to enhance liver function and reduce inflammation:

Fish oil. Omega-3 fatty acids and sesame lignans have been shown to reduce inflammation, which is a distinctive feature of liver disease and cirrhosis (Barham 2000; Dias 1995; Gronn 1992; Shimizu 1991; Chavali 1999; Utsunomiya 2000).
Studies have shown that reducing the ratio of omega-6 to omega-3 fatty acids prevents liver damage induced by total parenteral (intravenous) nutrition in newborn piglets, rats, and humans (Van Aerde 1999; Yeh 1997; Chen 2003; Alwayn 2005). Thus, it may be prudent for patients with cirrhosis to take fish oil supplements and lower their consumption of omega-6 fats, such as those found in corn oil.

It is important that any increase in fatty acids be accompanied by an increase in vitamin E. Without supplemental vitamin E, even fish oil can be detrimental. Diets containing 35 percent of calories from fish oil are likely to exacerbate liver damage due to alcohol and other toxins because fish oil’s polyunsaturated bonds are so readily oxidized by free radicals (Nanji 1989,1989,1994).

Monounsaturated oils, such as olive oil, should be the major source of fat calories for those with cirrhotic liver disease. Monounsaturated oils are preferable since saturated fats from animal sources usually contain considerable amounts of arachidonic acid, the precursor to inflammatory prostaglandins. For those whose main source of fat calories is animal fat, supplementation with eicosapentaenoic acid (EPA) may help reduce the buildup of pro-inflammatory arachidonic acid and reduce levels of inflammatory mediators (Barham 2000).

In addition to using olive oil instead of corn oil or animal fats, people with liver disease would most likely benefit from supplementation with a dose of fish oil high enough to inhibit inflammatory prostaglandin synthesis without providing a significant target for reactive oxygen species (ROS). While more work is needed to determine how much fish oil is too much, the nutrition studies cited above suggest that supplementation with fish oil should be limited to about 10 percent of total calories (Nanji 2001). Also, maintaining high levels of antioxidant nutrients such as vitamin E will help limit oxidant damage from polyunsaturated fats.

S-Adenosylmethionine (SAMe). By increasing oxidative stress, many liver toxins (e.g., alcohol and acetaminophen) deplete glutathione and other important antioxidant molecules. As a result, SAMe, a glutathione precursor, is also decreased (Lieber 2002). In both rodents and nonhuman primates, depletion of antioxidants occurs at early stages of liver disease. Supplementation with SAMe restores levels of glutathione and decreases liver damage in animals; it has been recommended as an area of study for humans with early liver disease or chronic exposure to liver toxins, including alcohol (Lieber 2002; Vendemiale 1989).

In one clinical trial, 123 patients with alcoholic liver cirrhosis were given either a placebo or 1,200 mg daily of oral SAMe. At the end of the two-year trial, 30 percent of the placebo-treated patients had died, compared with 16 percent of the SAMe group. When patients with the most severe disease were excluded from the calculation, these numbers became 29 percent in the placebo group and 12 percent in the SAMe group (Mato 1999). The livers of those patients with the most advanced cirrhosis may have been too damaged to respond to the SAMe.

Polyenylphosphatidylcholine (PPC). Phosphatidylcholine is produced in the liver through a process involving SAMe. Supplementing alcohol-treated rats or baboons with PPC during alcohol feeding prevents the depletion of SAMe (Aleynik 2003).

In rats, PPC treatment accelerated regression of preexisting fibrosis (Ma 1996). In a baboon study, none of the animals fed 2.8 g PPC per 1,000 calories (about 2 g daily per 20 kg body weight) developed fibrosis or cirrhosis, even after 6.5 years of alcohol feeding, whereas 10 out of 12 untreated baboons developed fibrosis or cirrhosis (Lieber 1994). In addition to preventing alcohol-induced oxidative stress, PPC stimulates the enzyme responsible for the breakdown of liver collagen (Lieber 1994).

Among humans, two years of treatment of alcoholic cirrhosis patients with 4.5 g daily of PPC resulted in favorable changes in two blood parameters of liver damage, bilirubin and liver transaminases, among certain subgroups. Fibrosis, however, continued to progress, leading the authors to conclude that while PPC is effective in preventing liver damage among animals, it is less effective among humans with long histories of drinking (Lieber 2003).

Silymarin. A standardized plant extract from milk thistle, silymarin contains about 60 percent silibinin (Boigk 1997). Silymarin appears to inhibit the formation of mediators of inflammation, such as leukotrienes (Dehmlow 1996). In animal studies, silymarin protected the liver from carbon tetrachloride damage and slowed the accumulation of scar tissue in the biliary tract (Kravchenko 2000; Batakov 2001; Boigk 1997). In baboons, silymarin slowed the progression of alcohol-induced liver fibrosis (Lieber 2003).

Some placebo-controlled human trials have shown promising results. In one study, mortality was 39 percent among alcoholic cirrhosis patients treated with Legalon (a proprietary standardized product containing 70 to 80 percent silymarin) after 24 to 41 months. Mortality was 58 percent in placebo-treated patients (Ferenci 1989). In another clinical study, this same silymarin preparation normalized blood levels of bilirubin and other markers of liver disease after six months (Feher 1989). Favorable changes in blood chemistry were noticed in as little as four weeks (Salmi 1982).

Improvements were also observed with a silymarin-phospholipid complex in patients with chronic active hepatitis (Buzzelli 1993). Recently, an Italian firm has developed a proprietary preparation of silibinin complexed with both vitamin E and phospholipids. The complex successfully protected rat livers against necrosis and inhibited collagen formation in rats after bile duct obstruction (Di Sario 2005).

Antioxidants. Since cirrhosis is the result of chronic injury to the liver from free radicals, antioxidant therapy may slow the progression of the disease. Studies have found that people with cirrhosis have low levels of vitamin C and vitamin E (Prakash 2004).
In one remarkable study, patients with hepatitis C were given seven oral antioxidants, glycyrrhizin (500 mg twice daily), schisandra (500 mg three times daily), silymarin (250 mg three times daily), ascorbate (2 g three times daily), lipoic acid (150 mg twice daily), L-glutathione (150 mg twice daily), and alpha-tocopherol (800 IU daily) for 20 weeks. Four different intravenous antioxidant preparations, including glycyrrhizin (120 mg), ascorbic acid (10 g), L-glutathione (750 mg), and B-complex (1 mL; composition not specified), were also administered twice weekly for the first 10 weeks. No significant side effects were observed. Normalization of liver enzymes, which indicated reduced liver injury, occurred in 44 percent of patients. One-fourth of the patients showed viral load decreases of 90 percent or more. Histologic improvement was noted in 36 percent of patients (Melhem 2005).

Consistent with these findings, an Italian study demonstrated that eating foods high in antioxidants (fruits and vegetables) decreased the progression of cirrhosis, while a high level of fatty animal products and sugar from non-fruit sources increased it (Corrao 2004).
Animal products are high in arachidonic acid, a precursor to inflammatory mediators such as prostaglandins and leukotrienes, and sugars from non-fruit sources are more likely to increase insulin levels because fiber is not present to slow the absorption of sugar. High insulin levels stimulate the conversion of arachidonic acid into inflammatory prostaglandins. The resulting inflammation generates high levels of ROS. Thus, cirrhotic patients should avoid non-fruit sources of sugar or consume additional fiber when non-fruit sugars are consumed.

Selenium, a potent antioxidant, appears to protect against hepatic cancers. In a four-year trial, selenium-enhanced table salt reduced primary liver cancer 35 percent in study participants compared with controls. In a study involving hepatitis B patients, one 200 mcg tablet of selenium daily reduced the incidence of primary liver cancer to zero. When selenium supplementation ceased, primary liver cancer incidence began to rise, indicating that hepatic carcinoma risk may be minimized with selenium supplementation (Yu 1997).

N-Acetylcysteine (NAC). NAC is a slightly modified version of the sulfur-containing amino acid cysteine. When taken internally, NAC replenishes intracellular levels of the natural antioxidant glutathione (GSH), helping to restore cells’ ability to fight damage from ROS (Borges-Santos 2012).

Schisandra and melon pulp concentrate. As the body loses its natural primary antioxidant mechanisms, it accumulates lipid peroxidation products, and liver mitochondria begin to fail. Purified extract from a non-GMO Cucumis melo melon has been found to be rich in superoxide dismutase (SOD), the first enzyme in your body's mitochondrial oxidant protection system (Vouldoukis 2004; Lester 2009). Melon-derived SOD quickly converts primary free oxygen radicals into hydrogen peroxide. That hydrogen peroxide must be rapidly converted into water to complete the mitochondrial oxidant detoxification process. That task is handled by a second liver-protective agent, an extract of the Chinese vine Schisandra chinensis.

Schisandra extract has been known to protect liver function for more than 4 decades (Li 1991), but it is only recently that we have learned that it does so by boosting mitochondrial antioxidant function (Lam 2010). In that fashion, the extract confers powerful protection against a host of oxidative liver toxins (including mercury) (Lam 1010; Kim 2008; Ip 2000; Ko 1995; Ip 1996; Zhu 1999; Stacchiotti 2009).

In an open label trial of 56 patients with acute or chronic hepatitis, cirrhosis, or fatty liver (steatosis), 22.5 mg per day of schisandrins resulted in decreased serum markers of liver cell injury, even in patients with cirrhosis (Akbar 1998). A placebo-controlled study of the same extract formulation in patients with chronic hepatitis (a condition that imposes extreme oxidant stress on liver tissue) resulted in significant decreases in liver damage markers after just one week (Akbar 1998). Neither study detected any side effects of the extract.

Branched-chain amino acids. Branched-chain amino acids (BCAAs) are essential amino acids (i.e., must be obtained in the diet because the human body cannot make them). BCAAs include leucine, isoleucine, and valine. Cirrhotic patients have an increased energy requirement that BCAAs seem to fill better than glucose or amino acids (Kato 1998). Supplementing the diet with these amino acids lowers hospital admission rates and improves nutritional parameters, liver function tests, and overall quality of life in patients with liver disease (Marchesini 2003). In addition, supplementing with BCAAs after surgery for hepatic carcinoma shortens hospital stays and improves the return of liver function (Meng 1999). Encephalopathy is also alleviated after treatment with BCAAs (Marchesini 1990).