The Hope Institute - http://www.smile.org.au/OtherMedicalTherapies/HepatitisC.htm#boost

In an extensive literature review, studies were found that show a drug may have indications of efficacy for HCV because it normalizes transaminases. Other studies point out that normalization of transaminases (liver function tests on blood work) has no relationship to outcome or progression of disease in hepatitis C. Yet other studies, sometimes criticizing nontraditional therapies, mention that normalizing transaminases does not prove drug effectiveness. The normalization of transaminases probably does have a beneficial effect, although the exact nature of this beneficial effect has not yet been exactly characterized. Certainly, if a drug decreases viral RNA copy count, it is beneficial.

Some of the nondrug therapies mentioned will only improve transaminase values. A study by Schalm et al. 1999 stated: "For the many patients who still do not respond with viral clearance despite new approaches (with drugs), the goal of therapy might be shifted towards persistent ALT (alanine-aminotransferase) normalization in order to reduce the progression of liver disease. Drugs that can normalize serum ALT such as interferon, ursodeoxycholic acid, ribavirin, and glycyrrhizin should be evaluated for this objective."

Like numerous other disease processes, hepatitis C is mediated by oxidative stress. Both the acute (new) and chronic (ongoing) events of tissue injury due to disease are encouraged by increased oxidative stress (Sumida et al. 2001). Increased levels of chemicals that indicate higher oxidative stress are found in hepatitis C. Thus, a good antioxidant regimen is warranted. A substance that quenches free radicals is potentially helpful in optimizing response to treatment.

Ursodeoxycholic Acid
Ursodeoxycholic acid is a naturally occurring bile acid found in small quantities in the liver. A synthetic form known as ursodiol helps to dissolve gallstones in those who cannot have gallbladder surgery or who do not need surgery. Ursodiol has low liver toxicity. When taken as a medication, it replaces some of the more toxic liver bile salts. In research related to hepatitis C, ursodiol in combination with licorice extract has helped normalize transaminase levels in HCV patients who are resistant to interferon (Tsubota et al. 1999).

In an earlier study, researchers tested 91 patients (47 males and 44 females) with chronic HCV liver disease. Patients were not positive for HIV or hepatitis B and had not taken interferon. They were randomly assigned to receive ursodiol (450 mg) at bedtime for 6 months (44 patients) or no treatment (47 patients). No relevant side effects were reported. They found that ursodiol was able to significantly reduce serum ALT and gamma-glutamyltransferase (GGT) levels that were at least twice the upper limit of normal on three different occasions over the previous 12 months (reductions of 36.7% for ALT and 47.6% for GGT) as compared to the control group. These results led researchers to hypothesize that ursodiol might be a possible alternative for patients who do not respond to interferon or who relapse once it is discontinued (Puoti et al. 1993).

Polyenylphosphatidylcholine (PPC)
The addition of PPC in regard to rehabilitating an infirmed liver is indicated in the overall treatment of hepatitis C (Lieber 2001). PPC is a naturally occurring phospholipid that is found throughout the body, particularly in cell membranes. It has been demonstrated that orally administered PPC can be incorporated into the liver cell membrane to enhance its integrity. PPC assists the cell membrane in determining what is safe to enter the cell as nutrients and what should be hampered from entry, as toxins. Hepatocytes (liver cells) are prime examples of cells needing the protection of a vigilant cell membrane (Oneta et al. 1999).

Membrane lipids such as PPC appear to prolong the survival of adult rat hepatocytes by controlling morphologic degeneration, such as a change in shape or size of the cell, enlargement of the cell surface, degranulation of cytoplasm, and multinucleation. These positive effects appear to be related to the sta-bilization of the plasma membrane (Ipatova et al. 1998).

In addition to the benefits observed in improved plasma membrane efficiency, histological evidence of disease activity was also significantly reduced in chronic active hepatitis patients maintained on phospholipid therapy (Holoman et al. 1998) . Liver cell regeneration was also greater in those receiving PPC because worn-out liver cells were replaced with youthful cells. The introduction of orally administered PPC, a constituent of lecithin, may have, because of its multifaceted nature, the potential of arresting and reversing liver damage (Abakumova et al. 1996).

PPC has a history of not only protecting the liver, but also enhancing the bio-availability of various herbs and nutrients. The increased power of silibinin, vitamin E, and interferon complexed with PPC corroborates this finding (Werner et al. 1990; Reizis et al. 1992).

When PPC is administered in conjunction with interferon, there is an increase in both their therapeutic values. In one study, individuals with abnormal serum ALT values, more than twice the upper normal, received 3 million IU of interferon subcutaneously, administered 3 times a week for 24 weeks. Various participants in the study were randomly selected to receive 1800 mg of PPC in addition to the interferon. To be classified as a responder, more than a 50% reduction in ALT was required, compared to pretreatment values. All responders were treated for an additional 24 weeks with either PPC or a placebo. Evaluation of the numbers at completion of the study, involving 92 in the PPC group and 84 in the placebo group, revealed a greater than 50% ALT reduction in 71% of patients who were treated with PPC, compared to 56% in those patients receiving the placebo. Although both hepatitis B and hepatitis C patients were included in this clinical trial, only those individuals with hepatitis C and receiving PPC observed the increased response rate ( Leich Study Group 1998).

In another study, a silymarin (milk thistle) and phosphatidylcholine complex, referred to as IdB1016, was dispensed among individuals with chronic active hepatitis with the following laboratory changes. After 7 days, 20 patients (mean age 52.5) observed a decrease in aspartate aminotransferase (AST) from 88.0 to 65.9. ALT dropped from 115.9 to 82.5, GGT from 51.4 to 41.3, total bilirubin from 0.76 to 0.53 and alkaline phosphatase from 143.4 to 137.5. The results relating to malonaldehyde (MDA), a marker reflecting lipid peroxidation, were inconsistent. Some reports showed no significant changes, while other researchers noted a 36% reduction in MDA while on IdB1016 (Buzzelli et al. 1993).

Because the liver vigorously defends against blatant signs of liver degeneration, a liver panel may not always reveal a liver under stress. Every measure should be employed to assist the liver in its attempts to hold the line. The watchful selection of foods, beverages, supplements, and environment can contribute to the liver's commitment to last a lifetime. Considering the fact the PPC is well tolerated and without major risk factors, it appears a prudent gesture for both the chronic active hepatitis patient, as well as those without overt liver symptoms to consider the benefits of 1800 mg a day of PPC supplementation.

Selenium
In areas of China with high rates of hepatitis B and primary liver cancer, epidemiological surveys demonstrated that high levels of dietary selenium reduce liver cancer incidence and hepatitis B infection. Animal studies showed that selenium supplementation reduced hepatitis B infection by 77.2% and precancerous liver lesions by 75.8% (Yu et al. 1997).

In an 8-year follow-up trial in 130,471 Chinese, those who were given a selenium-spiked table salt showed a 35.1% reduction in primary liver cancer, compared with the group given salt without the added selenium. A clinical study of 226 hepatitis B-positive people showed that one 200-mcg tablet a day of selenium reduced primary liver cancer incidences down 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. Selenium has demonstrated antiviral properties, and it appears to be effective in suppressing HCV (Yu et al. 1997).

Boosting Liver Glutathione Levels
Glutathione is the most important antioxidant used and manufactured by the liver. It kills bacterial invaders, acts as a cellular detoxifier, and helps prevent free-radical damage. In patients with hepatitis C, particularly those who are HIV-positive, a systemic depletion of glutathione is present, especially in the liver. This depletion may be a factor underlying the resistance to interferon therapy. This finding represents a biological basis for supplementing with the following nutrients that raise glutathione levels (Moriya et al. 2001).

Although the supplements listed above will help raise vital glutathione levels, people with compromised liver functioning such as those with hepatitis C may wish to take supplemental glutathione as well.

Liver Protecting Nutrients
Silymarin and its chief active ingredient silibinin are derived from milk thistle, a member of the daisy family. Both substances help prevent toxic liver damage and help the liver regenerate faster if damage is done. Silymarin and silibinin actually accelerate the rate of protein synthesis in the liver, leading to faster cell regeneration (Sonnenbichler et al. 1984, 1986a, 1986b, Valenzuela et al. 1994). Silymarin and silibinin act in the ribosomes, special cellular organelles where protein synthesis takes place. It was discovered that silibinin can bind the receptor for an important enzyme called DNA-dependent RNA polymerase I. This brings an increase in ribosomal RNA, which then leads to more protein synthesis (Sonnenbichler et al. 1984, 1986a, 1986b).

Some clinicians have found that a combination of silymarin and silibinin, PPC, SAMe, selenium, and several glutathione-boosting supplements not only improves outcomes of patients who are treated, but also decreases the patient dropout rate due to fewer side effects from conventional antiviral therapy (interferon and ribavirin).

Long-term use of licorice root extract (glycyrrhizin) has been shown to be helpful in preventing inflammation, liver cirrhosis, and hepatocellular carcinoma in Japanese hepatitis C patients (Guyton et al. 2002; Kumada 2002b). However, licorice flavoring is not effective. A possible side effect associated with ingestion of large amounts of licorice is hypertension. Therefore, blood pressure should be monitored regularly if taking licorice root.

Reducing Iron Stores
Elevated serum iron levels are often found in people with HCV, causing further oxidative damage to the liver. Certain nutritional supplements have shown evidence of reducing serum iron levels.

To help keep serum ferritin levels in the low normal range of between 30-80 nanograms/dL, high doses of green tea polyphenols and high-allicin garlic may be beneficial.

Lactoferrin, a subfraction of whey protein, may be especially beneficial as an adjunctive treatment for serum iron overload in hepatitis patients. Lactoferrin is a potent antioxidant, antiviral agent, and scavenger of free iron. In addition, lactoferrin is directly involved in the upregulation of natural killer (NK) cell activity, making it a natural modulator of immune function (Yi et al. 1997; Ikeda et al. 1998, 2000).

Taking 300 mg of elemental calcium can reduce iron absorption by as much as 50%. When eating iron-rich foods, consider taking a high-potency calcium supplement at the same time (Hallberg et al. 1991).

Preventing Free-Radical Damage
In addition to conventional drug therapy, broad spectrum antioxidant supplementation will help protect the liver against free-radical damage.

A study in the January 2002 issue of the Journal of Hepatology demonstrated that oxidative stress to the liver is a significant feature of hepatitis C infection. The results of this research strongly support the use of antioxidants such as vitamins A, C, and E (and selenium, as well as glutathione-boosting supplements) (Jain et al. 2002).

Some hepatitis C patients cannot tolerate beta carotene, vitamin A, or niacin found in many multinutrient formulas including the popular Life Extension Mix formula. Blood tests (ALT, AST, GGT) that measure liver enzymes can determine patient tolerance to these substances. People who cannot take multinutrient supplements such as Life Extension Mix can take individual supplements to provide optimal nutritional support. Vitamins C and E and grape seed-skin extract are powerful antioxidants shown to protect against free-radical damage.

Avoiding Liver Toxicity
Some herbs are metabolized in the liver and can be toxic to the liver, especially in high doses. The following herbal products have demonstrated liver toxicity: germander, comfrey, chapparal leaf, ma huang, pennyroyal, skullcap, and mistletoe. If one desires to use any of these herbal products, it is advisable to do so under the care of a physician and with careful monitoring of liver enzymes and hepatitis C viral counts (Harvey et al. 1981; Gossrau et al. 1990).

SUMMARY

Conventional physicians administer a two-drug combination consisting of interferon and ribavirin in an attempt to eradicate HCV. While this drug therapy is very effective in some patients, it fails in many others. The consequence of treatment failure is a chronic hepatitis C infection that silently damages the liver, thereby increasing the risk of lethal liver cirrhosis and/or liver cancer.

HCV latches on to iron to inflict free-radical damage to liver cells. One way of reducing these toxic free radicals is to lower the amount of iron in the liver. Another way of protecting the liver is to consume the proper antioxidant nutrients to protect cells against the damaging effects of free radicals. A healthy immune system may keep HCV in check. Supplements that help maintain youthful immune function are of particular importance.

If there is evidence of chronic HCV activity in the body, it is critical that liver-protecting agents be used on a consistent basis to minimize the amount of cellular damage.

An integrated treatment protocol follows:

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Comments (1)

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Improved AST and ALT happens steadily on these nutritional protocols. I am always surprised when TX normalises them quickly, while people still feel bad; I would expect them to normalise once the liver starts to heal, after Tx. As they are liver enzymes, could it be that Tx only inhibits their synthesis at first?

George , April 15, 2008 | url

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