Hepatitis C is an infectious disease caused by the hepatitis C virus, which infiltrates the liver and other organs. It causes inflammation and damage to DNA regulatory genes.
According to a 2007 report, hepatitis C (HCV) causes more deaths each year in the U.S. than human immunodeficiency virus (HIV). HCV is a primary reason why people need liver transplants. More than 4 million Americans are infected with HCV (NIH 2009; Rosen 2011; Holmberg 2011; Rubin 2011).
Approximately 75%-85% of people infected with HCV develop a chronic infection and face the risk of advanced liver fibrosis, cirrhosis, cancer, and other complications (Chen 2006).
Many people have the disease for decades before it is diagnosed. This is because HCV infection usually causes only minor symptoms until liver damage is advanced (Mayo Clinic 2011).
In some cases, liver abnormalities detected during routine blood work can suggest to a physician that a patient might have an HCV infection. This may allow treatment to begin before the disease reaches a critical stage. Therefore, proactive blood testing could be helpful in discovering an undetected HCV infection (McDonald 2010).
Though current standard of care has met with somewhat limited success and is burdened by considerable side effects, exciting findings reveal potential for underutilized drug strategies, such as metformin and thymosin alpha-1, to complement conventional treatment and improve outcomes in hepatitis C (Poo 2008; Baek 2007; Ciancio 2010; Yu 2012; Romero-Gómez 2009; Nkontchou 2011).
In this protocol, you will learn about how the hepatitis C virus is transmitted and the consequences of an infection. You will also discover that many people may not realize they are infected, and early detection can save lives. Lastly, you will find out about breakthroughs on the horizon that promise to vastly improve medical treatment outcomes as well as several natural compounds that target multiple aspects of hepatitis C.
How the Hepatitis C Virus is Transmitted
HCV is transmitted primarily via exposure to infected blood or blood products. Any HCV carrier can potentially transmit the infection (World Health Organization 2012). The most common mode of transmission is sharing contaminated needles during intravenous (IV) drug use (Williams 2011). Having had a blood transfusion before 1992 is a known risk factor as well. Other possible risk factors include body piercing, tattooing, and exposure to contaminated items such as toothbrushes, razor blades, or nail clippers (CDC 2012a; Cavalheiro 2007). While sexual transmission of HCV is possible, rates are low (Cavalheiro 2007; Vandelli 2004; Fierer 2008; Schmidt 2011).
Approximately 4% of infants born to HCV-infected mothers acquire the infection during childbirth. Transmission risk increases 2- to 3-fold if the HCV infected mother also has human immunodeficiency virus (HIV). Breastfeeding does not increase the risk of transmission (CDC 2011).
Disease Course and Outcomes
Acute phase
The first six months of HCV infection encompass the acute phase (Chakravarty 2010). Because it passes with few, if any signs or symptoms in most cases, this stage of the illness is usually dismissed by the patient. About 20% to 30% of adults with acute HCV infection may develop clinical symptoms. The symptomatic onset ranges from 3 to 12 weeks after exposure (Chen 2006; Dooley 2011). Patients may experience fever, fatigue, tenderness in the liver area, nausea or decreased appetite, and jaundice (Chakravarty 2010; Chen 2006).
Chronic phase
Approximately 75%-85% of HCV-infected persons will progress to chronic HCV infection (Chen 2006).
The chronic phase is generally established when HCV genetic material (RNA) persists in the patient's serum for 6 months or more (Dooley 2011; Chen 2006).
Numerous factors appear to affect the likelihood of developing chronic HCV infection. Females are more likely to clear the virus, for example, as are people who develop jaundice during the acute phase. In contrast, the virus appears to be more likely to persist in patients co-infected with HIV (Chen 2006; Dooley 2011).
Although the disease is transmittable during the chronic phase through blood, HCV carriers may not recognize they have an infection for up to 20 years because symptoms during this time are often mild (NIH-NDDIC 2012).
While elevations of alanine transaminase (ALT) - a liver enzyme that increases in response to liver cell death (Chen 2006) - may be observed, at least one-third of patients may exhibit normal levels (McDonald 2010). Eventually, nonspecific symptoms such as fatigue usually prompt the patient to visit a physician.
Outcomes
Within the first 20 years of infection, advanced liver disease may develop. During this timeframe, roughly 10% to 15% of patients develop cirrhosis of the liver – the replacement of healthy liver tissue by dysfunctional fibrous tissue and nodules (Dooley 2011; Chen 2006).
Up to 4% of patients with HCV-related liver cirrhosis develop liver cancer each year (Cheifetz 2011). Liver cancer may be suspected in someone with advanced HCV-related liver cirrhosis that experiences sudden weight loss, elevation in liver function tests, or pain or fullness in the right upper abdomen (Hepatitis C Technical Advisory Group 2005)
More than a third of liver transplants are a consequence of hepatitis C (Angelico 2011; Gordon 2009). Although five year survival following transplant is good (up to 85%), most hepatitis C patients who receive liver transplants have a recurrence of the virus (Gordon 2009; Narang 2010).
Diagnosis
HCV infection is usually detected during routine blood testing. Elevated levels of the liver enzyme alanine transaminase (ALT) would alert a physician to a possible infection with HCV. If a doctor suspects HCV, hepatitis C testing typically begins with a blood test to detect the presence of antibodies to the hepatitis C virus (Wilkins 2010, CDC 2012a).
The disease can be diagnosed by the presence of HCV antibodies or the direct presence of the virus or viral products in the blood. If the screen is positive, a liver biopsy may also be recommended to assess the severity of the disease and guide treatment decisions (Wilkins 2010).
Baby boomers (people born between 1946 and 1964) in particular are urged to get tested because rates of HCV infection are particularly high in this population (CDC 2012c).
Conventional Treatment
The goal of HCV infection therapy is to slow or halt progression of fibrosis and prevent the development of advanced cirrhosis (Wilkins 2010).
Standard treatment for hepatitis C centers upon pegylated interferon plus ribavirin (PEG-IFN/RBV).
- Interferons occur naturally and help the immune system recognize and attack viruses. Pegylated interferon is a chemically altered interferon that remains active in the body for a long time and helps mount robust immunity against HCV.
- Ribavirin is an antiviral drug that interferes with viral replication.
- The combination of the two drugs is more effective than either alone.
During pegylated interferon plus ribavirin treatment, physicians routinely test levels of liver enzymes, HCV antibodies, and the virus itself in the bloodstream. Monitoring these levels can help measure the effectiveness of treatment and determine prognosis (Fort 2012; Munir 2010; Wilkins 2010).
This combination treatment is ineffective in over 40% of HCV patients, leaving these individuals to seek additional approaches to eradicate the virus and/or protect against its damaging effects. Moreover, the contraindications and severe side-effects associated with interferon (e.g., depression, anemia, leukopenia and sepsis) can make treatment challenging (Wilkins 2010; Alkhouri 2012).
Sustained virologic response is the surrogate marker to evaluate the effectiveness of treatment. If HCV treatment is successful, the patient will achieve a sustained virologic response; this occurs when HCV RNA cannot be detected in serum 24 weeks after treatment ends (Alkhouri 2012).
Emerging Therapies
Only about 40% of patients with HCV genotype 1 infection (the most common genotype in North America) achieve sustained virologic response with pegylated interferon plus ribavirin (PEG-IFN/RBV) therapy (Zeuzem 2011; Alkhouri 2012). Therefore, rigorous research efforts are aimed at developing more effective treatment strategies.
Direct-acting Antivirals (DAAs)
Telaprevir and boceprevir, direct-acting antivirals (DAAs) that inhibit HCV replication, received FDA approval in 2011. They are used in combination with pegylated interferon plus ribavirin to treat chronic genotype 1 HCV infection (Kim 2012; Feret 2011).
Telaprevir
In chronic HCV-infected patients who had either not been treated or for who conventional treatment was unsuccessful, adding telaprevir to pegylated interferon plus ribavirin therapy resulted in significantly higher sustained virologic response rates (Jacobson 2011; Zeuzem 2011).
The rate of chronic HCV infection is notably high in the African American population (CDC 2012b). Research showed when telaprevir was used in combination with pegylated interferon plus ribavirin in African Americans, the sustained virologic response rate was 61% versus 25% without telaprevir (American College of Gastroenterology 2011).
Additional evidence indicates using telaprevir may shorten treatment time (Sherman 2011). Being able to shorten treatment duration is extremely important, as some patients stop complying with treatment over time or may need to stop treatment due to adverse events (Lo Re 2011; Kim 2012). If prolonged exposure to these therapies can be minimized, this might encourage patient compliance.
Boceprevir
Adding boceprevir to pegylated interferon plus ribavirin treatment has also yielded major improvements in sustained virologic response rates (Poordad 2011). In previously untreated patients, treatment with boceprevir plus pegylated interferon plus ribavirin therapy yielded high sustained virologic response rates in most patients at 28 weeks; boceprevir was also found to be safe and effective for up to 48 weeks (when necessary). Having a 4-week lead-in period of pegylated interferon plus ribavirin treatment before adding boceprevir yielded a better sustained virologic response as well as decreased viral breakthrough and relapse over a 48-week duration (Kwo 2010).
Limitations of DAAs include a greater frequency of adverse events than pegylated interferon plus ribavirin (Ghany 2011), complex dosing regimen (Lo Re 2011), potential for drug-drug interactions (Ghany 2011), and the emergence of treatment-resistant HCV strains (Sarrazin 2010; Kim 2012; Susser 2009; Kuntzen 2008). Also, neither drug is equally effective against all HCV genotypes. New therapies are being developed to address a broader range of genotypes (Shiffman 2012).
Metformin: More than a Diabetes Drug
Life Extension has been reporting on the benefits of metformin for years. New research indicates metformin, normally used to treat diabetes, may be a useful therapy for HCV patients. In vitro data suggests metformin may have a suppressive effect on HCV replication (Nakashima 2011). In women with HCV genotype 1 infection who were found to exhibit insulin resistance, taking metformin in addition to standard HCV therapy resulted in a doubled sustained virologic response and greater decrease in viral load compared to placebo in the first 12 weeks of treatment (del Campo 2010). A number of other clinical studies have also shown improved sustained virologic response rates among insulin-resistant HCV patients receiving metformin in addition to standard therapy (Yu 2012; Romero-Gómez 2009). Metformin use was also correlated with a significantly better prognosis among 99 diabetic HCV patients with cirrhosis. Compared to non-use, metformin treatment was associated with an 81% reduction in risk of hepatocellular carcinoma and a 78% reduction of liver-related death or need for liver transplant (Nkontchou 2011).
Ezetimibe: A cholesterol-lowering Drug that Inhibits HCV Viral Entry
New findings reveal certain cholesterol medications may be useful in HCV treatment. Niemann-Pick C1-like 1 (NPC1L1) receptors are important mediators of cholesterol absorption in the human body. Interestingly, scientists recently found NPC1L1 receptors also help the HCV virus enter cells.
The cholesterol drug ezetimibe specifically targets NPC1L1 receptors. Researchers tested its effects on HCV and found it inhibits infection by all major HCV genotypes. Moreover, in mice with human liver grafts, ezetimibe slowed the establishment of HCV genotype 1b infection. These findings represent a breakthrough discovery by identifying an entry factor for HCV and revealing a new treatment target (Sainz 2012).
Interferon-Free Treatment
In a 2012 Phase II study, patients were treated with an investigational interferon-free therapy (combination of protease inhibitor BI 201335 and polymerase inhibitor BI 207127) with and without ribavirin and for varying treatment durations. Treatment for 28 weeks resulted in a viral cure in nearly 82% of patients with HCV genotypes 1a CC and 1b infection, the most common genotypes in Asia and Europe. Moreover, 68% of all patients in the study achieved a viral cure, including individuals with genotype 1a non-CC, which is normally very difficult to treat. If proven to be a viable treatment option, interferon-free therapy would eliminate interferon’s side effects. This, in turn, would potentially encourage patient compliance (Zeuzem 2012).
HCV Vaccination on the Horizon
A February 2012 report states Michael Houghton, one of the scientists who discovered HCV in 1989, developed a vaccine from a strain of HCV. The results have been overwhelmingly positive—patients who received this vaccine produced antibodies that neutralized all known strains of HCV, a feat previously thought impossible given the virulence of HCV. Although further testing will be needed, and it would likely take five to seven years before the vaccine could receive approval, preliminary findings are encouraging (Hanlon 2012).
Thymosin alpha-1
Life Extension has been reporting on the benefits of thymosin alpha-1 since the early 1980s. This immune-boosting agent has been studied for its potential role in treating cancer and viral hepatitis. Study results suggest thymosin alpha-1 in addition to pegylated interferon plus ribavirin treatment may improve the efficacy of treatment in patients who were previously not responsive to therapy (Poo 2008; Baek 2007). Other study findings have indicated taking thymosin in addition to standard HCV treatment might lower the rate of relapse (Ciancio 2010). Moreover, thymosin alpha-1 shows promise as a potential adjuvant therapy in difficult-to-treat patients with HCV, but more studies are needed (Sherman 2010). In another trial among 552 hepatitis C patients who were non-responders to standard care, addition of two 1.6 mg subcutaneous injections of thymosin alpha-1 per week to pegylated interferon plus ribavirin for 48 weeks resulted in a 41% sustained virologic response compared to 26% in placebo recipients (Ciancio 2012).
Targeted Natural Therapeutics
Boosting Liver Glutathione and Easing Oxidative Stress
Glutathione acts as a cellular detoxifier and helps prevent damage from free radicals (Cacciatore 2010). However, glutathione depletion is a common finding among HCV-infected patients (Tapryal 2010). The following compounds may help to increase glutathione levels.
N-acetyl-cysteine. N-acetyl-cysteine (NAC) is derived from L-cysteine, a conditionally essential amino acid. This powerful antioxidant diminishes free radicals and raises glutathione levels (Nguyen-Khac 2011). In conventional medicine, NAC has been used to treat acetaminophen poisoning. In children with acute liver failure from causes other than acetaminophen poisoning, receiving NAC was associated with a shorter hospital stay, greater incidence of liver recovery, and better survival after transplantation (Kortsalioudaki 2008). In an early trial, addition of NAC to interferon boosted glutathione levels in white blood cells of patients with chronic hepatitis C and normalized ALT levels in 41% of interferon non-responders (Beloqui 1993). While more recent trials have been unable to confirm the therapeutic role of NAC in chronic hepatitis C, they have established it is very well tolerated (Grant 2000; Gunduz 2003).
S-adenosyl-L-methionine. S-adenosyl-L-methionine (SAMe), a methyl donor for numerous methylation reactions, has been studied for its antidepressant properties (Nahas 2011). SAMe also regulates glutathione synthesis (Medici 2011). In HCV-infected patients who were non-responders to previous antiviral therapy, adding SAMe to a pegylated interferon plus ribavirin (PEG-IFN/RBV) regimen improved early viral response (Feld 2011). In a separate trial, SAMe and trimethyglycine (another methyl donor) were given along with pegylated interferon plus ribavirin to chronic hepatitis C patients. The treatment resulted in an early virological response (EVR) in 59% of subjects, whereas pegylated interferon plus ribavirin alone had previously achieved only a 14% EVR (Filipowicz 2010).
Lipoic acid. This free-radical scavenger helps to repair damage caused by oxidative stress, assisting in the regeneration of important antioxidants such as glutathione and vitamin E (Shay 2009). In animals, lipoic acid has been found to prevent fatty liver disease (Park 2008). In human trials, administration of antioxidant blends containing lipoic acid was shown to favorably modulate liver enzymes, HCV RNA levels, and liver biopsy score in HCV patients (Melhem 2005; Berkson 1999).
Whey protein. Whey protein boosts glutathione levels and improves the functioning of the immune system (El-Attar 2009). In an animal model of hepatitis, whey protein supplementation attenuated chemical-induced liver enzyme elevations (Kume 2006). Moreover, a clinical study found oral whey protein reduced viral load, decreased inflammation, lowered ALT levels, and exerted other beneficial effects in compensated chronic HCV-infected patients (El-Attar 2009).
Selenium. Selenium is an essential component of glutathione peroxidase, an enzyme that protects cells from free radical damage (Khan 2012). Patients with hepatitis C or B have been found to have lower serum selenium concentrations than healthy individuals (Khan 2012). Moreover, selenium deficiency is thought to contribute to insulin resistance in people with HCV-related chronic liver disease; and reduced selenium levels have been observed in patients with hepatocellular carcinoma (Rohr-Udilova 2012; Himoto 2011).
Glutathione. A 1989 study found consumption of oral glutathione increased plasma glutathione levels (Jones 1989). Preclinical trials found oral glutathione increases glutathione levels in tissues such as the lungs, liver, and kidneys (Hagen 1990; Kariya 2007; Aw 1991; Iantomasi 1997; Favilli 1997).
Targeting Excess Iron Levels
Lactoferrin. Lactoferrin, an iron-binding glycoprotein, may be beneficial as an adjunctive treatment for serum iron overload in hepatitis patients. Lactoferrin is a potent antioxidant, antiviral agent, and scavenger of free iron (Actor 2009). In addition, it is directly involved in the upregulation of natural killer cell activity, making it a natural mediator of immune function (Actor 2009). As an immune mediator, lactoferrin may work synergistically with interferon to reduce viral load (Ishii 2003). In another study among patients with chronic HCV, lactoferrin alone significantly lowered the HCV RNA titer and improved efficacy of subsequent treatment with interferon and ribavirin (Kaito 2007).
Green Tea. Epigallocatechin-3-gallate (EGCG) from green tea has been found to interrupt the first step of HCV infection by blocking the virus from entering target cells. In addition, EGCG inhibited cell-to-cell transmission of HCV. Both of these effects were observed regardless of the genotype tested. These findings carry important implications for the prevention of HCV re-infection in liver transplant patients (Ciesek 2011). In addition, green tea has been shown to inhibit iron absorption in intestinal cells (Ma 2011) and accumulation in liver tissue (Saewong 2010), which can contribute to excessive oxidative stress.
Elemental Calcium. Calcium inhibits iron absorption (Shawki 2010). Taking 600 mg of elemental calcium can reduce iron absorption by as much as 60% (Hallberg 1991).
Additional Natural Liver Protection
Milk Thistle. Silymarin and its chief active ingredient, silibinin, are derived from milk thistle, a member of the daisy family. Both substances help the liver avoid toxic damage and regenerate after injury.
Silymarin
Findings from several studies suggest silymarin has potential antiviral (Polyak 2007), antioxidant (Bonifaz 2009), anti-inflammatory (Polyak 2007; Morishima 2010), and antifibrotic (El-Lakkany 2012) effects within the liver. It may also improve liver enzyme levels in HCV patients (Mayer 2005).
In a recent cell culture study, silymarin inhibited entry of HCV into cells, inhibited viral RNA and protein expression, and decreased cell-to-cell transmission of HCV (Wagoner 2010).
A clinical study involving 1,145 HCV-infected participants showed patients using silymarin had fewer liver-related symptoms and somewhat higher quality-of-life scores (Seeff 2008). Doses greater than 700 mg may improve bioavailability of silymarin; and oral doses of up to 2.1 g per day have been found to be safe and well tolerated (Hawke 2010).
Silibinin
The antioxidant, antifibrotic, and metabolic effects of silibinin have been demonstrated in numerous studies (Loguercio 2011; Trappoliere 2009). Silibinin also has antiviral capabilities (Ahmed-Belkacem 2010; Ferenci 2008).
The clinical efficacy of oral silibinin in active chronic hepatitis C has not yet been clearly established (Loguercio 2011; Verma 2007). However, intravenous silibinin effectively treated HCV re-infection following liver transplantation in a small number of patients in one trial (Eurich 2011), and helped 85% of non-responders to standard of care achieve undetectable HCV RNA levels in another (Rutter 2011). Likewise, administering high doses of silibinin intravenously in addition to pegylated interferon plus ribavirin therapy lowered viral loads in HCV-infected patients who were previous non-responders to treatment (Ferenci 2008); and 1,400 mg of intravenous silibinin daily for 14 days successfully induced sustained virologic response (SVR) in a 57-year-old liver transplant patient (Neumann 2010).
A medical literature review found no significant side effects with silybin phytosome at doses up to 10 grams per day, and no significant interactions with other medications (Loguercio 2011).
Polyenylphosphatidylcholine. Polyenylphosphatidylcholine (PPC) is a major component of essential phospholipids (Okiyama 2009). In addition to improving liver enzymes in HCV (Singal 2011), PPC replenishes levels of S-adenosyl-L-methionine (SAMe), a precursor to the potent antioxidant glutathione (Lieber 2005). PPC protects against liver damage (Okiyama 2009) and improves liver function (Zhao 2011; Singal 2011). In animal studies, it has demonstrated antioxidant, cytoprotective, anti-inflammatory, and antifibrotic effects, inhibiting oxidative stress and the development of alcoholic liver disease (Okiyama 2009; Singal 2011). Numerous double blind, placebo-controlled clinical trials have shown essential phospholipids improve chronic hepatitis among human subjects (Gundermann 2011).
Schisandra chinensis. Berries from the Schisandra chinensis (S. chinensis) plant contain active ingredients that protect the liver (Azzam 2007). Crude schisandra and its extracts have traditionally held a role in Chinese and Japanese medicine (Azzam 2007), and S. chinensis has been used to treat chemical and viral hepatitis (Chien 2011). A study examining the effects of a Japanese herbal combination containing S. chinensisindicated Schisandra fruit could inhibit HCV infection (Cyong 2000). The seed extract from S. chinensisappears to have liver-detoxifying capabilities; components of the seed extract are thought to have anticancer, anti-inflammatory, liver-protective, anti-HIV, and immunomodulating effects (Wang 2007).
Licorice Root Extract. Licorice root extract (glycyrrhizin) is known to exert an antiviral effect against HCV (Ashfaq 2011). In Japanese HCV patients, the long-term use of glycyrrhizin has shown to be helpful in preventing inflammation, liver cirrhosis, and hepatocellular carcinoma (Guyton 2002; Kumada 2002). The broad anti-inflammatory activity (Schröfelbauer 2009) and antioxidant capabilities (Li 2011) of glycyrrhizin have also been observed. Adding a nutritional supplement containing vitamin C, glycyrrhizic acid, and other antioxidants to standard pegylated interferon plus ribavirin treatment has been linked to a notably higher rate of biochemical and histologic improvements in patients with chronic HCV (Gomez 2010; Vilar Gomez 2007). In chronic HCV patients, oxidative stress and immunological parameters showed marked improvement following treatment with this blend (Gomez 2010).
A preparation known as Stronger Neo-Minophagen C (SNMC) contains glycyrrhizin as an active component and has been used in Japan for more than 30 years to treat chronic hepatitis (Kumada 2002). In animals with HCV, SNMC has been found to prevent fatty liver disease (Korenaga 2011) and protect liver cells against carbon tetrachloride-induced oxidative stress by restoring depleted glutathione levels (Hidaka 2007). A possible side effect associated with ingestion of large amounts of licorice is hypertension (Nielsen 2012); therefore, blood pressure should be monitored regularly.
Vitamin D. Diminished vitamin D levels have been observed in HCV patients (Arteh 2010; Petta 2010). Low serum vitamin D levels are associated with severe fibrosis, as well as a low sustained virological response to pegylated interferon plus ribavirin treatment in patients with chronic HCV infection (Petta 2010); and vitamin D supplementation has been found to enhance HCV response to pegylated interferon plus ribavirin therapy (Abu-Mouch 2011). In a recent study involving patients with HCV genotype 2-3 receiving pegylated interferon plus ribavirin treatment, supplementing with oral vitamin D significantly improved viral response. Twenty-four weeks after treatment, 95% of the treatment (vitamin D) group was HCV RNA negative versus 77% of the control group (Nimer 2012).
Coffee. A recent study showed patients with advanced HCV-related chronic liver disease who drank 3 or more cups of coffee each day were about 3 times more likely to respond to pegylated interferon plus ribavirin treatment than non-drinkers. These patients were previous non-responders to interferon treatment (Freedman 2011). Published study reports have documented an association between coffee consumption and lowered risks of liver cirrhosis (Modi 2010; Klatsky 2006), hepatocellular carcinoma (Larsson 2007; Bravi 2007), liver disease progression in HCV infection (Freedman 2009), and lower serum ALT activity (Ruhl 2005a). Population studies have shown coffee drinking reduces the risk of clinically significant chronic liver disease (Ruhl 2005b). These effects may be due in part to the antiviral activity of chlorogenic acid, a coffee polyphenol found in especially high concentrations in green coffee extracts (Wang 2009).
Zinc and zinc-carnosine. Zinc has HCV-inhibiting capabilities (Yuasa 2006). Zinc supplementation has resulted in a higher reported rate of HCV eradication among patients receiving interferon treatment (Takagi 2001), decreased gastrointestinal disturbances and hair loss, and improved fingernail health in patients with chronic HCV. It may also improve patient tolerance to IFN-alpha-2a and ribavirin (Ko 2005b).
A chelate compound consisting of zinc and L-carnosine may induce anti-oxidative functions in the liver, thereby decreasing liver cell injury (Murakami 2007). Supplementation with chelated zinc-carnosine has been found to lessen the degree of liver damage and improve long-term outcome of patients with chronic HCV infection or liver cirrhosis (Matsuoka 2009). In patients with HCV-related chronic liver disease, it appears to have a beneficial anti-inflammatory effect on the liver by decreasing iron overload (Himoto 2007). In addition, fewer gastrointestinal side effects were observed when zinc-carnosine supplementation was added to combination pegylated interferon plus ribavirin therapy (Suzuki 2006).
Curcumin. Curcumin is a yellow pigment present in the curry spice turmeric. It possesses antioxidant, anti-inflammatory, anti-fungal, antibacterial, and anti-proliferative capabilities (Aggarwal 2003; Rahman 2006; Aggarwal 2007). In addition, curcumin has been found to exert antiviral activity against a variety of viruses including the human immunodeficiency virus (HIV) (Li 1993), influenza virus (Chen 2010), and coxsackievirus (Si 2007). One team of researchers found curcumin reduces HCV gene expression, and combining curcumin with IFN-alfa treatment had "profound inhibitory effects" on HCV replication. The authors concluded curcumin may be valuable as a novel anti-HCV agent (Kim 2010). Curcumin has also been shown to protect against liver cancer (Darvesh 2012).
Quercetin. Quercetin is a flavonoid present in fruit, vegetables, wine, and tea that has antioxidant and anti-inflammatory properties. Studies indicate it also possesses anti-hypertensive, anti-bacterial, anti-fibrotic, anti-atherogenic, and anti-proliferative properties (Boots 2008). Quercetin has also been found to attenuate HCV virus production (Gonzalez 2009; Bachmetov 2012).
L-carnitine. Chronic HCV patients received pegylated interferon plus ribavirin plus the amino acid L-carnitine or pegylated interferon plus ribavirin alone for 12 months. A significant improvement in sustained virologic response was observed in 50% of the L-carnitine group versus 25% of the non-L-carnitine group (Malaguarnera 2011a). Supplementing pegylated interferon plus ribavirin treatment with L-carnitine has also been associated with decreased mental and physical fatigue, as well as improved health-related quality of life in patients with chronic HCV. These latter outcomes could potentially improve patient compliance with pegylated interferon plus ribavirin treatment (Malaguarnera 2011b).
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