Glutathione is a powerful antioxidant that helps the body defend against toxicity, and it is most needed by those living with chronic liver disease. Because the stress of chronic liver disease also depletes this valuable antioxidant, learn why supplementing with one of its precursors helps defend against future liver damage.
A powerful antioxidant found within every cell in your body, glutathione has many supportive functions. One of glutathione’s best-known roles is to defend the cell it inhabits against damage from wastes and toxins. Since the hepatic cells of those with chronic liver disease are consistently stressed as they deflect poisons, the cells’ quantity of glutathione becomes even more important. Even used as an emergency medicine tactic, one of glutathione’s building blocks has been extensively revered for protecting the liver from damaging toxins.
Clinical studies have documented that glutathione is essential for detoxification and that its depletion is associated with increased risks of toxicity and chronic disease. As this antioxidant is depleted, the body has fewer resources to protect itself from oxidation – a process defined by unstable oxygen molecules damaging cell membranes. Needed by other antioxidants to scavenge and neutralize free radicals, glutathione is the body’s primary defender against oxidative stress. Many experts believe that a deficiency of hepatic glutathione is one of the leading contributors to the progression of liver disease.
Glutathione levels decline naturally as people age, fight a chronic disease or are exposed to excessive amounts of toxins. Insufficient glutathione levels reduce the liver’s ability to break down drugs, chemicals and other toxins, enhancing the probability of liver damage. Several studies document the role glutathione depletion plays in advancing liver disease:
· After measuring levels of glutathione in the liver, blood and lymphocytes of patients with chronic Hepatitis C, Italian researchers found that the less glutathione present, the more severe their liver disease was.
· By studying people with hepatitis, scientists from Pamplona, Spain suggested that replenishing glutathione levels improves their response to interferon treatment.
· Researchers from the Oklahoma Medical Research Foundation confirmed that oxidative stress occurs in patients with chronic hepatitis. In addition, they demonstrated that the levels of free radicals corresponded directly with hepatitis activity.
· After studying the effects of high doses of intravenous glutathione in patients with fatty livers secondary to alcoholic hepatitis or viral hepatitis, Italian investigators concluded that glutathione resulted in marked improvement in patients’ liver tests.
The evidence connecting glutathione depletion with a poor liver disease outcome is clear. To capitalize on this understanding, many educated people with liver disease have taken it upon themselves to increase their odds by fortifying their glutathione levels.
Although glutathione is available as an over-the-counter pill, its absorption into cells when taken orally has been repeatedly questioned. Most experts on glutathione supplementation suggest that people with chronic liver disease supplement with its amino acid building blocks. Because it is readily absorbed and rapidly metabolized to glutathione, N-Acetyl Cysteine (NAC) is the glutathione building block most favored by healthcare practitioners. In the case of an acetaminophen overdose, NAC is administered by physicians to detoxify the drug before it destroys too many liver cells and becomes fatal. In addition, NAC has been shown to increase blood glutathione in HIV-infected patients with low levels of glutathione due to their chronic infection.
Despite the supportive literature, there have been few, large, well-designed trials advocating the use of NAC to retard liver disease. While the demand for more proof continues to grow, there are a few recently published trials:
· Published in the November 2006 journal Apoptosis, one such trial investigated whether NAC could prevent oxidative stress and inhibit liver cell death in fulminant hepatic failure. Based on an animal model, the researchers concluded that NAC demonstrates a hepatoprotective role for this severe type of liver failure.
· As published in the January 2008 journal Liver Transplantation, a retrospective study found that children treated with NAC for acute liver failure (not caused by acetaminophen poisoning) had a better outcome than matched controls not treated with NAC.
Since the hepatic cells of people with chronic liver disease have to fend off more than their share of waste and toxins, their cells’ glutathione levels drain quickly. Unfortunately, this depletion makes them more susceptible to the advancement of liver disease. When the liver is consistently insulted, the facts support NAC supplementation to replenish glutathione levels. Restoring glutathione levels is an effective way to refuel a person with liver disease’s ammunition, a replenishment that can help them defend against incurring any further liver damage.
Editor’s Note: Diabetes patients should check with their physician before taking NAC. Supplementing with NAC may disrupt insulin and interfere with its effectiveness.
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Kortsalioudaki, C, et al., Safety and efficacy of N-acetylcysteine in children with non-acetaminophen-induced acute liver failure, Liver Transplantation, January 2008.
San-Miguel B, et al., N-acetyl-cysteine protects liver from apoptotic death in an animal model of fulminant hepatic failure, Apoptosis, November 2006.
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www.hepatitis-central.com, HCV and the Body's Most Important Antioxidant, Nicole Cutler, L.Ac., Natural Wellness, 2008.
www.medscape.com, NAC Slows Early-Stage Non-Acetaminophen-Related Liver Failure, Medscape Medical News, 2007.
www.sciencedaily.com,. Treatment With NAC Is Associated With Better Outcomes For Children With Liver Failure, Study Suggests, ScienceDaily LLC, 2008.
www.spinalrehab.com.au, Oxidative Stress in Chronic Liver Disease: The Role of Glutathione, Theodore Hersh, MD, MACG, hyperMED, 2008.
www.thebody.com, Antioxidants, Oxidative Stress, and NAC, Carole Lemens and Craig Sterrit, The Body, December 1998.
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