N-Acetylcysteine improves non-acetaminophen induced acute liver failure recovery in children

January 24, 2008

A new study describes the findings of medical researchers at King’s College Hospital in London that NAC, an amino acid used to treat acute liver failure caused by toxicity with the commonly used pain relieving drug acetaminophen also aids in the recovery from non-acetaminophen induced acute liver failure.
NAC is an antioxidant that replenishes glutathione stores in the liver and the nutrient also improves detoxification. While widely used for many years to treat acetaminophens toxicity to the liver, NAC was first introduced as a treatment for acute liver failure not caused by the drug in 1995 at King's College Hospital.
The scientists evaluated the medical records of 170 King's College Hospital patients under the age of eighteen who were treated for non-acetaminophen induced acute liver failure. Children who received intravenous NAC along with standard care were compared with those who received standard care only.
Ten year survival was 75 percent among children who received NAC compared with 50 percent of those who received standard care only.
The team also found that 43 percent of those who received NAC did not need a liver transplant, compared with just 22 percent of those who did not receive the compound. Sixteen percent who received NAC died following liver transplant, compared with 39 percent of those who received standard care. Treatment with NAC was also linked with shorter hospital stays, and fewer and shorter intensive care stays.
“Our data demonstrates that NAC has minor, self-limited adverse effects and can be safely administered to children with non-acetaminophen induced acute liver failure,” the authors write The study is published in the January, 2008 issue of the journal Liver Transplantation.

NAC important in worsening obstructive lung disease

In this study 123 patients with acute exacerbation (drastic-sudden worsening of symptoms) of their chronic obstructive pulmonary disease (COPD) were placed on NAC 600mg or NAC 1200mg once a day, or inactive placebo for 10 days. The study was double-blinded, double-dummy, randomized and of course placebo controlled; the gold standard for research.
In these attacks a protein is released into the bloodstream known as CRP; this is a measure of the amount of inflammation and severity of attack. IL-8, is an inflammatory component of the immune system that is released into the blood stream causing worsening of symptoms. NAC 600mg normalized the level of CRP in 52% of the patients, and NAC 1200mg normalized CRP levels in 90% of the patients whereas only 19% of the patients on placebo achieved normal levels of CRP. NAC 1200mg was also superior in reducing the level of IL-8 and improving expectoration over 600mg and of course over placebo.
Both 600mg and 1200mg of NAC improved lung function, reduced cough intensity, and the sound of the lungs when listened with a stethoscope.
Conclusion; Treatment with NAC improved inflammatory-clinical markers and lung function in patients with acute worsening of COPD. The study is published in the journal Clinical Drug Investigation, 2005;25(6).

Add GliSODin to your list of select supplements before major or invasive surgery

In invasive surgery, a surgery which is complex and requires penetration into internal areas of the body, blood flow is interrupted and then reintroduced to the involved tissues. This generates a large volume of cell destroying free radicals that lead to tissue damage. This damage is called ischemia-reperfusion injury; to put this in perspective similar damage occurs after a stroke or heart attack due to the reintroduction of blood. The spinal cord and the kidneys are the most vulnerable organs to this form of damage. If the organs and tissues can be protected from the free radicals they will suffer less damage.
In this study one group of swine were supplemented with GliSODin for two weeks and the second group received placebo (swine have similar antioxidant profiles to humans). Then a major invasive procedure was performed. GliSODin significantly reduced the damage caused by the reintroduction of blood flow; DNA damage was decreased in cells. And spinal cord cell death was decreased. Additionally, venous acidosis was decreased; a condition where the blood becomes acidic, this acidosis is harmful to heart function. Organ function was not impaired with GliSODin supplementation. The study is published on line ahead of print in the journal Intensive Care Medicine, January 20th, 2007.

Evidence that GliSODin protects the kidneys in diabetes

Diabetes often causes kidney damage and can lead to kidney failure and the need for dialysis to remove waste products from the blood. Free radical damage to kidney cells is implicated in the progression of disease. GliSODin (oxykine in Japan) is the cantaloupe melon derived SOD covered by chains from wheat protein (polymeric films of wheat matrix gliadin). SOD is a powerful anti-inflammatory/antioxidant that is well absorbed by humans (SOD is normally destroyed in the digestive tract).
In this study researchers at the Molecular Gastroenterology and Hepatology Department in the Graduate School of Medical Science in Kyoto, Japan treated rodents with diabetes with GliSODin; an important time to supplement because kidney damage already starts in pre-diabetes; they are catching it early on before gross damage occurs. Giving GliSODin over a 12 week period significantly inhibited the leakage of protein into the animals’ urine vs. non-supplemented animals. The kidney cells of the supplemented animals were also significantly healthier. Diabetic animals not supplemented with GliSODin also had more inflammation in their kidneys. The study is published in the journal Biofactors, 2005;23(2).