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NAC article
- Thread starter Jane
- Start date
So I know Amy is taking NAC, others take GSH, if I'm understanding NAC produces more GSH in the body and if NAC is toxic but GSH is okay why would you choose one over the other?
I'm just trying to understand the difference more because I need something to help me out right now, I started taking GSH (oral) but should I take NAC? and how much? Thanks<img src="i/expressions/face-icon-small-smile.gif" border="0">
I'm just trying to understand the difference more because I need something to help me out right now, I started taking GSH (oral) but should I take NAC? and how much? Thanks<img src="i/expressions/face-icon-small-smile.gif" border="0">
So I know Amy is taking NAC, others take GSH, if I'm understanding NAC produces more GSH in the body and if NAC is toxic but GSH is okay why would you choose one over the other?
I'm just trying to understand the difference more because I need something to help me out right now, I started taking GSH (oral) but should I take NAC? and how much? Thanks<img src="i/expressions/face-icon-small-smile.gif" border="0">
I'm just trying to understand the difference more because I need something to help me out right now, I started taking GSH (oral) but should I take NAC? and how much? Thanks<img src="i/expressions/face-icon-small-smile.gif" border="0">
So I know Amy is taking NAC, others take GSH, if I'm understanding NAC produces more GSH in the body and if NAC is toxic but GSH is okay why would you choose one over the other?
I'm just trying to understand the difference more because I need something to help me out right now, I started taking GSH (oral) but should I take NAC? and how much? Thanks<img src="i/expressions/face-icon-small-smile.gif" border="0">
I'm just trying to understand the difference more because I need something to help me out right now, I started taking GSH (oral) but should I take NAC? and how much? Thanks<img src="i/expressions/face-icon-small-smile.gif" border="0">
warwick explains why on my blog <img src="i/expressions/face-icon-small-smile.gif" border="0"> <img src="i/expressions/face-icon-small-smile.gif" border="0"> <img src="i/expressions/face-icon-small-smile.gif" border="0"> i'm too lazy to type all of it out or cut and paste.
warwick explains why on my blog <img src="i/expressions/face-icon-small-smile.gif" border="0"> <img src="i/expressions/face-icon-small-smile.gif" border="0"> <img src="i/expressions/face-icon-small-smile.gif" border="0"> i'm too lazy to type all of it out or cut and paste.
warwick explains why on my blog <img src="i/expressions/face-icon-small-smile.gif" border="0"> <img src="i/expressions/face-icon-small-smile.gif" border="0"> <img src="i/expressions/face-icon-small-smile.gif" border="0"> i'm too lazy to type all of it out or cut and paste.
Try this article, it's what originally got me thinking about taking it.
<a target=_blank class=ftalternatingbarlinklarge href="http://www.webmd.com/content/article/120/113562.htm">NAC Article</a>
March 14, 2006 -- In its first test against cystic fibrosis, high doses of a drug called NAC were 'safe' for short-term use, researchers report.
NAC, or N-acetylcysteine, has a "proven safety record over long-term use at high doses in several chronic inflammatory conditions and has minimal interaction with other drugs," write the researchers. They included Rabindra Tirouvanziam, PhD, of Stanford University.
However, they aren't recommending NAC for cystic fibrosis. NAC needs more testing as a cystic fibrosis treatment, note Tirouvanziam and colleagues.
"It is important to warn patients against uncontrolled use of the drug," they write in Proceedings of the National Academy of Sciences.
Why NAC?
In their report, the researchers trace their interest in NAC as a cystic fibrosis treatment.
Cystic fibrosis is a chronic, progressive condition that primarily affects the body's respiratory and digestive systems. It is due to a gene defect that causes the body to produce abnormally thick mucous.
That mucous clogs the lungs, leading to recurring infections of the lungs and sinuses. It also makes breathing difficult.
In cystic fibrosis, the lungs have an unusually high number of neutrophils, a type of white blood cell. Those neutrophils prompt inflammation, setting the stage for more damage.
Tirouvanziam and colleagues noticed that neutrophils in cystic fibrosis patients were short on an antioxidant called glutathione. NAC is a building block for glutathione. The scientists wanted to see if NAC could boost glutathione, which in turn might curb lung inflammation.
Drug's First Test for Cystic Fibrosis
The researchers checked NAC's short-term safety. Participants were 18 children with cystic fibrosis who were at least 10 years old.
Every day for four weeks, the patients took three high doses of NAC by mouth. "We used doses in excess of 1.8 grams per day, which had never been used in [cystic fibrosis patients] before," write Tirouvanziam and colleagues.
The treatment appeared to be safe. The scientists note "very mild and infrequent drug-related adverse effects" including heartburn, nausea, and a bad taste from the drug.
Especially in patients with lung inflammation before taking NAC, neutrophils in the lungs became less active and had a rise in glutathione during NAC treatment. Lung function didn't improve, which didn't surprise the researchers because the test was so short.
Next Steps
Those findings could be an important cellular link in understanding cystic fibrosis, write the researchers.
However, they note that they didn't test NAC's effectiveness and long-term safety. That work will come later.
NAC's structure "prevents proper quality control of most commercial formulations available over the counter," the researchers caution. They call for "carefully designed and controlled clinical studies" of NAC and cystic fibrosis.
<a target=_blank class=ftalternatingbarlinklarge href="http://www.webmd.com/content/article/120/113562.htm">NAC Article</a>
March 14, 2006 -- In its first test against cystic fibrosis, high doses of a drug called NAC were 'safe' for short-term use, researchers report.
NAC, or N-acetylcysteine, has a "proven safety record over long-term use at high doses in several chronic inflammatory conditions and has minimal interaction with other drugs," write the researchers. They included Rabindra Tirouvanziam, PhD, of Stanford University.
However, they aren't recommending NAC for cystic fibrosis. NAC needs more testing as a cystic fibrosis treatment, note Tirouvanziam and colleagues.
"It is important to warn patients against uncontrolled use of the drug," they write in Proceedings of the National Academy of Sciences.
Why NAC?
In their report, the researchers trace their interest in NAC as a cystic fibrosis treatment.
Cystic fibrosis is a chronic, progressive condition that primarily affects the body's respiratory and digestive systems. It is due to a gene defect that causes the body to produce abnormally thick mucous.
That mucous clogs the lungs, leading to recurring infections of the lungs and sinuses. It also makes breathing difficult.
In cystic fibrosis, the lungs have an unusually high number of neutrophils, a type of white blood cell. Those neutrophils prompt inflammation, setting the stage for more damage.
Tirouvanziam and colleagues noticed that neutrophils in cystic fibrosis patients were short on an antioxidant called glutathione. NAC is a building block for glutathione. The scientists wanted to see if NAC could boost glutathione, which in turn might curb lung inflammation.
Drug's First Test for Cystic Fibrosis
The researchers checked NAC's short-term safety. Participants were 18 children with cystic fibrosis who were at least 10 years old.
Every day for four weeks, the patients took three high doses of NAC by mouth. "We used doses in excess of 1.8 grams per day, which had never been used in [cystic fibrosis patients] before," write Tirouvanziam and colleagues.
The treatment appeared to be safe. The scientists note "very mild and infrequent drug-related adverse effects" including heartburn, nausea, and a bad taste from the drug.
Especially in patients with lung inflammation before taking NAC, neutrophils in the lungs became less active and had a rise in glutathione during NAC treatment. Lung function didn't improve, which didn't surprise the researchers because the test was so short.
Next Steps
Those findings could be an important cellular link in understanding cystic fibrosis, write the researchers.
However, they note that they didn't test NAC's effectiveness and long-term safety. That work will come later.
NAC's structure "prevents proper quality control of most commercial formulations available over the counter," the researchers caution. They call for "carefully designed and controlled clinical studies" of NAC and cystic fibrosis.
Try this article, it's what originally got me thinking about taking it.
<a target=_blank class=ftalternatingbarlinklarge href="http://www.webmd.com/content/article/120/113562.htm">NAC Article</a>
March 14, 2006 -- In its first test against cystic fibrosis, high doses of a drug called NAC were 'safe' for short-term use, researchers report.
NAC, or N-acetylcysteine, has a "proven safety record over long-term use at high doses in several chronic inflammatory conditions and has minimal interaction with other drugs," write the researchers. They included Rabindra Tirouvanziam, PhD, of Stanford University.
However, they aren't recommending NAC for cystic fibrosis. NAC needs more testing as a cystic fibrosis treatment, note Tirouvanziam and colleagues.
"It is important to warn patients against uncontrolled use of the drug," they write in Proceedings of the National Academy of Sciences.
Why NAC?
In their report, the researchers trace their interest in NAC as a cystic fibrosis treatment.
Cystic fibrosis is a chronic, progressive condition that primarily affects the body's respiratory and digestive systems. It is due to a gene defect that causes the body to produce abnormally thick mucous.
That mucous clogs the lungs, leading to recurring infections of the lungs and sinuses. It also makes breathing difficult.
In cystic fibrosis, the lungs have an unusually high number of neutrophils, a type of white blood cell. Those neutrophils prompt inflammation, setting the stage for more damage.
Tirouvanziam and colleagues noticed that neutrophils in cystic fibrosis patients were short on an antioxidant called glutathione. NAC is a building block for glutathione. The scientists wanted to see if NAC could boost glutathione, which in turn might curb lung inflammation.
Drug's First Test for Cystic Fibrosis
The researchers checked NAC's short-term safety. Participants were 18 children with cystic fibrosis who were at least 10 years old.
Every day for four weeks, the patients took three high doses of NAC by mouth. "We used doses in excess of 1.8 grams per day, which had never been used in [cystic fibrosis patients] before," write Tirouvanziam and colleagues.
The treatment appeared to be safe. The scientists note "very mild and infrequent drug-related adverse effects" including heartburn, nausea, and a bad taste from the drug.
Especially in patients with lung inflammation before taking NAC, neutrophils in the lungs became less active and had a rise in glutathione during NAC treatment. Lung function didn't improve, which didn't surprise the researchers because the test was so short.
Next Steps
Those findings could be an important cellular link in understanding cystic fibrosis, write the researchers.
However, they note that they didn't test NAC's effectiveness and long-term safety. That work will come later.
NAC's structure "prevents proper quality control of most commercial formulations available over the counter," the researchers caution. They call for "carefully designed and controlled clinical studies" of NAC and cystic fibrosis.
<a target=_blank class=ftalternatingbarlinklarge href="http://www.webmd.com/content/article/120/113562.htm">NAC Article</a>
March 14, 2006 -- In its first test against cystic fibrosis, high doses of a drug called NAC were 'safe' for short-term use, researchers report.
NAC, or N-acetylcysteine, has a "proven safety record over long-term use at high doses in several chronic inflammatory conditions and has minimal interaction with other drugs," write the researchers. They included Rabindra Tirouvanziam, PhD, of Stanford University.
However, they aren't recommending NAC for cystic fibrosis. NAC needs more testing as a cystic fibrosis treatment, note Tirouvanziam and colleagues.
"It is important to warn patients against uncontrolled use of the drug," they write in Proceedings of the National Academy of Sciences.
Why NAC?
In their report, the researchers trace their interest in NAC as a cystic fibrosis treatment.
Cystic fibrosis is a chronic, progressive condition that primarily affects the body's respiratory and digestive systems. It is due to a gene defect that causes the body to produce abnormally thick mucous.
That mucous clogs the lungs, leading to recurring infections of the lungs and sinuses. It also makes breathing difficult.
In cystic fibrosis, the lungs have an unusually high number of neutrophils, a type of white blood cell. Those neutrophils prompt inflammation, setting the stage for more damage.
Tirouvanziam and colleagues noticed that neutrophils in cystic fibrosis patients were short on an antioxidant called glutathione. NAC is a building block for glutathione. The scientists wanted to see if NAC could boost glutathione, which in turn might curb lung inflammation.
Drug's First Test for Cystic Fibrosis
The researchers checked NAC's short-term safety. Participants were 18 children with cystic fibrosis who were at least 10 years old.
Every day for four weeks, the patients took three high doses of NAC by mouth. "We used doses in excess of 1.8 grams per day, which had never been used in [cystic fibrosis patients] before," write Tirouvanziam and colleagues.
The treatment appeared to be safe. The scientists note "very mild and infrequent drug-related adverse effects" including heartburn, nausea, and a bad taste from the drug.
Especially in patients with lung inflammation before taking NAC, neutrophils in the lungs became less active and had a rise in glutathione during NAC treatment. Lung function didn't improve, which didn't surprise the researchers because the test was so short.
Next Steps
Those findings could be an important cellular link in understanding cystic fibrosis, write the researchers.
However, they note that they didn't test NAC's effectiveness and long-term safety. That work will come later.
NAC's structure "prevents proper quality control of most commercial formulations available over the counter," the researchers caution. They call for "carefully designed and controlled clinical studies" of NAC and cystic fibrosis.
Try this article, it's what originally got me thinking about taking it.
<a target=_blank class=ftalternatingbarlinklarge href="http://www.webmd.com/content/article/120/113562.htm">NAC Article</a>
March 14, 2006 -- In its first test against cystic fibrosis, high doses of a drug called NAC were 'safe' for short-term use, researchers report.
NAC, or N-acetylcysteine, has a "proven safety record over long-term use at high doses in several chronic inflammatory conditions and has minimal interaction with other drugs," write the researchers. They included Rabindra Tirouvanziam, PhD, of Stanford University.
However, they aren't recommending NAC for cystic fibrosis. NAC needs more testing as a cystic fibrosis treatment, note Tirouvanziam and colleagues.
"It is important to warn patients against uncontrolled use of the drug," they write in Proceedings of the National Academy of Sciences.
Why NAC?
In their report, the researchers trace their interest in NAC as a cystic fibrosis treatment.
Cystic fibrosis is a chronic, progressive condition that primarily affects the body's respiratory and digestive systems. It is due to a gene defect that causes the body to produce abnormally thick mucous.
That mucous clogs the lungs, leading to recurring infections of the lungs and sinuses. It also makes breathing difficult.
In cystic fibrosis, the lungs have an unusually high number of neutrophils, a type of white blood cell. Those neutrophils prompt inflammation, setting the stage for more damage.
Tirouvanziam and colleagues noticed that neutrophils in cystic fibrosis patients were short on an antioxidant called glutathione. NAC is a building block for glutathione. The scientists wanted to see if NAC could boost glutathione, which in turn might curb lung inflammation.
Drug's First Test for Cystic Fibrosis
The researchers checked NAC's short-term safety. Participants were 18 children with cystic fibrosis who were at least 10 years old.
Every day for four weeks, the patients took three high doses of NAC by mouth. "We used doses in excess of 1.8 grams per day, which had never been used in [cystic fibrosis patients] before," write Tirouvanziam and colleagues.
The treatment appeared to be safe. The scientists note "very mild and infrequent drug-related adverse effects" including heartburn, nausea, and a bad taste from the drug.
Especially in patients with lung inflammation before taking NAC, neutrophils in the lungs became less active and had a rise in glutathione during NAC treatment. Lung function didn't improve, which didn't surprise the researchers because the test was so short.
Next Steps
Those findings could be an important cellular link in understanding cystic fibrosis, write the researchers.
However, they note that they didn't test NAC's effectiveness and long-term safety. That work will come later.
NAC's structure "prevents proper quality control of most commercial formulations available over the counter," the researchers caution. They call for "carefully designed and controlled clinical studies" of NAC and cystic fibrosis.
<a target=_blank class=ftalternatingbarlinklarge href="http://www.webmd.com/content/article/120/113562.htm">NAC Article</a>
March 14, 2006 -- In its first test against cystic fibrosis, high doses of a drug called NAC were 'safe' for short-term use, researchers report.
NAC, or N-acetylcysteine, has a "proven safety record over long-term use at high doses in several chronic inflammatory conditions and has minimal interaction with other drugs," write the researchers. They included Rabindra Tirouvanziam, PhD, of Stanford University.
However, they aren't recommending NAC for cystic fibrosis. NAC needs more testing as a cystic fibrosis treatment, note Tirouvanziam and colleagues.
"It is important to warn patients against uncontrolled use of the drug," they write in Proceedings of the National Academy of Sciences.
Why NAC?
In their report, the researchers trace their interest in NAC as a cystic fibrosis treatment.
Cystic fibrosis is a chronic, progressive condition that primarily affects the body's respiratory and digestive systems. It is due to a gene defect that causes the body to produce abnormally thick mucous.
That mucous clogs the lungs, leading to recurring infections of the lungs and sinuses. It also makes breathing difficult.
In cystic fibrosis, the lungs have an unusually high number of neutrophils, a type of white blood cell. Those neutrophils prompt inflammation, setting the stage for more damage.
Tirouvanziam and colleagues noticed that neutrophils in cystic fibrosis patients were short on an antioxidant called glutathione. NAC is a building block for glutathione. The scientists wanted to see if NAC could boost glutathione, which in turn might curb lung inflammation.
Drug's First Test for Cystic Fibrosis
The researchers checked NAC's short-term safety. Participants were 18 children with cystic fibrosis who were at least 10 years old.
Every day for four weeks, the patients took three high doses of NAC by mouth. "We used doses in excess of 1.8 grams per day, which had never been used in [cystic fibrosis patients] before," write Tirouvanziam and colleagues.
The treatment appeared to be safe. The scientists note "very mild and infrequent drug-related adverse effects" including heartburn, nausea, and a bad taste from the drug.
Especially in patients with lung inflammation before taking NAC, neutrophils in the lungs became less active and had a rise in glutathione during NAC treatment. Lung function didn't improve, which didn't surprise the researchers because the test was so short.
Next Steps
Those findings could be an important cellular link in understanding cystic fibrosis, write the researchers.
However, they note that they didn't test NAC's effectiveness and long-term safety. That work will come later.
NAC's structure "prevents proper quality control of most commercial formulations available over the counter," the researchers caution. They call for "carefully designed and controlled clinical studies" of NAC and cystic fibrosis.
Here's the whole article: I highlighted sections I thought were interesting.
For Release: March 14, 2006
STANFORD, Calif-- <b>A compound that has shown promise in combating some chronic inflammatory diseases may be useful in preserving lung function in cystic fibrosis patients, say researchers at the Stanford University School of Medicine and Lucile Packard Children's Hospital. The researchers have recently completed a Phase 1 clinical trial of the compound and have begun a Phase 2 clinical trial to test its efficacy in a larger number of patients.</b>
"These people basically destroy their lungs through ongoing inflammation and infection," said research associate Rabindra Tirouvanziam, PhD, the first author of the study. "We're optimistic that, with further research, we may be able to inhibit this process." The findings were published in the early online edition of the Proceedings of the National Academy of Sciences on March 13.
Cystic fibrosis is the most common disease caused by a recessive gene in Caucasians; about one in 2,500 infants are affected. Although the disorder was formerly fatal in childhood, the expected lifespan of sufferers has been increasing steadily with the advent of new treatments. But the attendant lung inflammation and scarring still results in the loss of three to four percent of lung function every year.
"If we can make any headway into relieving or cutting back on the amount of inflammation on a day-to-day basis, we could impact their health in a big way," said Carol Conrad, MD, a pediatric pulmonologist at Packard Children's and an assistant professor of pediatrics at Stanford medical school. Ibuprofen can slow the decline, but long-term use at high doses can negatively affect the kidney and gastrointestinal tract as well as other organs.
The researchers gave 18 cystic fibrosis patients, including seven children ten years or older, high oral doses of a compound called N-acetylcysteine, or NAC, for four weeks. NAC is utilized by the body to make glutathione, the body's main naturally occurring anti-oxidant. It has been tested with some success in people with other inflammatory lung problems, including chronic bronchitis, chronic obstructive pulmonary disease and a condition called idiopathic pulmonary fibrosis.
People with cystic fibrosis have a defective or missing version of a protein responsible for, among other things, releasing glutathione into the extracellular spaces. This problem is particularly acute in the airways, where bacteria accumulate. White blood cells called neutrophils are summoned to the lungs to fight infection but stumble into a biological ambush. Although it isn't clear why, the arriving neutrophils are doomed. They act strangely and begin to die.
Before they expire, they secrete a factor called interleukin-8, which recruits yet more neutrophils to the scene. They also pepper the surrounding cells with high levels of oxidants and other tissue-damaging molecules, and, in a final blow, release DNA and a protein called elastase, both of which increase the sticky, disease-trapping properties of the airway mucous. It's a vicious, viscous circle that leaves sufferers gasping for breath and prone to infection.
NAC treatment throws a wrench into this process. The researchers found that circulating neutrophils from cystic fibrosis patients contained significantly less glutathione than did neutrophils from healthy patients. They theorize that neutrophils must depend on cells around them to maintain their glutathione levels. In cystic fibrosis patients, that help is not forthcoming, and the neutrophils do not function properly.
<b>Four weeks of oral NAC treatment not only increased the amount of glutathione in circulating neutrophils, it also decreased the number of neutrophils and the levels of elastase and interleukin-8 in the airways. It was safe and well tolerated by the trial participants, who said they felt better during the study.</b>
<b>"The amount of decrease in the inflammatory markers we saw in this preliminary trial was rather astounding," said Conrad. "Many of those who had just completed the study asked if they could continue the treatment." The researchers recently began a 24-week placebo-controlled Phase II trial of NAC in cystic fibrosis patients to confirm their findings. Enrollment for that trial is now closed.</b>
Despite the improvement and the relatively safe profile of NAC, Conrad and Tirouvanziam strongly caution cystic fibrosis patients against self-medicating with NAC or any other drug. Although NAC can sometimes be found as a food supplement, many of these formulations contain little or no active compound, and some even contain a form of NAC that is potentially harmful to cystic fibrosis patients. The NAC that was used in this study is specially formulated for medical use by a Canadian company and is not licensed for sale in the United States.
Other Stanford and Packard Children's researchers involved in the research include Leonore Herzenberg, PhD; Leonard Herzenberg, PhD, and Richard Moss, MD. Teodoro Bottiglieri, PhD, of Baylor's Institute for Metabolic Diseases also contributed to the study. The Stanford researchers are listed as inventors on a provisional patent application covering NAC as a therapeutic agent for cystic fibrosis. Two of the authors (Leonore and Leonard Herzenberg) hold a small amount of equity in BioAdvantex (Mississauga, ONT, Canada), which sells European GMP NAC and provided this NAC for the current
study.
For Release: March 14, 2006
STANFORD, Calif-- <b>A compound that has shown promise in combating some chronic inflammatory diseases may be useful in preserving lung function in cystic fibrosis patients, say researchers at the Stanford University School of Medicine and Lucile Packard Children's Hospital. The researchers have recently completed a Phase 1 clinical trial of the compound and have begun a Phase 2 clinical trial to test its efficacy in a larger number of patients.</b>
"These people basically destroy their lungs through ongoing inflammation and infection," said research associate Rabindra Tirouvanziam, PhD, the first author of the study. "We're optimistic that, with further research, we may be able to inhibit this process." The findings were published in the early online edition of the Proceedings of the National Academy of Sciences on March 13.
Cystic fibrosis is the most common disease caused by a recessive gene in Caucasians; about one in 2,500 infants are affected. Although the disorder was formerly fatal in childhood, the expected lifespan of sufferers has been increasing steadily with the advent of new treatments. But the attendant lung inflammation and scarring still results in the loss of three to four percent of lung function every year.
"If we can make any headway into relieving or cutting back on the amount of inflammation on a day-to-day basis, we could impact their health in a big way," said Carol Conrad, MD, a pediatric pulmonologist at Packard Children's and an assistant professor of pediatrics at Stanford medical school. Ibuprofen can slow the decline, but long-term use at high doses can negatively affect the kidney and gastrointestinal tract as well as other organs.
The researchers gave 18 cystic fibrosis patients, including seven children ten years or older, high oral doses of a compound called N-acetylcysteine, or NAC, for four weeks. NAC is utilized by the body to make glutathione, the body's main naturally occurring anti-oxidant. It has been tested with some success in people with other inflammatory lung problems, including chronic bronchitis, chronic obstructive pulmonary disease and a condition called idiopathic pulmonary fibrosis.
People with cystic fibrosis have a defective or missing version of a protein responsible for, among other things, releasing glutathione into the extracellular spaces. This problem is particularly acute in the airways, where bacteria accumulate. White blood cells called neutrophils are summoned to the lungs to fight infection but stumble into a biological ambush. Although it isn't clear why, the arriving neutrophils are doomed. They act strangely and begin to die.
Before they expire, they secrete a factor called interleukin-8, which recruits yet more neutrophils to the scene. They also pepper the surrounding cells with high levels of oxidants and other tissue-damaging molecules, and, in a final blow, release DNA and a protein called elastase, both of which increase the sticky, disease-trapping properties of the airway mucous. It's a vicious, viscous circle that leaves sufferers gasping for breath and prone to infection.
NAC treatment throws a wrench into this process. The researchers found that circulating neutrophils from cystic fibrosis patients contained significantly less glutathione than did neutrophils from healthy patients. They theorize that neutrophils must depend on cells around them to maintain their glutathione levels. In cystic fibrosis patients, that help is not forthcoming, and the neutrophils do not function properly.
<b>Four weeks of oral NAC treatment not only increased the amount of glutathione in circulating neutrophils, it also decreased the number of neutrophils and the levels of elastase and interleukin-8 in the airways. It was safe and well tolerated by the trial participants, who said they felt better during the study.</b>
<b>"The amount of decrease in the inflammatory markers we saw in this preliminary trial was rather astounding," said Conrad. "Many of those who had just completed the study asked if they could continue the treatment." The researchers recently began a 24-week placebo-controlled Phase II trial of NAC in cystic fibrosis patients to confirm their findings. Enrollment for that trial is now closed.</b>
Despite the improvement and the relatively safe profile of NAC, Conrad and Tirouvanziam strongly caution cystic fibrosis patients against self-medicating with NAC or any other drug. Although NAC can sometimes be found as a food supplement, many of these formulations contain little or no active compound, and some even contain a form of NAC that is potentially harmful to cystic fibrosis patients. The NAC that was used in this study is specially formulated for medical use by a Canadian company and is not licensed for sale in the United States.
Other Stanford and Packard Children's researchers involved in the research include Leonore Herzenberg, PhD; Leonard Herzenberg, PhD, and Richard Moss, MD. Teodoro Bottiglieri, PhD, of Baylor's Institute for Metabolic Diseases also contributed to the study. The Stanford researchers are listed as inventors on a provisional patent application covering NAC as a therapeutic agent for cystic fibrosis. Two of the authors (Leonore and Leonard Herzenberg) hold a small amount of equity in BioAdvantex (Mississauga, ONT, Canada), which sells European GMP NAC and provided this NAC for the current
study.
Here's the whole article: I highlighted sections I thought were interesting.
For Release: March 14, 2006
STANFORD, Calif-- <b>A compound that has shown promise in combating some chronic inflammatory diseases may be useful in preserving lung function in cystic fibrosis patients, say researchers at the Stanford University School of Medicine and Lucile Packard Children's Hospital. The researchers have recently completed a Phase 1 clinical trial of the compound and have begun a Phase 2 clinical trial to test its efficacy in a larger number of patients.</b>
"These people basically destroy their lungs through ongoing inflammation and infection," said research associate Rabindra Tirouvanziam, PhD, the first author of the study. "We're optimistic that, with further research, we may be able to inhibit this process." The findings were published in the early online edition of the Proceedings of the National Academy of Sciences on March 13.
Cystic fibrosis is the most common disease caused by a recessive gene in Caucasians; about one in 2,500 infants are affected. Although the disorder was formerly fatal in childhood, the expected lifespan of sufferers has been increasing steadily with the advent of new treatments. But the attendant lung inflammation and scarring still results in the loss of three to four percent of lung function every year.
"If we can make any headway into relieving or cutting back on the amount of inflammation on a day-to-day basis, we could impact their health in a big way," said Carol Conrad, MD, a pediatric pulmonologist at Packard Children's and an assistant professor of pediatrics at Stanford medical school. Ibuprofen can slow the decline, but long-term use at high doses can negatively affect the kidney and gastrointestinal tract as well as other organs.
The researchers gave 18 cystic fibrosis patients, including seven children ten years or older, high oral doses of a compound called N-acetylcysteine, or NAC, for four weeks. NAC is utilized by the body to make glutathione, the body's main naturally occurring anti-oxidant. It has been tested with some success in people with other inflammatory lung problems, including chronic bronchitis, chronic obstructive pulmonary disease and a condition called idiopathic pulmonary fibrosis.
People with cystic fibrosis have a defective or missing version of a protein responsible for, among other things, releasing glutathione into the extracellular spaces. This problem is particularly acute in the airways, where bacteria accumulate. White blood cells called neutrophils are summoned to the lungs to fight infection but stumble into a biological ambush. Although it isn't clear why, the arriving neutrophils are doomed. They act strangely and begin to die.
Before they expire, they secrete a factor called interleukin-8, which recruits yet more neutrophils to the scene. They also pepper the surrounding cells with high levels of oxidants and other tissue-damaging molecules, and, in a final blow, release DNA and a protein called elastase, both of which increase the sticky, disease-trapping properties of the airway mucous. It's a vicious, viscous circle that leaves sufferers gasping for breath and prone to infection.
NAC treatment throws a wrench into this process. The researchers found that circulating neutrophils from cystic fibrosis patients contained significantly less glutathione than did neutrophils from healthy patients. They theorize that neutrophils must depend on cells around them to maintain their glutathione levels. In cystic fibrosis patients, that help is not forthcoming, and the neutrophils do not function properly.
<b>Four weeks of oral NAC treatment not only increased the amount of glutathione in circulating neutrophils, it also decreased the number of neutrophils and the levels of elastase and interleukin-8 in the airways. It was safe and well tolerated by the trial participants, who said they felt better during the study.</b>
<b>"The amount of decrease in the inflammatory markers we saw in this preliminary trial was rather astounding," said Conrad. "Many of those who had just completed the study asked if they could continue the treatment." The researchers recently began a 24-week placebo-controlled Phase II trial of NAC in cystic fibrosis patients to confirm their findings. Enrollment for that trial is now closed.</b>
Despite the improvement and the relatively safe profile of NAC, Conrad and Tirouvanziam strongly caution cystic fibrosis patients against self-medicating with NAC or any other drug. Although NAC can sometimes be found as a food supplement, many of these formulations contain little or no active compound, and some even contain a form of NAC that is potentially harmful to cystic fibrosis patients. The NAC that was used in this study is specially formulated for medical use by a Canadian company and is not licensed for sale in the United States.
Other Stanford and Packard Children's researchers involved in the research include Leonore Herzenberg, PhD; Leonard Herzenberg, PhD, and Richard Moss, MD. Teodoro Bottiglieri, PhD, of Baylor's Institute for Metabolic Diseases also contributed to the study. The Stanford researchers are listed as inventors on a provisional patent application covering NAC as a therapeutic agent for cystic fibrosis. Two of the authors (Leonore and Leonard Herzenberg) hold a small amount of equity in BioAdvantex (Mississauga, ONT, Canada), which sells European GMP NAC and provided this NAC for the current
study.
For Release: March 14, 2006
STANFORD, Calif-- <b>A compound that has shown promise in combating some chronic inflammatory diseases may be useful in preserving lung function in cystic fibrosis patients, say researchers at the Stanford University School of Medicine and Lucile Packard Children's Hospital. The researchers have recently completed a Phase 1 clinical trial of the compound and have begun a Phase 2 clinical trial to test its efficacy in a larger number of patients.</b>
"These people basically destroy their lungs through ongoing inflammation and infection," said research associate Rabindra Tirouvanziam, PhD, the first author of the study. "We're optimistic that, with further research, we may be able to inhibit this process." The findings were published in the early online edition of the Proceedings of the National Academy of Sciences on March 13.
Cystic fibrosis is the most common disease caused by a recessive gene in Caucasians; about one in 2,500 infants are affected. Although the disorder was formerly fatal in childhood, the expected lifespan of sufferers has been increasing steadily with the advent of new treatments. But the attendant lung inflammation and scarring still results in the loss of three to four percent of lung function every year.
"If we can make any headway into relieving or cutting back on the amount of inflammation on a day-to-day basis, we could impact their health in a big way," said Carol Conrad, MD, a pediatric pulmonologist at Packard Children's and an assistant professor of pediatrics at Stanford medical school. Ibuprofen can slow the decline, but long-term use at high doses can negatively affect the kidney and gastrointestinal tract as well as other organs.
The researchers gave 18 cystic fibrosis patients, including seven children ten years or older, high oral doses of a compound called N-acetylcysteine, or NAC, for four weeks. NAC is utilized by the body to make glutathione, the body's main naturally occurring anti-oxidant. It has been tested with some success in people with other inflammatory lung problems, including chronic bronchitis, chronic obstructive pulmonary disease and a condition called idiopathic pulmonary fibrosis.
People with cystic fibrosis have a defective or missing version of a protein responsible for, among other things, releasing glutathione into the extracellular spaces. This problem is particularly acute in the airways, where bacteria accumulate. White blood cells called neutrophils are summoned to the lungs to fight infection but stumble into a biological ambush. Although it isn't clear why, the arriving neutrophils are doomed. They act strangely and begin to die.
Before they expire, they secrete a factor called interleukin-8, which recruits yet more neutrophils to the scene. They also pepper the surrounding cells with high levels of oxidants and other tissue-damaging molecules, and, in a final blow, release DNA and a protein called elastase, both of which increase the sticky, disease-trapping properties of the airway mucous. It's a vicious, viscous circle that leaves sufferers gasping for breath and prone to infection.
NAC treatment throws a wrench into this process. The researchers found that circulating neutrophils from cystic fibrosis patients contained significantly less glutathione than did neutrophils from healthy patients. They theorize that neutrophils must depend on cells around them to maintain their glutathione levels. In cystic fibrosis patients, that help is not forthcoming, and the neutrophils do not function properly.
<b>Four weeks of oral NAC treatment not only increased the amount of glutathione in circulating neutrophils, it also decreased the number of neutrophils and the levels of elastase and interleukin-8 in the airways. It was safe and well tolerated by the trial participants, who said they felt better during the study.</b>
<b>"The amount of decrease in the inflammatory markers we saw in this preliminary trial was rather astounding," said Conrad. "Many of those who had just completed the study asked if they could continue the treatment." The researchers recently began a 24-week placebo-controlled Phase II trial of NAC in cystic fibrosis patients to confirm their findings. Enrollment for that trial is now closed.</b>
Despite the improvement and the relatively safe profile of NAC, Conrad and Tirouvanziam strongly caution cystic fibrosis patients against self-medicating with NAC or any other drug. Although NAC can sometimes be found as a food supplement, many of these formulations contain little or no active compound, and some even contain a form of NAC that is potentially harmful to cystic fibrosis patients. The NAC that was used in this study is specially formulated for medical use by a Canadian company and is not licensed for sale in the United States.
Other Stanford and Packard Children's researchers involved in the research include Leonore Herzenberg, PhD; Leonard Herzenberg, PhD, and Richard Moss, MD. Teodoro Bottiglieri, PhD, of Baylor's Institute for Metabolic Diseases also contributed to the study. The Stanford researchers are listed as inventors on a provisional patent application covering NAC as a therapeutic agent for cystic fibrosis. Two of the authors (Leonore and Leonard Herzenberg) hold a small amount of equity in BioAdvantex (Mississauga, ONT, Canada), which sells European GMP NAC and provided this NAC for the current
study.
Here's the whole article: I highlighted sections I thought were interesting.
For Release: March 14, 2006
STANFORD, Calif-- <b>A compound that has shown promise in combating some chronic inflammatory diseases may be useful in preserving lung function in cystic fibrosis patients, say researchers at the Stanford University School of Medicine and Lucile Packard Children's Hospital. The researchers have recently completed a Phase 1 clinical trial of the compound and have begun a Phase 2 clinical trial to test its efficacy in a larger number of patients.</b>
"These people basically destroy their lungs through ongoing inflammation and infection," said research associate Rabindra Tirouvanziam, PhD, the first author of the study. "We're optimistic that, with further research, we may be able to inhibit this process." The findings were published in the early online edition of the Proceedings of the National Academy of Sciences on March 13.
Cystic fibrosis is the most common disease caused by a recessive gene in Caucasians; about one in 2,500 infants are affected. Although the disorder was formerly fatal in childhood, the expected lifespan of sufferers has been increasing steadily with the advent of new treatments. But the attendant lung inflammation and scarring still results in the loss of three to four percent of lung function every year.
"If we can make any headway into relieving or cutting back on the amount of inflammation on a day-to-day basis, we could impact their health in a big way," said Carol Conrad, MD, a pediatric pulmonologist at Packard Children's and an assistant professor of pediatrics at Stanford medical school. Ibuprofen can slow the decline, but long-term use at high doses can negatively affect the kidney and gastrointestinal tract as well as other organs.
The researchers gave 18 cystic fibrosis patients, including seven children ten years or older, high oral doses of a compound called N-acetylcysteine, or NAC, for four weeks. NAC is utilized by the body to make glutathione, the body's main naturally occurring anti-oxidant. It has been tested with some success in people with other inflammatory lung problems, including chronic bronchitis, chronic obstructive pulmonary disease and a condition called idiopathic pulmonary fibrosis.
People with cystic fibrosis have a defective or missing version of a protein responsible for, among other things, releasing glutathione into the extracellular spaces. This problem is particularly acute in the airways, where bacteria accumulate. White blood cells called neutrophils are summoned to the lungs to fight infection but stumble into a biological ambush. Although it isn't clear why, the arriving neutrophils are doomed. They act strangely and begin to die.
Before they expire, they secrete a factor called interleukin-8, which recruits yet more neutrophils to the scene. They also pepper the surrounding cells with high levels of oxidants and other tissue-damaging molecules, and, in a final blow, release DNA and a protein called elastase, both of which increase the sticky, disease-trapping properties of the airway mucous. It's a vicious, viscous circle that leaves sufferers gasping for breath and prone to infection.
NAC treatment throws a wrench into this process. The researchers found that circulating neutrophils from cystic fibrosis patients contained significantly less glutathione than did neutrophils from healthy patients. They theorize that neutrophils must depend on cells around them to maintain their glutathione levels. In cystic fibrosis patients, that help is not forthcoming, and the neutrophils do not function properly.
<b>Four weeks of oral NAC treatment not only increased the amount of glutathione in circulating neutrophils, it also decreased the number of neutrophils and the levels of elastase and interleukin-8 in the airways. It was safe and well tolerated by the trial participants, who said they felt better during the study.</b>
<b>"The amount of decrease in the inflammatory markers we saw in this preliminary trial was rather astounding," said Conrad. "Many of those who had just completed the study asked if they could continue the treatment." The researchers recently began a 24-week placebo-controlled Phase II trial of NAC in cystic fibrosis patients to confirm their findings. Enrollment for that trial is now closed.</b>
Despite the improvement and the relatively safe profile of NAC, Conrad and Tirouvanziam strongly caution cystic fibrosis patients against self-medicating with NAC or any other drug. Although NAC can sometimes be found as a food supplement, many of these formulations contain little or no active compound, and some even contain a form of NAC that is potentially harmful to cystic fibrosis patients. The NAC that was used in this study is specially formulated for medical use by a Canadian company and is not licensed for sale in the United States.
Other Stanford and Packard Children's researchers involved in the research include Leonore Herzenberg, PhD; Leonard Herzenberg, PhD, and Richard Moss, MD. Teodoro Bottiglieri, PhD, of Baylor's Institute for Metabolic Diseases also contributed to the study. The Stanford researchers are listed as inventors on a provisional patent application covering NAC as a therapeutic agent for cystic fibrosis. Two of the authors (Leonore and Leonard Herzenberg) hold a small amount of equity in BioAdvantex (Mississauga, ONT, Canada), which sells European GMP NAC and provided this NAC for the current
study.
For Release: March 14, 2006
STANFORD, Calif-- <b>A compound that has shown promise in combating some chronic inflammatory diseases may be useful in preserving lung function in cystic fibrosis patients, say researchers at the Stanford University School of Medicine and Lucile Packard Children's Hospital. The researchers have recently completed a Phase 1 clinical trial of the compound and have begun a Phase 2 clinical trial to test its efficacy in a larger number of patients.</b>
"These people basically destroy their lungs through ongoing inflammation and infection," said research associate Rabindra Tirouvanziam, PhD, the first author of the study. "We're optimistic that, with further research, we may be able to inhibit this process." The findings were published in the early online edition of the Proceedings of the National Academy of Sciences on March 13.
Cystic fibrosis is the most common disease caused by a recessive gene in Caucasians; about one in 2,500 infants are affected. Although the disorder was formerly fatal in childhood, the expected lifespan of sufferers has been increasing steadily with the advent of new treatments. But the attendant lung inflammation and scarring still results in the loss of three to four percent of lung function every year.
"If we can make any headway into relieving or cutting back on the amount of inflammation on a day-to-day basis, we could impact their health in a big way," said Carol Conrad, MD, a pediatric pulmonologist at Packard Children's and an assistant professor of pediatrics at Stanford medical school. Ibuprofen can slow the decline, but long-term use at high doses can negatively affect the kidney and gastrointestinal tract as well as other organs.
The researchers gave 18 cystic fibrosis patients, including seven children ten years or older, high oral doses of a compound called N-acetylcysteine, or NAC, for four weeks. NAC is utilized by the body to make glutathione, the body's main naturally occurring anti-oxidant. It has been tested with some success in people with other inflammatory lung problems, including chronic bronchitis, chronic obstructive pulmonary disease and a condition called idiopathic pulmonary fibrosis.
People with cystic fibrosis have a defective or missing version of a protein responsible for, among other things, releasing glutathione into the extracellular spaces. This problem is particularly acute in the airways, where bacteria accumulate. White blood cells called neutrophils are summoned to the lungs to fight infection but stumble into a biological ambush. Although it isn't clear why, the arriving neutrophils are doomed. They act strangely and begin to die.
Before they expire, they secrete a factor called interleukin-8, which recruits yet more neutrophils to the scene. They also pepper the surrounding cells with high levels of oxidants and other tissue-damaging molecules, and, in a final blow, release DNA and a protein called elastase, both of which increase the sticky, disease-trapping properties of the airway mucous. It's a vicious, viscous circle that leaves sufferers gasping for breath and prone to infection.
NAC treatment throws a wrench into this process. The researchers found that circulating neutrophils from cystic fibrosis patients contained significantly less glutathione than did neutrophils from healthy patients. They theorize that neutrophils must depend on cells around them to maintain their glutathione levels. In cystic fibrosis patients, that help is not forthcoming, and the neutrophils do not function properly.
<b>Four weeks of oral NAC treatment not only increased the amount of glutathione in circulating neutrophils, it also decreased the number of neutrophils and the levels of elastase and interleukin-8 in the airways. It was safe and well tolerated by the trial participants, who said they felt better during the study.</b>
<b>"The amount of decrease in the inflammatory markers we saw in this preliminary trial was rather astounding," said Conrad. "Many of those who had just completed the study asked if they could continue the treatment." The researchers recently began a 24-week placebo-controlled Phase II trial of NAC in cystic fibrosis patients to confirm their findings. Enrollment for that trial is now closed.</b>
Despite the improvement and the relatively safe profile of NAC, Conrad and Tirouvanziam strongly caution cystic fibrosis patients against self-medicating with NAC or any other drug. Although NAC can sometimes be found as a food supplement, many of these formulations contain little or no active compound, and some even contain a form of NAC that is potentially harmful to cystic fibrosis patients. The NAC that was used in this study is specially formulated for medical use by a Canadian company and is not licensed for sale in the United States.
Other Stanford and Packard Children's researchers involved in the research include Leonore Herzenberg, PhD; Leonard Herzenberg, PhD, and Richard Moss, MD. Teodoro Bottiglieri, PhD, of Baylor's Institute for Metabolic Diseases also contributed to the study. The Stanford researchers are listed as inventors on a provisional patent application covering NAC as a therapeutic agent for cystic fibrosis. Two of the authors (Leonore and Leonard Herzenberg) hold a small amount of equity in BioAdvantex (Mississauga, ONT, Canada), which sells European GMP NAC and provided this NAC for the current
study.
I personally use both....mainly because the glutathione I take comes with NAC in the capsule. If I had the time, I think I would use immunocal to boost gsh instead of NAC because it is proven to raise glutathione levels with no adverse reactions...no heart burn, no liver enzyme issues. Larry Lands, a cf researcher in Canada, who was asked to join 10 anti-oxidant researchers around the world who specialize in cf and pulmonary issues, believes it is byfar the safest and he has been doing actual studies with it much longer than the Stanford researchers have been using high dose NAC. NAC has a long history of use but it is contra-indicated in many issues including people with poor liver function....umm, hello, that is more than 13% of cf patients. Also, if you look into the actual research by the Stanford researcher Rabindra Tirouvanziam, there is evidence to suggest that the problem with just NAC is that it produces gsh...but this researcher concludes that once produced the defect in the cftr channel does not allow the gsh to travel to the outside cell wall. Basically, you are raising your glutathione, but it can't go anywhere because the channel is broken. To quote the NAC research study....
<b> People with cystic fibrosis have a defective or missing version of a protein responsible for, among other things, releasing glutathione into the extracellular spaces. This problem is particularly acute in the airways, where bacteria accumulate. White blood cells called neutrophils are summoned to the lungs to fight infection but stumble into a biological ambush. Although it isn't clear why, the arriving neutrophils are doomed. They act strangely and begin to die.
</b>
The true question is how do you get the glutathione to extra-cellular spaces? The answer is to supplement glutathione....
It is astounding that this debate is still going on in the research community.
<b> People with cystic fibrosis have a defective or missing version of a protein responsible for, among other things, releasing glutathione into the extracellular spaces. This problem is particularly acute in the airways, where bacteria accumulate. White blood cells called neutrophils are summoned to the lungs to fight infection but stumble into a biological ambush. Although it isn't clear why, the arriving neutrophils are doomed. They act strangely and begin to die.
</b>
The true question is how do you get the glutathione to extra-cellular spaces? The answer is to supplement glutathione....
It is astounding that this debate is still going on in the research community.
I personally use both....mainly because the glutathione I take comes with NAC in the capsule. If I had the time, I think I would use immunocal to boost gsh instead of NAC because it is proven to raise glutathione levels with no adverse reactions...no heart burn, no liver enzyme issues. Larry Lands, a cf researcher in Canada, who was asked to join 10 anti-oxidant researchers around the world who specialize in cf and pulmonary issues, believes it is byfar the safest and he has been doing actual studies with it much longer than the Stanford researchers have been using high dose NAC. NAC has a long history of use but it is contra-indicated in many issues including people with poor liver function....umm, hello, that is more than 13% of cf patients. Also, if you look into the actual research by the Stanford researcher Rabindra Tirouvanziam, there is evidence to suggest that the problem with just NAC is that it produces gsh...but this researcher concludes that once produced the defect in the cftr channel does not allow the gsh to travel to the outside cell wall. Basically, you are raising your glutathione, but it can't go anywhere because the channel is broken. To quote the NAC research study....
<b> People with cystic fibrosis have a defective or missing version of a protein responsible for, among other things, releasing glutathione into the extracellular spaces. This problem is particularly acute in the airways, where bacteria accumulate. White blood cells called neutrophils are summoned to the lungs to fight infection but stumble into a biological ambush. Although it isn't clear why, the arriving neutrophils are doomed. They act strangely and begin to die.
</b>
The true question is how do you get the glutathione to extra-cellular spaces? The answer is to supplement glutathione....
It is astounding that this debate is still going on in the research community.
<b> People with cystic fibrosis have a defective or missing version of a protein responsible for, among other things, releasing glutathione into the extracellular spaces. This problem is particularly acute in the airways, where bacteria accumulate. White blood cells called neutrophils are summoned to the lungs to fight infection but stumble into a biological ambush. Although it isn't clear why, the arriving neutrophils are doomed. They act strangely and begin to die.
</b>
The true question is how do you get the glutathione to extra-cellular spaces? The answer is to supplement glutathione....
It is astounding that this debate is still going on in the research community.
I personally use both....mainly because the glutathione I take comes with NAC in the capsule. If I had the time, I think I would use immunocal to boost gsh instead of NAC because it is proven to raise glutathione levels with no adverse reactions...no heart burn, no liver enzyme issues. Larry Lands, a cf researcher in Canada, who was asked to join 10 anti-oxidant researchers around the world who specialize in cf and pulmonary issues, believes it is byfar the safest and he has been doing actual studies with it much longer than the Stanford researchers have been using high dose NAC. NAC has a long history of use but it is contra-indicated in many issues including people with poor liver function....umm, hello, that is more than 13% of cf patients. Also, if you look into the actual research by the Stanford researcher Rabindra Tirouvanziam, there is evidence to suggest that the problem with just NAC is that it produces gsh...but this researcher concludes that once produced the defect in the cftr channel does not allow the gsh to travel to the outside cell wall. Basically, you are raising your glutathione, but it can't go anywhere because the channel is broken. To quote the NAC research study....
<b> People with cystic fibrosis have a defective or missing version of a protein responsible for, among other things, releasing glutathione into the extracellular spaces. This problem is particularly acute in the airways, where bacteria accumulate. White blood cells called neutrophils are summoned to the lungs to fight infection but stumble into a biological ambush. Although it isn't clear why, the arriving neutrophils are doomed. They act strangely and begin to die.
</b>
The true question is how do you get the glutathione to extra-cellular spaces? The answer is to supplement glutathione....
It is astounding that this debate is still going on in the research community.
<b> People with cystic fibrosis have a defective or missing version of a protein responsible for, among other things, releasing glutathione into the extracellular spaces. This problem is particularly acute in the airways, where bacteria accumulate. White blood cells called neutrophils are summoned to the lungs to fight infection but stumble into a biological ambush. Although it isn't clear why, the arriving neutrophils are doomed. They act strangely and begin to die.
</b>
The true question is how do you get the glutathione to extra-cellular spaces? The answer is to supplement glutathione....
It is astounding that this debate is still going on in the research community.
I never bothered with NAC because i read about all of that 3 and a half years ago and i figured.... rather than take something to make the body produce something it cant use correctly, i decided to take what it needs directly.... which is the GSH. Made a noticeable difference for me .