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N Acetyl l cysteine (also spelled acetylcysteine, N Acetyl L Cysteine or N-acetylcyteine) is made from the amino acid cysteine joined to an acetyl group. Acetylcysteine (sometimes abbreviated as N-A-C or NAC) is a strong antioxidant. It donates the amino acid cysteine to help form the antioxidant glutathione. Glutathione is a powerful antioxidant normally found in the body.
N
Acetyl Cysteine
is an amino acid and antioxidant. N Acetyl l cysteine is a precursor in the
body to the critical antioxidant glutathione, which is produced within
cells, particularly by the liver.
Acetylcysteine
is significantly more cost
effective than taking glutathione.
This product contains
Acetylcysteine
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Acetyl Cysteine
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N Acetyl Cysteine Benefit
An excellent review article in the April 1998
issue of Alternative Medicine Reviews summarizes the known effects of acetylcysteine. The author writes, “N-acetylcysteine is an
excellent source of sulfhydryl groups, and is converted in the body into
metabolites capable of stimulating glutathione synthesis, promoting
detoxification, and acting directly as a free radical scavenger.
Administration of acetylcysteine has historically been as a mucolytic
[mucus dissolving] agent in a variety of respiratory illnesses; however,
it appears to also have beneficial effects in conditions characterized by
decreased glutathione or oxidative stress, such as HIV infection, cancer,
heart disease, and cigarette smoking.”
Acetylcyteine may also prevent toxicity to the kidneys
during x-ray testing after injection with a contrast material in the
bloodstream.
Patients with acute myocardial
infarction undergoing primary angioplasty are at high risk for
contrast-medium–induced nephropathy because of hemodynamic instability,
the need for a high volume of contrast medium, and the lack of effective
prophylaxis. We investigated the antioxidant N-acetylcysteine for the
prevention of contrast-medium–induced nephropathy in patients undergoing
primary angioplasty. We randomly assigned 354 consecutive patients undergoing primary
angioplasty to one of three groups: 116 patients were assigned to a
standard dose of N-acetylcysteine (a 600-mg intravenous bolus before
primary angioplasty and 600 mg orally twice daily for the 48 hours after
angioplasty), 119 patients to a double dose of N-acetylcysteine (a 1200-mg
intravenous bolus and 1200 mg orally twice daily for the 48 hours after
intervention), and 119 patients to placebo.
Results The serum creatinine concentration increased 25 percent or more
from baseline after primary angioplasty in 39 of the control patients (33
percent), 17 of the patients receiving standard-dose N-acetylcysteine (15
percent), and 10 patients receiving high-dose N-acetylcysteine. Overall in-hospital mortality was higher in patients with
contrast-medium–induced nephropathy than in those without such nephropathy
(26 percent vs. 1 percent. Thirteen patients (11 percent) in the
control group died, as did five (4 percent) in the standard-dose N-acetylcysteine
group and three (3 percent) in the high-dose N-acetylcysteine group. The rate for the composite end point of death, acute renal
failure requiring temporary renal-replacement therapy, or the need for
mechanical ventilation was 21 (18 percent), 8 (7 percent), and 6 (5
percent) in the three groups, respectively.
Conclusions: Intravenous and oral N-acetylcysteine may prevent
contrast-medium–induced nephropathy with a dose-dependent effect in
patients treated with primary angioplasty and may improve hospital
outcome.
Dr. Sahelian says: As a resident, I prescribed intravenous
acetylcysteine to patients with liver damage due to acetaminophen
(Tylenol) overdose. It protected the liver quite well.
N-Acetylcysteine and cocaine
craving
Dr. Peter W. Kalivas from the Medical University of South Carolina,
Charleston evaluated the effects of N-Acetylcysteine on cue-induced cocaine
craving of 15 people with cocaine dependence. Those who were taking the N-Acetylcysteine
supplements had less cocaine craving and interest evoked by depictions of
cocaine use on photographic slides. The neurotransmitter system involved
may be glutamate transmission. Dr. Peter W. Kalivas is now starting a
double-blind study is being conducted to evaluate the effect of N-Acetylcysteine
on relapse rates and also evaluating the effects of N-Acetylcysteine on
nicotine and marijuana craving.
Is cocaine desire reduced by N-acetylcysteine?
Am J Psychiatry. 2007 Jul;164(7):1115-7. LaRowe SD, Myrick H, Hedden
S, Mardikian P, Saladin M, McRae A, Brady K, Kalivas PW, Malcolm R.
Department of Psychiatry and Behavioral Sciences, Medical University of
South Carolina, Charleston, SC 29425,
In this double-blind, placebo-controlled trial, 15 volunteers received
acetylcysteine or placebo during a 3-day hospitalization. Participants
were crossed over to receive the opposite condition on a second, identical
3-day stay occurring 4 days later. During each hospital stay, participants
completed a cue-reactivity procedure that involved collecting
psychophysical and subjective data in response to slides depicting cocaine
and cocaine use. While taking N-acetylcysteine, participants reported less
desire to use and less interest in response to cocaine slides and watched
cocaine slides for less time.
An open-label trial of N-acetylcysteine for the
treatment of cocaine dependence: a pilot study.
Prog Neuropsychopharmacol Biol Psychiatry. 2007 Mar 30;31(2):389-94.
Mardikian PN, LaRowe SD, Hedden S, Kalivas PW, Malcolm RJ. Center for Drug
and Alcohol Programs, Department of Psychiatry and Behavioral Sciences,
Medical University of South Carolina, 67 President Street, Charleston, SC
29425, USA.
Twenty three treatment-seeking cocaine-dependent patients participated in
a 4-week medication trial and received N-acetylcysteine
at doses of 1200 mg/day, 2400 mg/day or 3600 mg/day. Results suggested
that the three doses were well tolerated. Overall, the retention rates
appeared to favor higher doses of NAC (2400 mg/day and 3600 mg/day). The
majority of subjects who completed the study either terminated use of
cocaine completely or significantly reduced their use of cocaine during
treatment.
Acetylcysteine Side Effects
Other than large doses causing nausea, acetylcysteine does not have
any significant side effects and appears to be a safe nutrient as long as
the dosage is kept to less than 500 mg. I experienced nausea for a few minutes within an hour
of taking three 600 mg pills on an empty stomach.
Counteracting Tylenol
Toxicity
Regular use of the painkiller acetaminophen is associated with
higher rates of asthma and chronic obstructive pulmonary disease and
reduced lung function. Animal experiments have suggested that
acetaminophen might lower antioxidant activity in the lungs, and causes
harm to the liver and kidneys.
My comments: With hundreds of people each year dying
from acetaminophen overdose, thousands more with liver damage or other
health problems, why is acetaminophen still available for sale without a
prescription whereas regulators have tried to pull away certain
nutritional supplements that are far less toxic?
Those who need to take acetaminophen for a health
condition should consider Acetylcysteine, a nutrient that protects the
liver from this drug's toxicity. The antidote for acetaminophen poisoning
is N acetyl cysteine. Acetylcysteine is thought to work through a number
of protective mechanisms. Acetylcysteine is a precursor of glutathione
and increases glutathione availability. Acetylcysteine also functions as
an anti-inflammatory and antioxidant and has positive inotropic effects.
Acetylcysteine increases local nitric oxide concentrations, and this vasodilatory effect on microcirculatory blood flow enhances local oxygen
delivery to peripheral tissues. These vasodilating effects decrease
morbidity and mortality even in the setting of established liver damage.
Acetylcysteine Recommendations
Acetyl cysteine is sold in dosages ranging from 250 to 600 mg.
Acetylcysteine can help form the powerful antioxidant glutathione but the
formation of glutathione synthesis is under feedback control.
Administration of acetylcysteine with the resulting increase in
glutathione levels may cause a feedback inhibition in glutathione
synthesis. Thus, it may be best to take acetylcysteine every other day. The use of acetylcysteine certainly
should be considered as an additional supplement in protecting various
cells from damage in the elderly and those with Parkinson’s disease. If
you are planning to use acetylcysteine along with other antioxidants,
limit your daily dosage to 100 to 500 mg and don’t take it all the time. Acetylcysteine could protect the liver
in those who take acetaminophen on
a regular basis.
Acetylcysteine Research Update
Thiolic antioxidant supplementation of the diet reverses age-related
behavioural dysfunction in prematurely ageing mice.
Pharmacol Biochem Behav. 2005 Jan;80(1):45-51.
We have studied in a model of premature ageing in mice based on their
impaired behavioural response in a simple T-maze test the effect of the
ingestion of thioproline (TP) plus N-acetylcysteine (0.1% w/w of each
antioxidant) by female and male mice of Swiss and BALB/c strains on
performance in two behaviour tests. The antioxidant treatment (4 weeks in
two different periods of life, i.e., adult and old age) protected all
animals against early-age-associated behavioural impairment, but this
improvement was more evident in the prematurely ageing mice (PAM) in
comparison to the control group or non-prematurely ageing mice (NPAM).
These effects could be due to the glutathione precursor role of
acetylcysteine and thioproline that replenish the intracellular reduced
glutathione (GSH) levels despite advancing age. In conclusion, diet
supplementation with acetylcysteine and thioproline appears to be an
effective therapy for protection against early behavioural decline in
prematurely ageing mice.
A patient-tailored N-acetylcysteine protocol for acute acetaminophen
intoxication.
Clin Ther. 2005 Mar;27(3):336-41.
Hepatotoxicity as a result of acetaminophen (APAP) intoxication has
become an important problem, but early intervention with N-acetylcysteine
(Acetylcysteine) is effective in preventing hepatic injury. Two
Acetylcysteine regimens are currently approved for acute APAP
intoxication: Acetylcysteine administered orally every 4 hours for 72
hours, and Acetyl cysteine administered intravenously for 20 hours within
8 to 10 hours after ingestion of a potentially hepatotoxic amount of APAP.
However, clinical observations suggest that a variable treatment duration
may be more appropriate than use of these predetermined, fixed-duration
protocols. This study investigated the tolerability and
efficacy of a patient-tailored N Acetylcysteine protocol for acute APAP
intoxication by comparing the incidence of hepatotoxicity in patients
receiving this protocol and in historical controls receiving 1 of 2
fixed-duration protocols: oral Acetylcysteine for 72 hours and intravenous
Acetylcysteine for 20 hours within 8 to 10 hours after ingestion of a
potentially hepatotoxic amount of APAP. This was a retrospective
case series study that included all patients admitted through the
emergency department (ED) of the National Taiwan University Hospital with
a diagnosis of APAP intoxication between October 1997 and October 2002.
According to the patient-tailored protocol, which had been used in the ED
since 1997, patients with a serum APAP concentration above the limit for
possible risk based on a modified Rumack-Matthew nomogram received oral
treatment with Acetylcysteine 140 mg/kg, followed by maintenance doses of
70 mg/kg every 4 hours. Acetylcysteine treatment was discontinued when the
APAP concentration was <10 mg/L and serum aspartate aminotransferase (AST)
was <40 IU/L. For the purposes of assessing clinical outcomes, patients
were divided into 3 groups based on duration of treatment: the
short-course group (</=36 hours), the intermediate-course group (37-72
hours), and the long-course group (>/=73 hours). The primary outcome
measure was development of hepatotoxicity, defined as a serum AST or
alanine aminotransferase concentration >1000 IU/L. Twenty-seven
patients were included in the study, 17 in the short-course group, 4 in
the intermediate-course group, and 6 in the long-course group. The mean
(SD) durations of Acetyl l cysteine treatment in the respective groups
were 22.1 (5.5) hours, 45.0 (8.2) hours, and 97.3 (33) hours. All 6
patients (22%) in the long-course group had hepatotoxicity (peak AST
range, 1083-9770 IU/L); their treatment duration ranged from 80 to 164
hours. No patients in the short- or intermediate-course group had evidence
of hepatotoxicity. One woman in the long-course group in whom initiation
of Acetylcysteine treatment was delayed by 28 hours died of fulminant
hepatic failure. The overall incidence of hepatotoxicity was similar to
that in the historical controls. CONCLUSIONS: In this retrospective case
series inpatients who received patient-tailored Acetylcysteine therapy for
acute APAP intoxication, the incidence of hepatotoxicity was low and
comparable to that in historical controls who received treatment with 1 of
2 fixed-duration regimens. Use of this protocol may have the potential to
shorten hospital stays without increasing the risk to patients. However,
the sample size was small, and the findings require confirmation in
prospective clinical trials.
Effect of dietary restriction and n acetyl cysteine supplementation on
intestinal mucosa and liver mitochondrial redox status and function in
aged rats.
Exp Gerontol. 2004 Sep;39(9):1323-32.
The age-related changes of glutathione (GSH) levels and the effect of
hypocaloric regimen and acetylcysteine supplementation were investigated
in intestinal mucosa and liver mitochondria of 28 months rats. Old rats
exhibited lower proteins, GSH and protein sulphydrils
concentrations, higher GSH-peroxidase (GSH-Px) activity and protein
carbonyl deposit, partial inhibition of succinate stimulated mitochondrial
state III respiration and decreased mitochondrial nitrosothiols
concentration. In conclusion, ageing
is characterized by a decrease of GSH concentrations, increased
protein oxidation and decreased mitochondrial NO content. Hypocaloric diet
ameliorated intestinal transport and, as well as acetylcysteine, was
effective in enhancing GSH levels but at different extent according to the
investigated districts. Both interventions reduced the age-associated
increase of GSH-Px and protein carbonyls and improved mitochondrial
respiration.
Treatment by acetylcysteine and melatonin
increases cardiac baroreflex and improves antioxidant reserve.
Am J Hypertens. 2004 Oct;17(10):947-54.
The aims of this study were to investigate the effects of
melatonin and acetylcysteine on the baroreflex sensitivity and to verify
whether those effects were correlated with their antioxidant capacity in
Wistar-Kyoto and spontaneously hypertensive rats (SHR). Rats were treated
with 30 mg/kg/day of melatonin or 4 g/kg/day of acetylcysteine
for 4 weeks. Changes in mean arterial pressure, heart rate, plasma
norepinephrine, and epinephrine were measured in conscious rats after an
intravenous injection of phenylephrine or sodium nitroprusside. RESULTS:
Melatonin and acetylcysteine produced a significant reduction in mean
arterial pressure and heart rate in SHR. Melatonin and acetylcysteine
improved bradycardic and tachycardic baroreflex responses in SHR without
modifying catecholamine responses. The antioxidant reserve, which was
reduced in SHR as reflected by the lower glutathione peroxidase activity
in plasma, was normalized by acetylcysteine and melatonin. Acetylcysteine
and melatonin increased glutathione peroxidase activity in erythrocytes
from SHR. The results of the present study suggest that
melatonin and acetylcysteine improve the baroreflex response in SHR in
correlation with the antioxidant effects of these substances.
N Acetyl cysteine in nephrology; contrast nephropathy
and beyond.
Curr Opin Nephrol Hypertens. 2004 Nov;13(6):649-54.
Since the first publication appeared in 2000 showing
that prophylactic oral administration of the antioxidant acetylcysteine,
along with adequate hydration, can prevent the reduction in renal function
induced by non-ionic, low-osmolality contrast agents, acetylcysteine has
rapidly become widely used in clinical practice. Meanwhile, other
applications of acetylcysteine in nephrology have been reported. This
review analyses recent literature on the effects of acetylcysteine on
radiocontrast-induced nephropathy, on plasma homocysteine concentrations,
and on cardiovascular events in patients with end-stage renal failure.
At least 19 randomized trials evaluating acetylcysteine
for the prevention of radiocontrast-induced nephropathy, at least five
meta-analyses, and several reviews on that topic have been published
within the past 4 years. One study recently indicated that the administration of acetylcysteine during a haemodialysis session significantly lowered plasma
homocysteine concentrations. Another study indicated that long-term
antioxidative treatment with acetylcysteine significantly reduced
cardiovascular events in patients with end-stage renal failure. SUMMARY:
Although there are controversies on dosing and timing, the use of
acetylcysteine together with hydration should be considered to protect
patients from radiographic contrast media-induced nephropathy. Long-term
antioxidative treatment with acetylcysteine in patients with end-stage
renal failure may also be useful to prevent adverse cardiovascular events.
Protective effect of n acetyl cysteine and deferoxamine on carbon
tetrachloride-induced acute hepatic failure in rats.
Crit Care Med. 2004 Oct;32(10):2079-2083.
Carbon tetrachloride (CCl4) is a lipid-soluble potent hepatotoxic;
thus, it widely is used as an animal model of severe hepatic failure.
We here describe the effects of acetylcysteine, deferoxamine, or both in
the treatment of CCl4-induced hepatic failure. SUBJECTS: Rats exposed to CCl4 were treated with acetylcysteine and/or deferoxamine
or vehicle. Acetylcysteine plus deferoxamine treatment significantly
attenuated hepatic and central nervous system oxidative damage after acute
hepatic failure induced by CCl4. In addition, the serum levels of alanine
aminotransferase, total bilirubin, and prothrombin time in the acetylcysteine
plus deferoxamine group were significantly lower than those in the acetylcysteine
or deferoxamine and saline groups. After acetylcysteine plus
deferoxamine treatment, hepatocellular necrosis and inflammatory
infiltration induced by carbon tetrachloride were greatly decreased.
Survival in untreated rats was 5%. Survival increased to 25% and 35%,
respectively, with acetylcysteine and deferoxamine treatment. In rats
treated with acetylcysteine plus deferoxamine, survival was 80%.
CONCLUSIONS:: Our data provide the first experimental demonstration that
acetylcysteine plus deferoxamine reduces mortality rate, decreases
oxidative stress, and limits inflammatory infiltration and hepatocyte
necrosis induced by CCl4 in the rat.
N acetyl cysteine
prevents cisplatin-induced ototoxicity in rats
Hearing Res 2004;July issue.
Treatment with acetylcysteine can
prevent the ototoxic effects often seen with cisplatin therapy. In the
current study, reported in the July issue of Hearing Research, the
researchers tested the benefits of acetylcysteine treatment in a newly
developed rat model of cisplatin-induced ototoxicity. Animals were treated
with acetylcysteine or saline 15 or 30 minutes before receiving cisplatin
or 4 hours afterward. The acetylcysteine-treated rats showed no
significant change in auditory brainstem response with cisplatin therapy.
In contrast, the saline-treated animals displayed marked ototoxicity.
N acetyl cysteine enhances muscle cysteine and glutathione
availability and attenuates fatigue during prolonged exercise in
endurance-trained individuals.
J Appl Physiol. 2004 Jun 11
The production of reactive oxygen species in skeletal muscle is linked with
muscle fatigue. This study investigated the effects of the antioxidant compound
acetylcysteine on muscle cysteine, cystine and glutathione, and on time
to fatigue during prolonged, submaximal exercise in endurance athletes. Eight
males completed a double-blind, crossover study, receiving acetylcysteine or placebo before
and during cycling for 45 min at 71%VO2peak, then to fatigue at 92%VO2peak.
Acetylcysteine was intravenously infused
for 20 min prior to and throughout exercise. Arterialized venous blood was
analyzed for acetylcysteine, glutathione status and cysteine concentration. A vastus
lateralis biopsy was taken pre-infusion, at 45 min exercise and fatigue and
analysed for acetylcysteine, total glutathione, reduced glutathione (GSH) cysteine
and cystine. Time to fatigue at 92%VO2peak was reproducible in preliminary
trials and with acetylcysteine was enhanced . Acetylcysteine increased muscle total and reduced acetylcysteine at
both 45 min and fatigue. Muscle cysteine and cystine were unchanged
during CON, but were elevated above pre-infusion levels with acetylcysteine. Muscle TGSH declined and muscle GSH tended to decline during
exercise. Both were greater with acetylcysteine. Neither exercise nor acetylcysteine affected
whole blood TGSH. Whilst blood GSH was decreased and calculated oxidised
glutathione increased with exercise, both were unaffected by acetylcysteine. In conclusion, acetylcysteine improved performance in well-trained individuals, with
enhanced muscle cysteine and GSH availability a likely mechanism.
Counteracting Tylenol Toxicity
In addition to its antioxidant properties,
acetylcysteine is currently used in a variety of other ways: to counteract
the effects of an overdose of acetaminophen (i.e., Tylenol®), to break up
mucus in respiratory ailments, to lessen the symptoms of colds or the flu,
and even to reduce the effects of hangovers.
Regular use of the painkiller acetaminophen is
associated with higher rates of liver and kidney toxicity, asthma, and
chronic obstructive pulmonary disease and reduced lung function.
My comments: With hundreds of people each year dying
from acetaminophen overdose, thousands more with liver damage or other
health problems, why is
acetaminophen still available for sale without a prescription whereas
regulators have tried to pull away certain nutritional supplements that
are far less toxic?
Those who need to take acetaminophen for a health
condition should consider acetylcysteine, a nutrient that protects the
liver from this drug's toxicity.
Acetylcysteine and Cocaine
Addiction
A study funded by the National Institutes of Health (NIH) suggests
that acetylcysteine can reduce the cravings associated with chronic
cocaine use. This research, released at the American College of
Neuropsychopharmacology's (ACNP) annual conference is among the first to
identify N-acetylcysteine (NAC) as a potential agent to modulate the
effects of cocaine addiction. There is also early evidence in animal
models of addiction to suggest that this chemical works similarly in the
treatment of heroin addiction, and possibly alcoholism. NAC is available
over the counter as an herbal supplement known for its antioxidant
effects. In the first phase of the study, the research team conditioned
rats on a regimen of cocaine to establish their addiction. The rats in the
treatment group were then treated with N acetylcysteine. After treatment,
the cocaine-addicted rats exposed to N-acetylcysteine were significantly
less likely to seek out cocaine than those without N acetylcysteine. Those
treated with NAC ceased to actively seek cocaine, but showed normal
food-seeking behaviors.
In the second phase of the study, acetylcysteine treatment was
investigated in a small inpatient study (n=15) involving non-treatment
seeking cocaine-dependent subjects. In this phase of research, subjects
were asked to look at pictures that were either neutral (e.g., trees,
boats) or cocaine-related (e.g., drug paraphernalia). Those individuals
treated with N-acetylcysteine reported less craving for cocaine and spent
less time looking at the cocaine-related pictures. In addition, when using
a functional magnetic resonance imaging test, subjects treated with
acetylcysteine had reduced brain activity in the prefrontal cortex, the
area of the brain activated during cocaine craving and used to modulate
the addictive behavior of chronic cocaine use. An open label trial, which
was recently completed, indicated that cocaine-dependent patients could
take N-acetyl cysteine on an extended outpatient basis, with minimal side
effects. More importantly, patients taking higher doses of NAC were more
likely to complete the trial, providing further indication of the
potential benefits of N-acetylcysteine.
N Acetyl Cystiene emails
Q. I was wondering if I could "overdose" on NAC. What is the safest
maximum per-day dosage??
A. Each person has a different threshold for N acetyl cysteine, but as with most supplements, more is not better, there could be
a feedback loop, or tolerance, or displacement of other crucial nutrients,
etc. I personally prefer not to exceed 250 mg of acetylcysteine a few
times a week, but a different doctor may have a different opinion.
Q. Hi, what exactly is the difference between
Cysteine and N Acetyl cysteine ? Which one is better to take?
A. Most often, aceytylcysteine is the one taken since
it has stronger antioxidant potential, however it depends on the condition
being treated. Acetylcysteine has an additional acetyl group which makes
it more potent as an antioxidant.
Q. What is the right n acetylcysteine dosage as a
daily supplement?
A. There are no accepted guidelines on the appropriate
n acetylcysteine daily dosage. Some people may need none, others may
benefit from taking 500 mg of n acetylcysteine a few days a week. If you
are taking other antioxidants, we suggest you reduce your dosage of n
acetylcysteine. Some people think that the more antioxidants they take the
healthier they will be, but there is no proof of this.
Q. Should one take n acetyl l cysteine if they are taking Tylenol
(acetaminophen) ? I understand that acetaminophen can damage the liver and
n acetylcysteine can protect the liver from Tylenol harm.
A. This is a good question. If your doctor approves, it
may be a good idea to take a small daily amount or a few times a week of a
n acetylcysteine supplement, although there is little research to guide us
on how much is needed and how often one should take the acetylcysteine.
Q. I would like to use acetylcysteine to protect my
liver from the amount of acetaminophin I am required to take on a daily
basis due to my injuries. How much would I need to take of acetylcysteine?
A. We have not seen any studies regarding the long term
use of acetaminophen and acetylcysteine, however a dose of 100 mg a day
would seem reasonable.
Q. I am a mild asthmatic, adult onset, female, age
54. I have been taking 500 mg of NAC (N Acetyl Cysteine) daily for about
six months. It has helped me manage my symptoms and reduce inhaled
corticosteroids ICS required by reducing the amount and thickness of both
chest and sinus mucus/phlegm. Now a clinical study and follow up comments
from the Univ. of VA have forced me to stop using the N Acetyl Cysteine as
it has been linked to the development of pulmonary arterial hypertension.
N-acetylcysteine (NACi), an antioxidant commonly used in nutritional and
body building supplements, can form a red blood cell derived molecule that
makes blood vessels think they are not getting enough oxygen. This leads
to pulmonary arterial hypertensioni (PAH), a serious condition
characterized by high blood pressure in the arteries that carry blood to
the lungs. The results appear in the September, 2007 issue of the Journal
of Clinical Investigation. "NAC fools the body into thinking that it has
an oxygen shortage," said Dr. Ben Gaston, UVa Children's Hospital
pediatrician and researcher who led the study. "We found that an NAC
product formed by red blood cells, know as a nitrosothiol, bypasses the
normal regulation of oxygen sensing. It tells the arteries in the lung to
'remodel'; they become narrow, increasing the blood pressure in the lungs
and causing the right side of the heart to swell." I am not a medical
professional and I cannot entirely understand the full implications of
this study; but it does seem to suggest caution re using acetylcysteine.
Can you please share your expert opinion on these new studies re NAC?
http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pubmed&pubmedid=17786245
http://www.medicalnewstoday.com/articles/81503.php
A. I am not aware of any clinical studies in humans that show N
acetylcysteine causes pulmonary arterial hypertension. Perhaps it does if
used daily in high dosages for prolonged periods. Most of the time we
recommend users to take this supplement every other day. We also suggest,
as a general rule, for people to take a few days or a week off each month
from the use of a particular supplement.
I cannot determine from reading the study what the total amount of
NAC the rodents were exposed to daily except it says 10 mg of NAC per ml
of water. When researchers do studies in
rodents, they often use dosages several times higher (per weight ratio)
than what humans would normally consume. Also, the metabolism of rodents
is different than that in humans. Although a lot can be learned from
studying the influence of nutrients and drugs in rodents and other
animals, this does not necessarily give us the exact effect these
nutrients and medicines would have in the human body.
I will wait for human studies to learn for certain what kind of
benefits and side effects N acetylcysteine has if used for prolonged
periods. In the meantime, using lower dosages and taking breaks appears to
be a reasonable approach.
Q. The article states 10mg/ml of water. An
average mouse drinks 30 ml water each day = about 300 mg NAC per day. Avg.
mouse weighs 1.5 oz = 200 mg/oz of NAC per oz of weight. Extrapolate that
dose level to a 140 lb human (140 x 16 oz x 200mg). A human would have to
take in 448,000 mg of NAC per day to = this level of mouse intake. I
realize this is not perfect, but it is in the ball park. It seems to
indicate that at normal human doses, there should be no problem.
A. Yes, assuming all the water
they were drinking had n-acetylcysteine, then it does mean that the mice
were exposed to extremely high amounts. I appreciate findings from rodent
studies but I realize also many of the findings may not apply well to
humans.