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N-acetylcysteine (NAC)
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In one pass NAC (N-acetylcysteine) is a stable form of cysteine, which the body uses to make glutathione (GSH), the molecule cells rely on to neutralize oxidative junk and toxins.
Educational content, not medical advice — consult a clinician.
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Chapter 1
A stable form of cysteine
(N-acetylcysteine) is a stable form of cysteine, which the body uses to make glutathione (GSH), the molecule cells rely on to neutralize oxidative junk and toxins. Glutathione is built from three amino acids. The body is rarely short of glutamate and glycine; what often runs low is cysteine, because there is not much of it in the diet and detoxification uses up a lot of it.
NAC puts a protective acetyl coat on cysteine. Inside the cell, enzymes called amidases strip the coat off and release free cysteine, giving GCL, the rate-limiting enzyme of synthesis, the raw material it needs.
If someone has swallowed too much paracetamol (acetaminophen, found in many cold remedies) at one time, go to the emergency department immediately, even if they feel fine for now. The antidote hospitals use is NAC itself; it works best the earlier it is given, and taking it at home is no substitute.
NAC puts a protective acetyl coat on cysteine. Inside the cell, enzymes called amidases strip the coat off and release free cysteine, giving GCL, the rate-limiting enzyme of synthesis, the raw material it needs.
If someone has swallowed too much paracetamol (acetaminophen, found in many cold remedies) at one time, go to the emergency department immediately, even if they feel fine for now. The antidote hospitals use is NAC itself; it works best the earlier it is given, and taking it at home is no substitute.
Myth · Why swallowing glutathione does not work
Why not just take cysteine? Swallowed cysteine is used up quickly in the gut and liver and does not stay in the blood; it is also more toxic than and oxidizes more easily. NAC adds an acetyl group to the amino group, a kind of protective coat. Once inside the cell, amidases remove the acetyl group and release free cysteine.Glutathione itself is a tripeptide, written γ-Glu-Cys-Gly: three amino acids strung together, with an unusual γ-peptide bond in the middle.
Glutamate (Glu): the body is not short of itGlycine (Gly): the body is not short of itCysteine (Cys): the piece that limits everything
So every mechanistic story about NAC comes down to one thing: raising the cysteine pool inside cells so that GCL, the enzyme doing the synthesis, has raw material to work with.
Some sellers offer reduced glutathione capsules to swallow, at several times the price of NAC. But a single oral dose of glutathione barely reaches the blood:
As a tripeptide, it is cut back into three free amino acids by peptidases (such as γ-glutamyl transferase) in the stomach and gutThose amino acids are absorbed separately, and cells then rebuild glutathione from them: a long detour that ends at the same bottleneck, the supply of cysteineWitschi 1992 (EJCP) gave 7 healthy volunteers a single oral dose of about 3 g of glutathione. Over the next 270 minutes, plasma glutathione, cysteine, and glutamate did not rise significantly, and the authors concluded that the systemic availability of oral glutathione is negligible
The evidence on a single oral dose is clear; whether taking it every day for a long time slowly raises the body's stores is being studied, and the results so far disagree. So if the goal is more glutathione inside cells, giving cells cysteine (NAC, for example) is more direct, cheaper, and easier to control than giving them glutathione.
NAC is not an antioxidant itself; it is the raw material for an antioxidant (glutathione). The distinction is often blurred on the supplement shelf, and once it is clear, glutathione capsules become much less persuasive.
Chapter 2
How it helps cells make glutathione
Glutathione in cells is not used once and thrown away; it keeps going round a cycle. It is made, sent out to neutralize junk, and then repaired to its original form. The rate-limiting step in making it depends on whether there is enough cysteine, and that is exactly where comes in. While working, glutathione itself is oxidized, and repairing it uses up , a coenzyme that supplies reducing power in cells.
Its use as an antidote works by enlarging the glutathione pool through this one entrance; thinning mucus relies mainly on its own thiol group breaking the disulfide bonds in mucus directly, and the mechanisms proposed in psychiatry go beyond this one route. The loop also needs NADPH to turn back, so people born short of the enzyme G6PD, who make less NADPH, should think one step further before taking high doses of NAC.
Its use as an antidote works by enlarging the glutathione pool through this one entrance; thinning mucus relies mainly on its own thiol group breaking the disulfide bonds in mucus directly, and the mechanisms proposed in psychiatry go beyond this one route. The loop also needs NADPH to turn back, so people born short of the enzyme G6PD, who make less NADPH, should think one step further before taking high doses of NAC.
Mechanism · How four enzymes pass the baton
Glutathione (GSH) in cells keeps going round a cycle: it is made, sent out to neutralize junk, and repaired back to its original form, again and again. Four enzymes pass the work along.Step 1 · Make it (two steps, both spending )
First the rate-limiting enzyme GCL (γ-glutamylcysteine ligase) joins glutamate to cysteine (Cys); then GSS (glutathione synthetase) adds glycine to complete glutathione. The first step is the key one: how fast GCL works depends on the concentration of cysteine in the cell, and that is exactly where comes in. Raise cysteine, GCL's limit loosens, and more glutathione gets made.
Step 2 · Use it (neutralizing junk)
GPx (glutathione peroxidase) leads this step: glutathione neutralizes hydrogen peroxide, lipid peroxides, and various electrophilic toxins that stick to cell components (such as NAPQI, which forms in a paracetamol overdose). In doing so, glutathione itself is oxidized into its used form, GSSG (oxidized glutathione, two molecules joined together).
Step 3 · Repair it (closing the loop)
GR (glutathione reductase) then turns GSSG back into fresh glutathione, and the repair uses up , the coenzyme that supplies reducing power in cells. NADPH comes mainly from the pentose phosphate pathway, whose first enzyme is G6PD, so the whole glutathione system depends indirectly on your glucose metabolism and on G6PD activity.
Where NAC comes in: at the cysteine supply at the entrance to step 1. Its use against paracetamol poisoning enlarges the glutathione pool through this one entrance; thinning mucus relies mainly on its own thiol group breaking disulfide bonds, not on this route.
Safety · What G6PD deficiency changes
G6PD (glucose-6-phosphate dehydrogenase) deficiency is an inherited condition that is relatively common in people of African, Mediterranean, Middle Eastern, and Southeast Asian ancestry, and not rare in southern China either (where it is known as favism). The cells most affected are red blood cells.The mechanism: G6PD is the first enzyme of the pentose phosphate pathway and produces , the coenzyme that supplies reducing power in cells. Red cells rely on NADPH to keep the glutathione recycling loop running, which protects their membranes from oxidation. When G6PD is lacking, NADPH cannot keep up, the glutathione pool in red cells falls, and oxidative stress (eating fava beans, certain drugs, an infection) can damage the cells and cause hemolytic anemia.
How this relates to :
NAC raises cysteine and supplies more raw material for glutathione, which by mechanism should helpBut used glutathione becomes GSSG, which needs NADPH to be repaired. People with G6PD deficiency already have less NADPH, so the theoretical worry is that the harder the loop runs, the more strain falls on that stepThis worry comes mainly from reasoning about the mechanism; there are few human data specifically testing whether NAC is safe in people with G6PD deficiency. In hospitals, G6PD deficiency is not a contraindication to using NAC for paracetamol poisoningIn practice: if you know you have G6PD deficiency and want to take NAC yourself at high doses over a long period, ask a doctor first
This is the real-world price of a supplement with a clear mechanism: it really does change your biochemistry, so it really can cause problems in some people. A supplement with a vague mechanism that works like a placebo is the opposite: it does not harm you, but it does not help you either.
Self-check: does your ancestry come from the Mediterranean, the Middle East, Africa, Southeast Asia, or southern China? Have you ever had unexplained jaundice, or fallen ill after eating fava beans? If so, before taking NAC long term, you can ask a doctor whether to have your G6PD activity checked.
Chapter 3
The antidote for paracetamol overdose
is the hospital antidote for paracetamol (acetaminophen) poisoning, and this is its most solid clinical role. At normal doses, paracetamol mostly goes through harmless metabolic routes in the liver. In an overdose, the excess is oxidized into NAPQI, a toxin that attacks cells. Glutathione in the liver normally neutralizes it, but once glutathione runs out, NAPQI starts destroying liver cells.
In hospital, NAC raises cysteine and rebuilds the glutathione pool before the liver is overwhelmed. Do not take NAC at home for an overdose; the dose, the time window, and the monitoring all have to be handled in a clinical setting. The earlier treatment starts, the better it works: people who start within 10 hours of taking the drug have much less liver damage than those who start after 16 hours.
In hospital, NAC raises cysteine and rebuilds the glutathione pool before the liver is overwhelmed. Do not take NAC at home for an overdose; the dose, the time window, and the monitoring all have to be handled in a clinical setting. The earlier treatment starts, the better it works: people who start within 10 hours of taking the drug have much less liver damage than those who start after 16 hours.
Clinical · How NAC rescues a paracetamol overdose
is the US FDA-approved antidote for poisoning with paracetamol (known as acetaminophen in the US, with brands such as Tylenol), and this is its most solid clinical role.The toxicology chain:
1. At therapeutic doses (under 4 g a day for adults), paracetamol is cleared mainly by the liver through glucuronidation and sulfation, which are harmless routes
2. In an overdose (more than 10 g at once, or 4-6 g a day over a long period combined with drinking or malnutrition), those harmless routes saturate, and the liver enzyme CYP2E1 oxidizes the excess into NAPQI, a reactive toxin that binds to cell components
3. Small amounts of NAPQI are immediately neutralized by glutathione in liver cells, and no harm is done
4. But if NAPQI is produced in large amounts for a long time, the glutathione pool runs out, and the excess NAPQI binds to liver proteins, causing widespread death of liver cells (mainly around the center of each liver lobule), then acute liver failure, and in severe cases death or an emergency liver transplant
How NAC rescues the patient:
NAC raises cysteine, GCL speeds up glutathione synthesis, and the glutathione pool is rebuilt quicklyIt keeps neutralizing NAPQI before the toxin overwhelms the liver, and the liver cells survive
The clinical evidence:
Prescott 1977 (Lancet): 15 patients with paracetamol poisoning were given intravenous NAC (300 mg/kg in total over 20 hours). Of the 12 who started treatment within 10 hours of taking the drug, 11 had normal or only mildly disturbed liver tests; the remaining 1, and all 3 who started after more than 10 hours, developed severe liver damageRumack 1981: in 662 consecutive paracetamol overdoses, those judged at risk from their blood levels on a nomogram were given oral NAC. Among those who started within 10 hours of ingestion, 7% had a transient rise in liver enzymes; the figure was 29% for those starting at 10–16 hours and 62% for those starting at 16–24 hours. Among patients treated within 24 hours, there were no deaths apart from one homicide victimThe Rumack-Matthew nomogram: the emergency decision tool. The blood level is measured against the time since ingestion, and if it lies above the treatment line on the chart, NAC is givenThe US FDA approved oral NAC (Mucomyst) for this use in 1985 and the intravenous form (Acetadote) in 2004
Paracetamol remains the most common cause of acute liver failure in the United States, and NAC is the proven, standard antidote on that path.
Among molecules you can buy on a supplement shelf, evidence at this actually saves lives level is very rare.
Safety · Alcohol and paracetamol together
Why long-term drinkers need extra care with paracetamol has two layers of mechanism:Long-term heavy drinking clearly upregulates the liver enzyme CYP2E1. It is one of the liver's main alcohol-processing enzymes, and it is also the very enzyme that turns paracetamol into NAPQIAt the same time, long-term drinking and alcohol-related liver disease often come with a low glutathione pool (used up by oxidative stress, plus too little cysteine and protein in the diet)Put the two together: more NAPQI is made and less glutathione is available to neutralize it, so by mechanism these people could develop liver toxicity even close to normal doses
Know the limits of the evidence: among the 662 overdose patients in Rumack 1981, a history of chronic drinking made no consistent difference to liver toxicity, while people who had been drinking at the time had milder toxic reactions (during acute drinking, alcohol and paracetamol compete for the same enzyme). So the danger comes from long-term heavy drinking, not from one night of drinking.
Clinical reminders:
Common clinical advice is that long-term heavy drinkers should take no more than 2 g of paracetamol a day, and should ask a doctor or pharmacist before using itTaking 4-8 g in a day is already above the adult limit of 4 g a day, and that is an overdose whether or not you have been drinkingI just took a pill for a headache plus I have been drinking quite a lot for years: put together, these two statements are a risk that is often underestimated
In practice:
Every painkiller has a cost after heavy drinking: paracetamol needs its dose limit respected, and anti-inflammatory painkillers such as ibuprofen and aspirin combined with alcohol irritate the stomach and can cause stomach bleeding. The safest course is to drink less, and to ask a doctor or pharmacist when you need medicineLong-term drinkers who often have headaches: see a doctor for an assessmentDo not take every day to prevent drunkenness or hangovers: no reliable randomized trial supports this, and it may make you less careful about how much you drink. NAC is a rescue tool, not a license to overindulge.
Chapter 4
Thinning mucus and psychiatric uses
Beyond its role as an antidote, has evidence on two quite different fronts, though of very different strength. Mucus in sputum is a thick gel held together by disulfide bonds, and NAC's thiol group can break those bridges and thin the sputum; in chronic bronchitis and , a pooling 13 studies found that it reduces flare-ups. In psychiatry it is being studied as an add-on treatment, because oxidative stress and glutamate imbalance are part of the shared pathology, but a review concluded that its effectiveness is not yet established, and none of these uses is a first-line treatment on its own.
Useful is not the same as universal: during COVID it was promoted as an antiviral miracle, and clinical trials did not bear that out.
Useful is not the same as universal: during COVID it was promoted as an antiviral miracle, and clinical trials did not bear that out.
Evidence · How good the lung and psychiatry data are
Beyond treating paracetamol poisoning, has real evidence of uneven strength in two quite different fields.1. Thinning mucus in chronic airway disease (chronic bronchitis, )
NAC carries a free sulfhydryl (-SH, thiol) groupThe mucin proteins in sputum form a thick, elastic gel held together by disulfide bondsNAC's thiol group can break those disulfide bonds, thinning the mucus so it is easier to cough upThe by Cazzola 2015 (European Respiratory Review): 13 studies and 4155 patients. People on NAC had clearly fewer flare-ups of chronic bronchitis or COPD ( 0.75, about a quarter fewer). The protective effect was more obvious in people without airflow limitation, but high doses (more than 600 mg a day) also worked in patients whose COPD was confirmed by lung-function testing. The authors recommend at least 1200 mg a day when there is airflow limitation, and say 600 mg a day seems enough when there is not. Side effects did not depend on doseItaly, Spain, and some central European countries prescribe it routinely for long-term COPD care; it is used less in the US, where inhaled bronchodilators and steroids are the mainstream treatmentCertainty of evidence: moderate to high (a meta-analysis of randomized trials), for patients who already have the diagnosis
2. Psychiatry
NAC has been studied in many psychiatric conditions, because they share part of their pathology with oxidative stress and an imbalance in the glutamate system:
Obsessive-compulsive disorder, hair-pulling disorder (trichotillomania), and compulsive skin-picking: several small randomized trials suggest that about 2400 mg a day may reduce compulsive behaviorsAdd-on treatment for bipolar disorder or depression: small, inconsistent signals; not a mainstream recommendationCutting down on addictive substances (cocaine, cannabis, tobacco): some small trials saw reduced craving, possibly through effects on the cystine-glutamate exchangerCognitive symptoms of schizophrenia: a signal, awaiting replication in larger trials
The review by Smaga 2021 (BJP) concludes that the effects in animal models are good, but clinical effectiveness in people is not yet fully established; it remains a promising candidate for add-on treatment. Certainty of evidence: low; these are all add-on findings, not first-line treatments on their own.
3. When NAC is not appropriate
G6PD deficiency (see above): ask a doctor before long-term high dosesAn acute asthma attack: inhaled (nebulized) NAC can actually trigger bronchospasm (it temporarily increases mucus and irritates the airway)Anticoagulant treatment (warfarin and similar) combined with long-term high-dose NAC: there are individual case reports of a slight rise in (a clotting test), so monitoring is neededPregnancy and breastfeeding: data are lacking (note: intravenous NAC for paracetamol poisoning in pregnancy is a different matter; that is emergency treatment)
Myth · When NAC was sold as a COVID cure
During the COVID pandemic of 2020–2022, online marketing promoted as an anti-COVID miracle drug:The hypothesis: NAC raises glutathione, so it should counter the oxidative stress caused by the virus, dampen the cytokine storm, and help clear mucusPushed by social media and podcasts, online NAC sales rose sharplyAround 2022, the US FDA went back and forth on whether NAC could be sold as a dietary supplement (it was first approved as a drug); go by the FDA's current documents for where this stands
What the clinical evidence actually shows:
Several small randomized trials gave inconsistent results, with no consistent improvement in such as hospitalization, ICU admission, or deathNone of the main COVID treatment guidelines lists NAC as a standard treatment
This episode is worth remembering. NAC is a genuinely useful molecule, but useful is not the same as universal. Selling it as a miracle drug in a new setting without strong evidence is a common supplement-marketing pattern: a plausible mechanism, media amplification, rising sales, trial results that do not follow, and then the marketing quietly moves on to the next molecule.
So a clear mechanism does not mean clinical effectiveness. The same NAC has very different evidence in different settings: for paracetamol poisoning, it has been the clinical standard for decades; for reducing flare-ups, there is a of randomized trials; for compulsive behaviors, there are only small trials; for COVID, there is no reliable evidence of benefit. Judging a supplement is not judging a molecule; it is judging how that molecule performs in one specific situation.
Chapter 5
Who needs it
Whether is worth buying depends first on the situation. An acute paracetamol overdose means going to the emergency department immediately; do not try it at home. For diagnosed or compulsive-spectrum conditions, discuss it with a specialist as an add-on. For healthy people who want antioxidant or anti-aging effects, there is no hard-endpoint evidence.
It acts on glutathione, the hub of the antioxidant system, so when there is a clear indication it is one of the few options that can be recommended, but it is not a default item on a wellness list. The dose depends on the situation, and a few groups should not buy it for themselves. If the aim is fighting oxidation, the first steps are quitting smoking, drinking less, sleeping enough, eating more vegetables and fruit, and exercising; supplements come after those.
It acts on glutathione, the hub of the antioxidant system, so when there is a clear indication it is one of the few options that can be recommended, but it is not a default item on a wellness list. The dose depends on the situation, and a few groups should not buy it for themselves. If the aim is fighting oxidation, the first steps are quitting smoking, drinking less, sleeping enough, eating more vegetables and fruit, and exercising; supplements come after those.
In practice · Who needs NAC, and how much
Do you need ?Q1 Which situation are you in?
Acute paracetamol overdose (intentional or accidental) → go to the emergency department immediately; do not try NAC at home (the dose, the time window, and the monitoring all have to be clinical)Diagnosed or chronic bronchitis → discuss NAC at 600-1200 mg a day with your lung specialist; it may reduce flare-upsObsessive-compulsive disorder, hair-pulling disorder, compulsive skin-picking → discuss NAC at 2400 mg a day with your psychiatrist as an add-on (not a replacement for standard treatment)Healthy people who want antioxidant or anti-aging effects → the evidence is insufficient and it is not a priority; see Q2 belowLong-term drinkers who sometimes take paracetamol → do not count on NAC to prevent harm; cut down on alcohol and keep the drug dose in check
Q2 Do you want to take NAC for wellness?
There is no human evidence on (lifespan, cardiovascular disease, cancer) supporting long-term NAC in healthy peopleSignals from small randomized trials: it raises the glutathione pool in the short term and improves some oxidative markers, but clinical endpoints do not differSide effects: stomach and gut discomfort is fairly common; allergy is rare; take extra care with long-term high doses alongside anticoagulants, or if you have G6PD deficiencyIf you insist on trying it: 600 mg a day, watch for 1-3 months, and do not stack several antioxidant supplements at once
Q3 How the doses are tiered:
600 mg a day: a general maintenance dose1200 mg a day: the clinical dose for COPD2400 mg a day: the dose used in psychiatric research (in divided doses)Intravenous use in emergencies: the dose is calculated by body weight (Prescott 1977 used 300 mg/kg in total over 20 hours) and is given only in hospital
Q4 People who should not buy it for themselves:
People whose ancestry comes from regions where G6PD deficiency is common (the Mediterranean, the Middle East, Africa, Southeast Asia, southern China) and who have never been tested: ask a doctor before long-term high dosesPeople whose chronic asthma is currently flaringPeople on continuous anticoagulant treatmentPregnancy and breastfeedingI have a cold and want to fight the virus: there is no evidence for this; drink fluids and rest. The evidence for vitamin C and zinc is limited too; they are just cheaper
Price: ordinary NAC capsules are not expensive, and far better value than glutathione capsules.
In practice · Where it ranks among antioxidants
If you want to fight oxidation, this is the easiest path to get lost on in the supplement aisle: glutathione, , vitamin E, vitamin C, alpha-lipoic acid, coenzyme , quercetin, curcumin, resveratrol, pterostilbene, and more.First, face one fact: several large randomized trials (HOPE, SELECT, and some cancer chemoprevention trials) have shown that high-dose antioxidant supplements on their own do not work on such as cardiovascular disease, cancer, and death, and are sometimes even slightly harmful. The vitamin E story covers this lesson of a perfect mechanism and trials that came up empty (see Vitamin E).
A real antioxidant strategy, ranked by payoff:
1. Do not smoke, and drink less: these are the biggest sources of oxidative stress
2. Sleep 7-9 hours a night
3. Eat a variety of vegetables and fruit every day (400-500 g): you take in the whole combination of polyphenols, carotenoids, and vitamin C, which is closer to what has clinical evidence than any single-molecule supplement
4. Regular aerobic exercise plus strength training: it upregulates the body's own antioxidant system (the NRF2 pathway) and is more sustainable than adding antioxidants from outside
5. If you have a specific indication (paracetamol poisoning, ): NAC is one of the few items on this list that can be recommended, because it acts on the glutathione system, the hub of antioxidant defense; for compulsive behaviors there are only small trials, so it is only an add-on to discuss with a psychiatrist
6. If you already do items 1-5 and still want to add one thing: take NAC at 600 mg a day for a while, and watch whether you notice a real difference
What not to stack:
NAC plus oral glutathione, cystine powder, high-dose vitamin E, alpha-lipoic acid, coenzyme Q10, and so on: swallowing an antioxidant salad does not make you more protected against oxidation, and it may interfere with the body's normal reactive oxygen species () signals (adaptation to exercise and immune responses both need those signals)
The antioxidant system is the body's own finely tuned feedback network. Your job is not to shovel raw materials in from outside, but not to break that system.
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References · 6
- Atkuri, K. R., Mantovani, J. J., Herzenberg, L. A., & Herzenberg, L. A. (2007). N-Acetylcysteine — a safe antidote for cysteine/glutathione deficiency. Current Opinion in Pharmacology, 7(4), 355-359. 10.1016/j.coph.2007.04.005
- Witschi, A., Reddy, S., Stofer, B., & Lauterburg, B. H. (1992). The systemic availability of oral glutathione. European Journal of Clinical Pharmacology, 43(6), 667-669. 7 healthy volunteers, one oral dose of glutathione 0.15 mmol/kg (about 3 g): plasma glutathione, cysteine and glutamate did not rise significantly over 270 min; the authors conclude systemic availability of oral glutathione is negligible because intestinal and hepatic gamma-glutamyltransferase hydrolyse it (abstract, PMID 1362956). 10.1007/BF02284971
- Prescott, L. F., Park, J., Ballantyne, A., Adriaenssens, P., & Proudfoot, A. T. (1977). Treatment of paracetamol (acetaminophen) poisoning with N-acetylcysteine. The Lancet, 2(8035), 432-434. 15 patients with paracetamol poisoning given IV N-acetylcysteine 300 mg/kg over 20 h, with no control group: liver-function tests stayed normal or only slightly disturbed in 11 of the 12 treated within 10 h; severe liver damage developed in the other one and in all 3 treated more than 10 h after ingestion (abstract, PMID 70646). 10.1016/S0140-6736(77)90612-2
- Rumack, B. H., Peterson, R. C., Koch, G. G., & Amara, I. A. (1981). Acetaminophen overdose: 662 cases with evaluation of oral acetylcysteine treatment. Archives of Internal Medicine, 141(3), 380-385. 662 consecutive acetaminophen overdoses; those at risk by the study nomogram got oral acetylcysteine (an open case series, no control group). Transient SGOT elevations in 7% of potentially toxic patients treated within 10 h, 29% at 10-16 h and 62% at 16-24 h; no deaths among those treated within 24 h apart from one alleged gunshot homicide (abstract, PMID 7469629). 10.1001/archinte.1981.00340030112020
- Cazzola, M., Calzetta, L., Page, C., Jardim, J., Chuchalin, A. G., Rogliani, P., & Matera, M. G. (2015). Influence of N-acetylcysteine on chronic bronchitis or COPD exacerbations: a meta-analysis. European Respiratory Review, 24(137), 451-461. 13 studies, 4155 COPD patients (NAC 1933, placebo or control 2222): fewer exacerbations with NAC, RR 0.75 (0.66-0.84), more apparent in patients without airway obstruction; high doses (over 600 mg/day) were also effective in spirometry-confirmed COPD (RR 0.75); adverse reactions not dose-dependent. The authors recommend at least 1200 mg/day with documented obstruction and 600 mg/day without (abstract, PMID 26324807). 10.1183/16000617.00002215
- Smaga, I., Frankowska, M., & Filip, M. (2021). N-acetylcysteine as a new prominent approach for treating psychiatric disorders. British Journal of Pharmacology, 178(13), 2569-2594. 10.1111/bph.15456