Knocking on Wood

@rvan.rvan I would hope too. I used to be very breathless. I have never gone on the big 3. My path has been just 7% saline, correcting my Gerd, excercising very regularly and eating well and I now breathe like a champ. (Oh, and I also take NAC for my lungs) I was originally haphazardly diagnosed by my GP as having COPD but later a pulmonologist found MAC and Bronchiectas.... Shortness of breath had been a problem for several years prior to diagnosis but cleared pretty shortly after addressing the Gerd and really taking care of my general health with a good diet and excercise. I am hopeful that you will get there. Sorry this is a winded response...but it is hard to say any one thing was responsible. Kate

@alleycatkate Hello Kate could you please give more info on the NAC? brand, strength, and timing would be great. Thanks Bill

@alleycatkate Hello Kate could you please give more info on the NAC? brand, strength, and timing would be great. Thanks Bill

@poodledoc and @rvan ...Hi Bill and Ryan...well, another lenghly response from me. Seems my norm. 🙂
I googled MAC & NAC ...afraid of getting a cheezy recipe. Although none directly related to MAC, there are so many articles on NAC in relation to lung health, clearance, reduction of exacerbations etc. and mycobacterias...Following is one I found particularly interesting and I am posting an excerpt from the article: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5084440/ It is entitled N-acetyl-cysteine exhibits potent anti-mycobacterial activity in addition to its know anti-oxidative functions. I personally take NAC 600 mg 2x a day..made by NOW. Gee...if ever there was a go to supplement for our ills, I would think it would be NAC. Kate

N-acetyl-cysteine (NAC) is included in the World Health Organization’s list of essential medicines; a list that details the most relevant medications needed for a basic health system [1]. Acetyl-cysteine is a derivative of cysteine in which an acetyl group is attached to nitrogen. Due to its disulfide reducing activity, NAC is used as a mucolytic agent to promote expectoration [2]. NAC is commonly prescribed as an adjunct therapy in patients with a wide range of respiratory diseases characterized by formation of thick mucus, such as cystic fibrosis [2–4]. At high doses, NAC results in significantly improved small airway function and decreased exacerbation frequency in patients with stable chronic obstructive pulmonary disease (COPD) [3, 4]. NAC’s mucolytic activity is also the basis of its use in liquefying sputum samples for the microscopic detection of acid-fast bacilli (AFB) in suspected pulmonary tuberculosis (TB) patients [5]. Furthermore, in both experimental animal models and clinical studies, NAC displays a protective effect on acute liver injury induced by anti-TB drugs in acetaminophen-dependent or independent conditions [6–11]. In patients with type 2 diabetes, NAC holds promise in primary prevention of cardiovascular complications and systemic inflammation [12–14].

In addition to the above clinical applications, NAC has been employed as a potent anti-oxidant in several experimental models of infection and cancer in vitro and in vivo [15–20]. In these settings, NAC serves as a pro-drug to L-cysteine, which is a precursor to the biologic antioxidant glutathione. This anti-oxidant property of NAC is associated with strong anti-inflammatory effects, which have been suggested to inhibit the activation of nuclear factor-κB (NF-κB) with subsequent inhibition of cytokine synthesis [2, 21, 22]. In a mammalian model of Mycobacterium tuberculosis infection, NAC has been shown to diminish TB-driven lung pathology and inflammatory status, as well as to reduce mycobacterial infection loads in the lung [23]. These effects were attributed to the drug’s anti-oxidant properties and immune regulatory activities. Whether NAC limits M. tuberculosis infection in this situation through a direct microbicidal effect on M. tuberculosis was not addressed. Indeed, NAC has been shown to exhibit anti-microbial activity against a number of bacterial pathogens including Pseudomonas aeruginosa, Staphylococcus aureus, Helicobacter pylori, Klebsiella pneumoniae and Enterobacter cloacae [17, 24–26].

In this study, we demonstrate that NAC directly impairs the growth of several species of mycobacteria in vitro independent of its inhibitory effects on the host NADPH oxidase system. This anti-mycobacterial effect was also observed in an experimental model in vivo. Thus, NAC may limit M. tuberculosis infection and disease both through suppression of the host oxidative response and through direct antimicrobial activity. This dual host and pathogen directed function makes the drug an interesting candidate for use as adjunct therapy for tuberculosis.

@goddard Hi Granny...There has been lots of discussion on this site about 3% vs 7% saline solution. If you can tolerate the 7, it seems to be superior. I am attaching a site that has a chart showing that the 7% is effective in killing MAC invitro. I think it speaks volumes to the efficacy of the higher solution vs the 3%. Please check chart 2 in the article. Best of luck to you. Kate
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4850692/

@poodledoc and @rvan ...Hi Bill and Ryan...well, another lenghly response from me. Seems my norm. 🙂
I googled MAC & NAC ...afraid of getting a cheezy recipe. Although none directly related to MAC, there are so many articles on NAC in relation to lung health, clearance, reduction of exacerbations etc. and mycobacterias...Following is one I found particularly interesting and I am posting an excerpt from the article: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5084440/ It is entitled N-acetyl-cysteine exhibits potent anti-mycobacterial activity in addition to its know anti-oxidative functions. I personally take NAC 600 mg 2x a day..made by NOW. Gee...if ever there was a go to supplement for our ills, I would think it would be NAC. Kate

N-acetyl-cysteine (NAC) is included in the World Health Organization’s list of essential medicines; a list that details the most relevant medications needed for a basic health system [1]. Acetyl-cysteine is a derivative of cysteine in which an acetyl group is attached to nitrogen. Due to its disulfide reducing activity, NAC is used as a mucolytic agent to promote expectoration [2]. NAC is commonly prescribed as an adjunct therapy in patients with a wide range of respiratory diseases characterized by formation of thick mucus, such as cystic fibrosis [2–4]. At high doses, NAC results in significantly improved small airway function and decreased exacerbation frequency in patients with stable chronic obstructive pulmonary disease (COPD) [3, 4]. NAC’s mucolytic activity is also the basis of its use in liquefying sputum samples for the microscopic detection of acid-fast bacilli (AFB) in suspected pulmonary tuberculosis (TB) patients [5]. Furthermore, in both experimental animal models and clinical studies, NAC displays a protective effect on acute liver injury induced by anti-TB drugs in acetaminophen-dependent or independent conditions [6–11]. In patients with type 2 diabetes, NAC holds promise in primary prevention of cardiovascular complications and systemic inflammation [12–14].

In addition to the above clinical applications, NAC has been employed as a potent anti-oxidant in several experimental models of infection and cancer in vitro and in vivo [15–20]. In these settings, NAC serves as a pro-drug to L-cysteine, which is a precursor to the biologic antioxidant glutathione. This anti-oxidant property of NAC is associated with strong anti-inflammatory effects, which have been suggested to inhibit the activation of nuclear factor-κB (NF-κB) with subsequent inhibition of cytokine synthesis [2, 21, 22]. In a mammalian model of Mycobacterium tuberculosis infection, NAC has been shown to diminish TB-driven lung pathology and inflammatory status, as well as to reduce mycobacterial infection loads in the lung [23]. These effects were attributed to the drug’s anti-oxidant properties and immune regulatory activities. Whether NAC limits M. tuberculosis infection in this situation through a direct microbicidal effect on M. tuberculosis was not addressed. Indeed, NAC has been shown to exhibit anti-microbial activity against a number of bacterial pathogens including Pseudomonas aeruginosa, Staphylococcus aureus, Helicobacter pylori, Klebsiella pneumoniae and Enterobacter cloacae [17, 24–26].

In this study, we demonstrate that NAC directly impairs the growth of several species of mycobacteria in vitro independent of its inhibitory effects on the host NADPH oxidase system. This anti-mycobacterial effect was also observed in an experimental model in vivo. Thus, NAC may limit M. tuberculosis infection and disease both through suppression of the host oxidative response and through direct antimicrobial activity. This dual host and pathogen directed function makes the drug an interesting candidate for use as adjunct therapy for tuberculosis.

what is difference between NAC and mucinex, and is NAC more effective as mucolytic?