Knocking on Wood

Thanks for forwarding citation. I agree this study says that 7% can be used therapeutically to kill MAC, but that 3% doesn't. . I will have to find the study my doc at UCLA referenced when my MAC was diagnosed in 2018, which said 3% was was as good--I think maybe the point of it (I cant remember) was whether 3% worked as well as mycolytic, thinning mucus (but not looking at whether saline was killing it). BTW, no doc has ever said anything about killing MAC with saline to me. After 15 years of totally dry cough, last spring I started having nagging productive cough instead of dry cough; in CT scan April 2020 some of mucus in little spots in middle lobe where I have bronchiectasis was gone, compared to some earlier scans. In 2018, I went to a doc who took the time to look at my CT scans from 2009-2018, and he said it waxed and waned over the years, would get better and worse. Im not sure if he meant the little spots of mucous were waxing and waning--

Here is cite to MSKCC discussion on NAC. https://www.mskcc.org/cancer-care/integrative-medicine/herbs/n-acetylcysteine

Is it your understanding that the GERD causes the bronchiectasis? which in turn sets you up for MAC by not allowing you to expel the MAC you've breathed in from normal air. Its my understanding that all sorts of people at any particular time might have some MAC bugs in their lungs because they are so common, but only those with MAC disease keep them in lungs, act as host to the bug. Is that your understanding? I had my most recent MAC doc tell me she thought I had GERD. But I dont have signs of it in my esophagus. I did not do the 24 hour test.

If it is NTM OR aspiration-- are they both MAC?

@goddard MAC (mycobacterium avium complex) is an NTM (non-tuberculosis mycobacterium). There are over 170 different types of mycobacterium; tuberculosis is one and, believe it or not, leprosy is also one. The different types vary in contagion and their effect on us. Bronchiectasis is damage to the bronchial tubes. It can be idiopathic, (unknown cause), or caused by many things; such as GERD (gastric esophageal reflux disease), silent aspiration of gastric acid, constant bronchitis, pneumonia, inhaling something damaging, or you can be born with it. If you have bronchiectasis, as many of us on this forum do, it makes you susceptible to getting MAC and/or getting sick from it with varying symptoms; constant cough, fever, weight loss, fatigue, night sweats. When the infection is active, it also causes additional lung damage such as cavities in the lungs. It may also contribute to getting lung nodules. Lung nodules can also caused by any type of inflammation in the lungs; inhaling something irritating or hazardous, silent aspiration, GERD, etc. Some of us, with bronchiectasis and a diagnosis of MAC or MAI (mycobacterium avium intercellular), don’t have any other symptoms besides the cough. Some people take antibiotics for a long time to get rid of the NTM infections. Most of us inhale some percentage of hypertonic saline since studies have shown that it helps control the NTM infection. To my knowledge, there is no cure for bronchiectasis and it is progressive. You can slow the progression by daily lung clearance, exercise, good diet, but having it makes you susceptible to lung infections. So basically — NTMs, bronchiectasis, GERD, cavities, nodules, are all somewhat connected. There doesn’t seem to be a consensus as to which comes first or which causes what. Although I can explain it, (I think accurately), that doesn’t really mean I actually understand it. Lol. I hope this helps.
Gina

@goddard MAC (mycobacterium avium complex) is an NTM (non-tuberculosis mycobacterium). There are over 170 different types of mycobacterium; tuberculosis is one and, believe it or not, leprosy is also one. The different types vary in contagion and their effect on us. Bronchiectasis is damage to the bronchial tubes. It can be idiopathic, (unknown cause), or caused by many things; such as GERD (gastric esophageal reflux disease), silent aspiration of gastric acid, constant bronchitis, pneumonia, inhaling something damaging, or you can be born with it. If you have bronchiectasis, as many of us on this forum do, it makes you susceptible to getting MAC and/or getting sick from it with varying symptoms; constant cough, fever, weight loss, fatigue, night sweats. When the infection is active, it also causes additional lung damage such as cavities in the lungs. It may also contribute to getting lung nodules. Lung nodules can also caused by any type of inflammation in the lungs; inhaling something irritating or hazardous, silent aspiration, GERD, etc. Some of us, with bronchiectasis and a diagnosis of MAC or MAI (mycobacterium avium intercellular), don’t have any other symptoms besides the cough. Some people take antibiotics for a long time to get rid of the NTM infections. Most of us inhale some percentage of hypertonic saline since studies have shown that it helps control the NTM infection. To my knowledge, there is no cure for bronchiectasis and it is progressive. You can slow the progression by daily lung clearance, exercise, good diet, but having it makes you susceptible to lung infections. So basically — NTMs, bronchiectasis, GERD, cavities, nodules, are all somewhat connected. There doesn’t seem to be a consensus as to which comes first or which causes what. Although I can explain it, (I think accurately), that doesn’t really mean I actually understand it. Lol. I hope this helps.
Gina

@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.