Do you have asthma? Do you know or love someone who does?

Here’s how to use supplemental glutathione (reduced, liposomal, and nebulized) to help with this condition.

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  1. My naturopath used a nebulizer with glutathione and it helped me immensely. It smelled a bit strange though….like sulfur….

  2. So here’s my understanding, as a non-scientist, of the inhaled glutathione issue. Chris, please tell me whether this is correct.
    The study David cites says the glutathione solution caused symptoms because the subjects were sensitive to sulfite. But glutathione doesn’t include a sulfite ion. If it undergoes a reaction that produces sulfite, some of it is no longer glutathione. It can’t act as an antioxidant, and it can’t form the bond to make nitrosoglutathione, because the sulfur atom is no longer where it needs to be to perform those functions. Clearly it’s more stable than that inside the body, or we wouldn’t have evolved to rely on it so heavily. Also, not all sulfite-sensitive asthmatics need medication every day, so we aren’t constantly getting triggered by our own lung fluid.
    So what degraded the glutathione in the study? My guess is its own acidity. The paper reports that the solution was acidic. That means the glutathione molecules experienced significantly different conditions than they would in the body, so that looks like a likely culprit.
    That study is so old they apparently didn’t recognize the role of nitrosoglutathione yet. Nowadays at least one source mentions adding sodium bicarbonate to glutathione for inhalation, in order to buffer the acidity. I’m guessing this prevents it from forming sulfite when mixed with water. This would make it safe for sulfite-sensitive patients.
    But as patients, we don’t actually need to know all these details that aren’t in the video. Inhaled glutathione is not a change in diet, it’s a medical treatment. It should be prescribed by a health care practitioner, and that practitioner will know how to prescribe it to be formulated correctly.

    1. Acidity stabilizes glutathione.

      You are right that it does not contain sulfite. But the cysteine can be catabolized to sulfite, and if molybdenum is deficient, the sulfite can accumulate.

      I have no idea how likely that is to occur in the lungs upon direct inhalation. Perhaps something in the solution was an irritant.

      1. Thanks for the information. I don’t know enough about this stuff to even form reasonable hypotheses; that’s why we need experts like you.
        Sure, people with impaired sulfur catabolism should also work on that. I personally feel significantly better since I read the free preview of the Cheat Sheet and started managing my molybdenum. But what if that problem isn’t fixed yet? Is it safer to fix the sulfite sensitivity first and wait to use supplemental glutathione, whether it’s oral or inhaled? That’s what I really want to know.
        So has inhaled glutathione been used safely in patients known to be sensitive to sulfite? If it has, even if it’s just anecdotal evidence, it should be safe to say, “Oh, the Marrades et al. study must have done something that didn’t work, even if we don’t know what went wrong,” and not conclude that the treatment is contraindicated. In that case, the sensible course of action for patients would be to try it carefully, starting with a low dose, under medical supervision, and see if it helps.

        1. I don’t think anyone has broken down sulfite-sensitive and non-sensitive people for GSH inhalation. I’m simply listing it as something to try, when other avenues for increasing GSH levels have proven inadequate, and to do so with medical supervision. Yes, it is definitely best to fix any deficiencies before going to something pharmaceutical in nature.

  3. Thanks for answering my question Chris, I know it was a deep observation. If you get the chance to check out Dr. Pall’s work (there are several presentations on youtube about this topic), I would love to hear your feedback!

  4. Hi Chris,

    Are you familiar with Dr. Martin Pall’s work regarding the Nitric Oxide/Peroxynitrite (NO/ONOO) cycle? He believes this cycle can get stuck in a negative feedback loop after mold, chemical exposure, etc. in certain individuals that then creates a cascade of free radicals leading to more sensitivity to said triggers.

    It is my understanding through your work that glutathione + NO help alleviate asthma. I have suffered from mold sensitivity for years that keeps getting worse and even now some asthmatic symptoms upon exposure. Is it possible to boost NO in the lungs specifically to treat asthma but not affect the NO/ONOO cycle systemically? I know this is an out there question but I am trying to bridge two schoools of thought and have yet to find anyone who can answer my question.

    Thanks for all you do!

    1. I am not, but I can see the loop idea making sense, because oxidative stress makes the enzyme make superoxide instead of NO, which causes more oxidative stress.

    2. And no I don’t know how to isolate a treatment to the lungs. Except obviously inhalation but I don’t know what increases NO by that route.

        1. See these comments by Jones et al:

          In light of these observations, two studies have attempted to administer GSH via inhalation to subjects with asthma. In the first study, a 600-mg glutathione solution (composition unclear) was administered by nebulization to 12 young adults with mild-to-moderate asthma in a double-blind, placebo-controlled, cross-over study (16). Subjects with asthma were pretreated with the glutathione solution or placebo and then immediately underwent challenge with ultrasonically nebulized distilled water. Compared to placebo, the glutathione solution attenuated the fall in the forced expiratory volume in one second resulting from the challenge (6.04 L decline vs. 20.41 L decline for glutathione solution vs. placebo) (16). However, in another study involving eight adults with mild asthma, a similar glutathione solution (600 mg, composition unknown) administered by nebulization resulted in increased airway resistance, decreased pulmonary function measured by the forced expiratory volume in one second, and increased asthma symptoms, including severe wheezing and breathlessness (n=1), breathlessness (n=2), and cough (n=4) (213). The reasons underlying the bronchoconstricting effect of the glutathione solution are not clear but may be related to sulfite sensitivity since the hypertonic acid solution that served as the placebo resulted in cough in only one subject (213). These findings are in contrast with those from other studies, which did not reveal toxic or adverse effects with similar inhaled glutathione solutions (300–600 mg) administered to subjects with cystic fibrosis (32, 118, 128, 283), chronic otitis media (314), idiopathic pulmonary fibrosis (39), human immunodeficiency virus (138), and chronic rhinitis (313). In those studies, nebulization of the glutathione solution resulted in lower airway GSH deposition (118) in treated subjects with a significant increase in epithelial lining fluid GSH concentrations (39, 118, 138, 283). Increased airway GSH availability in those studies was further associated with decreased O•2− release by airway alveolar macrophages (39, 283), decreased airway prostaglandin E2 synthesis (128), and increased circulating T cells in the bronchoalveolar lavage of treated subjects (128). A small randomized, double-blind, placebo-controlled pilot study of glutathione inhalation in children with cystic fibrosis also demonstrated greater peak expiratory flows and improved respiratory symptoms in the glutathione-treated group (32). While meta-analyses have found no evidence to recommend the routine clinical use of nebulized glutathione or thiol derivatives (240), these analyses were limited by the quality of the trials conducted. Given the profound GSH/GSSG balance that accompanies asthma, further research on the safety and efficacy of inhaled glutathione solutions for asthma may be warranted.

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