Aspirin And Asthma

[Wagner83]

I noticed worse breathing with small amounts of aspirin a few times now, I'm considering dropping the oj and see how my breathing during exercise changes:

Aspirin and Other Drugs That May Trigger Asthma

Aspirin Sensitivity, Asthma, and Nasal Polyps. Some people with asthma cannot take aspirin or NSAIDs because of what’s known as Samter’s triad -- a combination of asthma, aspirin sensitivity, and nasal polyps. Nasal polyps are small growths that form inside the nasal cavity. This aspirin sensitivity occurs in about 30% to 40% of those who have asthma and nasal polyps. Many people with Samter's triad have nasal symptoms, such as runny nose, postnasal drip , and congestion, along with asthma symptoms, such as wheezing, cough, and shortness of breath. Talk to your doctor about options other than aspirin and NSAIDs if you have this.
​

Nasal polyps are part of my family, but I don't think I have any, at least I didn't check and prefer ignorance as my diagnosis.

Aspirin-Exacerbated Respiratory Disease: Evaluation and Management

Abstract
The clinical syndrome of aspirin-exacerbated respiratory disease (AERD) is a condition where inhibition of cyclooxygenase-1 (COX-1) induces attacks of upper and lower airway reactions, including rhinorrhea and varying degrees of bronchospasm and laryngospasm. Although the reaction is not IgE-mediated, patients can also present with anaphylactic hypersensitivity reactions, including hypotension, after exposure to COX-1 inhibiting drugs. All patients with AERD have underlying nasal polyps and intractable sinus disease which may be difficult to treat with standard medical and surgical interventions. This review article focuses on the management of AERD patients with a particular emphasis on aspirin desensitization and continuous treatment with aspirin.​

Aspirin-induced asthma - Wikipedia

The symptoms of respiratory reactions in this syndrome are hypersensitivity reactions to NSAIDs rather than the typically described true allergic reactions that trigger other common allergen-induced asthma, rhinitis, or hives. The NSAID-induced reactions do not appear to involve the common mediators of true allergic reactions, immunoglobulin E or T cells.[4] Rather, AERD is a type of NSAID-induced hypersensitivity syndrome.

Spoiler: Guesswork on the causes

The disorder is thought to be caused by an anomaly in the arachidonic acid metabolizing cascade which leads to increased production of pro-inflammatory cysteinyl leukotrienes, a series of chemicals involved in the body's inflammatory response. When medications like NSAIDs or aspirin block the COX-1 enzyme, production of thromboxane and some anti-inflammatory prostaglandins is decreased, and in patients with aspirin-induced asthma this results in the overproduction of pro-inflammatory leukotrienes to causes severe exacerbations of asthma and allergy-like symptoms.[13][14][15][16][17][18] The underlying cause of the disorder is not fully understood, but there have been several important findings:

• Abnormally low levels of prostaglandin E2 (PGE2), which is protective for the lungs, has been found in patients with aspirin-induced asthma and may worsen their lung inflammation.[19] (@Travis, this one was written for you)
• In addition to the overproduction of cystinyl leukotrienes, overproduction of 15-lipoxygenase-derived arachidonic acid metabolites viz., 15-hydroxyicosatetraenoic acid and eoxins by the eosinophils isolated from the blood of individuals with AERD; certain of these products may help promote the inflammatory response.[20][21]
• Overexpression of both the cysteinyl leukotriene receptor 1[22] and the leukotriene C4 synthase[23] enzyme has been shown in respiratory tissue from patients with aspirin-induced asthma, which likely relates to the increased response to leukotrienes and increased production of leukotrienes seen in the disorder.
• The attachment of platelets to certain leukocytes in the blood of patients with aspirin-sensitive asthma has also been shown to contribute to the overproduction of leukotrienes.[24]
• There may be a relationship between aspirin-induced asthma and TBX21, PTGER2, and LTC4S.[25]
• Eosinophils isolated from the blood of aspirin-induced asthma subjects (as well as severe asthmatic patients) greatly overproduce 15-hydroxyicosatetraenoic acid and eoxin C4 when challenged with arachidonic acid or calcium ionophore A23187, compared to the eosinophils taken from normal or mildly asthmatic subjects; aspirin treatment of eosinophils from aspirin intolerant subjects causes the cells to mount a further increase in eoxin production.[20] These results suggest that 15-lipoxygenase and certain of its metabolites, perhaps eoxin C4, as contributing to aspirin-induced asthma in a fashion similar to 5-lipoxygenase and its leukotriene metabolites.

@tca300 I think you said you take aspirin and experienced issues with oj, on your thread @Diokine shared his interpretation of potential issues from too much salicylates (CO, oj, aspirin..). On the other hand Travis has spoken about the anti-fungal effects of aspirin, and I think the properties of coconuts and coconut oil have been investigated by a few members and Ray Peat so that I don't have anything to add. It would be interesting to know if the worsened asthma/breathing issues and allergic reactions are from "die-off" effects:

Medication
The preferred treatment for many patients is desensitization to aspirin, undertaken at a clinic or hospital specializing in such treatment. In the United States, the Scripps Clinic in San Diego, CA,[27] the Massachusetts General Hospital in Boston, MA,[28] the Brigham and Women's Hospital in Boston, MA,[29] National Jewish Hospital in Denver [30] and Stanford University Adult ENT Clinic have allergists who routinely perform aspirin desensitization procedures for patients with aspirin-induced asthma. Patients who are desensitized then take a maintenance dose of aspirin daily and while on daily aspirin they often have reduced need for supporting medications, fewer asthma and sinusitis symptoms than previously, and many have an improved sense of smell. Desensitization to aspirin reduces the chance of nasal polyp recurrence, and can slow the regrowth of nasal polyps. Even patients desensitized to aspirin may continue to need other medications including nasal steroids, inhaled steroids, and leukotriene antagonists.
​

PS: a guess from gbol with aspirin use.

 

[Travis]

I noticed worse breathing with small amounts of aspirin a few times now, I'm considering dropping the oj and see how my breathing during exercise changes:

Aspirin and Other Drugs That May Trigger Asthma

Aspirin Sensitivity, Asthma, and Nasal Polyps. Some people with asthma cannot take aspirin or NSAIDs because of what’s known as Samter’s triad -- a combination of asthma, aspirin sensitivity, and nasal polyps. Nasal polyps are small growths that form inside the nasal cavity. This aspirin sensitivity occurs in about 30% to 40% of those who have asthma and nasal polyps. Many people with Samter's triad have nasal symptoms, such as runny nose, postnasal drip , and congestion, along with asthma symptoms, such as wheezing, cough, and shortness of breath. Talk to your doctor about options other than aspirin and NSAIDs if you have this.
​

Nasal polyps are part of my family, but I don't think I have any, at least I didn't check and prefer ignorance as my diagnosis.

Aspirin-Exacerbated Respiratory Disease: Evaluation and Management

Abstract
The clinical syndrome of aspirin-exacerbated respiratory disease (AERD) is a condition where inhibition of cyclooxygenase-1 (COX-1) induces attacks of upper and lower airway reactions, including rhinorrhea and varying degrees of bronchospasm and laryngospasm. Although the reaction is not IgE-mediated, patients can also present with anaphylactic hypersensitivity reactions, including hypotension, after exposure to COX-1 inhibiting drugs. All patients with AERD have underlying nasal polyps and intractable sinus disease which may be difficult to treat with standard medical and surgical interventions. This review article focuses on the management of AERD patients with a particular emphasis on aspirin desensitization and continuous treatment with aspirin.​

Aspirin-induced asthma - Wikipedia

The symptoms of respiratory reactions in this syndrome are hypersensitivity reactions to NSAIDs rather than the typically described true allergic reactions that trigger other common allergen-induced asthma, rhinitis, or hives. The NSAID-induced reactions do not appear to involve the common mediators of true allergic reactions, immunoglobulin E or T cells.[4] Rather, AERD is a type of NSAID-induced hypersensitivity syndrome.

Spoiler: Guesswork on the causes

The disorder is thought to be caused by an anomaly in the arachidonic acid metabolizing cascade which leads to increased production of pro-inflammatory cysteinyl leukotrienes, a series of chemicals involved in the body's inflammatory response. When medications like NSAIDs or aspirin block the COX-1 enzyme, production of thromboxane and some anti-inflammatory prostaglandins is decreased, and in patients with aspirin-induced asthma this results in the overproduction of pro-inflammatory leukotrienes to causes severe exacerbations of asthma and allergy-like symptoms.[13][14][15][16][17][18] The underlying cause of the disorder is not fully understood, but there have been several important findings:

• Abnormally low levels of prostaglandin E2 (PGE2), which is protective for the lungs, has been found in patients with aspirin-induced asthma and may worsen their lung inflammation.[19] (@Travis, this one was written for you)
• In addition to the overproduction of cystinyl leukotrienes, overproduction of 15-lipoxygenase-derived arachidonic acid metabolites viz., 15-hydroxyicosatetraenoic acid and eoxins by the eosinophils isolated from the blood of individuals with AERD; certain of these products may help promote the inflammatory response.[20][21]
• Overexpression of both the cysteinyl leukotriene receptor 1[22] and the leukotriene C4 synthase[23] enzyme has been shown in respiratory tissue from patients with aspirin-induced asthma, which likely relates to the increased response to leukotrienes and increased production of leukotrienes seen in the disorder.
• The attachment of platelets to certain leukocytes in the blood of patients with aspirin-sensitive asthma has also been shown to contribute to the overproduction of leukotrienes.[24]
• There may be a relationship between aspirin-induced asthma and TBX21, PTGER2, and LTC4S.[25]
• Eosinophils isolated from the blood of aspirin-induced asthma subjects (as well as severe asthmatic patients) greatly overproduce 15-hydroxyicosatetraenoic acid and eoxin C4 when challenged with arachidonic acid or calcium ionophore A23187, compared to the eosinophils taken from normal or mildly asthmatic subjects; aspirin treatment of eosinophils from aspirin intolerant subjects causes the cells to mount a further increase in eoxin production.[20] These results suggest that 15-lipoxygenase and certain of its metabolites, perhaps eoxin C4, as contributing to aspirin-induced asthma in a fashion similar to 5-lipoxygenase and its leukotriene metabolites.

@tca300 I think you said you take aspirin and experienced issues with oj, on your thread @Diokine shared his interpretation of potential issues from too much salicylates (CO, oj, aspirin..). On the other hand Travis has spoken about the anti-fungal effects of aspirin, and I think the properties of coconuts and coconut oil have been investigated by a few members and Ray Peat so that I don't have anything to add. It would be interesting to know if the worsened asthma/breathing issues and allergic reactions are from "die-off" effects:

Medication
The preferred treatment for many patients is desensitization to aspirin, undertaken at a clinic or hospital specializing in such treatment. In the United States, the Scripps Clinic in San Diego, CA,[27] the Massachusetts General Hospital in Boston, MA,[28] the Brigham and Women's Hospital in Boston, MA,[29] National Jewish Hospital in Denver [30] and Stanford University Adult ENT Clinic have allergists who routinely perform aspirin desensitization procedures for patients with aspirin-induced asthma. Patients who are desensitized then take a maintenance dose of aspirin daily and while on daily aspirin they often have reduced need for supporting medications, fewer asthma and sinusitis symptoms than previously, and many have an improved sense of smell. Desensitization to aspirin reduces the chance of nasal polyp recurrence, and can slow the regrowth of nasal polyps. Even patients desensitized to aspirin may continue to need other medications including nasal steroids, inhaled steroids, and leukotriene antagonists.
​

PS: a guess from gbol with aspirin use.

Hey Mito. A few studies I'd read only about a week ago indicated that the pharmacological inhibition of lipoxygenase had increased prostaglandins by freeing-up more arachidonate available for cyclooxygenase: This enzyme and its prostaglandins products gets the most attention, yet the lipoxygenase enzymes and its leukotrienes produced are also very important. I think it's logical to assume the converse would also hold, that this aspirin-mediated reaction could stem from an increase in leukotrienes consequent of cyclooxgenase inhibition. This idea gets support from the role leukotrienes play in the body, which act like powerful beacons for mononuclear leukocytes (i.e. basophils, eosinophils, neutrophils). Leukotriene B₄'s ability to attract leukocytes more than any other lipid has been demonstrated in countless studies going back decades.

Asthma is mediated by leukotriene B₄ and 13-hydroxylinoleic acid, the latter being a product of the enzyme 15-lipoxygenase; this has roughly 66% of the chemotactic potency as leukotriene B₄. Why 15-lipoxygenase adds a hydroxyl group onto linoleic acid's carbon №13, and not carbon №15 as perhaps supposed, is because this enzyme's was numbered using arachidonic acid as reference—which is two carbons longer. The leukotrienes are produced through the enzyme 5-lipoxygenase, and this does not have a hormonal linoleic acid product.

But don't take my word for it. A person can always go to Google Scholar and view for themselves the quality and quantity of articles resulting from the search-term: 'asthma and leukotriene B₄.' Increased levels are always found via bronchial lavage, and simply inhaling these atomized lipids will certainly cause symptoms. The increased presence of leukotriene B₄ in the asthmatic lung is really all that is needed to explain the concomitant eosinophilia, and the metabolite 13-hydroxylinoleic acid as been shown to cause bronchoconstriction through the capsaicin receptor. Inhibiting prostaglandin synthesis could logically be though to increase leukotriene B₄ synthesis through this substrate-shuttling mechanism, and the fact that you had any side-effects at all might indicate that you still have ω−6 fatty acids in your body! [Has Mito been eating eggs and chicken again?]

The plant molecules esculetin and baicalein inhibit lipoxygenase and decrease this type of asthma symptoms: The more acute reactions appear to be on account of histamine released from mast cell degranulation and eosinophil basic protein from its eponymous leukocyte. The eosinophil basic protein binds strongly the muscarinic acetylcholine receptor type II, a regulatory receptor controlling acetylcholine production (the inhibition of which increases acetylcholine). Some of the most powerful and classic asthma drugs, such as atropine and pilocarpine, work on this receptor.

So basically leukotriene B₄ works by attracting eosinophils, which degranulate and release toxic proteins, and 13-hydroxylinoleic works by doing this but also by binding capsaicin receptors.

Since inhibition of lipoxygenase increases prostaglandins and the inhibition of cyclooxygenase increases leukotrienes, the only two options are to inhibit both simultaneously or to eliminate ω−6 fatty acids entirely; I would strongly suggest doing the latter, and that more I read about them the more I tend to avoid them.

 

[michael94]

aspirate

 

[Wagner83]

Hey Mito. A few studies I'd read only about a week ago indicated that the pharmacological inhibition of lipoxygenase had increased prostaglandins by freeing-up more arachidonate available for cyclooxygenase: This enzyme and its prostaglandins products gets the most attention, yet the lipoxygenase enzymes and its leukotrienes produced are also very important. I think it's logical to assume the converse would also hold, that this aspirin-mediated reaction could stem from an increase in leukotrienes consequent of cyclooxgenase inhibition. This idea gets support from the role leukotrienes play in the body, which act like powerful beacons for mononuclear leukocytes (i.e. basophils, eosinophils, neutrophils). Leukotriene B₄'s ability to attract leukocytes more than any other lipid has been demonstrated in countless studies going back decades.

Asthma is mediated by leukotriene B₄ and 13-hydroxylinoleic acid, the latter being a product of the enzyme 15-lipoxygenase; this has roughly 66% of the chemotactic potency as leukotriene B₄. Why 15-lipoxygenase adds a hydroxyl group onto linoleic acid's carbon №13, and not carbon №15 as perhaps supposed, is because this enzyme's was numbered using arachidonic acid as reference—which is two carbons longer. The leukotrienes are produced through the enzyme 5-lipoxygenase, and this does not have a hormonal linoleic acid product.

But don't take my word for it. A person can always go to Google Scholar and view for themselves the quality and quantity of articles resulting from the search-term: 'asthma and leukotriene B₄.' Increased levels are always found via bronchial lavage, and simply inhaling these atomized lipids will certainly cause symptoms. The increased presence of leukotriene B₄ in the asthmatic lung is really all that is needed to explain the concomitant eosinophilia, and the metabolite 13-hydroxylinoleic acid as been shown to cause bronchoconstriction through the capsaicin receptor. Inhibiting prostaglandin synthesis could logically be though to increase leukotriene B₄ synthesis through this substrate-shuttling mechanism, and the fact that you had any side-effects at all might indicate that you still have ω−6 fatty acids in your body! [Has Mito been eating eggs and chicken again?]

The plant molecules esculetin and baicalein inhibit lipoxygenase and decrease this type of asthma symptoms: The more acute reactions appear to be on account of histamine released from mast cell degranulation and eosinophil basic protein from its eponymous leukocyte. The eosinophil basic protein binds strongly the muscarinic acetylcholine receptor type II, a regulatory receptor controlling acetylcholine production (the inhibition of which increases acetylcholine). Some of the most powerful and classic asthma drugs, such as atropine and pilocarpine, work on this receptor.

So basically leukotriene B₄ works by attracting eosinophils, which degranulate and release toxic proteins, and 13-hydroxylinoleic works by doing this but also by binding capsaicin receptors.

Since inhibition of lipoxygenase increases prostaglandins and the inhibition of cyclooxygenase increases leukotrienes, the only two options are to inhibit both simultaneously or to eliminate ω−6 fatty acids entirely; I would strongly suggest doing the latter, and that more I read about them the more I tend to avoid them.

Hey Travishnu,
I do eat a couple of egg yolks pretty regularly but given all the efforts I have done compared to the average joe, the fact that my fat intake is pretty low but mostly saturated, that I'm rather lean (e.g. waist-line is a bit crowded but the abs above it are visible), as well as tca300's experience (most PUFAs-depleted member award?) I wonder if the issues may stem from elsewhere, as you suggested yourself here (I do have tongue coating) :

In the absence of dietary ω−6 fatty acids, their formation in the body can still occur. Although humans don't have a Δ⁶-desaturase enzyme, helminths and fungi do. The pathological yeast/fungi Candida albicans is known to synthesize arachidonic acid de novo, which it will even form prostaglandin E₂ with despite not having a genetic sequence homologous to mammalian cyclooxygenase. The B-series leukotrienes would be expected to form in the process, and even nonenzymatically as they are simply hydroxylated lipids (and especially in the presence of a neutrophil attack, which releases superoxide towards the pathogen). Since primate leukocytes have evolved in the tropics where both helminth infections are more common and plants do not synthesize ω−6 fatty acids, I maintain that the relatively potent chemoattraction of leukotriene B₄ on leukocytes had more-or-less evolved as a fungi- and helminth-seeking device. The fact that eosinophils will follow a leukotriene B₄ gradient while also containing a toxic cargo in its cytosol—containing eosinophil basic protein, eosinophil neurotoxin, and eosinophil peroxidase—which has been shown to kill helminths upon degranulation further this idea. Accepting this line of line of thinking eventually leads to the thought that the unnatural ω−6-derived leukotriene B₄ will decrease immunological sensitivity by increasing background levels over that found in the vicinity of helminths and yeast. Eosinophils have also been shown to be attracted to 13-hydroxylinoleic acid with roughly ²⁄₃·leukotriene B₄ potency, but even this reduced attraction is far greater than even the most powerful ω−3 and ω−9 derivatives.

Then comes the avoidance of almonds, grains, seeds, olive oil, avocados . . . and the egg yolks start going down the sink.​

For the record, bromelain, 500 mg, 5000GDU, did help get rid of the symptoms, I just made sure not to ingest it too close to the aspirin to avoid over-thinning the blood. I wonder what the difference between an allergic, histamine-mediated reaction is and asthma? I think it is well accepted that high histamine foods may lead to exaggerated reactions of the body (cheese, wine..). The reason for such a sensitivity in certain individuals is an other story, but wouldn't asthma be a low-to-high grade continuous allergic reaction? If I understood what you wrote, you suggested that the histamine reaction is a downstream effect of the harm done by leukotrienes and 13-hydroxylinoleic acid, the latter being a metabolite of the former and not produced (therefore, no broncho-constriction) if there are no out-of-control fungus within the body as well as dietary w-6 fatty acids. It would still mean that leukotrienes, are, for some reason, present in high numbers in asthmatic lungs.

 

[fradon]

salycylate sensitivies...as too much depletes sulphate and not enough sulphate well you start having problems in all areas, intestinal, leaky gut.

 

[postman]

Hey Travishnu,
I do eat a couple of egg yolks pretty regularly but given all the efforts I have done compared to the average joe, the fact that my fat intake is pretty low but mostly saturated, that I'm rather lean (e.g. waist-line is a bit crowded but the abs above it are visible), as well as tca300's experience (most PUFAs-depleted member award?) I wonder if the issues may stem from elsewhere, as you suggested yourself here (I do have tongue coating) :



For the record, bromelain, 500 mg, 5000GDU, did help get rid of the symptoms, I just made sure not to ingest it too close to the aspirin to avoid over-thinning the blood. I wonder what the difference between an allergic, histamine-mediated reaction is and asthma? I think it is well accepted that high histamine foods may lead to exaggerated reactions of the body (cheese, wine..). The reason for such a sensitivity in certain individuals is an other story, but wouldn't asthma be a low-to-high grade continuous allergic reaction? If I understood what you wrote, you suggested that the histamine reaction is a downstream effect of the harm done by leukotrienes and 13-hydroxylinoleic acid, the latter being a metabolite of the former and not produced (therefore, no broncho-constriction) if there are no out-of-control fungus within the body as well as dietary w-6 fatty acids. It would still mean that leukotrienes, are, for some reason, present in high numbers in asthmatic lungs.

Bromelain cured your aspirin asthma?

 

[Wagner83]

Bromelain cured your aspirin asthma?

It helped with the symptoms. At some point I started reacting to aspirin and even oj but now I'm fine. Perhaps it had to do with the overall quantity as well as springtime, temporary healthstate..

 

[Faith]

Citrus is a histamine liberator.

 

[Lizb]

Citrus is a histamine liberator.

So what do I drink instead?

 

[Faith]

I have had asthma for over 40 years ( I'm 50 ), and have developed a histamine sensitivity. I have been modifying my diet quite a bit trying to be more "Peaty", but citrus and eggs just don't work for me. I have skin reactions to both unfortunately. I too would like to know how I can get the benefits of citrus from something else. Just FYI asthma is mediated by many different things, not just leukoteine. Histamine promotes bronchospasm and mucus production and can definitely cause an asthma attack. As far as the aspirin goes, I think the salycilate would be the problem.

 

[Lizb]

I have had asthma for over 40 years ( I'm 50 ), and have developed a histamine sensitivity. I have been modifying my diet quite a bit trying to be more "Peaty", but citrus and eggs just don't work for me. I have skin reactions to both unfortunately. I too would like to know how I can get the benefits of citrus from something else. Just FYI asthma is mediated by many different things, not just leukoteine. Histamine promotes bronchospasm and mucus production and can definitely cause an asthma attack. As far as the aspirin goes, I think the salycilate would be the problem.

I definitely have a salycilate intolerance but thought it was only from green juices (really bad - lungs fill with mucous) but I'm wondering if, having heard you mention orange juice whether it might be a problem too. I have bronchiectasis so it's quite difficult to know exactly what's going on, unless it's extreme. Thanks for the heads up - I'll drop the orange juice for a bit to see it there's a different.

 

[Faith]

Lizb - I'm brand new to this forum (or any forum), and I know we can all help each other. Discovering my histamine intolerance changed my life. My quality of life was not good before that. Reducing my histamine burden allows me to have some higher histamine foods occasionally, and I want so much to be able to have fresh orange juice - hoping that continuing to improve my health will eventually resolve the histamine intolerance.