Asthma episode coincides with high ETCO2 (End Tidal Carbon Dioxide), high temperatures, and need to hyperventilate

[tastyfood]

I have been recently been posting about my asthmatic episodes, likely due to continued high dose aspirin. I've been trying to prevent the attacks from happening this last week, and have noticed that certain things are sending me to a respiratory acidosis state. I have two cases of taking high vitamin K and a dose of B vitamins (Energin) sending me to state of having to hyperventilate to get my breathing back to normal.

When I get the asthma attack is when I seem to be exhaling more carbon dioxide. I have a capnometer that goes up to 72 mmHG while I'm having difficulty breathing and feel a need to hyperventilate. These episodes also coincide with very high temperatures, close to 100F.

Is this a normal reaction to pushing the production of carbon dioxide too far? The need to hyperventilate kicks in as a way to bring balance back?

Thank you!

 

[redsun]

Hypercapnia: An Aggravating Factor in Asthma

Asthma is a common chronic respiratory disorder with relatively good outcomes in the majority of patients with appropriate maintenance therapy. However, in a small minority, patients can experience severe asthma with respiratory failure and hypercapnia, ...

www.ncbi.nlm.nih.gov

"Recent discoveries indicate that hypercapnia increases airway contractility, impairs the innate immune response, and promotes adipogenesis, which likely underlies the negative effects of elevated carbon dioxide (CO2) on airway contraction, respiratory infections and obesity in patients with asthma."

 

[tastyfood]

Thanks @redsun. Finding interesting posts about hypercapnia in the forum now.

I had my blood bicarbonate (what the lab calls serum CO2) tested, and it wasn't high (26, top of the normal range is 30), which makes me think these hypercapnia episodes have been short-lived.

 

[redsun]

Thanks @redsun. Finding interesting posts about hypercapnia in the forum now.

I had my blood bicarbonate (what the lab calls serum CO2) tested, and it wasn't high (26, top of the normal range is 30), which makes me think these hypercapnia episodes have been short-lived.

I think its actually the opposite problem. Aspirin causes metabolic acidosis because of the fact that it is an acid and due to its ability to cause uncoupling as well which then leads to lactic acidosis lowering blood pH. The body hyperventilates in order to raise blood pH by making you breathe out CO2, causing respiratory alkalosis. Thats why your ETCO2 is high when this happens. You actually get hypocapnia because of the acidosis caused by aspirin which forces the body to excrete more CO2 to control blood pH.

Salicylic Acid (Aspirin)

A publicly available article also appearing in PubMed about Salicylic Acid (Aspirin)

www.statpearls.com

"Aspirin causes high anion gap metabolic acidosis and respiratory alkalosis. The high anion gap comes from the addition of salicylic acid as well as the generation of lactic acid (due to uncoupling of oxidative phosphorylation causing anaerobic respiration). The respiratory alkalosis is due to direct stimulation of the respiratory center."

This is basically what happens when you have hypoxia or have a mitochondrial defect. In this case your ATP synthesis is impaired due to aspirin which mimics a mitochondrial defect. The mitochondria are not defective, its due to the uncoupling making them not produce as much ATP.

 

[tastyfood]

I think its actually the opposite problem. Aspirin causes metabolic acidosis because of the fact that it is an acid and due to its ability to cause uncoupling as well which then leads to lactic acidosis lowering blood pH. The body hyperventilates in order to raise blood pH by making you breathe out CO2, causing respiratory alkalosis. Thats why your ETCO2 is high when this happens. You actually get hypocapnia because of the acidosis caused by aspirin which forces the body to excrete more CO2 to control blood pH.

Salicylic Acid (Aspirin)

A publicly available article also appearing in PubMed about Salicylic Acid (Aspirin)

www.statpearls.com

"Aspirin causes high anion gap metabolic acidosis and respiratory alkalosis. The high anion gap comes from the addition of salicylic acid as well as the generation of lactic acid (due to uncoupling of oxidative phosphorylation causing anaerobic respiration). The respiratory alkalosis is due to direct stimulation of the respiratory center."

This is basically what happens when you have hypoxia or have a mitochondrial defect. In this case your ATP synthesis is impaired due to aspirin which mimics a mitochondrial defect. The mitochondria are not defective, its due to the uncoupling making them not produce as much ATP.

Respiratory alkalosis is related to low measurements of ETCO2. I am getting very high amounts when I have these shortness of breath plus hyperventilation episodes. The high amounts are considered respiratory acidosis.

The hypercapnia concept matches my airway contractility symptoms better.

Also, how do you explain that my temperatures goes up to 100F while I'm having the episode, plus my oxygen saturation drops?

I haven't taken aspirin in more than 2 weeks. The worst asthma episodes came after taking vitamin K and B vitamins, two pro-metabolic things.

Thanks for the comments.

 

[yerrag]

Thanks @redsun. Finding interesting posts about hypercapnia in the forum now.

I had my blood bicarbonate (what the lab calls serum CO2) tested, and it wasn't high (26, top of the normal range is 30), which makes me think these hypercapnia episodes have been short-lived.

Serum bicarbonate isn't the same as serum CO2. It is drawn from the veins for one, and when drawn from the arteries, in hospitals, it is painful, and I don't know why bicarbonates are not measured but the pressure of oxygen and CO2 (in mm Hg , to determine serum pH.

I'm not certain of this, but I would rather use my breathe rate to determine my serum pH. It, however, isn't quantitative but qualitative but it serves my purpose.

So, if breath rate is 14, my blood pH would be optimal at 7.4. If lower, it is acidic and if higher, it is alkaline. So, if my breath rate is say 22, I would say I'm very acidic. Then I would use it as a starting point and ask why. Is it metabolic or is it respiratory?

And if it is alkaline, that isn't good either as it means low CO2 and low CO2 is serotogenic as the platelets won't hold serotonon and you would have a lot of serotonin running amuck. And free serotonin could cause the capillaries to be permeable such that your alveoli becomes edematous with water, and thus their ability for gas exchange of CO2 and oxygen would be impaired. The details of serotonin and its effects on the lungs are well discussed by Peat in one of his newsletters.

 

[tastyfood]

Serum bicarbonate isn't the same as serum CO2.

Agreed, and there are lengthy discussions about that in the forum. That's why I said "what the lab calls CO2", which in reality is a test for bicarbonate. My result was just "normal" in the blood test, which I take as a good sign. Given the episodes and all the problems recently, I thought there was going to be something wrong with that.

 

[redsun]

Respiratory alkalosis is related to low measurements of ETCO2. I am getting very high amounts when I have these shortness of breath plus hyperventilation episodes. The high amounts are considered respiratory acidosis.

The hypercapnia concept matches my airway contractility symptoms better.

Also, how do you explain that my temperatures goes up to 100F while I'm having the episode, plus my oxygen saturation drops?

I haven't taken aspirin in more than 2 weeks. The worst asthma episodes came after taking vitamin K and B vitamins, two pro-metabolic things.

Thanks for the comments.

Fever is always triggered by pyrogens acting on the hypothalamus to change the temperature setpoint. Likely pyrogens are being released due to the asthma attack. Plasma norepinephrine spikes during asthma attacks which further stimulates metabolism, making you use up the oxygen in your blood faster. Norepinephrine is also involved in increasing thermogenesis and increasing vasoconstriction to preserve heat for the new setpoint.

Do you consume caffeinated beverages? Have you observed these effects after them as well? Hyperventilation, increased body temp?

 

[tastyfood]

Fever is always triggered by pyrogens acting on the hypothalamus to change the temperature setpoint. Likely pyrogens are being released due to the asthma attack. Plasma norepinephrine spikes during asthma attacks which further stimulates metabolism, making you use up the oxygen in your blood faster. Norepinephrine is also involved in increasing thermogenesis and increasing vasoconstriction to preserve heat for the new setpoint.

Do you consume caffeinated beverages? Have you observed these effects after them as well? Hyperventilation, increased body temp?

Looks like endotoxin is the most common pyrogen?

I do get two cups of coffee per day. No issues. No hyperventilation, and just a slight increase in body temperature because of the prometabolic effects.

 

[tastyfood]

Any tests you would recommend to bring clarity to this situation?

I had high eosinophils which are related to asthma and allergies. I need to retest to confirm that they went down. My electrolytes, liver enzymes, and all the basic things were fine, including bicarbonate.

 

[redsun]

Looks like endotoxin is the most common pyrogen?

I do get two cups of coffee per day. No issues. No hyperventilation, and just a slight increase in body temperature because of the prometabolic effects.

It can't be endotoxin since its not happening from food. Endogenous pyrogens such as Il-1 or TNF which may be released when the asthma attack is triggered.

Any tests you would recommend to bring clarity to this situation?

I had high eosinophils which are related to asthma and allergies. I need to retest to confirm that they went down. My electrolytes, liver enzymes, and all the basic things were fine, including bicarbonate.

Yeh I didnt know you stopped aspirin. Since you are no longer taking aspirin, the acidic and uncoupling effect of aspirin is no longer the immediate cause so its actually irrelevant here. But the lingering effects of aspirin on cyclooxygenase enzymes still matter and are what is behind it.

Bs and K2 increase CO2 formation in the cells. Because of the aspirin-induced asthma making your airways narrow and increasing mucus production, you have compromised air flow, making it harder to expel CO2. Thats when your symptoms get triggered.

Researchers propose its due to increased cysteinyl leukotriene production caused by aspirin. So it will probably take time for your levels to normalize. High eosinophils could be due to parasites but its probably high because of the aspirin (unless it was high before you ever took aspirin).

Aspirin-induced asthma: clinical aspects, pathogenesis and management - PubMed

Aspirin (acetylsalicylic acid)-induced asthma (AIA) consists of the clinical triad of asthma, chronic rhinosinusitis with nasal polyps, and precipitation of asthma and rhinitis attacks in response to aspirin and other NSAIDs. The prevalence of the syndrome in the adult asthmatic populations is...

pubmed.ncbi.nlm.nih.gov

"The aetiology of AIA is complex and not fully understood, but most evidence points towards an abnormality of arachidonic acid (AA) metabolism. Cyclo-oxygenase (COX), the rate-limiting enzyme in AA metabolism, exists as two main isoforms. COX-1 is the constitutive enzyme responsible for synthesis of protective prostanoids, whereas COX-2 is induced under inflammatory conditions. A number of theories regarding its pathogenesis have been proposed. The shunting hypothesis proposes that inhibition of COX-1 shunts AA metabolism away from production of protective prostanoids and towards cysteinyl leukotriene (cys-LT) biosynthesis, resulting in bronchoconstriction and increased mucus production. The COX-2 hypothesis proposes that aspirin causes a structural change in COX-2 that results in the generation of products of the lipoxygenase pathway. It is speculated that this may result in the formation of mediators that cause respiratory reactions in AIA. Related studies provide evidence for abnormal regulation of the lipoxygenase pathway, demonstrating elevated levels of cys-LTs in urine, sputum and peripheral blood, before and following aspirin challenge in AIA patients."

 

[yerrag]

Any tests you would recommend to bring clarity to this situation?

I had high eosinophils which are related to asthma and allergies. I need to retest to confirm that they went down. My electrolytes, liver enzymes, and all the basic things were fine, including bicarbonate.

How high?

How about considering the presence of parasites? What about fungal parasites?

How about fungi that lives inside your blood, and its spores constantly being released into blood? And your platelets always being low because they are constantly being used to eat away these spores, and this causes free serotonin to impair your lung function?

Sorry I don't have links for you to read to give you that ounce of credence you need. Always consider the strong possibility that the journals in concert with Google curate what is kosher and not for your eyes and mind, and why Ray Peat and Gilbert Ling and Bechamp are not in the hallowed halls of Oxford, Harvard, and not Nobel laureates while scumbags like Obama are.

 

[tastyfood]

How high?

Lab range for absolute numbers is 0.0-0.4 (measured in x10E3/uL). Mine were 1.0.

How about considering the presence of parasites? What about fungal parasites?

I had the same exact problem with eosinophils and asthma a year ago. They went down after asthma subsided. The Dr. tested me for all the known parasites that are known for driving eosinophils up, and the results were negative. Since the pattern with asthma and allergy is the same this year, I want to believe it's not parasites.

And your platelets always being low because they are constantly being used to eat away these spores, and this causes free serotonin to impair your lung function?

Platelets were ok in the test results. Middle of the range, which was comforting.

Bs and K2 increase CO2 formation in the cells. Because of the aspirin-induced asthma making your airways narrow and increasing mucus production, you have compromised air flow, making it harder to expel CO2. Thats when your symptoms get triggered.

This makes sense. Again, my two worst episodes came right after taking these two substances. In the case of K2, I had taken a hefty dose thinking there wasn't an upper limit for K2. Between all the aspirin, some minocycline I had taken to rule out TLR4-induced asthma, I thought I might have depleted K2, and decided to do 40mg in one take. It was a lot, and sent me into overdrive. Had never happened before and I have a lot of experience taking lots of K2 orally in olive oil. I took one dose of Energin from Idealabs thinking the niacinamide, B1, and B6 would help me with possible serotonin-induced asthma. The Bs also sent me into overdrive. That prosultiamine from the new Energin formulation is really strong. It looks I had it all wrong. I should have focused in taking a break from everything, just like I did with aspirin. Now I know what's triggering me.

Researchers propose its due to increased cysteinyl leukotriene production caused by aspirin. So it will probably take time for your levels to normalize. High eosinophils could be due to parasites but its probably high because of the aspirin (unless it was high before you ever took aspirin).

It's not parasites. I dealt with asthma in the winter time last year (not aspirin related), and my eosinophils also went up. I tested for parasites and it was all negative. Eosinophils went down as soon as the asthma was gone.

"The aetiology of AIA is complex and not fully understood, but most evidence points towards an abnormality of arachidonic acid (AA) metabolism. Cyclo-oxygenase (COX), the rate-limiting enzyme in AA metabolism, exists as two main isoforms. COX-1 is the constitutive enzyme responsible for synthesis of protective prostanoids, whereas COX-2 is induced under inflammatory conditions. A number of theories regarding its pathogenesis have been proposed. The shunting hypothesis proposes that inhibition of COX-1 shunts AA metabolism away from production of protective prostanoids and towards cysteinyl leukotriene (cys-LT) biosynthesis, resulting in bronchoconstriction and increased mucus production. The COX-2 hypothesis proposes that aspirin causes a structural change in COX-2 that results in the generation of products of the lipoxygenase pathway. It is speculated that this may result in the formation of mediators that cause respiratory reactions in AIA. Related studies provide evidence for abnormal regulation of the lipoxygenase pathway, demonstrating elevated levels of cys-LTs in urine, sputum and peripheral blood, before and following aspirin challenge in AIA patients."

This is very interesting, thanks. And thanks for all the comments.

 

[Chad_Catholic]

What is the state of your digestive health? Has it changed since experiencing these breathing episodes?

 

[redsun]

This makes sense. Again, my two worst episodes came right after taking these two substances. In the case of K2, I had taken a hefty dose thinking there wasn't an upper limit for K2. Between all the aspirin, some minocycline I had taken to rule out TLR4-induced asthma, I thought I might have depleted K2, and decided to do 40mg in one take. It was a lot, and sent me into overdrive. Had never happened before and I have a lot of experience taking lots of K2 orally in olive oil. I took one dose of Energin from Idealabs thinking the niacinamide, B1, and B6 would help me with possible serotonin-induced asthma. The Bs also sent me into overdrive. That prosultiamine from the new Energin formulation is really strong. It looks I had it all wrong. I should have focused in taking a break from everything, just like I did with aspirin. Now I know what's triggering me.

Yeh that'll definitely do it. I dont think K2 is that effective at increasing CO2. But at that dose I am sure it is. And B vitamins of course directly do it through the krebs cycle and ETC.

You may find zinc supplementation helpful to deal with this for now. The enzyme carbonic anhydrase is a zinc metalloenzyme that helps bicarbonate and CO2 convert into each other as needed. CO2 leaves the cell, converts to bicarbonate using CA enzyme and travels to the lungs. When it reaches the lungs, CA converts it back to CO2 so it can be expelled when you exhale.

Zinc is also a positive allosteric modulator of the beta 2 receptor, meaning it increases the receptors affinity for epinephrine. Beta 2 agonists such as clenbuterol are actually used for asthma since they promote bronchodilation. So zinc itself may help alone by increasing beta 2 receptor activity and it would also potentiate the effects of asthma medications like clen in case you needed to use those.

 

[tastyfood]

What is the state of your digestive health? Has it changed since experiencing these breathing episodes?

It was good before, and it's been good through this rough patch of the last 2 weeks as well. The TLR4 connection suspicion was likely unfounded because all I eat is foods that digest well, I have good and frequent bowel movements, and I'm not bloated.

 

[tastyfood]

Yeh that'll definitely do it. I dont think K2 is that effective at increasing CO2. But at that dose I am sure it is. And B vitamins of course directly do it through the krebs cycle and ETC.

Yeah exactly. The night before I had taken "some" K2, and I already noticed something. Then the night after I went overboard and doubled the vitamin K2 dose to 40mg, which led to an "oh ***t" moment. I was put in a state where I thought I had to go to the ER. Thankfully, I stayed put, kept breathing, and even managed to sleep a bit in prone position. The B vitamins, I think due to the strong prosultiamine, did exactly the same to me.

You may find zinc supplementation helpful to deal with this for now. The enzyme carbonic anhydrase is a zinc metalloenzyme that helps bicarbonate and CO2 convert into each other as needed. CO2 leaves the cell, converts to bicarbonate using CA enzyme and travels to the lungs. When it reaches the lungs, CA converts it back to CO2 so it can be expelled when you exhale.

I've been eating some canned oysters through this last week, and they've been helpful I think .

Beta 2 agonists such as clenbuterol are actually used for asthma since they promote bronchodilation. So zinc itself may help alone by increase beta 2 receptor activity and it would also potentiate the effects of asthma medications like clen in case you needed to use those.

I have the albuterol sulfate inhaler at home, and the interesting thing is that it wasn't really giving me relief with the mild asthmatic symptoms. I think I was at a point where I would need to do a lot of puffs, which I'd rather avoid. The doctor prescribed a corticosteroid inhaler, which is stronger, and that's what I used during the two/three bad episodes. Similarly, I'd rather avoid continued use for obvious reasons.

 

[redsun]

Yeah exactly. The night before I had taken "some" K2, and I already noticed something. Then the night after I went overboard and doubled then vitamin K2 dose to 40mg, which led to a "oh ***t" moment. I was put in a state where I thought I had to go to the ER. Thankfully, I stayed put, kept breathing, and even managed to sleep a bit in prone position. The B vitamins, I think due to the strong prosultiamine, did exactly the same to me.



I've been eating some canned oysters through this last week, and they've been helpful I think .



I have the albuterol sulfate inhaler at home, and the interesting thing is that it wasn't really giving me relief with the mild asthmatic symptoms. I think I was at a point where I would need to do a lot of puffs, which I'd rather avoid. The doctor prescribed a corticosteroid inhaler, which is stronger, and that's what I used during the two/three bad episodes. Similarly, I'd rather avoid continued use for obvious reasons.

That sounds like a terrible experience. Fortunately you were able to wait it out.

Thats good you ended up getting zinc from oysters. Forgot to mention high dose aspirin also seems to reduce zinc levels. Hopefully with some more time you'll get back to normal.

 

[tastyfood]

Thats good you ended up getting zinc from oysters. Forgot to mention high dose aspirin also seems to reduce zinc levels. Hopefully with some more time you'll get back to normal.

Would it make sense to test zinc levels in blood as a way to verify status? I was also planning to send hair to Idealabs in a month or so to see where things are. I was also wondering if it made sense to test salycilate levels in blood to see how "overdosed" I am? I am hoping to be able to benefit from aspirin again in the near future (at smaller doses of course).

To summarize the situation (thanks for all the comments), I think it went down like this:

- Continued high dose (3g+) daily aspirin ended up giving me asthmatic symptoms.
- In addition to the effect on COX metabolism, it is more than possible that I wasn't buffering the aspirin with sufficient baking soda. When taking that much, the alka-seltzer type proportions should be followed. Aspirin can also deplete glycine, which apparently contributes to glutathione metabolism which protects the lungs.
- With the asthma, sputum started to accumulate, leading to infection in the lungs, and reduced airflow.
- Reduced airflow means poorer ability of expelling the CO2.
- Between all the wheezing, excessive mucus in the lungs, restricted airflow, CO2 has been accumulating, leading to more respiratory acidosis.
- While exploring different asthma-inducing routes such as a serotonin, I engaged in supplementation of things that further pushed me in the CO2 producing territory, which aggravated the problem, leading to episodes of extreme asthma, need to hyperventilate.
- Given my recent test results, all the symptoms, and how I have been reacting to things, I probably just need to take a break from taking all these different things, let the salicylate levels go down on their own, and build back up.

 

[Chad_Catholic]

Have you tried a high dose of progesterone for its anti-estrogen properties? Estrogen steals oxygen from mitochondria.