Reducing Stomach Acid Decreases Intracellular Co2

[Spondive]

This study might show that reducing acid production in stomach Luman reduces co2 intracellularly and that co2 protects the mucosal barrier of the stomach. Important to note not extra cellular or in Luman but metabolically and within the cell.

Another thought I had is I have seen studies that disrupted blood flow to the gut will cause damage to mucosa.. Is it possible if tissue concentrations of co2 are lower vasoconstriction and reduced blood flow will occur?


Metabolic base production and mucosal vulnerability during acid inhibition in a mammalian stomach in vitro. - PubMed - NCBI

 

[haidut]

This study might show that reducing acid production in stomach Luman reduces co2 intracellularly and that co2 protects the mucosal barrier of the stomach. Important to note not extra cellular or in Luman but metabolically and within the cell.

Another thought I had is I have seen studies that disrupted blood flow to the gut will cause damage to mucosa.. Is it possible if tissue concentrations of co2 are lower vasoconstriction and reduced blood flow will occur?


Metabolic base production and mucosal vulnerability during acid inhibition in a mammalian stomach in vitro. - PubMed - NCBI

This is extremely interesting, as one of the drugs that has been shown to protect the stomach very well is famotidine. Famotidine is a carbonic anhydrase inhibitor and also increases blood flow in the mucosa. So, this may explain its protective effects a lot better than the official H2-antagonism mechanism.
Famotidine inhibits carbonic anhydrase (CA) | Ray Peat Forum
Studies on the mechanism for the gastric mucosal protection by famotidine in rats. - PubMed - NCBI
Famotidine prevents canine gastric blood flow reduction by NSAIDs. - PubMed - NCBI

 

[Spondive]

Thanks Haidut..I think you posted something that ppi also increases co2 in the tissues and that maybe why certain percentage of people get better on them

 

[Spondive]

I also wonder if because co2 is low in the tissues does nitric oxide increase and causes the relaxation of the lower esophageal sphincter causing worsening reflux

 

[haidut]

I also wonder if because co2 is low in the tissues does nitric oxide increase and causes the relaxation of the lower esophageal sphincter causing worsening reflux

That is also a great observation. Whenever CO2 is low, NO will rise as an emergency vasorelaxant. This inappropriate relaxation is also seen in varicose veins, and their cause estrogen has many of the vasodilating properties of NO. So, I would not be surprised if prolactin or estrone are elevated in people with GERD but I think doing an NO test with the saliva strips would the first thing I'd try.

 

[Spondive]

I look forward to reading all your comments Haidut! Keep up the great work!

 

[marikay]

So would bag breathing help when experiencing GERD?

 

[tara]

Is it possible if tissue concentrations of co2 are lower vasoconstriction and reduced blood flow will occur?

I believe so. I think reduced systemic CO2 levels reduce blood flow to the whole digestive system, in favour of skeletal muscles.
If hypocapnic, raising CO2 levels should increase circulation and oxygen delivery to the digestive system.

 

[NathanK]

I also wonder if because co2 is low in the tissues does nitric oxide increase and causes the relaxation of the lower esophageal sphincter causing worsening reflux

Thats a very interesting theory. I think its as plausible as any

 

[michael94]

This is extremely interesting, as one of the drugs that has been shown to protect the stomach very well is famotidine. Famotidine is a carbonic anhydrase inhibitor and also increases blood flow in the mucosa. So, this may explain its protective effects a lot better than the official H2-antagonism mechanism.
Famotidine inhibits carbonic anhydrase (CA) | Ray Peat Forum
Studies on the mechanism for the gastric mucosal protection by famotidine in rats. - PubMed - NCBI
Famotidine prevents canine gastric blood flow reduction by NSAIDs. - PubMed - NCBI

I think the h2 antagonism is the better explanation or at least just as good. Molecular Hydrogen as an Energy Source for Helicobacter pylori | Science

Thats a very interesting theory. I think its as plausible as any

Another thing low stomach acid does is allow bacteria/candida overgrowth in the stomach ( specifically h pylori ) and these produce ammonia to further reduce stomach acid and make the environment even more hospitable ( vicious cycle ). Here's a quote from peat

Ammonia suppresses respiratory, and stimulates glycolytic, activity.

So the low stomach acid allows ammonia producing bacteria to ramp up which increases glycolysis ( reduced c02 ) and inhibits respiration.

edit: and of course there's all the downstream effects of poor nutrient absorption from weak digestion.

 

[What-a-Riot]

"Acid inhibition reduced metabolic co2 production by 29%"

So I don't know enough to know: would this mean that famotidine, which we've established improves glucose tolerance would in fact interfere with glucose metabolism? Or is this co2 production separate from metabolism of energy substrates?

I know by inhibiting carbonic anhydrase, famotidine can increase co2 retention, which is of course good, and in the context of controlled breathing or exogenous co2 supplementation could definitely increase co2 levels, but if it's at the expense of co2 production that seems like a significant problem.

 

[Diokine]

So would bag breathing help when experiencing GERD?

Definitely. If I experience heartburn or indigestion, breathing exercises are the first thing I go to. They are extremely effective. A 1/4tsp of salt is also very effective.

I also wonder if because co2 is low in the tissues does nitric oxide increase and causes the relaxation of the lower esophageal sphincter causing worsening reflux

Bingo! I think it's safe to say that NO may be one of the causes of relaxed LES tone. There is some evidence out there to support this idea. Histamine has a big role as well. The primary pathology ultimately is a disruption in cholinergic activity in the vagal nerve, there is also a bioenergetic component (disruption of proper calcium metabolism and inability of LES to relax by over excitation) caused by hydrogen peroxide and prostaglandins.

In addition, hydrogen peroxide seems to be involved in the mechanism of LES relaxation by inhibiting both the influx of calcium into cells and mobilization from calcium stores [33]. In another study on the effects of exposure to acid using esophageal sections including the mucosa and muscle coat [34], IL-1 and IL-6 were found to induce hydrogen peroxide, which was involved in the contraction of the esophageal muscle coat. The authors also performed the same series of studies using human LES tissues. They concluded that mucosal inflammation induced hydrogen peroxide production, which stimulates the synthesis of PAF and PGE2 and is involved in LES relaxation [35]. These reports are interesting in that the authors demonstrated an important role of oxidative stress in reflux due to impaired LES function.

Inflammation and Oxidative Stress in Gastroesophageal Reflux Disease

I posted some studies a while back detailing the stabilization of mast cells (of which there is a very large concentration in the stomach!) by CO2, which reinforces the idea that proper CO2 production is critical for healthy tissue ANYWHERE in the body.

CO2 Decreases Mast Cell Sensitivity