Causes of Hypochlorhydria

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I haven’t done a real test. Basing this off the fact that one cap of betaine hcl doesn’t produce a warming sensation (even 15 dont sometimes), my skin repair, quality of my nails and my hair indicating that I’m not getting any protein, failing baking soda test, I’m low on dopamine histamine acetylcholine everything, have to supplement all the b vitamins in large quantities including B12, need 60+ mg of zinc to not get white spots on nails, I could go on. I did have an endoscopy and colonoscopy and the report says they found a normal amount of gastric juice in my stomach. However the quantity can be normal but the pH not. There were other problems further down my digestive tract due to infection from undercooked meat, which happens in the first place when stomach acid is inadequate. However before the infection I had moments when I could feel my stomach was functioning and after that stay in the hospital my stomach was never the same. I Suspect due to the IV antibiotic They gave me causing me beri beri

I don’t eat gluten or beans. Liver triggers multiple skin issues in me badly, more than 2 yolks a week are a problem too. Dairy is the worst trigger by far. Making red meat a staple protein is too ambitious when dealing with hypochlorhydria. So I eat white fish and pray to absorb something

I find if you have acidosis and high cortisol supplementing betaine hcl exacerbates the problem and you need tons of potassium and bicarbonate to compensate. I’ve tried dissolving it and it still injured my lining.
Not sure if you have answered this before, but what happens when you drink Coca Cola after eating meat? Does it help at all with digestion? I personally find I benefit from it. Interestingly, it has to be Coca Cola. Pepsi for some reason doesn't work well for this, in my experience.
 

Apple

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Maybe the baking soda test is inaccurate.
So you had the proper test in a hospital at 17 years old and it showed low levels?
Didn’t even know this was possible to test. Would really like to do that
little update here...
I did another baking soda test today in 5 min after drinkng a cup of coffee (no sugar, no milk, in the morning).
It worked this timed, I burped in several minutes.
It confirmes that Coffee does induce/increase stomach acid.
Good thing for me as I don't like dependence on supplements.
I may test diferent types of coffee (and other substances) to see which have a stronger effect.
For example, caffeinated ground coffee appeared to stimulate more acid secretion than decaffeinated ground coffee, whilst their instant counterparts did not differ in their acid-stimulating ability. In relation to gastrin secretion, ground caffeinated coffee and freeze-dried instant coffee both appeared to stimulate higher gastrin levels.
Interestingly, a dark brown roast coffee blend is less effective at stimulating gastric acid secretion compared to a medium roast market blend.

No wonder I always feel good after drinking coffee after a meal.
 
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Motif

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little update here...
I did another baking soda test today in 5 min after drinkng a cup of coffee (no sugar, no milk, in the morning).
It worked this timed, I burped in several minutes.
It confirmes that Coffee does induce/increase stomach acid.
Good thing for me as I don't like dependence on supplements.
I may test diferent types of coffee (and other substances) to see which have a stronger effect.
For example, caffeinated ground coffee appeared to stimulate more acid secretion than decaffeinated ground coffee, whilst their instant counterparts did not differ in their acid-stimulating ability. In relation to gastrin secretion, ground caffeinated coffee and freeze-dried instant coffee both appeared to stimulate higher gastrin levels.
Interestingly, a dark brown roast coffee blend is less effective at stimulating gastric acid secretion compared to a medium roast market blend.

No wonder I always feel good after drinking coffee after a meal.

Update?
 
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ursidae

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Not sure if you have answered this before, but what happens when you drink Coca Cola after eating meat? Does it help at all with digestion? I personally find I benefit from it. Interestingly, it has to be Coca Cola. Pepsi for some reason doesn't work well for this, in my experience.
Sorry, didn’t see this question before. I have not experimented with drinking Coca Cola. I find benefit from freshly juiced Lemon ginger celery. I think I’m gonna trial celery juice again. Last time I did it daily for 2 weeks it improved my skin issues a lot
 

Motif

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Sorry, didn’t see this question before. I have not experimented with drinking Coca Cola. I find benefit from freshly juiced Lemon ginger celery. I think I’m gonna trial celery juice again. Last time I did it daily for 2 weeks it improved my skin issues a lot
How much celery juice and did you only drink it in the morning or over the day ?
 
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ursidae

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3B85A205-2352-4E71-A7F5-87B68B03277C.jpeg


the reference range is to the right

55C20EEF-3261-40EB-9012-7DAAA11A5331.jpeg


Will be doing more H Pylori tests.
 
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ursidae

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I think I might have botched the test. I asked at the lab if I had to be fasted and they said no in a way that made me slightly doubtful. I had eaten than day. And I had taken betaine hcl and bromelain the days before. The reference range for gastrin is strange but several sources state that normal is above 20
 
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ursidae

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Also I did the baking soda test a couple of days ago. No burping for two hours until I took a sip of fresh squeezed orange juice which provoked a strong belch
 

Apple

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I think I might have botched the test. I asked at the lab if I had to be fasted and they said no in a way that made me slightly doubtful. I had eaten than day. And I had taken betaine hcl and bromelain the days before. The reference range for gastrin is strange but several sources state that normal is above 20
I think your results look good and you did everything ok.

" What Should I Do During the Esophageal pH Test?
Eat your regular meals at the usual times and eat the way you normally do. If you do not eat during the monitoring period, your stomach will not produce acid as usual, and the test results will not be accurate."
 
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ursidae

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I didn’t do an esophageal pH test but looking at my PG1/2 ratio I might be okay even though it’s tested when fasted

Based on the predefined criteria for classifying the EGT results, 303 (47%) of the 627 enrolled subjects were classified as having hypochlorhydria; in particular, 155 (24%) had profound hypochlorhydria, whereas 66 (10%)
had hyperchlorhydria.
Fig. 4 shows the ROC curve for discriminating the
hypochlorhydric patients from the other patients in the entire cohort or in the subgroups according to H. pylori infection status. In the entire cohort, the AUC (95% CI) values determined for the PG I level, PG II level, and PG I/ II ratio were 0.72 (0.68-0.76), 0.44 (0.39-0.48), and 0.86 (0.83-0.89), respectively, indicating that the PG I/II ratio showed the best and excellent diagnostic accuracy for the discrimination of hypochlorhydric patients. The combined evaluation with the PG I level and PG I/II ratio (AUC [95% CI], 0.86 [0.83-0.89]) did not further improve the diagnos-
tic accuracy compared with the evaluation using the PG I
Figure 4
76.4% and 78.7%, respectively (Table 1). Meanwhile, the results of the ROC analysis differed according to H. pylori infection status, as expected based on the above-mentioned correlation between the serum PG values and gastric acid secretion levels. In particular, although the PG I/II ratio showed the best diagnostic accuracy for the discrimination of hypochlorhydric subjects from the subjects with H. pylori infection based on an AUC (95% CI) of 0.87 (0.84- 0.90) (Fig. 4B), the PG I level rather than the PG I/II ratio showed the best diagnostic accuracy in the subjects without H. pylori infection based on an AUC (95% CI) of 0.80 (0.73-0.88) (Fig. 4C). Accordingly, the best cutoff PG I/II ratio for predicting hypochlorhydria in the subjects with H. pylori infection was 2.7, at a corresponding sensitivity of 79.2% and specificity of 76.3% (Table 1). Meanwhile, the best cutoff PG I level for predicting hypochlorhydria in the subjects without H. pylori infection was 35 ng/mL, at a cor- responding sensitivity and specificity of 70.0% and 76.3%, respectively (Table 1).


However

Serum PG values
Blood samples were obtained from each patient under fasting conditions, and the serum was separated and stored at −20°C. Fasting serum PG I and PG II levels were measured by chemiluminescent enzyme immunoassay using commercial kits (Lumipulse PG I and II, Fujirebio Inc., Tokyo) (Kikuchi et al. 2011).
 
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ursidae

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I can’t find a single study where PG 1 and 2 were NOT tested fasted. Crap. They’re probably not gonna return my money for this
 

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- Inhibition of restraint ulcers in the rat by pyridoxine deficiency

"Histamine is formed from the decarboxylation of histidine, a reaction catalyzed by the enzyme histidine decarboxylase, and its coenzyme pyridoxal-5-phosphate.[15,16] Pyridoxine deficiency decreases histamine-forming capacity in tissues.[17] These experiments suggest that it is the pyridoxine deficiency that reduces histamine formation, and circumstantially that this reduction in histamine-forming capacity is responsible for the observed decrease in the incidence of ulcerations in the stomach. Since two pyridoxine-deficient animals with normal levels of gastric HFC [Histamine-forming Capacity] were the ones that developed ulcers, histamine may be one of the mediators of restraint ulceration."

"The present finding of a decreased HFC after pyridoxine deficiency is more striking than those of Kahlson, et al, whose experimental animals ate a pyridoxine-deficient diet for only two weeks.[17] The reduced HFC was not the result of a reduction in histidine decarboxylase, but rather of the pyridoxal-5-phosphate cofactor; when pyridoxal-5-phosphate was added to the homogenate in vitro, normal levels of activity resulted."

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"It must be kept in mind that pyridoxal-5-phosphate is a coenzyme for many other reactions, being required for practically all the reactions involving the non-oxidative degradation and interconversion of free amino acids.[18] A block in some other pathway dependent on pyridoxal-5-phosphate might be responsible for the results noted here."

Glad your research brought this to light. If this were a way to increase gastric juice production, I wonder if -

- supplemental arginine would result in increased gastric juice production, and be helpful in addressing acid reflux issue; as I wonder if this arginine supplementation would be able to break a vicious cycle involving faulty digestion involving low acidity by providing a boost in stomach acidity to improve digestion and helping in delivery of nutrients to the blood stream. Concurrent with intake of soda water for its carbon dioxide content to provide for vascular availability of carbon dioxide, while simultaneously aiding the kidneys in excreting acidity from the system, to the effect that a more alkaline acid-base balance would allow room for the conversion of CO2 to carbonic acid, as the lower pH would allow this to take place. If say there is high lactate in the system that needs to be excreted by the kidneys, then making it possible for ammonium lactate to be excreted would relieve the system of a lot of acidity that can only be done by the kidneys, as in an extreme case of metabolic acidosis, there isn't any H+ ions to spare for excretion and this makes it impossible to excrete ammonium lactate, and instead potassium phosphate is excreted, which doesn't relieve the system of acidity much (the reason H+ is unavailable is because H+ ions have transferred to cells and K+ ions replacing it in the blood/ecf as the body's way of lowering the ecf acidity). It may be that high thiamine supplementation is needed as thiamine can enable conversion of lactate into pyruvate and into glucose in the Cori cycle. I'm not sure if i'm right about this though, but I'm hoping that tregular hiamine supplementation can slowly remove lactate from the system and eventually the ecf would not be so acidic, and at this point, the K+ ions can fo back to the cel, and the H+ ions back to the ecf, and then the kidneys can go back to excreting ammonium lactate. So if this is correct, we would have a stack that could be used for fixing acid reflux, as a start, on the way to restoring acid-base balance along with fixing hypothyroid, with some additional tweaks.

Does this make sense to you?
- Agmatine: Clinical applications after 100 years in translation (Fig. 2a; another decrapoxylase that depends on pitytoxine)
- The interdependence of gastric secretion and the CO2 content of the blood
 
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ursidae

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I’ve experimented with baking soda, lower protein diet abundant in citrus fruit, and I take 30 mg benfotiamine/thiamine hcl (and TTFD once a week) and 25 mg p-5-p daily. I can get arginine tomorrow and try the whole stack.
Is sparkling water the same as soda?
 

lvysaur

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Type A blood
 

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PaRa

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Type A blood
bruuuh

its bull****
I’m A myself and my stomach acid is stronger than ever, thanks to histamine


both histamine and thyroid function upregulate gastric HCL


fact is that high dairy diet isnt effective for all and it can smash your gastric acid
 
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