Aquí os dejo un estupendo resumen de las razones por la cuales normalmente en el SFC solemos tener bajo ácido estomacal (HCL). Recordar que yo lo necesito tomar para poder comer (literalmente), pues de lo contrario puedo hacer digestiones de 10 horas...Fue un gran descubrimiento diagnosticarme la hipocloridia! :
There are no published studies of stomach acid levels in CFS. There is onestudy showing a slow rate of emptying of the stomach, particularly of liquids,
in CFS (Burnet and Chatterton, 2004), and this might be explained by low stomach
acid production, since stomach acid entry into the duodenum with food is what
normally signals the excretion of pancreatic digestive juice and bile, which
govern the rate of digestion and hence, via feedback, the rate of emptying of
the stomach.
Anecdotal reports from several PWCs (based on the bicarbonate—burp test or other
more sophisticated stomach acid measurements) suggest that low stomach acid is a
common phenomenon in CFS. If so, it could help to explain some of the other
issues involving the digestive system that are often observed in CFS, such as
intestinal yeast infections and bacterial dysbiosis, as well as low levels of
pancreatic enzymes (chymotrypsin or elastase) in the stools. Stomach acid
normally kills yeasts and deleterious bacteria that come in with food, as well
as stimulating excretion of pancreatic enzymes. Stomach acid also normally
begins the digestion of proteins by converting pepsinogen to pepsin in the
stomach.
The question arises as to what is the immediate cause of the low stomach acid in
CFS. Stomach acid (hydrochloric acid) is normally produced by the parietal
cells (also called oxyntic cells) in the wall of the stomach. These cells
import chloride ions from the blood and pass them into the lumen (cavity) of the
stomach. At the same time, they pump hydrogen ions (protons) into the lumen of
the stomach as well, forming hydrochloric acid.
The hydrogen ions are derived from ionization of carbonic acid, which the
parietal cells obtain from the reaction of carbon dioxide and water, catalyzed
by the enzyme carbonic anhydrase. (The parietal cells are actually net
importers of CO2 from the blood, even though they produce CO2 in their
mitochondria, as do other types of cells. They export bicarbonate back to the
blood.)
The hydrogen ions are transported into the lumen of the stomach by
hydrogen-potassium ATPase molecules in the cell membrane that faces the lumen of
the stomach. These "proton pumps" exchange potassium from the lumen of the
stomach for hydrogen ions from the parietal cells. The hydrogen ions must be
pumped against a strong pH gradient, since the pH of the stomach acid may be
below pH1, while the pH in the cytoplasm of the parietal cells is over pH7. The
proton pumps are powered by ATP, which is produced by the large number of
mitochondria in the parietal cells.
Zinc is particularly important for the parietal cells, because carbonic
anhydrase requires it, and also because the gene expression of
hydrogen-potassium ATPase requires "zinc-finger" molecules. So zinc deficiency
could be a possible reason for low stomach acid production. There is some
published evidence that the absorption of zinc is hindered by low stomach acid,
so this could be a self-perpetuating mechanism.
I think that the other main suspect for causing low stomach acid in CFS is
glutathione depletion. There is considerable evidence now for glutathione
depletion in CFS. Glutathione depletion in the mitochondria of the parietal
cells could cause partial blocks in the Krebs cycle and the respiratory chain
due to elevation of oxidizing free radicals. This would lower the rate of
production of ATP, and that could hinder the ability of the proton pumps to move
hydrogen ions into the lumen of the stomach, thus resulting in low stomach acid.
It is interesting to note that one of the main mechanisms of the drugs used to
lower stomach acid production ("proton pump inhibitors") is to oxidize cysteine
residues to cystine in the part of the hydrogen-potassium ATPase molecules that
is exposed to the stomach lumen, and that glutathione acts to prevent this
oxidation. So there may be two ways in which glutathione could act to improve
stomach acid production: increasing the rate of production of ATP, and
preventing oxidation of cysteine residues in hydrogen-potassium ATPase
molecules.
It is usually not recommended to take ordinary (non-liposomal) glutathione
orally, because there are enzymes in the wall of the small intestine that
decompose it into its constitutive amino acids before they are absorbed.
However, glutathione is able to survive in the stomach. I don't know whether
the parietal cells can utilize glutathione directly from the stomach, but
perhaps taking oral glutathione might help to raise stomach acid levels.
As far as I know, this has not been tried, but it might be possible to determine
whether or not it would work by doing a baking soda—burp test before and after
taking oral glutathione for a few days. I don't know what dosage of glutathione
would be appropriate, so this may take some experimentation.
The baking soda—burp test involves drinking a glass of water into which
one-quarter teaspoon of baking soda (sodium bicarbonate) has been mixed, and
then timing to see if a burp occurs within two minutes. If it does, it
indicates that there is stomach acid present; if not, it indicates low stomach
acid.
If taking zinc and glutathione do not restore stomach acid levels, one can still
use the approach of taking a hydrochloric acid solution orally (properly diluted
so as not to damage the mouth, throat and esophagus, but to still be strong
enough to help in the stomach) such as the product sold by Allergy Research
Group. (Using a drinking straw and rinsing the mouth with water afterward will
protect the enamel on the teeth.) Taking betaine-HCl is another possibility,
but I have not been able to resolve the question as to whether the betaine in
this supplement would speed up the BHMT alternative pathway in the liver and
kidneys too much, at the expense of the methionine synthase pathway, which is
partially blocked, and which the methylation cycle treatment seeks to speed up.