I determined that I have low stomach acidity based on the symptoms. I found this site that suggested using high dose niacin to stimulate HCL secretion. There was even a nice argument differentiating between having a deficiency or a dependency (having a higher metabolic need) of a nutrient. The theory seemed to hold and I thought I had found a simple, inexpensive solution to a HUGE problem in my life right now.
http://orthomolecula...6n04-p225.shtml
However, upon further research, I found that taking niacin >3g/day(in any form, apparently) can cause hepato-toxicity, decrease insulin sensitivity, cause blurry vision, increase homocysteine and the list goes on and on.
I searched pubmed for "niacin", "liver" and came up with many studies to confirm this.
I know I can treat low HCL by supplementing with Betaine HCL, bitters, digestive enzymes. Also, some people have found benefits by increasing histamine (which is needed for HCL production?) after supplementing with L-Histidine. However, according to wiki-
"Supplementation of Histidine has been shown to cause rapid zinc excretion in rats with an excretion rate 3 to 6 times normal. [2][3]Some people take histidine in an attempt to raise their histamine levels. Histamine is released under conditions of higher osmolality (dehydration\salt). Raising histamine may be more effective by adapting the body to a higher osmolality by eating sodium without greatly increasing water intake and taking supplements that help the body adapt to those conditions (zinc\taurine\B1\B12). Histidine supplementation likely tricks the body into believing it is producing less histamine and assumes it is well or overhydrated and is better off without the nutrients used to maintain cellular hydration in a hyperosmotic state. Histidine supplementation however is inadvisable because one of the hallmarks of today's chronic diseases (diabetes, Alzheimer's, Parkinson's) is zinc depletion."
This too is bad. Sigh.
However, my questions is this. In the article, they suggest that Niacin increases HCL production by increasing mitochondrial function is parietal cells, through mediation of NAD. This activity is independent of the availability of Histamine, which is my second reason for not wanting to use L-histidine.
Adequate HCl Secretion Requires Optimal Amounts of Vitamin B3
Niacin is a potent stimulator of histamine and PGD2(a vasodilator).51,52,53 When administered orally in amounts of 100 mg or greater, there is a release of histamine from storage sites (e.g., mast cells and basophils) through a complicated process of degranulation, and the release of PGD2 from dermal macrophages. There is evidence that the niacin flush is not mediated by the release of histamine from mast cells or other storage sites.52 Researchers discovered that niacin caused a markedly increased release of PGD2, but there was no concomitant release of histamine from mast cells (as would have been suggested by an increase in plasma levels of a histamine metabolite). They concluded that the niacin-induced vasodilation was primarily mediated by the release of PGD2.
The fact that niacin markedly improved symptoms suggestive of hypochlorhydria in these two patients indicates that niacin can be used therapeutically to increase functionally the secretion of HCl from parietal cells. It is conceivable that the niacin-induced release of PGD2 leads to the binding of this prostaglandin to receptors on parietal cells stimulating the release of HCl. This would mean that there is a gastric source of PGD2 other than dermal macrophages, and that the parietal cells contain receptors for PGD2. There is no current evidence addressing the niacinin-duced prostaglandin-mediated release of HCl. More likely, niacin ingestion causes the release of PGD2 from dermal macrophages and the release of histamine from gastric mast cells. The histamine release might be mediated by some of the niacin that gets absorbed within the stomach. The histamine released from gastric mast cells would then be available to bind to the H2 receptors on the parietal cells, thus stimulating the release of HCl.
Doses of niacin, such as 2-3 grams per day, will deplete histamine storage sites after a few days of continued use, and the flush typically goes away. If the histamine storage sites become depleted with continued use, how then does niacin benefit individuals with hypochlorhydria? Niacin and niacinamide are precursors to coenzymes that participate in a few hundred enzymatic reactions in the body, but their involvement in mitochondrial functioning may explain how both forms of vitamin B3 optimize HCl secretion. Both forms of vitamin B3 are precursors to NAD+, which is then converted to the energy-rich reduced coenzyme, NADH, that plays a critical role in complex I of the mitochondrial respiratory chain.54 Half the parietal cell volume is occupied by mitochondria,55 making the parietal cells the largest storehouse of mitochondria among all eukaryotic cells.56 Basic biochemistry has revealed to us that the free energy produced by oxidative phosphorylation within the mitochondria is used to produce ATP. A report by Spenney,55 elucidating the mechanisms of HCl secretion, has shown it to be an ATP-dependent process. The ATP synthesized from mitochondrial energy, once stimulated to breakdown, mediates HCl secretion, and provides the necessary fuel that facilitates the exchange of K+ for H+ occurring within the canalicular membrane of the parietal cell.55 Chloride ions are also actively transported into the lumen of the parietal cell where they combine with hydrogen ions to form HCl.57,58 The therapeutic use of niacin seems to restore the functional ability of the parietal cells by a mechanism of action unrelated to histamine. Like niacin, niacinamide has been shown to correct symptoms suggestive of hypochlorhydria, even though niacinamide’s pharmacologic actions do not involve the release of histamine from storage sites. The coenzymes formed from vitamin B3 allow for optimal mitochondrial functioning, leading to the production of ATP, and the necessary fuel to drive the process of releasing HCl from the parietal cells.
So I wonder If I can achieve increased HCL secretion by supplementing with NAD or NADH directly, instead of using Niacin?
This is a long shot but Low stomach acid, or hypochlorhydria is more common than we think...
Edited by Lufega, 24 October 2008 - 03:08 AM.
