Would you be so kind as to provide scientific reference to the above quote ? I'm not saying this sarcastically, but this is information I've been wondering about for a long time.
Thanks
Here's evidence of 5-HTP in the stomach being converted to serotonin in the stomach cells, which causes acetylcholine release. The second abstract explains how acetylcholine causes stomach acid secretion.
Eur J Pharmacol. 1986 Aug 15;127(3):179-85
Increased gastric cholinergic activity evoked by 5-hydroxy-L-tryptophan in the rat.
Sanger GJ, McClelland CM.
In gastrointestinal tissues such as rat stomach, exogenous 5-hydroxytryptamine (5HT) has little or no ability to affect nerve activity. However, endogenous 5HT might act differently, and this was investigated by stimulating 5HT synthesis using 5-hydroxy-L-tryptophan (5HTP). In longitudinal strips of rat forestomach, 5HTP (50 and 500 microM) increased cholinergically mediated contractions evoked by electrical field stimulation, probably by facilitating acetylcholine release; contractions evoked by exogenous acetylcholine were unaffected by 5HTP. The ability of 5HTP to increase electrically evoked contractions was long-lasting, required the presence of pyridoxal (a monoamine decarboxylase cofactor) and was reduced by the decarboxylase inhibitor carbidopa, but not by 6-hydroxydopamine. In the presence of paroxetine and nialamide, the 5HTP-induced increase in cholinergically mediated contractions was short-lasting. In anaesthetised rats 5HTP caused stimulation of gastric motility, which was blocked or reduced by atropine. These findings suggest that in the rat 5HTP stimulates gastric cholinergic activity, by increasing the concentration of 5HT at sites which normally synthesise 5HT.
PMID: 3019729
Curr Opin Gastroenterol. 2001 Nov;17(6):481-8.
Gastric secretion.
Schubert ML.
Department of Medicine, Division of Gastroenterology, Medical College of Virginia and McGuire VAMC, Richmond, Virginia 23249, USA. mitchell.schubert@med.va.gov
The influence of central and peripheral stimuli on gastric acid secretion is mediated via activation of histaminergic, gastrinergic, and cholinergic pathways coupled to intracellular second-messenger systems that determine the trafficking and activity of H+ K+-ATPase, the proton pump of the parietal cell. Histamine, released from enterochromaffin-like cells stimulates the parietal cell directly via H-2 receptors coupled to generation of cAMP. Gastrin, acting via cholecystokinin-2 receptors on enterochromaffin-like cells coupled to an increase in intracellular calcium, stimulates the parietal cell indirectly by activating histidine decarboxylase, releasing histamine, and inducing enterochromaffin-like cell hypertrophy and hyperplasia. Acetylcholine, released from gastric postganglionic intramural neurons, stimulates the parietal cell directly via M-3 receptors coupled to intracellular calcium release and calcium entry. The second-messenger systems activated in the parietal cell converge on H+ K+-ATPase that catalyzes the exchange of luminal K+ for cytoplasmic H+ and is responsible for gastric luminal acidification. The main inhibitor of acid secretion is somatostatin which, acting via sst2 receptors, exerts a tonic inhibitory influence on parietal, enterochromaffin-like, and gastrin cells. Acute infection with Helicobacter pylori results in hypochlorhydria, whereas chronic infection may be associated with either hypo- or hyperchlorhydria. Although prostaglandins are thought to play a physiologic role in the regulation of acid secretion and maintenance of gastric mucosal integrity, the precise roles of cyclooxygenase-1 and cyclooxygenase-2 in these processes still eludes us.
PMID: 17031207
There's also the possibility that the 5-HTP gastric lesions are initiated by reduced blood flow (due to vasoconstriction?), and that increased stomach acid merely aggravates things.
Pharmacol Res. 1999 Apr;39(4):261-7.
Role of endogenous serotonin and histamine in the pathogenesis of gastric mucosal lesions in unanaesthetised rats with a single treatment of compound 48/80, a mast cell degranulator.
Ohta Y, Kobayashi T, Ishiguro I.
Department of Biochemistry, School of Medicine, Fujita Health University, Toyoake, Aichi, 470-1192, Japan.
In unanaethetised rats with a single injection of compound 48/80, a mast cell degranulator (0.75 mg kg-1, i.p.), gastric lesions occurred with increased serum serotonin and histamine levels and reduced gastric mucosal blood flow at 0.5 h after the injection and developed at 3 h. Pretreatment with either cyproheptadine (a serotonin and histamine antagonist) or methysergide (a serotonin antagonist) prevented the formation of gastric mucosal lesions with attenuation of reduced gastric mucosal blood flow at 0.5 h after compound 48/80 injection, while pretreatment with either amitriptyline (a selective inhibitor of histamine release from mast cells), tripelennamine (a histamine H1-receptor antagonist), famotidine (a histamine H2-receptor antagonist) or cimetidine (a histamine H2-receptor antagonist) had no effect. Pretreatment with either cyproheptadine, methysergide, amitriptyline or tripelennamine prevented the development of gastric mucosal lesions at 3 h after compound 48/80 injection, while pretreatment with either famotidine or cimetidine had no effect. These results indicate that in unanaesthetised rats with a single compound 48/80 treatment, acutely released endogenous serotonin causes gastric mucosal lesions, while released endogenous histamine mainly contributes to the lesion development and that gastric acid plays little role in the pathogenesis of the compound 48/80-induced acute gastric lesions. Copyright 1999 The Italian Pharmacological Society.
PMID: 10208755