But why? I didn't know, so I didn't dig into it. However, life with young children tends to provide repeated opportunities to ponder the wherefores of gastroenteritis, and I've just had a couple of days to do that. About 3-4 days ago, my four year-old daughter had diarrhea despite not having any vomiting beforehand. I wondered briefly if she had just had a stomach bug go through her, but since I didn't know of any contacts of hers having stomach bugs, I stopped worrying about it.
Then yesterday, the two-year-old I babysit most afternoons couldn't come over because she had vomited. And it turned out that she had vomited five days ago, too. Out came the molybdenum for my whole family, for seven people in one household taking their turn vomiting is a nightmare I'd rather avoid. I've had intestinal gurgling for the past 24 hours, but no vomiting or nausea, and so far, no one else in the family has shown any signs of illness. The rest of the two-year-old friend's family hasn't been affected; her mom says that she made a barley (a very good source of molybdenum) soup for the family this past week that the two-year-old did not eat.
So, again, I'm wondering what is going on. Can molybdenum really get rid of nausea from gastroenteritis? Has it been overlooked as a nausea help because it tends to be mostly in foods that are difficult for an upset stomach to handle due to their lipid and fiber content? Barley water has been used as a traditional remedy for many things, including nausea, but it doesn't seem that anyone knew which components of barley helped with which ailments.
In the past decade, much research has been done on endogenous hydrogen sulfide (H2S), a catabolite of which is sulfite. It appears that H2S is part of the body's response to defend against inflammatory damage in the gastrointestinal tract:
Gastric mucosa expresses both CSE and CBS, which have the ability to mediate H2S synthesis (Fiorucci et al., 2005). In the gastrointestinal tract (GI), recent studies suggest that H2S may contribute to mucosal defense against injury caused by nonsteroidal anti-inflammatory drugs, and it also seems to play a significant role in regulating gastric mucosal blood flow. The mechanisms through which H2S exerts these anti-inflammatory properties are not fully understood. However, the involvement of ATP-sensitive potassium (KATP) channels must be considered (Fiorucci et al., 2006), because it was already demonstrated that H2S reduces leukocyte infiltration and edema formation via KATP channel activation (Zanardo et al., 2006). In contrast, Wallace et al. (2007) demonstrated that H2S promotes healing of gastric ulcers in rats by a mechanism that is not associated with KATPchannels, because neither glibenclamide (KATP channel antagonist) nor pinacidil (KATP channel activator) affected ulcer healing.
Our results confirmed that ethanol administration at high concentrations caused severe macroscopic and microscopic gastric mucosal damage, with hemorrhage, edema, and epithelial cell loss (Guslandi, 1987; Laine and Weinstein, 1988;Medeiros et al., 2008). In the present study, we observed that both H2S donor and H2S precursor (-cysteine) decreased ethanol-induced gastropathy. This effect was greatest after 30 min, persisted for 6 h, but was reversed 24 h after the H2S donor treatment. Furthermore, propargylglycine (an irreversible inhibitor of CSE) pretreatment prevented the protective effect of -cysteine on ethanol-induced gastric damage. These findings are consistent with the hypothesis that gastroprotective effects of -cysteine are correlated to increased H2S synthesis. Therefore, we could infer that H2S synthesis is essential to gastric protection against ethanol.
http://jpet.aspetjournals.org/content/330/3/764.long (See also https://www.ncbi.nlm.nih.gov/pubmed/17825973, https://www.ncbi.nlm.nih.gov/pubmed/25774496, and https://www.researchgate.net/publication/243968909_Protective_effect_of_hydrogen_sulfide_against_cold_restraint_stress-induced_gastric_mucosal_injury_in_rats for studies reporting hydrogen sulfide's protective effect in the GI tract.)
As part of our bodies' protection mechanisms from attack by the various viruses, bacterias, and parasites that we occasionally ingest, we might be increasing the amount of H2S in our stomach and intestines. If we are deficient in molybdenum, we will be deficient in the molybdoenzyme sulfite oxidase, which catalyzes the conversion of sulfite to sulfate; consequently, catabolism of hydrogen sulfide will be stopped at sulfite, which can lead to nausea and vomiting as our bodies try to expel the sulfite accumulating in the stomach and proximal intestine (as discussed...ad nauseum...in previous posts). Thus, in order to lessen nausea and vomiting in connection with stomach bugs, molybdenum supplementation should be an effective aid, preferably taken before the vomiting gets started, as absorption of any oral remedy is harder once vomiting has begun.
Does anyone out there know a cruise director, school nurse, or sleep-away camp director looking for a way to avoid a norovirus plague ruining their events? Send them my way, and I'll sing the praises of molybdenum to them. And when they look at me skeptically and ask, "Why haven't I heard of this being used as a nausea remedy before?", I will answer with another question, "Can you even pronounce molybdenum?" Outside the mining and metallurgy industries, few have paid more than passing attention to molybdenum until now, but I suspect recent findings on endogenous hydrogen sulfide will change that.