For some time, I've been wondering why young children under 5 years of age tend to be more severely afflicted by gastroenteritis. Per the Medscape website:
Acute gastroenteritis is a common cause of morbidity and mortality worldwide. Conservative estimates put diarrhea in the top 5 causes of deaths worldwide, with most occurring in young children in nonindustrialized countries.
https://emedicine.medscape.com/article/176515-overview
As I and several others have observed, molybdenum (given in the form molybdenum glycinate) successfully treats the nausea, vomiting, and diarrhea of viral gastroenteritis. (See
https://petticoatgovernment.blogspot.com/2018/01/molybdenum-for-gastroenteritis-nausea.html,
https://petticoatgovernment.blogspot.com/2018/01/molybdenum-and-diarrhea.html) The relatively high level of molybdenum in legumes--generally considered "poor man's food"--appears to be a plausible explanation for why travelers from wealthier countries often suffer to a much greater degree from viral gastroenteritis when visiting poorer countries than do the local people who eat a lot of legumes.
But children in these poorer, nonindustrialized countries are also being fed legumes....why are they dying from diarrhea in such large numbers even when their usual diet is relatively high in molybdenum? I think the tendency to avoid eating beans when feeling nauseated helps explain to some degree why people, including young children,
continue to feel nauseated after they are already vomiting and starting to have diarrhea. But why doesn't molybdenum ingested earlier and stored in the body have more of an ameliorative effect in very young children? We store molybdenum in many parts of the body, especially in the liver. (See references at
https://www.imoa.info/HSE/environmental_data/human_health/molybdenum_uptake.php.) Because the liver, via the biliary tract, is well-situated to deliver molybdenum to the part of the digestive tract where the action of vomiting starts (see
https://en.wikipedia.org/wiki/Retroperistalsis), the liver is the most logical source of stored molybdenum that could have an impact on emesis.
I think a clue to why very young children tend to be more severely affected by viral gastroenteritis symptoms might lie in the absence of CD10 in the liver bile capillaries (canaliculi) of infants and children under 2 years of age. (See
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5805126/ and
https://www.nature.com/articles/3700677.) CD10 is also absent in the liver bile capillaries of people with Alagille syndrome (
https://www.nature.com/articles/3700677), a major feature of which is liver bile ducts which are narrow, malformed, and reduced in number (
https://rarediseases.info.nih.gov/diseases/804/alagille-syndrome). Perhaps the tiny bile capillaries of small children, due to being without CD10 for the first two years of life, are malformed in such a way as to decrease the ability to mobilize molybdenum out of its liver-located storage; then after the bile capillaries start to have CD10 at about age 24 months, the livers continue to grow and liver cells undergo normal turnover, allowing substantial bypassing and repair of the earlier bile capillary defects by around age 5 years.
If insufficient delivery of molybdenum from the liver tissue to the proximal small intestine (duodenum) in very young children helps explain their greater mortality from gastroenteritis symptoms, then we should expect to see that obstructive jaundice--generally caused by an obstruction between the liver and the duodenum--is associated with nausea, vomiting, and diarrhea. It looks like that could indeed be the case, for nausea, vomiting, and diarrhea are noted as symptoms that have been observed to occur together with jaundice. (
https://www.medicinenet.com/jaundice_in_adults/article.htm#what_are_the_signs_and_symptoms_of_jaundice_in_adults,
https://www.merckmanuals.com/home/liver-and-gallbladder-disorders/manifestations-of-liver-disease/jaundice-in-adults). It would be interesting to investigate whether people with gallstones or other bile duct obstructions are more severely affected by norovirus than people without. It is already accepted that it is a bad thing to obstruct the biliary tract; maybe an impaired ability quickly to utilize molybdenum stores in the liver is an additional negative result of biliary obstruction. Due to the prevalence of parasites in many developing countries, it would also be interesting to investigate the effects of parasites on the transport of molybdenum within the biliary tract.
There is much new space opened up for inquiry into diseases of the gastrointestinal tract by the discovery of molybdenum's ameliorative effect on the viral gastroenteritis symptoms of nausea, vomiting, and diarrhea. Despite notifying many researchers and public health officials at the beginning of 2018, I have no knowledge to date of any researchers or medical practitioners following up on my reports of molybdenum glycinate's effectiveness in preventing/treating those symptoms. Molybdenum keeps working as I've been reporting, and the number of successes I hear about keeps ticking upward. I'm disappointed in the medical world. A housewife in Colorado shouldn't be the only one trying to fit all this together.
(Disclaimer: I do not prescribe the use of pharmaceutical drugs in any way. I am not a physician, and I reject out of hand any attempt to hold me liable for what boils down to a discussion of food. Any use of a molybdenum supplement should be prudent and guided by the tested tolerable upper intake levels for its usage (see
http://lpi.oregonstate.edu/mic/minerals/molybdenum for those limits). Any use of an isolated molybdenum supplement during pregnancy should be under the direction of a medical professional as such supplements have apparently not been tested during pregnancy.)
