Manganese Toxicity Concerns Refuted

Regarding the following article:

Manganese Toxicity (July, 2023) https://www.ncbi.nlm.nih.gov/books/NBK560903/

This article from July 2023 shows a wide array of mechanisms that can contribute to manganese toxicity, such as: being an infant, a woman low in iron, being elderly, having liver problems, low bile flow, diabetes, low pancreas function, being a welder, having Parkonson’s or any nerve or cognitive disorders, having any of a wide array of enzyme dysfunction, or being on TPN meaning getting fed via an IV line. A lot of that might be summed up as being low in copper, iodine, or B12, or all three. This appears to be new, emerging research. TPN appears to be the medical establishment’s version of our protocol, and they get a lot wrong, which can explain why manganese toxicity and or copper deficiency happens on TPN.

Next, I will go over the article more closely, “quoting them”, and my comments WILL BE IN ALL CAPS.

Before I continue, several mineral interaction effects should be understood. Zinc can lower manganese. And manganese can lower copper. Furthermore, low copper creates similar problems as manganese toxicity, such as the neurodegenerative problems, liver problems, enzyme dysfunction, and diabetes. Also TPN is notoriously low in copper, and is recognized to cause copper deficiency. I suspect that TPN is also low in iodine and B12, both of which also are strong nerve healers like copper. Therefore, it appears to me that for these reasons, copper, iodine, and B12 should all be protective against, and the antidotes to manganese toxicity, which is rare enough as it is. Furthermore, the problem of “low iron” is really a problem of low copper, as copper is needed for the body to actually use iron, and make many iron transport proteins that will appear low, and appear as if it’s low iron, when it’s really low copper.

“Manganese toxicity (manganism) is rarely encountered”

“The most often documented etiologies for the development of manganism include chronic total parenteral nutrition (TPN) use in critically ill patients, consumption of contaminated well-water, and exposure through work in welding, smelting, and mining.”

NOTE, THEY SPECIFICALLY DO NOT SAY THAT SUPPLEMENTATION CAUSES MANGANESE TOXICITY OR MANGANISM. FURTHERMORE, THERE ARE HUNDREDS OF POSITIVE REVIEWS OF MANGANESE SUPPLEMENTS OVER ON AMAZON.COM INDICATING A HIGH LEVEL OF SAFETY. FURTHERMORE, SOME OF THOSE SUPPLEMENT COMPANIES SUGGEST INTAKE LEVELS OF FROM 50 MG TO 200 MG, WELL ABOVE THE CUTOFF LEVELS IN WATER AT 0.4 MG/LITER. SO EXPLANATIONS ARE NEEDED TO EXPLAIN THESE WILDLY DIFFERENT POINTS OF VIEW.

I FEEL THAT “COPPER DEFICIENCY” MIGHT HELP EXPLAIN THINGS, COPPER DEFICIENCY IS KNOWN TO BE PROMINENT AMONG PEOPLE ON IV ADMINISTERED TPN, AS THEY ARE SICK. WATER SUPPLIES THAT ARE CONTAMINATED WITH OTHER TOXINS MIGHT ALSO FURTHER DEPLETE COPPER IN PEOPLE. AND WELDING FUMES AS A PROBLEM APPEAR TO BE SIGNIFICANTLY DIFFERENT THAN SUPPLEMENTATION.

“Ingested Mn from plant sources is normally filtered through the liver, and the excess is removed to avoid toxicity. In individuals with hepatic dysfunction, patients are at higher risk of Mn toxic accumulation in the bloodstream.[10][11]

LIVER TOXICITY CAN BE FROM COPPER DEFICIENCY. AND COPPER CAN CURE FATTY LIVER PROBLEMS. SEE: https://revealingfraud.com/2023/08/health/chapter-59-liver-disease-and-copper/

“Another common source of concern for manganism is drinking water. Well-water specifically can accrue excessive amounts of the metal via breakdown from adjacent rock beds. Postulated means of Mn excess include the presence of anoxic water tables, carbon-rich soil, agricultural fertilizers, and run-off from sites of human deposition of materials rich in Mn (incorrectly disposed batteries, waste from mining facilities, sewer water).[13]

OTHER TOXINS SUCH AS FERTILIZERS ALL DEPLETE COPPER.

MEASURING MANGANESE IN WATER AND ATTEMPTING TO CORRELATE THAT WITH MEASUREMENTS OF COGNITIVE ABILITY APPEARS TO IGNORE UP TO 50 OTHER POTENTIAL TOXINS THAT CAN BE IN WATER SUPPLIES, AND IS THUS A POOR INDICATOR OF POTENTIAL MANGANESE TOXICITY, AND SHOULD THUS BE IGNORED BECAUSE THE EVIDENCE IS TOO POOR.

FOR EXAMPLE, IF A MURDER TOOK PLACE, AND IT IS KNOWN THAT ONE OF 50 PEOPLE IN A ROOM DID IT, AND IF I’M ONE OF THE PEOPLE IN THE ROOM, THAT IS WOEFULLY INSUFFICIENT EVIDENCE TO CONVICT ME OF THE MURDER. SIMILARLY, WE CANNOT BLAME MANGANSE FROM THIS KIND OF EVIDENCE. THIS IS ONE OF THE REFERENCES IN THE STUDY WE ARE EVALUATING:

Neurobehavioral Function in School-Age Children Exposed to Manganese in Drinking Water https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4256698/

TO SUM UP, JUST BECAUSE THIS IS A CONCERN, DOES NOT MEAN IT IS A VALID CONCERN. IT IS FAR MORE REASONABLE TO BLAME PESTICIDES, FLUORIDE, AND SEWAR WATER THAN MANGANESE.

IT’S ALSO TOO LITTLE MANGANESE TO RIGHTLY BLAME MANGANESE.

NEXT:

“Given the lack of removal via pancreatic and biliary secretions, intravenous routes of Mn consumption can easily lead to toxic doses resulting in the feared neuropsychiatric complications described below.”

SO, A LACK OF BILE AND PANCREAS SECRETIONS, FROM NOT PUTTING FOOD INTO THE DIGESTIVE TRACT, BUT INTO THE VEINS, CAUSES A LACK OF THE BODY’S ABILITY TO EXCRETE MANGANESE THROUGH BILE THAT IS NOT BEING SECRETED TO DIGEST FOOD THAT IS NOT THERE. THIS IS A FALURE OF TYING TO INJECT FOOD INTO THE VEINS, AND AGAIN, NOT A SOLID PROOF OF MANANESE TOXICITY.

“The elderly are also postulated to be at increased risk for the acceleration of neurotoxicity beyond that of their age-related proclivity.”

POSTULATED MEANS THIS IS ONLY A GUESS. OR A SUGGESTION FOR FUTURE RESEARCH. THIS IS NOT EVIDENCE.

“lower levels of iron (Fe) present in the blood of females, which has been known to correlate with higher Mn levels.”

YES, BUT WE THINK MOST, IF NOT ALL, LOW IRON PROBLEMS ARE REALLY JUST LOW COPPER PROBLEMS.

IRON DEFICIENCY CONTRIBUTES TO MANGANESE TOXICITY:

“Transport of Mn3+ (oxidized form) is via transferrin in the bloodstream and transported across cell membranes via transferrin-receptor complexes. Transferrin receptors are located on cells of the BBB, neurons, and other cells of the central nervous system (CNS).[30] This ability of oxidized Mn to be carried via transferrin is one of the means that Fe deficiency contributes to manganism, given that transferrin levels are increased in the setting of iron deficiency.[31] Furthermore, deficiencies in Fe can lead to the up-regulation of Mn absorptive transporters in the intestines such as DMT-1, leading to Mn overload.[32]

“Cells utilize channels known as ATPase 13A2, SLC30A10, Ferroportin, and SPCA1 for the export of Mn. Relationships between deficiencies in these efflux channels have been linked to the development of hereditary Mn-induced parkinsonism in recent studies.”

THE STUDY OF REFRENCE:

Syndrome of Hepatic Cirrhosis, Dystonia, Polycythemia, and Hypermanganesemia Caused by Mutations in SLC30A10, a Manganese Transporter in Man https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3309187/

THIS IS A CASE STUDY. IT IS IMPOSSIBLE TO DRAW CONCLUSIONS OF CAUSALITY FROM CASE STUDIES, BECAUSE THE SAMPLE IS ONLY ONE PERSON.

“We have recently reported a suspected autosomal recessively inherited syndrome of hepatic cirrhosis, dystonia, polycythemia, and hypermanganesemia in cases without environmental Mn exposure.”

OK, SO IT IS TWO CASES. STILL NOT ENOUGH. ALSO, NOTE, THIS IN CASES WITHOUT ANY MANGANESE EXPOSURE, SO WHY BLAME MANGANESE. THEY DO THE SAME THING WITH COPPER, AND IT’S LIKELY THE SAME MISUNDERSTANDING. MN, LIKE COPPER, MAY WELL BUILD UP IN TISSUES WHEN THERE ARE OTHER TOXINS PRESENT, AND THIS DOES NOT MEAN THAT MN IS TOXIC, WHICH IS WHY YOU CAN’T RELY ON CASES STUDIES WHERE THERE IS NO MN OR COPPER EXPOSURES.

THEY WRITE THAT THIS MN BUILDUP HAPPENS WITH A BROKEN TRANSPORTER, “SLC30A10”. BUT THEY DID NOT PROVE THAT MN BROKE THE TRANSPORTER. IN FACT, IT LIKELY DIDN’T, BECAUSE THERE WAS NO MN EXPOSURE. THEY CLAIM THIS IS GENETIC, BUT IT COULD BE FROM A TOXIN, TOO, THEY JUST DON’T KNOW.

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ABOVE ALL, AT NO TIME, IN NO CASE, DO THEY HAVE ANY SITUATION WHERE A PERSON TOOK A MANGANESE SUPPLEMENT AND SUFFERED ANY TOXICITY.

THEIR CONCERNS ARE MOSTLY THEORETICAL, INVALID, OR INAPPLICABLE.

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