I hope this note finds You well
oxythiamine is an anti-metabolite which blocks the Essential B1 Vitamine Pathway
The body would perceive that as a severe Thiamine deficiency with all of its clinical presentations and complications
The mortality rate from a severe Thiamine deficiency is 30%
"Therefore, it is
conceivable that other groups of bacteria can exist in the gut that can mediate the reverse
process and produce oxythiamine. An intriguing possibility may be that altered gut
microflora in ESRD can lead to abnormal oxythiamine production and absorption with
subsequent functional thiamine deficiency in the face of normal or increased serum levels"
As has been reviewed, the text SILENCE, refers to the case where a Physician acquired a disease which was defined as non-curable, but after dialysis, disappeared
The implication was that Dr North's original diagnosis was erroneous
"Even more unusual is the way North’s recovery occurred. She was one of the first people to be tried on renal dialysis"
Should she have experienced gut bacteria which synthesized oxythiamine, which is dialyzable, or acquired that toxin from any source, eg some sort of fecalith there at the midwest, then she would have experienced a Thiamine deficiency because of that anti-metabolite
fatigue:depression::dementia:psychosis
We are now aware that deficiencies of Thiamine (B1), Niacin (B3), Folate (B9), and/or Cobalamin (B12) cause severe fatigue and dementia, which is often misdiagnosed as depression or psychosis
That would cause an expensive medical misadventure
Rumor is that jonathan makes his living off medical misadventures
Best wishes always
Thank you for your assistance with this matter
Cordially,
Joseph W Arabasz MD
S/P USAF, Top Secret 1964-69
University of Colorado at Boulder 1972, CU School of Medicine '75, '77, '83
Past Division Chairman, Anesthesiology, Cook County Hospital, Chicago, Illinois
Past Chairman, Respiratory Therapy, Cook County Hospital, Chicago
Diplomate ABA
Mensa
Sigma Xi, The Professional Science Research Society
PO Box 6939
Denver, CO 80206
USA
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Subject Title- Thiamine deficiency in end-stage renal disease- malnutrition despite ample nutrients
"In another study, Koeth et al
found that intake of L-carnitine (in red meat) can cause atherosclerosis via a similar
mechanism. Therefore, these authors have identified gut microbiota as a link between
dietary intake of nutrients and CVD (cardiovascular disease). Furthermore, it is well-known that dietary and
environmental factors can lead to alterations in intestinal microbiome, thereby contributing
to the pathogenesis of various clinical phenotypes. In fact, Vaziri et al
evaluated the microbiota of patients with ESRD (end stage renal disease) on hemodialysis using phylogenetic microarray and found
significant differences in the abundance of numerous bacteria between the ESRD
and control groups. Furthermore, there is a report of a specific form of Escherichia coli
(“thiamine-missing” mutant E coli) that can convert oxythiamine to thiamine 9
Therefore, it is
conceivable that other groups of bacteria can exist in the gut that can mediate the reverse
process and produce oxythiamine. An intriguing possibility may be that altered gut
microflora in ESRD can lead to abnormal oxythiamine production and absorption with
Moradi and Said
Author manuscript; available in PMC 2017 July 20
subsequent functional thiamine deficiency in the face of normal or increased serum levels.
Although overt symptoms and signs of B1 deficiency might not be present, functional
thiamine deficiency may contribute to various complications of ESRD including oxidative
stress, impaired energy metabolism, anemia, CVD, and ultimately increased mortality
(Figure 1). These novel mechanisms will need to be further examined in future studies
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