(Formerly Mag me with a spoon #1)
Ever wondered what happens when iron and magnesium get together and the effect of iron overload in the liver on magnesium status.
Some important clues:
- Cysteine dioxygenase has an iron atom at its core and in the same way that iron gets into the core of hemoglobin, I’m assuming that it’s bioavailable copper that enables that enzyme to work, as well When it doesn’t, then we have sulfate issues.
- There is an entirely different pathway with sulfite oxidase, which by the way relies on molybdenum, but folks can have issues with sulfates as well there.
- Rheumatoid arthritis is one of the 30+ autoimmune conditions that have exploded on the scene since the introduction of HFCS and GMO products that coupled with the enrichment of flour with iron filings have created untold stress for our livers. This has caused a massive loss of liver copper and build-up of liver iron. (You might look into the work of Mary Fields, PhD in the early 1980’s)
- Rheumatoid arthritis = low bioavailable copper (and by inference, high unbound iron.)
- When iron is out of control, and in a state of overload, it has a profound effect on both magnesium status and tumor necrosis factor alpha (TNFa):
— Magnesium deficiency is the metabolic precursor to the inflammatory cascades triggered by substance P when intracellular magnesium is too low:
Weglicki, W.B., Phillips, T.M. (1992). “Pathobiology of magnesium deficiency: a cytokine/neurogenic inflammation hypothesis.”
https://www.ncbi.nlm.nih.gov/pubmed/1384353
— Iron overload in the liver has a devastating effect on liver chemistry and causes a rise in TNFa:
Brown, K.E., et al. (2006). “Chronic iron overload stimulates hepatocyte proliferation and cyclin D1 expression in rodent liver.”
https://pubmed.ncbi.nlm.nih.gov/16890145/
— As you note later in this thread, there is a decided impact of sulfites on thiamine (B1) status and it turns out that thiamine deficiency drives an increase in iron:
Itokawa, Y. (1987). “Tissue minerals of magnesium-deficient rats with thiamine deficiency and excess.”
https://pubmed.ncbi.nlm.nih.gov/3821175/
Talk about a perfect metabolic storm! There are hundreds if not thousands of articles that tie magnesium deficiency to elevated TNFa and vice-versa. Which is the chicken, which is the egg? It would be an endless debate to some extent. We are in total agreement re the impact of too little magnesium.
We just need to pull the curtain back all the way to reveal that magnesium loss is always in response to a stressor. It is how we are wired as a species. As I study the cellular enzyme pathways, the impact of ROS (reactive oxygen species), the central role of antioxidant enzymes (which is produced in the liver) and the fact that low ceruloplasmin ==> high iron stored in the liver. Iron stress in the liver is a cellular nightmare and by inference, iron is especially toxic to magnesium status in the liver.
Given that information, I’m more inclined to say that the real threat is our exposure to dietary and supplemental iron, which is further aggravated by the twisted and false belief that folks are iron anemic, it creates a perfect metabolic storm.
In my world, based on my research and what I’ve been able to piece together from hundreds & hundreds of articles over 7 yrs of reading & reflection, the iron enriched wombs of women today are producing children who are iron dysregulated. The agricultural, food and medical systems only further that iron dysregulation. Vaccines only send this dysregulation into stratospheric orbit in a body that has low production of both copper-dependent antioxidant enzymes, as well as low magnesium.
I am convinced that iron is the 1st offender, and magnesium is taking it on the chin whenever we are under stress.
Hope that makes sense and connects some important mineral dots!
A votre sante!
MORLEY M. ROBBINS
For Facebook discussion:
https://www.facebook.com/groups/MagnesiumAdvocacy/permalink/1027207120680690/