Low Toxin Diet Copper antagonists and discussion

[Peater]

Can anyone add to the list of copper antagonists? Would love some discussion too.


Zinc
Molybdenum
Potassium
Manganese
Sulphur
Taurine

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9324259

In conclusion, we hypothesize that the excessive non-ceruloplasmin Cu in the body can result in a higher requirement for Mo, which becomes deficient. It results in low SUOX activity, disrupted Met metabolism and higher Aβ content. Consequently, the excess of Met can increase Aβ neurotoxicity [52]. So, although Mo is not directly involved in the formation of Aβ, such as Cu, the link with the Aβ hypothesis is indirect (Figure 2). Its harmful effects on metabolism trigger the other symptoms of AD-related diseases and, later, AD symptoms. That hypothesis is in line with the findings of the current review.

 

[Elie]

B6 is one.

I don't think it is about antagonizing it, it is just not uptaken by cells efficiently when certain nutrients and enzymes are lacking (as per the fibromyalgia doctor whose video was posted here).

 

[Peater]

B6 is one.

I don't think it is about antagonizing it, it is just not uptaken by cells efficiently when certain nutrients and enzymes are lacking (as per the fibromyalgia doctor whose video was posted here).

Thanks Elie! I didn't know that. You are right, antagonists wasn't the right word. "Balancing nutrients" maybe?

I don't take B6 anymore as I suspect I over-did it and gave myself some toxicity symptoms. I just mention it as something to watch out for.

 

[Peater]

Modification of vitamin A metabolism in rats fed a copper-deficient diet - PubMed

The liver is the main storage site of vitamin A and copper. Inverse relationships between copper and vitamin A liver concentrations have been suggested. We have investigated the consequences of a copper-deficient diet on liver and blood vitamin A storage in Wistar rats. Animals were fed either a...

pubmed.ncbi.nlm.nih.gov

I was wondering if depleting Vit A helps deal with excess copper as well, I was surprised to find this. Welcome any comments. Tagging @mosaic01 as you have a good eye for these studies.

The liver is the main storage site of vitamin A and copper. Inverse relationships between copper and vitamin A liver concentrations have been suggested. We have investigated the consequences of a copper-deficient diet on liver and blood vitamin A storage in Wistar rats. Animals were fed either a copper-deficient diet for 45 days from weaning, or an identical diet containing adequate amounts of copper. Concentrations of vitamin A were determined by isocratic high performance liquid chromatography using UV detection. We have observed in the liver of the rats fed a copper-deficient diet a significantly higher mean level of retinyl esters (148 +/- 37 micrograms/g of liver) and retinol (3.3 +/- 1.4 micrograms/g of liver) compared to the mean concentration of the retinyl esters (53 +/- 8.5 micrograms/g of liver) (p less than 0.01) and retinol (1.4 +/- 0.5 micrograms/g of liver) (p less than 0.01) in controls. Opposite results were observed in the serum of the group fed a copper-deficient diet as these rats had a significantly lower level of retinol (22 +/- 4 micrograms/100 ml) compared to the mean concentration in the controls (64 +/- 20 micrograms/100 ml) (p less than 0.01). These findings suggest that a copper-deficient diet may cause defective transport of vitamin A from liver to blood. This experimental model may be useful to further investigate unusual liver vitamin A and copper concentrations observed in children during various hepatobiliary diseases.