Iron Metabolism

youngsinatra

Member
Joined
Feb 3, 2020
Messages
3,148
Location
Europe

Healthseeker

Member
Joined
May 10, 2022
Messages
427
Location
WV
3-s2.0-B9780124177628500557-f42-51-9780124177628.jpg
 

youngsinatra

Member
Joined
Feb 3, 2020
Messages
3,148
Location
Europe

„Zn-induced neuronal death was also attenuated by addition of the energy substrate oxaloacetate, the activator of pyruvate dehydrogenase, dichloroacetate, or the inhibitors of NAD+ catabolism, niacinamide or benzamide. Acetyl carnitine, α-keto butyrate, lactate, and β-hydroxy-butyrate did not attenuate Zn2+-induced neurotoxicity, perhaps because they could not regenerate NAD+ or be used for energy production in the presence of glucose.“
 
OP
bruschi11

bruschi11

Member
Joined
Dec 20, 2016
Messages
470
really good stuff @youngsinatra . The pyruvate thing is nuts. It’s obvious though it makes sense why.

I’m going through hell here. I’m realizing manganese dropping at end of 2022 was the reason I was never able to get system back online. Why NAd in February 2023 didn’t work. Cuz I wasn’t getting histidine up. And I’ve needed histidine all year to get in control of the zinc. Manganese dropped in hair for the first time my entire history 6 years of htmas. At end of 2022. And even worse lately.

I didn’t get it. Now as I take manganese get methylation going my body is just using the zinc and I’m into extreme torture diabetic no appetite but starving at same time.

I can’t handle it. I want to write more about what myself and nutritionist I’m working with are putting together. The chemical depression is so bad. I cannot deal with it. I need my misery to end so ****** bad.


It’s basically nad+ manganese raises histidine. ATP. Folate cycle needs to work. Manganese uses carnosine to raise histidine.
 
Last edited:

youngsinatra

Member
Joined
Feb 3, 2020
Messages
3,148
Location
Europe
„Other energy substrates, NAD+catabolism inhibitors, and pyruvate dehydrogenase (PDH) cofactors [pyruvate, oxaloacetate, malate, succinate, lactate, β-hydroxy-butyrate, α-keto-butyrate, FBP, DHAP, acetyl-carnitine, niacinamide, benzamide, 3-aminobenzamide, dichloroacetate (DCA), riboflavin, thiamine, lipoic acid, and lipoic amide] were tested at optimal concentrations (concentration titration data not shown) for their ability to reduce Zn2+-induced or glucose deprivation-induced neuronal death. At these concentrations, none of the compounds were found to be toxic or to induce gross changes in cell volume. Oxaloacetate, niacinamide, benzamide, and 3-aminobenzamide were nearly as effective as pyruvate at attenuating Zn2+-induced neuronal death, but of these, only pyruvate and oxaloacetate were used as energy substrates (Table(Table3).3). Niacinamide, benzamide, and 3-aminobenzamide competitively inhibit all NAD+-catabolizing enzymes; niacinamide is also a precursor for NAD+ synthesis (for review, see Szabo and Dawson, 1998). In addition, DCA, which functions as an activator of the PDH complex (inhibiting the kinase that inhibits the complex), partially attenuated Zn2+ neurotoxicity without serving as an energy substrate. However, the other PDH complex cofactors, thiamine or lipoic acid, were ineffective against Zn2+neurotoxicity. The effect of DCA was synergistic with low levels of pyruvate (data not shown).
 
OP
bruschi11

bruschi11

Member
Joined
Dec 20, 2016
Messages
470
I did live blood analysis yesterday. I’m anemic. Just as Gbold said would happen in zinc toxicity. And what I’ve been theorizing for awhile. I’m not getting iron out of the liver. It’s trapped.
 
EMF Mitigation - Flush Niacin - Big 5 Minerals

Similar threads

Back
Top Bottom