Homemade mitosynergy copper (copper 1) Does it really work??

[youngsinatra]

Sorry I see you've detailed your process above. Interesting you have much better results than me. I can't get the deep orange colour. I might need to try pure copper glycinate powder. I have that product but with fillers so maybe that's why it's not working

Yeah. I personally use food-grade copper bisglycinate powder from a chemistry company. I paid 25€ for 25g IIRC.

By doing so everything dissolves perfectly in hot liquid, without visable remains. Even if the solution is deep yellow/orange, you can see cleary through it.

 

[youngsinatra]

Sorry I see you've detailed your process above. Interesting you have much better results than me. I can't get the deep orange colour. I might need to try pure copper glycinate powder. I have that product but with fillers so maybe that's why it's not working

A friend of mine was unable to do it with the crushed copper pill, probably due to the fillers.

 

[Ben.]

Sorry I see you've detailed your process above. Interesting you have much better results than me. I can't get the deep orange colour. I might need to try pure copper glycinate powder. I have that product but with fillers so maybe that's why it's not working

Mine is very intense orange. For a moment i thought it would become red even. Used copper sulphate (which is dirt cheap), ascorbic acid and baking soda.
I eyeballed sinatras 100mg on the AA and Baking Soda.

Altough how legit this is, i dont know.

Edit: Way to much copper. Dont replicate. Don't ingest.

 

[youngsinatra]

Mine is very intense orange. For a moment i thought it would become red even. Used copper sulphate (which is dirt cheap), ascorbic acid and baking soda.
I eyeballed sinatras 100mg.

Altough how legit this is, i dont know.

View attachment 35703

Interesting. How much copper did you use?

 

[ddjd]

Mine is very intense orange. For a moment i thought it would become red even. Used copper sulphate (which is dirt cheap), ascorbic acid and baking soda.
I eyeballed sinatras 100mg.

Altough how legit this is, i dont know.

View attachment 35703

Wow that looks legit. Is the copper sulphate food grade??

 

[Ben.]

Interesting. How much copper did you use?

Way to much. Woudn't suggest using it to make copper (I).

I did this now 6 times with different amounts. if i use 8mg copper sulphate its see trough pisslike. Barely any colour. When i go up to 100-200ish mg it gets stronger yellow but still not realy strong. At 1/8th of a teaspoon which is, if i didn't miscalculate completly c.a 36.000mg of actuall copper (0,9g copper sulphate). At that point it is already strong orangish with a yellow taint. At a full teaspoon its insanely orange. even more than the picture.

All of this in 100ml water with 150mg Ascorbic acid and sodium bicarbonate.

Obviously i didn't ingest any.


Soooooooo ... dont take the previous picture i posted seriously and dont go off buying anything. My apologies.

Wow that looks legit. Is the copper sulphate food grade??

99,8% purity. No, the vendor i bought it from did not sell it for ingestion.

 

[youngsinatra]

The low dose should be effective even if it‘s not that deeply colored.

A low dose of CuSO is also less blue than a supersaturated solution. (get‘s really darkblue)

 

[ddjd]

The low dose should be effective even if it‘s not that deeply colored.

A low dose of CuSO is also less blue than a supersaturated solution. (get‘s really darkblue)

I wonder why Charles Barker from mitosynergy used niacin in his formula. Maybe it adds to stability in some way

 

[youngsinatra]

I wonder why Charles Barker from mitosynergy used niacin in his formula. Maybe it adds to stability in some way

Charles Barker said that producing copper (I) as a powder was really difficult because of it‘s quick reduction to copper (II) and low shelf-life.

Probably adds stability.

 

[youngsinatra]

View: https://youtu.be/kxmyOD_Xo0g


A quick video on how I make mine.

Use a small amount of hot, almost boiling water
1. First add sodium bicarbonate (100mg)
2. Then add copper (II) bisglycinate (I used 30mg which equals to 10mg elemental copper) here
3. Add 15-30mg of ascorbic acid.

 

[Amazoniac]

Thank you for that report. I've tried copper sulphate the past 2 weeks but the antimicrobial effect from it seems to be to strong (stomacheache and nausea for example) and i get more negative effects than positives from it.

You make it with the ascorbic acid and sodium bicarbonate you've mentioned? Does it have to be bisglycinate or does another form work aswell to make copper (I)? I've copper sulphate on hand and a "komplex" in pill form with glycinate, gluconate and citrate in it.

Before my lack of knowledge in chemistry bites me in the **** here im thinking of purchasing some from mitosynergy.

It can be a symptom of harm and it's consistent with the idea that free copper(2) is problematic at the gut level, but there's more to it:

- Copper signalling: causes and consequences

"As Ctr1 cannot transport bivalent copper, some ingested Cu(II) avoids the liver and passes rapidly into the systemic circulation where can target albumin [135]. Following entry into hepatocytes, Cu(I) binds the initial acceptor GSH, which delivers it to the different copper chaperones, such as Atox1, CCS and COX17 that partition copper into distinct intracellular compartments [116]. Nevertheless, the landscape of Cu(I) trafficking to chaperons via GSH may change. Recent data on femtomolar [175] versus picomolar [148] affinities of GSH towards Cu(I) raise the role for [Cu4(GS)6] preserving Cu(I). In fact, the Cu(I) availability is highly associated with GSH level of the cell. Ogra et al. [214] observed that depletion of GSH led to decreased copper in the bile and blood but increased copper in the liver. The decreased GSH level resulted in an oxidative environment in the liver that made Cu(I) less bioavailable. In addition, the redox state of the cells influences the activity of copper pumps. GSH deficiency inhibits ATP7A and ATP7B resulting in the intracellular accumulation of copper [136]."​

However, a considerable fraction of food copper occurs in such oxidation state, yet there are not complaints about it, which is why I think that it's a matter of stability of the copper complex.

What was brought up elsewhere is that a reductase impairment may not be limited to the intestines. In this case, a hypothetical intestinal trap would be preferable to it happening once in the body; the person could be facilitating its uptake, it's going to eventually be oxidized to copper(2) when the ability to recycle it is compromised.

 

[Amazoniac]

- Extracellular Cu2+ pools and their detection: From current knowledge to next-generation probes

Spoiler

"In mammalian cells, the membrane transporters Ctr1/2 and ATP7A/7B regulate respectively the import and the export of Cu (as Cu+) into/from the cytosol. Intracellularly, the reduced Cu+ state is predominant due to the high abundance of reducing agents such as ascorbate, NADPH, and glutathione. The latter is a key regulator of cellular redox homeostasis, attaining 1–10 mM concentration. Glutathione exists in both reduced (thiol) GSH and oxidized (disulfide) GSSG form, the GSH:GSSG ratio being a marker of cellular redox status. The cytosolic and mitochondrial glutathione pools are highly reduced, with GSH:GSSG > 10000:1. Conversely, the glutathione pool is much more oxidized in the endoplasmic reticulum, with a GSH:GSSG ratio in the 1–15:1 range. Notwithstanding, reduced GSH is still the major species therein [2]. Such levels of the GSH:GSSG ratio imply a redox potential that contributes to keeping Cu in the reduced Cu+ state in all cell compartments. As a result, Cu2+ exists in the intracellular environment only transiently, in binding sites buried within cuproenzymes, where Cu cycles between Cu+ and Cu2+."

"Although an important role of GSH in Cu uptake has been suggested,[3] recent studies showed that intracellular ‘‘free” Cu+ is buffered at very low concentration (about 1 aM), below the threshold for Cu+-binding to GSH in mainly tetranuclear Cu-thiolate clusters. Actually, Cu+ is bound to proteins with attomolar affinity, called metallo-chaperones, each of which delivers Cu to a specific target (CCS to SOD1, Atox1 to ATP7A/B, Cox17 to COX). Only in case of Cu overload, GSH and metallothioneins (MTs), a family of thiol-rich proteins, could bind Cu. Indeed, although metallothioneins are the strongest Cu+ ligands in the cell (log Ka ~19–20), they are normally loaded with Zn2+ [4-6]."

"Conversely, in the extracellular space, Cu is carried mainly in the oxidised Cu2+ state. Herein, Cu2+ levels and speciation in different extracellular compartments, are thoroughly revised under both physiological and pathological conditions (see Section 2). Indeed, although a rigorous control of Cu levels and localization exists, failure of Cu homeostasis may occur, resulting in pathological states. For instance, genetic mutations on ATP7A or ATP7B genes result in two severe Cu-related diseases called Menkes’ (MD) and Wilson’s disease (WD), respectively. In MD, Cu accumulates in the intestine causing a systemic Cu deficiency, whereas in WD Cu accumulates mainly in the liver due to impaired biliary excretion. In addition, Cu dyshomeostasis or mislocalization has been also recognized in neurodegenerative disorders, such as Alzheimer’s and Parkinson’s disease, as well as in cancer [7]. As a result, altered Cu levels in biological fluids are observed in such Cu-related diseases. Remarkably, the portion of exchangeable (i.e., kinetically-labile) Cu, and not total Cu levels, appears to be increased in serum and urine of WD and AD patients [8]."

 

[youngsinatra]

- Extracellular Cu2+ pools and their detection: From current knowledge to next-generation probes

Spoiler

"In mammalian cells, the membrane transporters Ctr1/2 and ATP7A/7B regulate respectively the import and the export of Cu (as Cu+) into/from the cytosol. Intracellularly, the reduced Cu+ state is predominant due to the high abundance of reducing agents such as ascorbate, NADPH, and glutathione. The latter is a key regulator of cellular redox homeostasis, attaining 1–10 mM concentration. Glutathione exists in both reduced (thiol) GSH and oxidized (disulfide) GSSG form, the GSH:GSSG ratio being a marker of cellular redox status. The cytosolic and mitochondrial glutathione pools are highly reduced, with GSH:GSSG > 10000:1. Conversely, the glutathione pool is much more oxidized in the endoplasmic reticulum, with a GSH:GSSG ratio in the 1–15:1 range. Notwithstanding, reduced GSH is still the major species therein [2]. Such levels of the GSH:GSSG ratio imply a redox potential that contributes to keeping Cu in the reduced Cu+ state in all cell compartments. As a result, Cu2+ exists in the intracellular environment only transiently, in binding sites buried within cuproenzymes, where Cu cycles between Cu+ and Cu2+."

Spoiler

​

"Although an important role of GSH in Cu uptake has been suggested,[3] recent studies showed that intracellular ‘‘free” Cu+ is buffered at very low concentration (about 1 aM), below the threshold for Cu+-binding to GSH in mainly tetranuclear Cu-thiolate clusters. Actually, Cu+ is bound to proteins with attomolar affinity, called metallo-chaperones, each of which delivers Cu to a specific target (CCS to SOD1, Atox1 to ATP7A/B, Cox17 to COX). Only in case of Cu overload, GSH and metallothioneins (MTs), a family of thiol-rich proteins, could bind Cu. Indeed, although metallothioneins are the strongest Cu+ ligands in the cell (log Ka ~19–20), they are normally loaded with Zn2+ [4-6]."​

​

"Conversely, in the extracellular space, Cu is carried mainly in the oxidised Cu2+ state. Herein, Cu2+ levels and speciation in different extracellular compartments, are thoroughly revised under both physiological and pathological conditions (see Section 2). Indeed, although a rigorous control of Cu levels and localization exists, failure of Cu homeostasis may occur, resulting in pathological states. For instance, genetic mutations on ATP7A or ATP7B genes result in two severe Cu-related diseases called Menkes’ (MD) and Wilson’s disease (WD), respectively. In MD, Cu accumulates in the intestine causing a systemic Cu deficiency, whereas in WD Cu accumulates mainly in the liver due to impaired biliary excretion. In addition, Cu dyshomeostasis or mislocalization has been also recognized in neurodegenerative disorders, such as Alzheimer’s and Parkinson’s disease, as well as in cancer [7]. As a result, altered Cu levels in biological fluids are observed in such Cu-related diseases. Remarkably, the portion of exchangeable (i.e., kinetically-labile) Cu, and not total Cu levels, appears to be increased in serum and urine of WD and AD patients [8]."​

​

Thanks for sharing!

 

[Jing]

Ive been trying this out recently using copper biglycinate tablets , majority of the time I get it to turn to a deep orange colour but sometimes it just turns yellow or even green why could this be? Seems random I do the same stuff each time lol I'm using 200mg sodium bicarbonate, 9mg copper and 200mg ascorbic acid.

 

[youngsinatra]

Ive been trying this out recently using copper biglycinate tablets , majority of the time I get it to turn to a deep orange colour but sometimes it just turns yellow or even green why could this be? Seems random I do the same stuff each time lol I'm using 200mg sodium bicarbonate, 9mg copper and 200mg ascorbic acid.

I don‘t know. I always get the same result, but I use copper bisglycinate powder, so it completely dissolves in hot water.

 

[Jing]

Mine is very intense orange. For a moment i thought it would become red even. Used copper sulphate (which is dirt cheap), ascorbic acid and baking soda.
I eyeballed sinatras 100mg on the AA and Baking Soda.

Altough how legit this is, i dont know.

View attachment 35703

Edit: Way to much copper. Dont replicate. Don't ingest.

Been making this recently I have copper biglycinate powder and copper sulfate powder, copper sulfate powder turns to a deep orange like in your picture copper biglycinate turns to a lighter orange but only sometimes lots of the time copper biglycinate seems to turn green. Is it safe to consume copper sulfate? Also how much elemental copper is in copper sulfate ? How much copper sulfate do I use to get 3mg of elemental copper?

 

[youngsinatra]

 

[youngsinatra]

Speciation of copper in a range of food types by X-ray absorption spectroscopy - PubMed

Copper (Cu) is an essential element and the effects of diets deficient in it are well established. However, the effects of long-term high copper intake are less clear. The chemical form of copper from food sources and its resultant bioavailability is a potentially important factor in its...

pubmed.ncbi.nlm.nih.gov

So it seems that Cu(I) is the predominant copper found in foods, which to me supports the idea of Charlie Barker. Cacao seems to be predominantly Cu(II) though!

I chatted with Charlie Barker and he said that copper (II) + AA = copper (I) oxide, which gets hooked up by stomach acid (HCl) and created copper (I) chloride which has poor bioavailability.

I tried this in a solution and it is true. Mixing copper (II) + ascorbic acid turns it yellow/orange. Mixing some NaCl to it makes the solution completely transparent like water.

I know that the copper (I) nicotinate complex is synthesized by reacting copper (I) chloride and nicotinic acid. I‘ve talked to some who successfully made it that way. (Then the solution turns from transparent to dark orange again)

I tried mixing niacinamide + copper (I) chloride in hot solution, but it did not changed the color. Maybe it requires nicotinic acid. (the flush kind)

I chatted with someone who said that he uses pure Cu2O (copper (I) oxide) powder, nicotinic acid and HCl (4%) and he got copper (I) nicotinic acid out of it. He also said that his blood tests only improved after taking this.

The experimentation continues!

 

[Ben.]

Speciation of copper in a range of food types by X-ray absorption spectroscopy - PubMed

Copper (Cu) is an essential element and the effects of diets deficient in it are well established. However, the effects of long-term high copper intake are less clear. The chemical form of copper from food sources and its resultant bioavailability is a potentially important factor in its...

pubmed.ncbi.nlm.nih.gov

So it seems that Cu(I) is the predominant copper found in foods, which to me supports the idea of Charlie Barker. Cacao seems to be predominantly Cu(II) though!

I chatted with Charlie Barker and he said that copper (II) + AA = copper (I) oxide, which gets hooked up by stomach acid (HCl) and created copper (I) chloride which has poor bioavailability.

I tried this in a solution and it is true. Mixing copper (II) + ascorbic acid turns it yellow/orange. Mixing some NaCl to it makes the solution completely transparent like water.

I know that the copper (I) nicotinate complex is synthesized by reacting copper (I) chloride and nicotinic acid. I‘ve talked to some who successfully made it that way. (Then the solution turns from transparent to dark orange again)

I tried mixing niacinamide + copper (I) chloride in hot solution, but it did not changed the color. Maybe it requires nicotinic acid. (the flush kind)

I chatted with someone who said that he uses pure Cu2O (copper (I) oxide) powder, nicotinic acid and HCl (4%) and he got copper (I) nicotinic acid out of it. He also said that his blood tests only improved after taking this.

The experimentation continues!

Wow. Thanks alot for sharing. I felt the yellow one was already "better" than the usuall copper 2 in terms of toleration and effect.

I actually have niacin here so i'll be trying it.

 

[youngsinatra]

Wow. Thanks alot for sharing. I felt the yellow one was already "better" than the usuall copper 2 in terms of toleration and effect.

I actually have niacin here so i'll be trying it.

Cool. Keep me updated!