37 replies to this topic

[ironfistx]

Wait, I am seriously confused.  Did you buy powder that was copper or something else?

[KBAnthis]

Wait, I am seriously confused.  Did you buy powder that was copper or something else?

I bought a gram of copper (1) niacin from mitosynergy. I really like it so far.

[ironfistx]

Is that type the only kind you can buy that is copper 1 organization?

Edited by ironfistx, 21 September 2018 - 02:13 AM.

[KBAnthis]

It is the only Copper 1 supplement I have found. So far I have noticed a vast difference. If you are looking for the best it is the best I have found and I would like to hear others opinions. The difference in energy is really noticeable. It is not like coffee or tea, but it is needed by the body.

[ta5]

There's another Copper(1) supplement now called "Cu1" Cuprous Nicotinic Acid:

https://www.amazon.c...t/dp/B09DZYSNL3

It's expensive at $1.85 per mg of copper. But, it is cheaper than MytoSynergy at $5.21 per mg of copper.

 

This is interesting: Sibannac, Inc.'s Copper 1 Supplier Seeks New Drug Application with FDA

 

[Sibannac, Inc] has been actively researching and developing a Copper1 niacin product through its licensing agreement with the patent owner, Mitosynergy. Mitosynegy has been awarded multiple U.S. patents for molecular compounds for bioavailable coppers, namely Cuprous Nicotinic Acid. These patented compounds involve the only known bioavailable Copper 1 in the Copper 1 oxidative state. (For additional information, Patent Nos.: WO2016/037181 and 20150224112.)

 

Mitosynergy had previously received a No Objection Letter: #910, from the FDA, allowing the Copper compound to be marketed as an Initial New Dietary Ingredient ("IND"). Now the company is moving forward in the process of submitting a New Drug Application with the FDA. Copper, in its optimal oxidative state, could be used as a pharmaceutical and nutraceutical. The company is pursuing the use of Copper 1 niacin as an immune modulator to pursue a therapeutic claim for long-COVID and blood born microaerophilic spirochete bacteria pathogens, such as Lyme Disease.

 

Sibannac is developing its Copper1 product through its Campus Co. platform and will likely produce the initial run in the Company's Scottsdale-based, FDA registered facility.

 

"Sibannac will be delivering best-in-class wellness products based on cutting-edge formulations. We're working with some of the best design people in the industry and moving toward offering clinically-proven ingredients in our products," said Sibannac's CEO, David Mersky.

 

Edited by ta5, 16 November 2022 - 03:42 AM.

[ta5]

I'm trying to figure out if Copper-2 is really bad or not since it's so expensive. If Copper-1 and -2 were the same price, of course I would get Copper-1. But, since chelated Copper-2 is only $0.05 per milligram and Copper-1 costs 37x more, I'd like to know if it's worth it.

 

This 2019 review presents evidence that Copper-2 should be avoided:

Avoiding Alzheimer's disease: The important causative role of divalent copper ingestion

Amyloid plaques are a consistent feature of the AD brain. These plaques consist of aggregates of amyloid beta (Aβ). Aβ is a piece of the amyloid precursor protein, and is clipped off the protein in normal brains, but does not accumulate and aggregate in normal brains as it does in the AD brain. It was shown two decades ago that copper-2 induced Aβ aggregation.24 This was elaborated on in further work where it was shown that copper-2 potentiates Aβ neurotoxicity.25 Aβ reduces copper-2 to copper-1 and in the process generates hydrogen peroxide (H2O2), which is a potent source of damaging oxidant radicals.25

 

A more recent line of investigation indicates glycation of Aβ may be involved.25 Glycation is the non-enzymatic addition of a sugar to an amino acid. It is an appealing mechanism because superoxide anion, a reactive oxygen species (ROS), is generated during the glycation process. In the presence of copper-2, superoxide is converted to hydroxyl radical, an ROS, which according to this group, is the source of oxidative damage in AD. Extensive glycation in AD is supported by the finding that large amounts of Aβ in the plaques of AD patients are found in the form of advanced glycation end-products (AGEs). According to this group, all three components of AD plaques, Aβ, sugars, and copper-2, are necessary for the resulting neuronal DNA damage.26 (Sugars provide the glycation substrate).

 

In all these proposed mechanisms of oxidant damage, copper-2 plays a necessary role. So, the direct absorption of copper-2 into the blood, as shown in the 64Cu studies cited,12 without liver processing to put the copper-2 in safe channels, with presumed more or less direct access of copper-2 to the brain, would be expected to be quite neurotoxic.

 

[...]

 

There are additional data which suggest there is an additional cause besides copper-2 of the AD epidemic, and it also involves copper, but copper in general, not a specific valency of copper. This stems from the work of Dr Rosanna Squitti and her group, in Italy. First, she and her group have shown that the fraction of copper in blood, known as “free copper,” is intimately involved with the pathogenesis of AD. By way of background, the blood copper can be thought of as in two pools. One pool, comprising about 90% of the total blood copper, is tightly (covalently) bound to the ceruloplasmin (Cp) molecule. The other 10% of copper is loosely bound to albumin and other molecules in the blood. This smaller fraction, known as non-Cp copper, and also known as free copper, is what the body uses for its day to day needs for copper. It is also this pool that is greatly expanded in a disease of copper accumulation and copper toxicity, Wilson’s disease (WD). The free copper is toxic when the pool is enlarged too much. Dr Squitti’s group has shown that the free copper pool is enlarged in AD,27 that the levels of the free copper correlate with measures of cognition in AD,28 that the levels of free copper predict rates of cognition loss over time in AD,29 and that free copper levels predict the risk of conversion of mild cognitively impaired (MCI) patients to full AD patients.30 These data indicate strongly that AD is, at least in most patients, a disease of copper toxicity. These data are neutral to the copper-2 hypothesis, because the free copper measured by Dr Squitti could be both copper-1 and copper-2. But the Squitti data are compatible with the direct absorption of copper-2 into the blood, as has been discussed, increasing the level of free copper in the blood, and causing toxicity to cognition.

 

Low copper-2 intake in Switzerland does not result in lower incidence of Alzheimer’s disease and contradicts the Copper-2 Hypothesis

Copper nutrition and biochemistry and human (patho)physiology (full article is on sci-hub.se)

In opposition to the hypothesis that elevated brain copper increases AD risk, other scientists have suggested that copper depletion may also play a role in the pathogenesis of AD. Supporting this postulate is the observation that AD patients have low brain copper levels and reduced activity of some cuproenzymes (Klevay, 2008). There is also limited published evidence demonstrating an inverse relationship between body copper levels and risk of developing AD; that is, those with higher copper levels had a lower incidence of AD (Siotto et al., 2016).

 

[ironfistx]

Also, I'm not sure whether I'm an over or under methlator. I have poor methyl. genetics. Some methl donors make me worse (like high dose methyl B12).

Same. Methyl b versions, or methyl B12 separately cause me to feel horrible.

[ironfistx]

Somewhere I heard the copper1 doesn't cause a change in serum copper. Is this suspect?

There's a group on Facebook that suggests taking 12mg copper per day.

It would be an error to interpret this as a recommendation, you know.

Edited by ironfistx, 20 November 2022 - 06:55 PM.