Shockingly Successful Trial Shows Copper Dissolved In Dmso Treats Als

haidut

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I posted some studies before showing that ALS is a disease of mitochondrial origin and delivering copper directly to the motor neurons may be a viable treatment. Here are some of the previous posts on that:
Copper May Treat Als | Ray Peat Forum
More evidence that diseases like ALS are mitochondrial | Ray Peat Forum

This latest study builds up on past research and will likely proceed into human trials. The notable difference in this study was that disease progression was fully halted while the animals received the treatment. I am not sure how this patented compound is better than simply eating extra liver, but it is still beneficial as it will remind people that conditions like ALS are energetic in origin and as such may have MANY treatments that doctors may not even consider right now. It also serves as a validation of my current approach of using DMSO as an effective carrier of various therapeutic substances including minerals. It should also alleviate some of the fears of neuro-toxcity of DMSO as if it had any they would probably manifested in these neurologically compromised animals. Finally, it should answer some questions about absorption - i.e. within 10min of applying to the skin substances dissolved in DMSO reach the bloodstream and the nervous system.

http://www.sciencedirect.com.sci-hub.bz/science/article/pii/S0969996116300201
ALS: 'Shockingly successful' Copper-ATSM mice trials show first signs of prolonging life

"...
A new treatment for ALS could be on the way, as researchers say they have stopped the progression of the disease in mice for two years. The treatment allowed the mice to live for 650 days – 500 days longer than any other previous treatment has managed. The results from Oregon State University, published in Neurobiology of Disease, were unexpectedly promising, say the scientists. The treatment, known as Copper-ATSM, was dissolved in the solvent dimethyl sulfoxide and applied directly to the skin of the mice on the back of their necks. It was absorbed within ten minutes, and scientists say the difference was noticeable almost immediately."
 
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Elie

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Would copper suspended in DMSO alone do the trick do you think? 1-3 mg perhaps?
 
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haidut

haidut

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Would copper suspended in DMSO alone do the trick do you think? 1-3 mg perhaps?

It should. The solution used in the study was 1.5% copper in pure DMSO.
 

nullredvector

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do you have any idea if we can get copper ASTM?

also you mentioned lipitor/statins linked to ALS. do you per chance have the link? thanks @haidut. my grandfather died of ALS (and he was on lipitor or some statin)

I have greying hair and neuromuscular issues... my grandfather also had really thick hair like me that was completely white.
 
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haidut

haidut

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do you have any idea if we can get copper ASTM?

also you mentioned lipitor/statins linked to ALS. do you per chance have the link? thanks @haidut. my grandfather died of ALS (and he was on lipitor or some statin)

I have greying hair and neuromuscular issues... my grandfather also had really thick hair like me that was completely white.

Statins, neuromuscular degenerative disease and an amyotrophic lateral sclerosis-like syndrome: an analysis of individual case safety reports from ... - PubMed - NCBI
http://www.psmag.com/health-and-behavior/statins-lou-gehrig-and-big-questions-27449
Statin Drugs Linked To Amyotrophic Lateral Sclerosis (ALS)
Statins Linked To Increased Fatigue
Medscape: Medscape Access

Last link is paywall so here is the actual partial text:
"...
New York, NY- Data analyzed by the World Health Organization (WHO), according to the Wall Street Journal (WSJ), have identified an association between those taking the cholesterol-lowering drugs and the risk of amyotrophic lateral sclerosis (ALS), also known as Lou Gehrig's disease, but experts are not convinced yet that the risk is real [1].

The identification of a possible statin-ALS interaction is the work of Dr Ralph Edwards, director of the WHO drug-monitoring center. Last fall, according to the WSJ, while sifting through a large database, Edwards discovered that of the 172 people who developed ALS or similar neurodegenerative diseases, 40 were taking statins.

"The number of Lou Gehrig's cases associated with statins struck Dr Edwards as high," writes reporter Avery Johnson. "He would have expected a number in the single digits, judging from how often other drugs in the database were linked to the disease. Still, the analysis didn't prove anything. Dr Edwards hesitated to publicize his finding, wary of creating a drug scare and mindful that statins have been shown to reduce heart attacks significantly."

Screaming too early . . .
The hesitation in publicizing his findings highlights an increasingly common problem, reports Johnson, as sophisticated software allows for the trolling of massive databases in search of possible drug dangers. Although "data mining" can identify risks not uncovered in clinical trials, there is a risk of raising unwarranted concerns, forcing regulators to divert resources from other legitimate dangers, he notes.

"People reach different judgments on when to shout and when not to shout," Dr Robert Temple (US Food and Drug Administration) told the WSJ. "It's the hardest single thing—the value and danger to screaming early."

More regulators are expanding access to their databases, including the FDA and other drug regulators that once kept adverse-event reports closely guarded, and we will likely see more and more possible safety risks start to emerge, writes Johnson. Last fall, Edwards checked the WHO database to see if there was a statin-ALS risk signal after hearing from an American doctor about an ALS-like case seemingly brought on by the cholesterol-lowering drugs. Using his software, Edwards discovered the 40 ALS cases and learned that the number was higher than expected. He speculates that muscle pain and weakness, a side effect of statins, and a link to peripheral neuropathy involve neuromuscular degeneration and that this might be triggered by statins in certain patients, the WSJ reports.

The real dilemma, however, was whether or not to publish his findings. ALS is rare, affecting one in 100 000 people, whereas statins have well-documented cardiovascular benefits in a vast number of patients. There was a concern the findings would raise unwarranted fears about the drugs. Meanwhile, about six months before Edwards noticed the risk of ALS with statins, scientists at the FDA also noticed the ALS-statin signal in a database that overlaps but isn't identical to the WHO database. Like Edwards, the FDA did not want to arouse premature concern, and instead of publishing its findings, pressed the drug companies, including Pfizer, the maker of atorvastatin, for all their clinical-trial data. Altogether, the long-term statin trials, including more than 120 000 patients, identified 20 ALS cases, a number spread evenly between those randomized to placebo and those randomized to a statin. The FDA study is expected to be published soon.

"The result of the analysis was very reassuring," Temple told the WSJ.

Not convinced
Edwards, however, is not so sure. He believes a signal wouldn't necessarily show up in the FDA data because ALS is rare. Speaking with experts in neurodegenerative disease, he was told the ALS signal was "worrisome and should be investigated." After later coming across a study suggesting the neurodegenerative effects of the drugs might be halted or reversed, Edwards decided to publish his findings, although the paper was rejected by the BMJ and the Lancet, reports Johnson. Drug Safety, a smaller journal, eventually published the findings. Edwards' study recommended that patients using statins should talk to their doctor about stopping the drug if they experience severe neuromuscular symptoms. The paper, he told the WSJ, is intended to prompt more research, not to cause cardiovascular patients on statins to stop taking their medication.

"Suppose you started to get symptoms and your doctor said, 'Now you have two years to live,' " Edwards told the WSJ. "Wouldn't you want to know that there's some possibility that the disease is linked to the drug so you could stop taking the drug?"

More evidence is expected soon. Some researchers are analyzing case reports of people who developed ALS-like symptoms after taking statins; others are currently looking at patient records kept by Kaiser Permanente to see whether people who developed ALS were more likely than control subjects to have used statins, writes Johnson."
 

pszamrej

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Hi everybody, this is my first post on this forum, however I'm reading it since a while and trying incorporate Ray Peat principles.
So my question is do someone know the dosage used in the study ?

Piotr
 
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haidut

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Hi everybody, this is my first post on this forum, however I'm reading it since a while and trying incorporate Ray Peat principles.
So my question is do someone know the dosage used in the study ?

Piotr

The dose was 30mg/kg ATSM daily for a mouse. That translates to about 2.5mg/kg daily for a human. They used 1.5% solution of the CuATSM in DMSO. This means dissolving 15mg CuATSM per 1ml DMSO, or 1.5g CuATSM per 100ml DMSO. The dose of 2.5mg/kg for a human is absolutely massive at first sight but since CuATSM is a complex molecule, only about 20% of it is actually copper. So, this 5mg/kg human dose gives about 0.5mg/kg elemental copper, which means most humans would end up getting 35mg - 50mg copper daily. While that is still a hgih dose, it is not unheard of in clinical trials. I have seen studies with oral copper at 20mg daily, and considering the copper-deficient state of ALS patients, the higher dose may very well be warranted. Whether using other copper salts would achieve the same effects as Cu-ATSM is unknown but given that the study on ALS talks about the benefit being due almost exclusively due to Cu-ATSM upregulating cytochrome C oxidase levels and activity, then probably regular copper would work as well as it does the same. Thyroid (T3), red light, and methylene blue have the same effects on cytochrome C, and are probably a much safer approach than absorbing 0.5mg/kg elemental copper daily, which is still a very high dose. But. again, in people with ALS there appears to be a drastic copper deficiency so such high doses may not be as toxic as they would be for non-deficient people.
 
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pszamrej

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Thanks a lot, do you think dosage for dog can be calculated from human or mouse values ?
I read somewhere that methylene blue can affect red blood cells in dogs. ( decrease them ).
Thyroid is supplemented right now with great success.
 
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haidut

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Thanks a lot, do you think dosage for dog can be calculated from human or mouse values ?
I read somewhere that methylene blue can affect red blood cells in dogs. ( decrease them ).
Thyroid is supplemented right now with great success.

Yes, you can calculate the dose for a dog from a mouse. See attached chart. Based on that the dose for a dog would be 1/6 of the mouse dose, so this means 5mg/kg Cu-ASTM for the dog and considering elemental copper this means 1mg/kg of elemental copper for a dog.
 

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pszamrej

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Wow thanks for the chart, it will be helpful. I'm not sure if my dog has Degenerative Myelopathy ( similar to ALS in humans ), but he is too old for MRI diagnosis, which require full anesthesia ( 13,5 y ), I will not risk it. I think I will try smaller dosages first, than progress to study dose. If anyone will be interested in the results, I will post it here.
There is one more thing I do not quite understand, why they say that copper administered that way is safe ?
 
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haidut

haidut

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Wow thanks for the chart, it will be helpful. I'm not sure if my dog has Degenerative Myelopathy ( similar to ALS in humans ), but he is too old for MRI diagnosis, which require full anesthesia ( 13,5 y ), I will not risk it. I think I will try smaller dosages first, than progress to study dose. If anyone will be interested in the results, I will post it here.
There is one more thing I do not quite understand, why they say that copper administered that way is safe ?

I don't know why they say it is safe. My guess would be that it avoids first pass metabolism to the liver and metals like copper and iron are most toxic to the liver upon ingestion. But this is just speculation, maybe you can email the author and ask them directly.
Please post results, I think many people will be genuinely interested.
 

pszamrej

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My guess would be that it avoids first pass metabolism to the liver and metals like copper and iron are most toxic to the liver upon ingestion.

Yes that's possible I think and ok, I will post the results. So far as I dosed thyroid daily ( 100mg of T4/2xday and few times a day of 5mcg of T3 ), he is stronger, has better proprioception of the hind legs.
I'm concerned about supplementation of Testosterone, I give him 100mg/week in order to stop muscle wasting, but I know Ray Peat do not recommend this, any idea how to stop muscle wasting without exogenous T ?
 
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haidut

haidut

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Yes that's possible I think and ok, I will post the results. So far as I dosed thyroid daily ( 100mg of T4/2xday and few times a day of 5mcg of T3 ), he is stronger, has better proprioception of the hind legs.
I'm concerned about supplementation of Testosterone, I give him 100mg/week in order to stop muscle wasting, but I know Ray Peat do not recommend this, any idea how to stop muscle wasting without exogenous T ?

Antiinflammatory drugs seem to reduce or stop cachexia. There are even trials right now with cancer patients taking NSAID to prevent wasting. However, the classic approach would be using a drug like cyproheptadine or ketotifen, which have proven track record for cachexia. Please don't ask for a dose, I don't know much about dosing these for animals.
 

pszamrej

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Yes I give him anti inflammatory supplements + 150mg of aspirin 2xday, also have started cyproheptadine few days ago 1mg/2xday.
What do you think about Testosterone supplementation ? Should I stop this in your opinion ?
 
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Bump. Anyone here succesfully dissolve copper in DMSO? Would simply putting copper filings in dmso and waiting a few hours be enough, or is there more to it?
 

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