haidut

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Peat has mentioned the Creutzfeldt-Jacob disease (CJD) / BSE in several of his articles and interviews and has explained how environmental stress, estrogen, PUFA, ionizing radiation, etc can cause metabolic derangements resulting in the same brain damage so characteristic of this pathology. The public is more familiar with that pathology under the name of mad cow disease (MCD) and it seems virtually every country in the world with large beef-producing industry is periodically hit by a wave of this pathology. What makes MCD relevant to humans is that it can actually cause the same disease in humans by virtue of consuming meat from animals inflicted by CJD/BSE. The official version is that the cause of the disease is unknown but it results in misfolded proteins that acquire infectious properties and can cause the same deformities in the brains of people who eat contaminated meat. How exactly small proteins not carrying genes (unlike, say, viruses) are capable of becoming infectious continues to baffle mainstream medicine. Some mainstream geneticists have proposed that the disease is caused by so-called "slow viruses", yet not such viruses have been found so far. As usual, the answer may be something much simpler and more fundamental. Namely, as the study below demonstrates, the CJD/BSE/MCD pathology may be simply a symptom/sign of mitochondrial failure. More importantly, the study is one of the few that states proper energy production is required for maintenance of a cell's structure (and not just function). As such, this disease may very well be treatable by interventions that improve mitochondrial function and shift the metabolism away from the oxidation of fat and towards the oxidation of glucose. That same approach has already been shown to be therapeutic in other neurodegenerative conditions such as multiple sclerosis (MS) and even the invariably lethal amyotrophic lateral sclerosis (ALS). I don't see a reason why it won't also work in CJD/BSE/MCD.

Mitochondrial respiratory chain deficiency correlates with the severity of neuropathology in sporadic Creutzfeldt-Jakob disease
https://medicalxpress.com/news/2020-05-brain-powerhouses-creutzfeldt-jacob-disease.html

"...A study performed by researchers from the University of Bergen, Norway, and the University of Vienna, Austria, shows damage of the mitochondria—the cell's microscopic powerhouses—in the brains of people with Creutzfeldt-Jacob disease. The researchers found that the mitochondrial power generator (known as the respiratory chain) is severely impaired in brain cells from people who died with Creutzfeldt-Jacob disease. "These mitochondrial defects were widespread in the brain and correlated with the severity of disease," says Professor Charalampos Tzoulis at the University of Bergen and Haukeland University Hospital, Bergen. Damaged mitochondria are no longer able to provide the energy required for neuronal maintenance and function. "These findings strongly suggest that mitochondrial failure contributes to the pathogenesis of Creutzfeldt-Jacob disease," says Tzoulis."
 
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Very interesting.I also came along the notion that Prionprotein itself,eufolded or misfolded, is related to Thiamine metabolism, hence parts of energymetabolism,B1s trafficking,allocation and other state of affairs and relations.
 

Eberhardt

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Hi. this is very interesting indeed. I have a question though. If this is true - which I have been leaning towards for a while - then how come it spreads in wild population. For example there have been outbrakes of prion disease in wild reindeer populations without any observable artificial trigger like say a radiation leak or similar. I assume the mitochondrial state of otherwise healthy animals to be fairly good so how does this happen then? @haidut ?
 

Perry Staltic

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Hi. this is very interesting indeed. I have a question though. If this is true - which I have been leaning towards for a while - then how come it spreads in wild population. For example there have been outbrakes of prion disease in wild reindeer populations without any observable artificial trigger like say a radiation leak or similar. I assume the mitochondrial state of otherwise healthy animals to be fairly good so how does this happen then? @haidut ?

It's been a while since I looked at it, but Mark Purdy's research revealed either high manganese soils, or local hunters using high manganese licks to make deer antlers grow larger in areas with clusters of deer wasting disease. He hypothesized that high manganese cattle feeds and use of the organophosphate pesticide Phosmet caused manganese poisoning that deformed prions. Dr. David Brown of Cambridge proved that manganese can deform prions exactly as observed in Mad Cow disease.

 

RealNeat

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It's been a while since I looked at it, but Mark Purdy's research revealed either high manganese soils, or local hunters using high manganese licks to make deer antlers grow larger in areas with clusters of deer wasting disease. He hypothesized that high manganese cattle feeds and use of the organophosphate pesticide Phosmet caused manganese poisoning that deformed prions. Dr. David Brown of Cambridge proved that manganese can deform prions exactly as observed in Mad Cow disease.

Interesting, there is some major CWD phobia around these parts but no one ever ties it to environmental exposure and once again just attributes it to a contagious disease (easy cop out without need of critical thought)

they feed them garbage and the deer eat higher PUFA foods especially when they are baited. They also munch all over sprayed greens and side of the road exposing themselves to break dust residue and the like...

it's telling when the most CWD is in and around the cities and not where I live (super rural)
 

Eberhardt

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Interesting, there is some major CWD phobia around these parts but no one ever ties it to environmental exposure and once again just attributes it to a contagious disease (easy cop out without need of critical thought)

they feed them garbage and the deer eat higher PUFA foods especially when they are baited. They also munch all over sprayed greens and side of the road exposing themselves to break dust residue and the like...

it's telling when the most CWD is in and around the cities and not where I live (super rural)
Also @Perry Staltic . I actually wrote to peat about it and he said that it fitted quite well with the delayed and not to forget accumulated effect of the chernobyl fallout. There's no baiting in Norway as far as I know but maybe it can affect it too. So far the only verified once of prion diseases have been connectable to radiation
 

tygreezytlb

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How then I'm curious does this explain lab leaks where someone is directly exposed to prions and then develops the disease 9 years later.

It clearly is an infectious protein
 

Eberhardt

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How then I'm curious does this explain lab leaks where someone is directly exposed to prions and then develops the disease 9 years later.

It clearly is an infectious protein
I have never heard of this, do you have any sources?
 

tygreezytlb

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Perry Staltic

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How then I'm curious does this explain lab leaks where someone is directly exposed to prions and then develops the disease 9 years later.

It clearly is an infectious protein

Can you provide an example? Sounds dubious.
Edit: n/m, I see post above
 

Perry Staltic

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Pure conjecture. Not credible evidence of infectious protein, i.e., prion.
 

tygreezytlb

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Pure conjecture. Not credible evidence of infectious protein, i.e., prion.

How so? Come on the coincidence level is pretty ridiculous. She works in a lab stabs herself with prions and gets CJD. What else would it be?! Your not really offering any better explanation.
 

Perry Staltic

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How so? Come on the coincidence level is pretty ridiculous. She works in a lab stabs herself with prions and gets CJD. What else would it be?! Your not really offering any better explanation.

Nine years elapsed. Could have been anything. Correlation, especially that weak, does not equal causation. Just because I don't have other explantions doesn't make the prion hypothesis more credible. There really is no compelling evidence that prions are infectious; just weak correlations like this
 

Jon2547

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How then I'm curious does this explain lab leaks where someone is directly exposed to prions and then develops the disease 9 years later.

It clearly is an infectious protein
No its not "clearly" an infectious protein.
 

Jon2547

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When we have discussions with those that believe in contagious pathogens that float thru the air and land on organisms causing apocalyptic plagues, the issue is not really the so-called micro organism. The real issue is the mind of the befuddle that believes such a thing. If you're not inferring arrogance from this, chances are, you are one of those that believes in such mythology.

I don't know how David Copperfield made the Statue of Liberty disappear into thin air. But just because I can't explain how he pulled off this illusion does not mean that the Statue of Liberty was made to vanish literally.
 

tygreezytlb

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I fear ur not honestly looking at this. Seems to be a confirmation bias. Im in agreement with how much of a role cellular integrity has so to speak but clearly these prions have an affect on the human body. To say otherwise without offering any alternative theory is pretty poor. If it were not a case of infection we would see far more cases of prion illness.

I'm going where the evidence leads you seemingly are denying the evidence. That is far too much of a coincidence in my opinion.
 

Perry Staltic

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I fear ur not honestly looking at this. Seems to be a confirmation bias. Im in agreement with how much of a role cellular integrity has so to speak but clearly these prions have an affect on the human body. To say otherwise without offering any alternative theory is pretty poor. If it were not a case of infection we would see far more cases of prion illness.

I'm going where the evidence leads you seemingly are denying the evidence. That is far too much of a coincidence in my opinion.

There is no quality evidence; just circumstantial. An alternative theory is manganese poisoning. Much more credible. They can't reproduce the same protein misfolding blamed on prions in animals fed tissues from animals that had "prion disease", but Dr. David Brown of Cambridge did reproduce exactly the same misfolding by exposing brain tissue to manganese. That's quality evidence. Research Mark Purdy + manganese.
 

tygreezytlb

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Okay well next question would be what are some implementations that would help fight this disease at all ? If any ? I see the article talks about mitochondria what in particular could one actually do.
 

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