My money was always on you being correct. Not necessarily because I understood the science (I did not) but because you were offering a highly provocative hypothesis but going unchallenged.
When Richard H. Ebright -- the bellicose but clearly capable Professor of Chemistry and Chemical Biology at Rutgers University -- refused to comment on your hypothesis that persuaded me all the more.
Sadly, the circumstances are such that no congratulations are in order. I had hoped you were wrong.
Alzheimer's and CJD have their cause in the mitochondria. I now know why the telomeres of cancer cells do not shorten. I searched because I wanted to know why this is so. This is more or less already stated in research reports. It is also clear from this that the vaccine can trigger everything.
"Our father and husband, Dr. Baselga, was a fighter and a believer in science. That's why, when he was diagnosed with Creutzfeldt-Jakob disease (CJD), a rapidly progressing, fatal neurodegenerative disease, our lungs dropped to our stomachs. The science behind CJD is a mystery and there are no treatments, which rendered his fighting spirit useless...
Patients, on average, live between 3 weeks and 6 months post the onset of symptoms. All that is known is that the disease begins when a protein, for some unknown reason, misfolds in the brain and becomes contagious, convincing all nearby proteins to rebel and misfold as well. Around one in one million people per year are diagnosed with CJD. Of those diagnosed, 10-15% acquire the disease genetically, a small minority contract the disease through iatrogenic contact, meaning that they had nervous system surgery with infected tools, and an even smaller minority contract it from eating contaminated meat. My father suffered from a fourth type of CJD, the most common, which is called sporadic CJD..."
""We can see that the spike protein, when affected by our own immune system, can produce amyloid structures, and that this can potentially affect our blood coagulation. We believe that this discovery is significant for many fields of research, and we hope that other researchers will examine the questions that it raises," says Sofie Nyström, who is an associate professor at IFM and the other author on the study. "
👏👏👏👏👏. You were right. Along with Stephanie Seneff. Now to know who will be most likely affected, look at the glysophate connection/reaction with SARS Cov2, within the body, prion creation and mitochondrial impact...
In a nutshell, the body replaces glycine molecules within the body with glysophate molecules, for those that are exposed to it. The ensueing chain reaction effect not only cripples mitochondrial function but also creates misfolded proteins....misfolded proteins can wind up as prions. Prions can cross barriers. Basically the body does not like misfolded proteins at any time, in any place.
Flooding the human body with spikes is a recipe for prion disease catastrophe. It is a very dangerous experiment that is going on in the world right now.
Fascinating that it takes people outside the “science” to figure this out. Brilliant work. Thank you- you’re saving many more lives than the faux scientists. You are a hero. ❤️
So what's the solution? I assume proteolytic enzymes (nattokinase, lumbrokinase, serrapeptase) would do a pretty good job of taking care of rogue spikes and amyloid proteins throughout most of the body, but they don't cross the BBB as far as I'm aware.
Mary, on a tangent, this January 2022 paper about Taurine's stabilizing effect on Lysozyme is interesting. The Italian authors designed their study referencing a wide knowledge-base. Parts of it read like a review of the literature with 74 papers cited.
"Lysozyme is a glycosidase ... [followed by chemical and shape descriptions]...widely known to undergo amyloid fibrillation."
"...the inhibitory ability of the molecule [Taurine] on amyloid fibrillation by following the kinetic of the aggregation process."
"In the present study we report on the ability of taurine to modify lysozyme stability, and to interphere [sic] with its amyloid aggregation propensity. Also, we explored taurine influence on the cytotoxicity of the resulting fibrils."
"SAXS experiments proved that even low amounts of taurine modified protein-protein interactions: the short-range attractive term decreases, as well as the long-range electrostatic repulsion between proteins decreases because the dielectric permittivity of the solvent increases at increasing taurine content."
The paper ends on a bit of a down-note:
"We determined an effect of taurine on lysozyme amyloidogenesis, but by our data it does not impact on aggregates cytotoxicity. When further similar studies on taurine effects on amyloid β peptide and tau aggregations will be performed, we believe that taurine role in AD should become clearer."
Happy to pass it along. Another thing about Taurine is its role in getting excess "vitamin a" out of the body. I'm running across a few papers referencing Retinoic Acid's involvement in thrombosis. RA is the teratogenic derivative of Retinol (itself quite dangerous beyond tissue thresholds).
One relevant snip from a paper on chemical modulators of Fibrinogen production:
"Many acquired or inherited factors can contribute to thrombosis. The acquired factors include medicines, hence the need to assess medication when evaluating thrombosis risk. RA is used topically to treat acne, and for acute promyelocytic leukemia (APL). There is a possible link between our data and clinical use of RA. Some APL patients were reported to have low plasma fibrinogen (<0.1 mg/mL in 61% of patients, n = 34) and suffer from hemorrhages. 39 In contrast, treatment with RA has been shown to give a rapid correction of fibrinogen levels and increase thrombotic events. 40 41 42 Apart from the plausible contribution of increased fibrinogen production, another potential source for this prothrombotic effect is thrombocytosis seen in RA-treated APL patients. 43 Here we also show that RA treatment increased thrombocyte cell fraction in a non-statistically significant manner. Effects of RA on platelet activity have also been reported. RA reduced platelet activation in diet-induced atherosclerosis in rabbits, 44 and inhibited platelet aggregation, spreading, dense-granule secretion, and clot retraction in vitro. 45 While we cannot exclude a contribution of the increased number of thrombocytes, possible direct effects of RA include thrombocyte responses to injury, or even an increased production of other key coagulation factors through the same mechanism as behind increased fibrinogen production (mediated by RA and the retinoid X nuclear receptors 36 ), our data showed a trend toward increased thrombocyte binding after RA treatment that correlated with increased fibrinogen."
Chemical Modulators of Fibrinogen Production and Their Impact on Venous Thrombosis
A pleasant surprise: I'm recently experimenting with 5-10 grams of Taurine spread out over 24 hours and have logged that my systolic blood pressure on average is down 12 points to 110, with diastolic down 4 points to 72. Those are 11% and 5% reductions respectively. One thing I really like is it has increased my pulse-rate by 17% to 64bpm. It's the only thing I've changed in weeks. My mother-in-law who is 97 has been showing some almost startling cognitive changes lately after we added a couple of grams of Taurine in her morning yogurt. More talkative, longer sentences, more vivid memories, out of the blue phrasing and words we've not heard before. I once coil-bound about a hundred abstracts of studies on Taurine. It's seemingly involved in just about everything and is unique compared to other amino acids, which apparently makes it quite versatile.
Of course you were. Why do you think we all subscribe? We know when someone is driving for truth
Thank you. 🙏
I will venture a guess that part of you very much did not want to be right.
Thank you for your research, insight and perseverance.
Please share any info you come up for detoxification for both C19 Long haul people and vaccine injured.
Thank you, Walter!
My money was always on you being correct. Not necessarily because I understood the science (I did not) but because you were offering a highly provocative hypothesis but going unchallenged.
When Richard H. Ebright -- the bellicose but clearly capable Professor of Chemistry and Chemical Biology at Rutgers University -- refused to comment on your hypothesis that persuaded me all the more.
Sadly, the circumstances are such that no congratulations are in order. I had hoped you were wrong.
Terrifying and now we need the cure. Thank you for your work
Alzheimer's and CJD have their cause in the mitochondria. I now know why the telomeres of cancer cells do not shorten. I searched because I wanted to know why this is so. This is more or less already stated in research reports. It is also clear from this that the vaccine can trigger everything.
Did you know the head of cancer research at AZ died last year of CJD at 61?
Here is the GoFundMe page with a note written by his wife & kids. (Supposedly the fundraiser was for CJD Research, not the family. )
https://www.gofundme.com/f/dr-baselga-funds-for-creutzfeldtjakob-disease
"Our father and husband, Dr. Baselga, was a fighter and a believer in science. That's why, when he was diagnosed with Creutzfeldt-Jakob disease (CJD), a rapidly progressing, fatal neurodegenerative disease, our lungs dropped to our stomachs. The science behind CJD is a mystery and there are no treatments, which rendered his fighting spirit useless...
Patients, on average, live between 3 weeks and 6 months post the onset of symptoms. All that is known is that the disease begins when a protein, for some unknown reason, misfolds in the brain and becomes contagious, convincing all nearby proteins to rebel and misfold as well. Around one in one million people per year are diagnosed with CJD. Of those diagnosed, 10-15% acquire the disease genetically, a small minority contract the disease through iatrogenic contact, meaning that they had nervous system surgery with infected tools, and an even smaller minority contract it from eating contaminated meat. My father suffered from a fourth type of CJD, the most common, which is called sporadic CJD..."
Uhhhhh
Maybe they should read Luc Montagnier's last article.
A more recent pharma death... age 64, Pancreatic Cancer.
https://www.fiercepharma.com/pharma/emergent-mourns-passing-founder-and-former-ceo-el-hibri
These guys aren't taking their own jabs, are they?
I would be ok with that.
Fair, but it would add a whole new level to the deception.
would you give a quick explanation of why the telomeres do not shorten?
Further back than the vaccine.
""We can see that the spike protein, when affected by our own immune system, can produce amyloid structures, and that this can potentially affect our blood coagulation. We believe that this discovery is significant for many fields of research, and we hope that other researchers will examine the questions that it raises," says Sofie Nyström, who is an associate professor at IFM and the other author on the study. "
👏👏👏👏👏. You were right. Along with Stephanie Seneff. Now to know who will be most likely affected, look at the glysophate connection/reaction with SARS Cov2, within the body, prion creation and mitochondrial impact...
Anyone got a breakdown of her latest paper? I watch all her interviews but still need some hand holding.
In a nutshell, the body replaces glycine molecules within the body with glysophate molecules, for those that are exposed to it. The ensueing chain reaction effect not only cripples mitochondrial function but also creates misfolded proteins....misfolded proteins can wind up as prions. Prions can cross barriers. Basically the body does not like misfolded proteins at any time, in any place.
Thank you. Some basic questions:
- Can any protein become misfolded, and if so, does that automatically make it a prion?
- Are prions mostly in the brain? What about the gut?
- How do you test for prions?
- Is this something that can only be seen at autopsy?
- If so, how do they diagnose something like CJD?
@Mn: See this article from 2021
https://www.countere.com/home/prions-are-going-to-end-the-world
Flooding the human body with spikes is a recipe for prion disease catastrophe. It is a very dangerous experiment that is going on in the world right now.
Also, clot shot similarities.
Walter, here's the pdf: https://pubs.acs.org/doi/pdf/10.1021/jacs.2c03925
I read the medical Express article. Well done Walter! 👏👏🥂
Fascinating that it takes people outside the “science” to figure this out. Brilliant work. Thank you- you’re saving many more lives than the faux scientists. You are a hero. ❤️
Walter, I love you
I just looked at the Ethical Skeptic's twitter feed and found this:
https://twitter.com/EthicalSkeptic/status/1528455553701249027/photo/1
and then this
https://twitter.com/EthicalSkeptic/status/1528442266037231617?cxt=HHwWgoC97ZKJj7YqAAAA
Does the S1 subunit of the vaccine-induced spike protein cause this same behavior after being cleaved?
Dr Fleming points to that being the case in this video:
https://brandnewtube.com/watch/dr-richard-fleming-how-the-vaxx-is-breaking-down-the-body_O6Vy9D1XVXc4Fn5.html
Were Cellular Powerhouses Once Parasites?
Mitochondria may have started out stealing energy rather than producing it
Impressive, Walter.
So what's the solution? I assume proteolytic enzymes (nattokinase, lumbrokinase, serrapeptase) would do a pretty good job of taking care of rogue spikes and amyloid proteins throughout most of the body, but they don't cross the BBB as far as I'm aware.
I agree. I was listening to a podcast from a few years (before Covid) ago n it mentioned the supplement TUDCA helps with Misfolded proteins.
Mary, on a tangent, this January 2022 paper about Taurine's stabilizing effect on Lysozyme is interesting. The Italian authors designed their study referencing a wide knowledge-base. Parts of it read like a review of the literature with 74 papers cited.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8779517/
snips:
"Lysozyme is a glycosidase ... [followed by chemical and shape descriptions]...widely known to undergo amyloid fibrillation."
"...the inhibitory ability of the molecule [Taurine] on amyloid fibrillation by following the kinetic of the aggregation process."
"In the present study we report on the ability of taurine to modify lysozyme stability, and to interphere [sic] with its amyloid aggregation propensity. Also, we explored taurine influence on the cytotoxicity of the resulting fibrils."
"SAXS experiments proved that even low amounts of taurine modified protein-protein interactions: the short-range attractive term decreases, as well as the long-range electrostatic repulsion between proteins decreases because the dielectric permittivity of the solvent increases at increasing taurine content."
The paper ends on a bit of a down-note:
"We determined an effect of taurine on lysozyme amyloidogenesis, but by our data it does not impact on aggregates cytotoxicity. When further similar studies on taurine effects on amyloid β peptide and tau aggregations will be performed, we believe that taurine role in AD should become clearer."
Thank you for this!
Happy to pass it along. Another thing about Taurine is its role in getting excess "vitamin a" out of the body. I'm running across a few papers referencing Retinoic Acid's involvement in thrombosis. RA is the teratogenic derivative of Retinol (itself quite dangerous beyond tissue thresholds).
One relevant snip from a paper on chemical modulators of Fibrinogen production:
"Many acquired or inherited factors can contribute to thrombosis. The acquired factors include medicines, hence the need to assess medication when evaluating thrombosis risk. RA is used topically to treat acne, and for acute promyelocytic leukemia (APL). There is a possible link between our data and clinical use of RA. Some APL patients were reported to have low plasma fibrinogen (<0.1 mg/mL in 61% of patients, n = 34) and suffer from hemorrhages. 39 In contrast, treatment with RA has been shown to give a rapid correction of fibrinogen levels and increase thrombotic events. 40 41 42 Apart from the plausible contribution of increased fibrinogen production, another potential source for this prothrombotic effect is thrombocytosis seen in RA-treated APL patients. 43 Here we also show that RA treatment increased thrombocyte cell fraction in a non-statistically significant manner. Effects of RA on platelet activity have also been reported. RA reduced platelet activation in diet-induced atherosclerosis in rabbits, 44 and inhibited platelet aggregation, spreading, dense-granule secretion, and clot retraction in vitro. 45 While we cannot exclude a contribution of the increased number of thrombocytes, possible direct effects of RA include thrombocyte responses to injury, or even an increased production of other key coagulation factors through the same mechanism as behind increased fibrinogen production (mediated by RA and the retinoid X nuclear receptors 36 ), our data showed a trend toward increased thrombocyte binding after RA treatment that correlated with increased fibrinogen."
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7982297/
Chemical Modulators of Fibrinogen Production and Their Impact on Venous Thrombosis
A pleasant surprise: I'm recently experimenting with 5-10 grams of Taurine spread out over 24 hours and have logged that my systolic blood pressure on average is down 12 points to 110, with diastolic down 4 points to 72. Those are 11% and 5% reductions respectively. One thing I really like is it has increased my pulse-rate by 17% to 64bpm. It's the only thing I've changed in weeks. My mother-in-law who is 97 has been showing some almost startling cognitive changes lately after we added a couple of grams of Taurine in her morning yogurt. More talkative, longer sentences, more vivid memories, out of the blue phrasing and words we've not heard before. I once coil-bound about a hundred abstracts of studies on Taurine. It's seemingly involved in just about everything and is unique compared to other amino acids, which apparently makes it quite versatile.