Took Grass fed brain capsules, Neurological symptoms still a week after stopping (Mad Cow!?)

[GenericName86]

I think you'll be okay, I do understand your concern though. Do you have health anxiety at all? The mind can do nasty stuff when you become convinced you have something wrong with you. I'm not trying to dismiss your concerns and you could of had a bad reaction to it but I in regards to the disease you're worried about I don't think you have it/will get it.

 

[tygreezytlb]

I have some health anxiety but ive never experienced anything like this, and i stopped a week ago, i only took them for maybe 2 weeks, i know the incubation period is supposed to be long but i often have adverse reactions and my blood brain barrier sucks, i wish ida done more research on this, im really struggling right now, my head feels hollow, headaches, cant think properly at all, hands are tingling on the right side, tired , and struggling to exert myself.

 

[S-VV]

Get an mri

 

[tygreezytlb]

its not that easy where i am, i was fine til i took these tablets.

Get an mri

 

[S-VV]

Go to the ER, don't mention anything about your anxiety or the tablets, and say that the symptoms started suddenly. They will do an mri/ct scan

 

[Belsazar]

First to calm your mind: Go to your doctor and get medical tests. Ancestral supplements get their brain tissues from New Zealand which never had any BSE cases (see source 1 & 2). Most cases had ties to the UK in the 90s (see source 3). Use your head (source 4).

Maybe write an official email to ancestral supplements with the batch date and ask them about this issue. Do they have any additional safety measures/tests for their brain tissues besides statement below and governmental surveillance? Maybe then they will make an (un)offical test of the batch you received to rule out any possibilities.

[ FACT: There has never been a case of mad cow disease in New Zealand. BSE (mad cow disease), scrapie and other known TSE’s, do not occur in New Zealand. A national surveillance programme is in place to provide comprehensive monitoring. ]

Source 1: Grass Fed Beef Brain Glandular From New Zealand [$52]

"New Zealand has never had a case of BSE."

Source 2: https://www.mpi.govt.nz/dmsdocument/19196/direct

"It is thought that they got the disease from eating food made from cows sick with BSE. Most of the people who have become sick with vCJD lived in the United Kingdom at some point in their lives. Only four lived in the U.S., and most likely, these four people became infected when they were living or traveling overseas."

Source 3: https://www.fda.gov/animal-veterinary/animal-health-literacy/all-about-bse-mad-cow-disease

“I hope these companies are using their heads,” the NIH’s Brown says, “and not the cattle’s heads.”

Source 4: https://abcnews.go.com/Health/story?id=118112&page=1

 

[tygreezytlb]

theres no real test for vCJD, thanks for the 4th one, now u really got me scared! Ive been in contact with the owner. But all he keeps touting is what those links say. Supposedly people have alot of false assumptions about prions. Yeh but when u have doctors advocating for these things and u can buy them on amazon.... u tell me, and they make claims like that. Crazy stuff.

 

[Belsazar]

theres no real test for vCJD, thanks for the 4th one, now u really got me scared! Ive been in contact with the owner. But all he keeps touting is what those links say. Supposedly people have alot of false assumptions about prions. Yeh but when u have doctors advocating for these things and u can buy them on amazon.... u tell me, and they make claims like that. Crazy stuff.

Tonsil biobsy? Creutzfeldt–Jakob disease

Consider onset of CJD after 1 week seems way too early - prions need to accumulate first which would take more time and those capsules only contain a small amount of tissue. I had a similar eposode of being convinced of having a certain disease (Hypochondriasis - Wikipedia) with unability to sleep and panic attacks - but it turned out it was only in my head. Do the tests you can to calm down your mind.

Have you researched what peat says about it? Im quite sure he has covered it in an radio interview, but can't recall now.

 

[Giraffe]

So Im kinda paranoid about mad cow right now. But anyway, I was having memory issues previous to taking these pills, which are ancestral supplements, grass fed brain and liver. And at the time which was like 2 weeks a go, they gave me more energy, but still having more issues, then I noticed my issues get alot worse, almost ataxia like symptoms. Struggling with remembering or being cognitiant altogether, grips on hands, and motor sensors seemingly spacey and a headache now for 5 days, with my head feeling hot all the time nearly. Almost like a racing mind, now mind u I have mitochondrial issues im sure, because I took statins a while back, and they messed me up ALOT. Im only 30, could this be mad cow?! regardless I dont know what to do. I dont know what to eat. etc. Looking for some advice thanks.

You may want to read the articles posted here:

BSE - mad cow - scrapie, etc.: Stimulated amyloid degeneration and the toxic fats

 

[tygreezytlb]

You may want to read the articles posted here:

BSE - mad cow - scrapie, etc.: Stimulated amyloid degeneration and the toxic fats

what is the purpose of this? what am i supposed to be extracting from that?

 

[Giraffe]

what is the purpose of this? what am i supposed to be extracting from that?

You say you are "paranoid about mad cow" after ingesting "ancestral supplements, grass fed brain and liver." I suggest you learn more about mad cow disease and Creutzfeld Jakob disease. I don't know what caused your problems, but I am sure it's not mad cow disease.

 

[tygreezytlb]

You say you are "paranoid about mad cow" after ingesting "ancestral supplements, grass fed brain and liver." I suggest you learn more about mad cow disease and Creutzfeld Jakob disease. I don't know what caused your problems, but I am sure it's not mad cow disease.

thats not true tho, it can sporadically occur, which can then infect someone. there was no evidence shown in what u posted to the contrary theres supposedly a lack of evidence... but nothing more than that.

 

[Giraffe]

thats not true tho, it can sporadically occur, which can then infect someone. there was no evidence shown in what u posted to the contrary theres supposedly a lack of evidence... but nothing more than that.

I tried to be helpful. If you prefer to believe that you suffer from a very rare mysterious disease that can't be treated instead of looking for alternative explanations ... Well, it's your choice. Have a good day!

 

[tygreezytlb]

i just dont feel right man. my mind is slipping i cant breathe properly.

 

[tygreezytlb]

Tonsil biobsy? Creutzfeldt–Jakob disease

Consider onset of CJD after 1 week seems way too early - prions need to accumulate first which would take more time and those capsules only contain a small amount of tissue. I had a similar eposode of being convinced of having a certain disease (Hypochondriasis - Wikipedia) with unability to sleep and panic attacks - but it turned out it was only in my head. Do the tests you can to calm down your mind.

Have you researched what peat says about it? Im quite sure he has covered it in an radio interview, but can't recall now.

Ive been messaging the owner of ancestral supplements... I got this response... then he unlisted his brain from the UK amazon site... so all his reviews are gone.

Amazon product ASIN B0756S6YGFView: https://www.amazon.co.uk/Ancestral-Supplements-Grass-Brain-Liver/dp/B0756S6YGF


anyone else find this suspicious? oh he didnt reply either when he said he would.

Ancestral Supplements​

Mon, Apr 26, 3:52 PM (1 day ago)

to me

Hi Ty,

I appreciate your concern and that you are part of a small group of individuals that cares more about the quality of our products. I know that you are searching for answers and I hope that to provide the peace of mind you are seeking.

Please allow me until the end of the day to gather more information and give you a proper answer... one that you need and deserve.

We will be in touch very soon, Ty. Talk to you soon!

 

[Belsazar]

Suspicious, but maybe he just wants to avoid that you write a review. The Us version is still there ...

You could also reach out to Masterjohn who advertises ancestral supplements.

 

[tygreezytlb]

Suspicious, but maybe he just wants to avoid that you write a review. The Us version is still there ...

You could also reach out to Masterjohn who advertises ancestral supplements.

Curious. Can you offer further reassurance on prion accumulation? or do we just not know enough to how they work, but my one worry is, I have a poor blood brain barrier, and general poor mitochondrial health im pretty sure, due to statin damage - I wonder - would that make a difference on the incubation period if I was exposed?

the owner got back to me anyway, said it was just a catalog issue, no plans to remove the product and he quoted pretty much what u quoted at this point. Anyway Im now focusing on my health in general regardless. As I said, I was having neurological/dysautonomia issues previous to this, but this has made it ALOT worse. Similar to what the previous poster said - The energy boost, and then the crash happened for me also. I came off the tablets cold turkey. Its possibly im sure the pituatary gland had something to do with it contained in the supplement?

Peat seems to think prion diseases are reversible or at least, improvable, and probably reflect more our own toxicity in the bodies inability to deal with them? at least thats what I got from them. But as you say whatever this is, has certainly messed me up, just hope its not neurodegenerative and I can improve and repair this seemingly damage done.

 

[Belsazar]

Statins May Cause Insulin Resistance By Depleting Vitamin K

A great study, which both highlights the dangers of statins while also providing a plausible mechanism for those side effects that both FDA and Big Pharma vehemently continue to dispute. This plausible mechanism involves the inhibition of vitamin K2 (MK-4) synthesis, which requires the same...

raypeatforum.com

BSE - mad cow - scrapie, etc.: Stimulated amyloid degeneration and the toxic fats

BSE mad cow, scrapie, etc.: Stimulated amyloid degeneration and the toxic fats

raypeat.com

Mad Cow Disease May Be A Mitochondrial/metabolic Issue

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...

raypeatforum.com

 

[tygreezytlb]

UPDATE: This has not improved, I am having auditory hallucinations (hearing phone ring constantly during the day), headaches persist, visual flashes, my heart is beating very hard, completely fatigued, and I have very little energy or appetite, vision has got worse, and Im having hyperreflexia at times, balance is off, a general feeling of being drunk.

THIS IS REALLY SCARY. WHAT THE HELL HAS HAPPENED. I can only draw a correlation to the brain tablets I was taking, similar symptoms became apparent around 10 days into taking them, when my grip and hand went numb at times, which developed into, breathing issues, one night after alchohol consumption felt very similar to how feeling now, but this has now persisted for nearly 4 weeks, while I have suffered with brain fog/memory issues. Nothing like this.

I am now taking a Energin, Cypro at ttimes, and B12, I have just ordered VIT E, and VIT K from idealabs. I am very scared, had to go to accident and emergency to tell them what is going on, spoke to them about the pills which they sort of dismissed, but suggested If I had had covid, I could be suffering from some sort of long covid neurological issue?! and Im hoping to see a neurologist soon. But nothing seems to help these issues at this point. Seem to become calmer on a night, I am still able to obviously function to some degree in terms of communication, and gather thoughts at this point, there is definitely muscle weakness and co-ordination problems.

Hyperreflexia seems to improve slightly with supplementation. I have order methlyne blue also. I definitely already had mitchondrial dysfunction which makes me wonder, a possibly exposure? could = rapid onset? I dont know... Any advice any tips, anything at all, what are other possibilities?

I emailed ray peat about prions.

FROM RAY

"I think all the “prion” diseases involve the activation of the prion protein and similar proteins by PUFA, released by injury, including radiation, and by prolonged excitation and fatigue. PLA2 inhibitors reduce fatty acid release; they include aspirin, progesterone, and flavonoids such as orange juice. Estrogen activates PLA2.


Bate C, Reid S, Williams A: Phospholipase A2 inhibitors or platelet activating factor antagonists prevent prion replication. J Biol Chem. 2004, 279: 36405-36411.

Docosahexaenoic and eicosapentaenoic acids increase prion formation in neuronal cells
Clive Bate, Mourad Tayebi, Luisa Diomede, Mario Salmona & Alun Williams
BMC Biology volume 6, Article number: 39 (2008)
Abstract
Background
The transmissible spongiform encephalopathies, otherwise known as prion diseases, occur following the conversion of the cellular prion protein (PrPC) to an alternatively folded, disease-associated isoform (PrPSc). Recent studies suggest that this conversion occurs via a cholesterol-sensitive process, as cholesterol synthesis inhibitors reduced the formation of PrPSc and delayed the clinical phase of scrapie infection. Since polyunsaturated fatty acids also reduced cellular cholesterol levels we tested their effects on PrPSc formation in three prion-infected neuronal cell lines (ScGT1, ScN2a and SMB cells).
Results
We report that treatment with docosahexaenoic acid (DHA), eicosapentaenoic acid (EPA) or the cholesterol synthesis inhibitor simvastatin reduced the amounts of free cholesterol in membrane extracts from prion-infected neuronal cells. Simvastatin reduced cholesterol production while DHA and EPA promoted the conversion of free cholesterol to cholesterol esters. Crucially, while simvastatin reduced PrPSc formation, both DHA and EPA significantly increased the amounts of PrPSc in these cells. Unlike simvastatin, the effects of DHA and EPA on PrPSc content were not reversed by stimulation of cholesterol synthesis with mevalonate. Treatment of ScGT1 cells with DHA and EPA also increased activation of cytoplasmic phospholipase A2 and prostaglandin E2 production. Finally, treatment of neuronal cells with DHA and EPA increased the amounts of PrPC expressed at the cell surface and significantly increased the half-life of biotinylated PrPC.
Conclusion
We report that although treatment with DHA or EPA significantly reduced the free cholesterol content of prion-infected cells they significantly increased PrPSc formation in three neuronal cell lines. DHA or EPA treatment of infected cells increased activation of phospholipase A2, a key enzyme in PrPSc formation, and altered the trafficking of PrPC. PrPC expression at the cell surface, a putative site for the PrPSc formation, was significantly increased, and the rate at which PrPC was degraded was reduced. Cholesterol depletion is seen as a potential therapeutic strategy for prion diseases. However, these results indicate that a greater understanding of the precise relationship between membrane cholesterol distribution, PrPC trafficking, cell activation and PrPSc formation is required before cholesterol manipulation can be considered as a prion therapeutic.
Background
Transmissible spongiform encephalopathies (TSEs), also known as prion diseases, include Creutzfeldt-Jakob disease and kuru in humans, scrapie in sheep and goats, and bovine spongiform encephalopathy in cattle. The central event in these diseases is thought to be the conversion of a host-encoded cellular prion protein (PrPC) into an abnormally folded disease-associated isoform, designated PrPSc [1]. Aggregates of PrPSc accumulate around neurons in affected brain areas [2], a process which is thought to lead to neuronal dysfunction and the clinical symptoms of infection. PrPSc constitutes the major and perhaps the only component of the infectious particle [3].
The process of prion replication has been studied extensively in prion-infected neuronal cell lines. Treatment with some cholesterol synthesis inhibitors reduced the production of PrPSc in scrapie-infected neuronal cells [4–6]. The anti-prion effect of such drugs is attributed to cholesterol depletion affecting the formation of specialised membrane micro-domains called lipid rafts [7]. These lipid rafts are highly enriched in cholesterol, sphingolipids and gangliosides, and contain specific proteins [8]. The presence of a glycosylphosphatidylinositol (GPI) anchor that mediates the attachment of proteins including PrPC and PrPSc to membranes, targets these proteins to lipid rafts [9].
Since cholesterol levels are a factor determining PrPSc formation [4–6], the effects of compounds reported to affect cellular cholesterol levels were examined. Polyunsaturated fatty acids (PUFA) are fatty acids which contain two or more double bonds within their hydrocarbon chain. They are taken as dietary supplements by large numbers of people for their perceived health benefits against a variety of diseases including coronary heart disease, hypertension, diabetes mellitus and rheumatoid arthritis [10]. The common PUFA include docosahexaenoic acid (DHA), eicosapentaenoic acid (EPA), arachidonic acid (AA), linoleic acid (LA) and linolenic acid (LNA) and in most cells PUFA are rapidly incorporated into phospholipids [11]. The incorporation of PUFA into phospholipids alters the composition and physical properties of cell membranes [12]. Since dietary PUFA reduce cellular cholesterol levels [13] the effects of PUFA on the composition of neuronal cell membranes and on the production of PrPSc were examined. We report that treatment with DHA or EPA significantly reduced the amounts of free cholesterol in ScGT1, ScN2a and SMB cells. However, in contrast to the effects of cholesterol synthesis inhibitors, treatment with DHA or EPA actually increased PrPSc formation. DHA or EPA treatment also increased the activity of phospholipase A2 (PLA2), an enzyme reported to affect PrPSc formation [14]. They also increased the amount of PrPC, that is essential for the development of prion diseases [15, 16], at the cell surface, a putative site for PrPSc formation. In conclusion our data indicate that cholesterol depletion per se does not reduce PrPSc formation.
Results
DHA and EPA increase PrPScin prion-infected neuronal cells
The effect of PUFA on the formation of PrPSc in ScGT1 cells was determined by daily treatment with 1 μM PUFA for 7 days. Significantly higher amounts of PrPSc were found in cells treated with DHA (14.2 ng/ml ± 1.7 compared with 8 ± 1, n = 15, P = 0.00000000001) or EPA (13.8 ng/ml ± 2.4 compared with 8 ± 1, n = 15, P = 0.00000002) than in untreated cells, or cells treated with AA, LA or LNA (Figure 1A). Treatment with DHA or EPA did not affect the survival of ScGT1 cells (data not shown). Immunoblots were used to verify the ELISA data; these showed that there were observable differences in the amounts of PrPSc between untreated cells and cells treated with 1 μM DHA or 1 μM EPA (Figure 1B). In contrast, the amounts of β-actin in untreated cells and cells treated with DHA or EPA were not significantly different. Determination of the effects of different PUFA on PrPSc formation in ScGT1 cells revealed that whereas treatment with either DHA or docosapentaenoic (DPA) significantly increased amounts of PrPSc present, treatment with docosatetraenoic acid (DTA) or LA did not. Similarly, while treatment with EPA increased the amounts of PrPSc in ScGT1 cells, treatment with eicosatetraenoic acid (ETA) did not. The effects of DHA, DPA and EPA on the PrPSc content of ScGT1 cells were dose-dependent (Figure 2).

Ann Agric Environ Med. 2007;14(2):225-8.
Expression of cellular isoform of prion protein on the surface of peripheral blood lymphocytes among women exposed to low doses of ionizing radiation
Piotr Kłuciński 1 , Bogdan Mazur, Antoni Hrycek, Ewa Maśluch, Paweł Cieślik, Jolanta Kaufman, Gayane Martirosian
Ionizing radiation affects the expression of adhesive and co-stimulatory molecules in lymphocytes. The physiological function of cellular isoform of prion protein (PrPc) is little known. Evidences indicate a link between lymphocytes activation and PrPc expression on their surface; however, no direct effect of radiation on PrPc level in these cells was investigated. The objective of this study was to determinate the effect of low doses of ionizing radiation on the expression of PrPc on the surface peripheral blood lymphocytes in the women operating X-ray equipment. In 36 female workers and 30 persons of the control group the PrPc expression on CD3 (T lymphocytes), CD4 (T helper), CD8 (T cytotoxic) and CD19 (B lymphocytes), as well as the percentage of lymphocytes with PrPc on their surface, were tested. Subgroups with respect to age and length of employment were selected. A significant increase was observed in PrPc expression on CD3 and CD4 with lowered PrPc level on CD8 and percentage of CD8 cells with PrPc in workers compared to control. The PrPc level did not show significant changes in subgroups in relation to age (below and over 40 years old) both in the investigated and control groups, whereas a lower percentage of PrPc expressing CD19 cells showed in employed women below 40 years of age. A significant decrease was found in PrPc expression on the surface of CD3, CD4 and CD8 cells in the subgroup employed for over 10 years than in the subgroup with less than 10 years of employment.

J Neurotrauma. 2019 Nov 15;36(22):3103-3114. doi: 10.1089/neu.2018.5918. Epub 2019 Jun 6.
Low-Field Magnetic Stimulation Restores Cognitive and Motor Functions in the Mouse Model of Repeated Traumatic Brain Injury: Role of Cellular Prion Protein
Sathiya Sekar 1 , Yanbo Zhang 2 , Hajar Miranzadeh Mahabadi 1 , Amirhassan Parvizi 1 , Changiz Taghibiglou 1
Traumatic brain injury (TBI)/concussion is a growing epidemic throughout the world. Memory and neurobehavioral dysfunctions are among the sequelae of TBI. Dislodgement of cellular prion protein (PrPc) and disruption of circadian rhythm have been linked to TBI. Low-field magnetic stimulation (LFMS) is a new noninvasive repetitive transcranial magnetic stimulation (rTMS) technique that generates diffused and low-intensity magnetic stimulation to deep cortical and subcortical areas. The role of LFMS on PrPc, proteins related to the circadian rhythm, and behavior alterations in a repeated TBI mouse model were studied in the present study. TBI was induced to the mice (right hemisphere) using weight-drop method, once daily for 3 days. LFMS treatment was given for 20 min once daily for 4 days (immediately after each TBI induction). The results showed that LFMS-treated TBI mice significantly improved cognitive and motor function as evidenced by open field exploration, rotarod, and novel location recognition tasks. In addition, a significant increase in PrPc and decreased glial fibrillary acidic protein levels were observed in cortical and hippocampal regions of LFMS-treated TBI mice brain compared with sham-treated TBI mice, while neuronal nuclei level was significantly increased in cortical region. In LFMS-treated mice, a decrease in proteins related to circadian rhythm were observed, compared with sham-treated TBI mice. The results obtained from the study demonstrated the neuroprotective effect of LFMS, which may be through regulating PrPc and/or proteins related to circadian rhythm. Thus, the present study suggests that LFMS may improve the subject's neurological condition following TBI.
Keywords: cellular prion protein; circadian rhythm proteins; low-field magnetic stimulation; motor and cognitive functions; repeated traumatic brain injury.

Review Acta Biochim Biophys Sin (Shanghai). 2013 Jun;45(6):485-93.
Role of lipid in forming an infectious prion?
Fei Wang, Jiyan Ma
Abstract
The infectious agent of the transmissible spongiform encephalopathies, or prion diseases, has been the center of intense debate for decades. Years of studies have provided overwhelming evidence to support the prion hypothesis that posits a protein conformal infectious agent is responsible for the transmissibility of the disease. The recent studies that generate prion infectivity with purified bacterially expressed recombinant prion protein not only provides convincing evidence supporting the core of the prion hypothesis, that a pathogenic conformer of host prion protein is able to seed the conversion of its normal counterpart to the likeness of itself resulting in the replication of the pathogenic conformer and occurrence of disease, they also indicate the importance of cofactors, particularly lipid or lipid-like molecules, in forming the protein conformation-based infectious agent. This article reviews the literature regarding the chemical nature of the infectious agent and the potential contribution from lipid molecules to prion infectivity, and discusses the important remaining questions in this research area.

 

[Spokey]

So Im kinda paranoid about mad cow right now. But anyway, I was having memory issues previous to taking these pills, which are ancestral supplements, grass fed brain and liver. And at the time which was like 2 weeks a go, they gave me more energy, but still having more issues, then I noticed my issues get alot worse, almost ataxia like symptoms. Struggling with remembering or being cognitiant altogether, grips on hands, and motor sensors seemingly spacey and a headache now for 5 days, with my head feeling hot all the time nearly. Almost like a racing mind, now mind u I have mitochondrial issues im sure, because I took statins a while back, and they messed me up ALOT. Im only 30, could this be mad cow?! regardless I dont know what to do. I dont know what to eat. etc. Looking for some advice thanks.

When every one was freaking out about that back in the 80s, a documentary mentioned the gestation time for mad cow was allegedly 30 years, so the time frame suggests not BSE. I don't buy the prion theory anyway, which also suggests it's not going to be mad cow and probably explains why there aren't now millions of people in their thirties with severe neurological issues living in the UK.