Young Mom Dying: Another Prion Case in the USA. "Mad Cow" or What?

On the heels of a news report about a 16 year-old boy in North Carolina who just died from a prion disease, comes another report of a 38 year-old mom in Maine also diagnosed with a prion disease - soon-to-be fatal. Two different cases in two different states, both in relatively young people.

What's happening? Reports about "Mad Cow" and other prion diseases started disappearing from the news after the media gagged Oprah back-when and then vanished completely, following Bush's gag order on scientists in 2005. Authorities have been insisting that unlike Britain, we do not have the problem here. But now, it looks like the lid is off. Why? What else aren't they telling us?

I suspect the 16 year-old originally was infected via epigenetic inheritance, consider airborne infection unlikely, think a more rapidly progressive strain must be considered - but most strongly suspect a super-imposed infection (probably flu) in both victims allowed already present prions to use the immune system to spread in the body.

My ongoing concern about epidemics and pandemics is precisely that -

prions use the immune system to spread in the body.

Given that infection with prions and other misfolded proteins is widespread, deaths are just the tip of the iceberg - the real problem is the burden of chronic disease unleashed in survivors.

And this, I think, is why doctors suddenly are reporting prion-related deaths. We're about to see an uptick in prion-related deaths triggered by other infections and as well, a huge surge in prion-related chronic disease.

NOTE: Protein misfolding can result in several different types of diseases, including diseases that are infectious, genetic, epigenetic, chronic, degenerative, and almost always debilitating. The list of "modern" diseases linked to prions, prion-related proteins and other misfolded proteins is long, and still growing. Besides "Mad Cow Disease" or vCJD, this list includes cancers; Alzheimer's and other dementias; diabetes; HIV/AIDS; Parkinson's; ALS; schizophrenia, depression, bipolar disorder, autism and other mental illnesses; myositis; arthritis; stomache ailments like Crohn's and colitis; and many, many other chronic debilitating diseases. In short, virtually any organ or body system can be affected, and few cases progress rapidly to encephalopathy.


The New Patient: A young 38 year-old mom.
Another fast progression with no explanation; diagnosed as a prion disease within 3 months. Her symptoms started in November with a cough and vertigo. Christmas Eve, stroke symptoms sent her to hospital, but doctors found no evidence of stroke. By mid-January, she had slurred speech, a loss of motor skills, deteriorating vision, memory loss and was unable to walk. Days later she developed encephalitis (swelling of the brain).

Family hopes for miracle after young mom struck by disease

After months of debilitating symptoms with no diagnosis, doctors this week say Sandi Tucker Kennedy, a 38-year-old wife and mom of four young children ages 2 to 9, is believed to have a prion disease, a family of rare progressive neurodegenerative disorders that take over the neurological system.

“She's actually very young for it,” …

“The neurological condition is going to continue. It's a rapid-moving disease,” Tucker said. “The prognosis is four to 12 months from the onset of symptoms and she's had symptoms for four months now.”

I thought it was interesting that in the comments under the article about the 38-year-old woman, there were several people who felt like she was suffering from Lyme Disease. I have heard that Lyme Disease is also difficult to diagnose, like the Prion disease. Is it just a coincidence that these people felt the symptoms had some similarity? Is there a connection between Lyme Disease and Prion Disease? Could this woman really be suffering from some very virulent form of Lyme Disease? I wonder if her doctors have tried large doses of antibiotics on her. Certainly couldn't hurt at this point...

Maybe the world line divergence John Titor spoke of is starting to converge. Mad Cow starts popping up, terror attacks at the olympics, and a civil war brought on by martial law style police tactics could be right around the corner.

reply to post by kaylaluv


Any kind of super-imposed infection can help spread prions in the body, including Lyme Disease - infection-triggered prion spread occurs because prions use the immune system to spread in the body, and inflammation attracts prions.

* Inflammation lets prions invade 'safe' tissue
* On the Road to Dementia: Inflammation, Prions, ...

Aguzzi and colleagues in Britain and the United States inoculated specially bred mice with prions and checked to see if the prions spread in their bodies when the mice had an inflammatory condition. This is because other studies had suggested that prions might be attracted to immune system inflammatory cells.

“In all cases, chronic lymphocytic inflammation enabled prion accumulation in otherwise prion-free organs,” the researchers wrote.

10. Central Nervous System Inflammation and Prion Disease Pathogenesis

The study of inflammation in the prion diseases is relatively new. Indeed, for a number of years the accepted dogma was that the prion diseases lacked an inflammatory response in the brain (1–3). This persists in spite of a number of studies showing that the pathological hallmarks of the prion diseases (PrPSc deposition, astrocytosis, vacuolation, and neuronal loss) are associated with the presence of activated microglia (4–7). At the heart of this discrepancy is a simple matter of what is meant by inflammation. The innate inflammatory response is the tissue’s response to injury or infection, and, as so succinctly put by Metchnikoff in the late ninetenth century, “The essential and primary element in typical inflammation consists in a reaction of the phagocytes against a harmful agent” (8). Given that the microglia are the brain’s resident macrophages (i.e., phagocytic cells), we believe that the presence of activated microglia in prion-affected brains represents an inflammatory response (9–11).
Affiliation(s): (1) CNS Inflammation Group, School of Biological Sciences, University of Southampton, Southampton, UK
Book Title: Molecular Pathology of the Prions

Brain Inflammation Likely Key Initiator to Prion and Parkinson's Disease

…researchers of the Computational Biology group at the Luxembourg Centre for Systems Biomedicine showed that neuro-inflammation plays a crucial role in initiating prion disease.

Prion diseases represent a family of neurodegenerative disorders associated with the loss of brain cells and caused by proteins called prions (derived from ‘protein’ and ‘infection’). The diseases are found in both humans and animals, such as Creutzfeld-Jakob disease and mad cow disease respectively. Although mostly harmless, prions can transform into infectious agents, which accumulate in the brain and destroy the nervous tissue.
But how exactly does the accumulation of prions cause destruction of the brain? “Understanding the process by which prions destroy neurons is critical for finding a cure for prion disease”, says Isaac Crespo, first author of the publication. He and his colleagues tackled this question with a computational approach: They ran their own computer programmes on experimental data generated by other research groups, and identified a set of 16 proteins that seems to control the onset of the disease. Interestingly, almost all of these proteins have known functions in neuro-inflammation.

Prion disease does seem to be one of the forerunner diseases out there, causing many diseases that seem to be unrelated to occur in people. That is what I read from some of my research on this too. It is hard to fathom but it is possible that much of what is going on has relations with prions taking over. But how come now, what has changed to lower our resistance to prions. They may be newly discovered but they were not much of a problem to humans before while they have always been around. I think something is causing us to be more susceptible to them now. Maybe something is making the cows more susceptible to mad cow disease too. What antidote aren't we naturally consuming these days, probably something we were told is not good for us in the past.

reply to post by rickymouse

...They may be newly discovered but they were not much of a problem to humans before while they have always been around. I think something is causing us to be more susceptible to them now. ...

Prions are an adaptive mechanism - an agent of evolutionary change - they result when proteins misfold in response to environmental change. So maybe, we're just dealing with a wholehelluvalot more environmental changes than we've ever had to face before.

reply to post by soficrow


That is probably it. We have changed the food we eat, the air we breath, and the soaps and perfumes we use quicker than in most other times in history. Our bodies need to understand how to detoxify these things, many of these things did not exist in nature before. Even being able to eat a mango requires genetic knowledge. The scents we smell cause reactions in our bodies in preparation of things. The chemistry in the body starts to build enzymes when we smell something cooking...these enzymes can become a problem sometimes if we eat something else. I think that things in our environment are interfering with our bodies ability to compensate for natural problems that are occurring.

A lot of the information on Prions is old yet there seems to be little research on these over the years...almost as if they want to avoid the issue.

reply to post by rickymouse


Have been reviewing the research - and it seems clear that human prion infections do take decades to manifest except when something like flu causes inflammation to the central nervous system. From 2007 (a research article):

...individuals incubating prion disease may be highly susceptible to CNS inflammation. ...During the years or decades of prion disease incubation, especially with low or subclinical prion titers, at-risk individuals are certain to encounter diverse pathological insults, such as viral and bacterial infections, autoimmune disease, or neoplastic processes, all of which may have an inflammatory component. These individuals may develop severe neurological diseases not immediately associated with prion infections due to the dissociation of the putative clinical findings from the accumulation of PrPSc. If so, then the effects of the bovine spongiform encephalopathy epidemic on the population should be looked upon differently.

Ed. to add:

A lot of the information on Prions is old yet there seems to be little research on these over the years...almost as if they want to avoid the issue.

Lots of new info - look for "proteinopathies" and "protein misfolding diseases" - the cover-up dates back, and involves restricting the "prion disease" definition to those involving the brain's "prion protein." Now, the few recognized prion diseases are considered to be "proteinopathies" and "diseases resulting from misfolded proteins" - along with a host of others.

reply to post by soficrow


So they have just done what they always seem to do. Split things up even though the cause is the same and the treatments are almost identical. Make ten diseases out of one even though the diseases have the same principals of origination.

Porphyria's are like that, they have scattered a bunch of diseases off this probable heavy metal poisoning origination yet most of the diseases have nearly the same cause and metabolic needs. If the red blood cells aren't forming right you can't eat certain foods. No big deal.

So I am interested to find how to avoid the prions from taking hold. It seems to me that the body should be able to id these things and cause atopsis of the cell. I think that our bodies are being confused by improper chemical consumption. Food is all chemistry and consumption of certain food chemistry in overabundance causes a problem with gene expression if it is in opposition of your hereditary changes. Now what would dampen the bodies ability to identify these misguided proteins and also cancer cells. Prion disease seems more like a symptom to me of a misfunctioning body, we should identify and destroy these misfolded proteins continuously.

It could just be a diet that has changed too fast and includes foods and food chemistry that the body cannot properly identify.

reply to post by rickymouse

...Prion disease seems more like a symptom to me of a misfunctioning body, we should identify and destroy these misfolded proteins continuously.

It could just be a diet that has changed too fast and includes foods and food chemistry that the body cannot properly identify.

Here's where you and I are going in two different directions. You are focused on the idea that prions are bad and need to be "cleared." I am more interested in their role as "evolutionary mechanisms" that are helping us adapt to environmental change - to me, the disease aspect is like a test-run with harmful effects mixed into the beneficial aspects. In this light, attempting a full override would be disastrous.

...There is a middle ground I know but I'm not ready to investigate it publicly.

reply to post by soficrow


I don't think we can successfully evolve that much in a generation though. Viruses can stimulate evolution without killing us but I doubt if prions could successfully succeed at that. I understand what you are thinking but I can't see it working properly. Even bacteria cause change in the body, sometimes this is good sometimes it is bad. We eventually would probably adapt in our offspring to utilize these prions. Many organisms live symbiotically with us but I don't think a misfolded protein would be one of them.

I could be wrong, but we interact with life that is made right a lot better than life that is misformed. I think this misfolding is a flaw in the structure myself, something that shouldn't be. I think lots of this is from mankind messing with things. We have been messing with things for many centuries. Even consuming a protein that the body does not recognize because we changed our diet is like consuming a misfolded protein. They assumed that we would not absorb these proteins but that has been proven false in the last twenty years. Adding new foods and preparation techniques for the food should be done slowly so we can adapt.

Sooner or later the misfolded proteins will no longer be harmful to us. Maybe this is what you are thinking, it is true, humans will evolve to be able to consume these eventually, killing a lot of people along the way.

reply to post by rickymouse

I don't think we can successfully evolve that much in a generation though.

No, we can't - prions start the evolutionary process via epigenetics. With yeast and bacteria for example, the unsuccessful tryouts disappear in 3-4 generations - the successful ones make it into DNA. So we need several generations to work out the kinks.

Viruses can stimulate evolution without killing us but I doubt if prions could successfully succeed at that.

Viruses transport prions. Also, viruses routinely "misfold" their own proteins - it's why they keep changing.

Many organisms live symbiotically with us but I don't think a misfolded protein would be one of them.

Organisms are constantly "sharing" information - one of the main mechanisms for this sharing is prions.

I could be wrong, but we interact with life that is made right a lot better than life that is misformed.

What is "right" in one environment is dead wrong misformed in another. Point being, we evolved to live in a particular environment then we changed that environment radically in roughly a century. We can't be thinking we can change our environment without changing ourselves too. We MUST change and adapt to survive.

I think this misfolding is a flaw in the structure myself, something that shouldn't be.

No. Protein misfolding is a response to environmental change. Whether it will be successful, and quickly enough is a different question.

We have been messing with things for many centuries. Even consuming a protein that the body does not recognize because we changed our diet is like consuming a misfolded protein. They assumed that we would not absorb these proteins but that has been proven false in the last twenty years. Adding new foods and preparation techniques for the food should be done slowly so we can adapt.

Proteins misfold inside our bodies - in response to changes in the micro-environments of our cells - not just elsewhere. Prion infection through ingestion is maybe 30% of the story, depending on the strain.

Sooner or later the misfolded proteins will no longer be harmful to us. Maybe this is what you are thinking, it is true, humans will evolve to be able to consume these eventually, killing a lot of people along the way.

Again, the prions we consume are not the whole problem, not even the biggest part of the problem. About 5-15% of prions are inherited either genetically or epigenetically; some are "acquired" from external sources through food, medicines, personal hygiene products and so on; and most, up to 85% depending on the strain, arise "sporadically" in the body - meaning they are created inside us in response to other things we have ingested, absorbed or inhaled.

Just a quick heads up.

Community creates fundraisers for young mom struck by rare, fatal disease

Sandi Tucker Kennedy, a 38-year-old wife and mom of four young children ages 2 to 9, has been diagnosed with a prion disease, a family of rare progressive neurodegenerative disorders that take over the neurological system.

The disease is rapidly progressing and Kennedy, who is now at her Kennebunk home surrounded by family, has been given a short time to live.

It took months of debilitating symptoms for doctors to reach the diagnosis, including many hospital visits and stays, and the fundraisers that have been set up are helping to defray those medical costs.

…A fundraising page has also been set up at youcaring.com where 100 percent of the funds raised will benefit the Kennedy family. To donate, visit www.youcaring.com and search for "Hope for Sandi."

This is a very significant thread for everyone simply because many doctors believe that Alzheimer's disease is Mad Cow Disease, just renamed or cloaked to avoid 'panic', as happened here in the UK when Mad Cow disease was first announced and the beef industry collapsed.

The prions are the clue / link.

Just slightly off course here, but I do believe the fabled 'time traveller', John Titor did mention that the true extent of mad Cow Disease would be hidden. In the UK we have an epidemic of elderly people suffering from Alzhemers / dementia.

It won't be the first illness that has had its 'True Nature' hidden from the population.

In the 'True Nature' of any illness we find the answers and the cures.


However, on a sadder note, your thread, Soficrow, reminded me of a dear friend, Helen.

About 12 years ago, Helen suffered a twitch that would not go away on one side of her face. Then it became worse. She started having seizures that would not stop and ended up in intensive care within an inch of her life. She had encephalitis. The doctors were mystified as to the cause. But Helen's condition continued to gradually degenerate until five years later she died of this degenerative illness.

No cause was ever given for her illness but her helplessness as her body failed her and her mind broke haunt me and her other friends to this day. I suspect a prion illness as do others who knew her well as it was something we discussed many times due to the helplessness of her doctors and many specialists.

a reply to: Elliot

I am sorry about your friend.

I suspect there are several (if not numerous) strains of the Mad Cow prion. Alzheimer's Disease involves a prion that affects the Tau(?) protein but not the so-called "prion protein." But it's the mechanism and process that count. Seems clear that prions are an epigenetic mechanism/factor, and modify proteins after the genes produce them. Much more to learn in this field. Here's an interesting take on what's happening - not the whole story, but likely an important part of the picture...

Alzheimer’s disease: an evolutionary approach

Summary - Alzheimer’s disease (AD) is a complex disease associated with advanced age whose causes are still not fully known. Approaching the disease from an evolutionary standpoint may help in understanding the root cause of human vulnerability to the disease. AD is very common in humans and extremely uncommon in other mammals, which suggests that the genetic changes underlying the alterations in cerebral structure or function that have taken place over the course of the evolution of the genus Homo have left specific neurons in the human brain particularly vulnerable to factors which trigger the disease. Most of the genes whose mutation leads to AD are involved in synaptic plasticity. Evidence has also been found relating AD to neuronal oxidative stress. Neurons in certain association areas of the human brain retain juvenile characteristics into adulthood, such as the increased expression of genes related to synaptic activity and plasticity, incomplete myelination and elevated aerobic metabolism, which can cause an increase in oxidative stress in these neurons. Oxidative stress can cause myelin breakdown and epigenetic changes in the promoter region of genes related to synaptic plasticity, reducing their expression. These changes may in some cases induce hyperphosphorylation of tau and β-amyloid deposits, which are characteristic of AD. The adaptation of humans to the cognitive niche probably required an increase in synaptic plasticity and activity and neuronal metabolism in neurons in areas related to certain cognitive functions such as autobiographical memory, social interaction and planning. The cost of these changes may have been the brain’s increased vulnerability to factors which can trigger AD. This vulnerability may have resulted from the evolutionary legacies that have occurred over the course of the evolution of the human brain, making AD a possible example of antagonistic pleiotropy. The evolutionary approach allows apparently unrelated data from different disciplines to be combined in a manner that may lead to an improved understanding of complex diseases such as Alzheimer’s.

I remember when there were barely any old folks homes.
I remember when elderly people rarely ever had dementia and Alzheimer's disease was almost unheard of.

So, what has changed?

Where did 'they' go wrong?

I suspect that if we follow the money we will find that profit seeking is the cause of a lot of human and animal suffering.

What's the answer?

I have an idea..........but I doubt it would ever happen. People who LOVE money.........LOVE money!

My mother in law irons flat all her money (notes of course) and would stoop to almost anything to acquire more money.

Now if this is true of an 'ordinary' person, what could be said for those so greedy for wealth and power that they literally would stoop to scrape the dross off the floor and feed it to their fellow man?

a reply to: Elliot

....they literally would stoop to scrape the dross off the floor and feed it to their fellow man?

Enter: processed "food" - hot dogs, sausages, nuggets.... . These days, you can't even count on a piece of "meat" being meat - half the time they glue scraps together for pretend steak or chicken breast.

....I think the key is epigenetics (including the epigenetic effects of prions) - epigenetics is best viewed as rapid response to environmental change. We have altered our environments dramatically over the past few hundred years - and now we're paying the price.

Time for everyone to own up, and start cleaning up the mess.

I think the problem lies in red meat.

Britons have been lectured about the hazards of eating too much red meat till they're blue in the face; and I think it's having an effect on choice of diet.

I get the impression that it's not quite the same on the other side of the pond.

Take it easy.

Eat something else.

originally posted by: CJCrawley
I think the problem lies in red meat.

You're wrong. Virtually any protein can misfold into an infectious disease-causing form - including plant proteins. And fyi - a lot of prion formation originates in the human body itself (referred to as "sporadic").

a reply to: soficrow

If I'm wrong, the science is too.

I didn't make it up.