Researchers have found abnormal prion protein in the skin of 23 people who died from Creutzfeldt-Jakob Disease (CJD). Meanwhile exposing mice to skin tissue taken from the CJD patients caused them to develop prion disease.
The study has raised questions about the possibility of prion diseases being transmitted during medical procedures that involve the skin, as well as the possibility of using skin samples to detect the diseases.
Creutzfeldt-Jakob disease (CJD)—the human equivalent of mad cow disease—is caused by rogue, misfolded protein aggregates termed prions, which are infectious and cause fatal damages in the patient’s brain. CJD patients develop signature microscopic sponge-like holes in their brains. The initial signs of CJD include memory loss, behavior changes, movement disorder, and vision problems, which usually rapidly progress to death. According to the National Institutes of Health (NIH), 90 percent of CJD patients die within one year of onset, and hundreds of Americans are diagnosed annually. There is no available treatment or cure.
There are numerous types of prion diseases in humans, and CJD is the most common. About 90 percent of CJD cases have a sporadic origin. Prion infectivity is highly concentrated in CJD patient brain tissue. Inter-personal CJD transmission has occurred after patients were exposed to surgical tools previously contaminated by CJD brain tissues.
In a Science Translational Medicine study published today, Case Western Reserve University School of Medicine researchers found that CJD patients also harbor infectious prions in their skin, albeit at lower levels. In the study, the researchers collected skin samples from 38 patients with assistance from the National Prion Disease Pathology Surveillance Center at Case Western Reserve School of Medicine and measured their prion levels. Using a highly sensitive in vitro assay developed and conducted by Byron Caughey’s group at the NIH, they detected prion protein aggregates in the skin samples from all of CJD patients. Prion levels were 1,000-100,000 times lower in the skin than in the brain, and only detectable by this extremely sensitive assay. The researchers further demonstrated that such skin prions are infectious, since they are capable of causing disease in humanized mouse models.
“It is well known that CJD is transmissible via surgical or medical procedures involving prion-infected brain tissue. Our finding of infectious prions in skin is important since it not only raises concerns about the potential for disease transmission via common surgeries not involving the brain, but also suggests that skin biopsies and autopsies may enhance pre-mortem and post-mortem CJD diagnosis,” said Wenquan Zou, Associate Professor of Pathology and Neurology and Associate Director of the National Prion Disease Pathology Surveillance Center at Case Western Reserve School of Medicine. Zou led the study involving a consortium of research groups and researchers across Case Western Reserve School of Medicine, University Hospitals Cleveland Medical Center, the NIH, and the People’s Republic of China.
“The level of prion infectivity detected in CJD skin was surprisingly significant, but still much lower than that in CJD brains,” cautioned Qingzhong Kong, Associate Professor of Pathology and Neurology at Case Western Reserve School of Medicine. “Prion transmission risk from surgical instruments contaminated by skin prions should be much lower than that of instruments contaminated by brain tissue.” In the study, the Kong group assisted by the Zou group demonstrated that CJD patient skin is infectious using humanized transgenic mouse models.
Current diagnostic tools for CJD rely on brain tissue samples collected at either biopsy or autopsy, or cerebral spinal fluid obtained by spinal taps. The new study may lay the foundation for less invasive techniques. “Using the skin instead of brain tissue for post-mortem diagnosis could be particularly helpful in cultures that discourage brain autopsy, such as China and India. These countries have the largest populations with the greatest number of patients, but brain autopsy is often not performed,” said Zou.
“Further investigation is necessary to determine whether extra precautions should be taken during non-neurosurgeries of CJD patients, especially when surgical instruments will be reused,” said Zou. Case Western Reserve School of Medicine researchers plan to further evaluate the potential risk of skin prion transmission through non-neurosurgeries, primarily using mouse models.
The study was conducted by scientists from the National Institute of Allergy and Infectious Diseases (NIAID) and various other collaborating groups.
Generally, people associate prion diseases with the brain, although it has been shown that clusters of the abnormal prion protein, which cause sponge-like holes in the brain, can accumulate in other organs including the liver, spleen, lungs and kidney. It is known that Sporadic CJD, which is the most common human prion disease, can be transmitted via invasive medical procedures involving the central nervous system and cornea, but transmission via the skin has not generally been considered a concern.
The authors want to study the risk of surgical instruments becoming contaminated and the risk associated with procedures that involve CJD patients. They also suggest the possibility of using the skin-based diagnostic test for prion diseases in humans and animals.
Crossbow Communications specializes in issue management and public affairs. Alzheimer’s disease, Creutzfeldt-Jakob disease, chronic wasting disease and the prion disease epidemic is an area of special expertise. Please contact Gary Chandler to join our coalition for reform firstname.lastname@example.org.
By the time Kay Schwister got her diagnosis last summer, she couldn’t talk anymore. But she could still scowl, and scowl she did.
After weeks of decline and no clue what was causing it, doctors had told Schwister — a 53-year-old vocational rehab counselor and mother of two from Chicago — that she had an incurable disease called Creutzfeldt-Jakob disease, or CJD.
The disease was shrinking Kay’s brain, and riddling it with holes. She would likely live only a few more weeks, the doctors said.
It was a diagnosis that no one could ever want. But the fact that Schwister was able to get a firm diagnosis while still alive is a relatively new development that represents a step forward in understanding a group of devastating neurological disorders. And, some biochemists say, it could lead to better ways of diagnosing brain diseases that are much more common, including Parkinson’s disease and Alzheimer’s disease.
For Kay Schwister, it all started in the spring of 2016, when she started getting headaches and feeling dizzy all the time. Aging, she told herself, just didn’t feel very good. Over the next few weeks, she got steadily worse.
“She got to the point where she was so nauseous and so dizzy that she stopped driving and working,” says her husband, Tim Schwister.
By the time Kay entered the emergency room last June, her speech had changed. She was enunciating things in a strange way, and finishing each sentence on a really high note.
Doctors drew blood and spinal fluid and tested it for things like multiple sclerosis and mercury poisoning. Those tests came back negative.
Soon, Kay couldn’t talk or walk.
“Not knowing what we were dealing with was probably one of the hardest things to ever go through in life,” says Tim. “We really wanted to know what we were up against, and if there was anything that we could do.”
Ultimately, Kay’s doctors ordered a newly developed test for Creutzfeldt-Jakob disease — a very rare condition that’s thought to kill about 1 in a million people worldwide every year, including about 300 deaths annually in the U.S.
That test came back positive. About a month after Kay entered the hospital, the Schwisters had their answer. It was ugly, but still an answer.
Normal proteins in Kay’s brain had started misfolding, bending themselves into an unnatural shape and coaxing other proteins to do the same, like some kind of malicious origami. These misshapen proteins, known as prions, formed clumps in the brain, causing neurons to die.
“It’s almost as if it starts to turn certain portions of your brain off,” says Tim.
The vast majority of CJD cases worldwide are like Kay’s, popping up for no apparent reason. Other cases seem to be inherited. A very small number of patients have contracted the illness through close contact with material from an infected person’s brain or nervous system — during certain transplant procedures or via contaminated surgical equipment, for example. And another form, variant CJD, is the human version of mad cow disease, and has been linked to eating infected beef.
There is no cure or treatment for CJD. All Tim could do for his life partner of 35 years was to try to make her as comfortable as possible. Still, having a diagnosis spurred the many people who loved Kay into action, Tim says. Family and friends flew in from all over the country to visit. She was rarely alone.
“Every day, it was nonstop,” Tim says. “People that were there to visit with her, just to try to keep her spirits up.”
She never went home. Kay Schwister died within seven weeks of entering the hospital.
Until recently, families like the Schwisters wouldn’t have known what their loved one was suffering from until it was all over, when an autopsy might have shown that the brain was smaller than expected. Under a microscope and using a special stain, a pathologist would have seen holes in the brain, along with tangles and clumps of misfolded proteins (prions).
But diagnosis after death is too late — not just for the patient and families, but also for researchers trying to study potential therapies to slow down or stop the progression of the disease. These same diagnostic frustrations apply to some of the most common forms of dementia, including Parkinson’s and Alzheimer’s disease, which are also associated with protein misfolding.
“The trouble with many of these diseases, some of which are incredibly prevalent, is that it can take months or years to diagnose,” says Byron Caughey, a biochemist at Rocky Mountain Laboratories in Hamilton, Mont., a part of the National Institute of Allergy and Infectious Disease.
A previous spinal fluid assay for CJD could identify brain cell injury, but not the cause of that injury. That’s why Caughey recently teamed up with scientists in Italy, Japan and the U.K. to develop a different test. It’s called RT-QuIC, which stands for “real-time quaking-induced conversion.”
The test, developed a few years ago and still available via only a few laboratories, harnesses the bad protein’s ability to induce normal, neighboring proteins to take on its twisted form. The test takes about 90 hours and involves getting a sample of spinal fluid, shaking it up with normal proteins and waiting to see if the normal proteins misfold.
Caughey and some Italian scientists have even figured out how to avoid the spinal tap; they can make the test work with a sample of cells taken from deep inside a patient’s nostril, from a spot that is separated from the brain by just a bony partition.
“So, we now have the ability to collect a little bit of spinal fluid or nasal brushing from patients while they’re still alive, and with quite a high degree of certainty, tell whether or not they have a prion disease,” says Caughey. In several studies now, he says, the RT-QuIC test has sensitively and specifically identified CJD prions in symptomatic patients; the test has since been distributed to CJD surveillance centers in multiple countries.
“Technologically, it’s a major new paradigm for testing protein misfolding,” says Dr. Jiri Safar, director of the National Prion Disease Pathology Surveillance Center at Case Western Reserve University in Cleveland and one of Caughey’s collaborators. Since the center started using the assay in April 2015, it has tested more than 5,000 samples from patients referred by doctors scattered around the U.S., Canada and Mexico. And within that group, Safar says, about 500 people tested positive for CJD. The assay costs about $50 to run.
“It’s a major game changer,” says Safar, who hopes wider use of the test in suspected cases will help to completely eliminate the possibility of transmitting CJD through infected blood, bodily fluids or organs.
Caughey, Safar and colleagues reported in late November in the journal Annals of Neurology that a second-generation version of their test was just as effective in diagnosing the disease as an autopsy or biopsy of a living brain (which is another diagnostic option, but a risky, invasive one).
Alison Green, a biochemist at the University of Edinburgh in the U.K., is now working on a modified version of the test that has been shown capable of detecting Parkinson’s disease and Lewy body dementia.
“It’s very important, because there is no other diagnostic test for Parkinson’s disease,” Green says. “It’s purely a clinical diagnosis at present.”
Parkinson’s is a chronic and progressive movement disorder that eventually includes symptoms of dementia in an estimated 50 to 80 percent of cases. Diagnosing it sometimes requires years of observation, at which point a patient has already lost a lot of neurons.
In a small study published last summer, Green used a version of RT-QuIC that looks for alpha-synuclein (a protein that’s associated with Parkinson’s) on 20 people who had a Parkinson’s diagnosis, and 15 people in a control group.
“And you can get a nice, clear-cut positive result after 120 hours,” she says. Nineteen out of 20 patients with Parkinson’s were correctly identified, and there were no false positives. Green is now replicating the study with 110 subjects.
If the test proves to be as reliable as it was in her first study, Green says, it could become an important diagnostic tool for doctors to rapidly identify a patient’s ailment and start therapies as soon as possible, when they might still make a difference.
“A lot of these drugs or therapies are being introduced way too late because patients aren’t diagnosed early enough,” Green explains. “And they may be effective treatments if you give them earlier.”
She’s also applied for funding to develop a test that would look for abnormal beta-amyloid peptides, possible indicators of Alzheimer’s disease.
The ultimate goal, says Green, is to have a whole bank of RT-QuIC assays so that patients with any kind of undiagnosed dementia can get answers.
Knowing the prognosis earlier, she says, could give some patients and families more choices.
“If you have early onset dementia, do you really want to spend the last few years of your life working, or do you want to take early retirement?” says Green.
And even for diseases that have no option of being slowed or reversed, she says, a firm and accurate diagnosis can still offer something essential to families — a spur to move beyond tests and treatments.
“We really, truly wanted to know if there was something that we could do for her,” says Tim Schwister of his wife, Kay. The diagnosis let him and his sons know that chasing further treatment at that point wouldn’t help, and that the best they could do was to turn their attention to making Kay comfortable, and spending time with her.
The diagnosis also helped the Schwisters connect with other families who’d gone through the same experience.
In a time of such great loss, Tim says, “it’s nice to know that you’re not alone.”
Crossbow Communications specializes in issue management and public affairs. Alzheimer’s disease, Creutzfeldt-Jakob disease, chronic wasting disease and the prion disease epidemic is an area of special expertise. Please contact Gary Chandler to join our coalition for reform email@example.com.
Science, Evidence Proving That Alzheimer’s A Transmissible Disease
If you think that you and your family are immune to the surging epidemic of neurodegenerative disease, think again. Neurodegenerative disease, including Alzheimer’s disease, is the fastest-growing cause of death in the world. It’s getting worse every day thanks to mismanagement and misinformation.
Infectious proteins known as prions are involved with most forms of neurodegenerative disease. Prion disease is known in neurology as transmissible spongiform encephalopathy (TSE). The operative word is “transmissible.” The global epidemic has more to do with the prion contagion than age.
Dr. Stanley Prusiner, an American neuroscientist from the University of California at San Francisco, earned a Nobel Prize in 1997 for discovering and characterizing deadly prions and prion disease. Prusiner claims that all TSEs, includingAlzheimer’s disease, are caused by prions.
President Obama awarded Prusiner the National Medal of Science in 2010 to recognize the importance of his research. According to Prusiner, TSEs are a spectrum disease. Creutzfeldt-Jakob disease, which is extremely aggressive and extremely transmissible, is at the extreme end of the spectrum. Unfortunately, Prusiner’s science is being ignored and we are facing a public health disaster because of the negligence.
Neurologists are just guessing when they make a diagnosis on the prion spectrum. If the patient exhibits memory problems, they are labeled with Alzheimer’s disease. If they have a movement disorder, they are diagnosed with Parkinson’s disease. If the person exhibits extreme symptoms of both, they are diagnosed with Creutzfeldt-Jakob disease (CJD). It’s far from a science. Neurologists don’t know where along the spectrum the disease becomes transmissible. The entire spectrum could represent a transmissible disease. Unfortunately, neurologists are not warning these patients and their caregivers about the risks of exposure. Even those with Creutzfeldt-Jakob disease are not quarantined. They are sent home, where they can infect friends, family, caregivers, clinics, dental offices, restaurants and entire communities.
“There has been a resurgence of this sort of thinking, because there is now real evidence of the potential transmissibility of Alzheimer’s,” says Thomas Wiesniewski M.D. a prion and Alzheimer’s researcher at New York University School of Medicine. “In fact, this ability to transmit an abnormal conformation is probably a universal property of amyloid-forming proteins (prions).”
A study published in the journal Nature renews concern about the transmissibility of Alzheimer’s disease between people. A second study released in early 2016 by the same scientist adds to the stack of evidence.
According to neuroscientist Laura Manuelidis, at least 25 percent of Alzheimer’s diagnoses are wrong. These misdiagnoses are actually CJD, which is further up the prion spectrum. CJD, without dispute, is extremely infectious to caregivers and loved ones.
Studies confirm that people and animals dying of prion disease contaminate the environment around them with prions because prions are in the urine, feces, blood, mucus and saliva of each victim. Each victim becomes an incubator and a distributor of the Pandora-like pathogen. Victims are contagious long before they exhibit clinical symptoms.
At the personal level, this is very bad news for caregivers, especially spouses, who are 600 percent more likely to contract neurodegenerative disease from patients (Duke University and Utah State University). A cough, sneeze, utensils and drinking glasses all become lethal pathways. Once an item is contaminated, it’s impossible to sterilize. The human prion is resistant to both heat and chemicals. It’s reported that prions released from people are up to a hundred thousand times more difficult to deactivate than prions from most animals. Prions are not alive, so they can’t be killed.
Wastewater treatment plants are collecting points for prions from infected humans. The sewage treatment process can’t stop prions from migrating, mutating and multiplying before being discharged into the environment where they can kill again. The bad news is that the prions are being released back into the environment and dumped openly on land. The wastewater is being reclaimed and used for irrigating crops, parks, golf courses. It’s even being recycled as drinking water.
Claudio Soto, PhD, professor of neurology at the University of Texas Medical School in Houston, and his colleagues confirmed the presence of prions in urine. Soto also confirmed that plants uptake prions and are infectious and deadly to those who consume the infected plants. Therefore, humans, wildlife and livestock are vulnerable to prion disease via plants grown on land treated with sewage sludge and reclaimed sewage water.
Prion researcher Dr. Joel Pedersen, from the University of Wisconsin, found that prions become 680 times more infectious in certain soils. Pedersen also found that sewage treatment does not inactivate prions. Therefore, prions are lethal, mutating, migrating and multiplying everywhere sewage is dumped.
“Our results suggest that if prions enter municipal wastewater treatment systems, most of the agent would bond to sewage sludge, survive anaerobic digestion, and be present in treated biosolids,” Pedersen said.
“Land application of biosolids containing prions represents a route for their unintentional introduction into the environment. Our results emphasize the importance of keeping prions out of municipal wastewater treatment systems. Prions could end up in sewage treatment plants via slaughterhouses, hospitals, dental offices and mortuaries just to name a few of the pathways. The disposal of sludge represents the greatest risk of spreading prion contamination in the environment. Plus, we know that sewage sludge pathogens, pharmaceutical residue and chemical pollutants are taken up by plants and vegetables.”
Thanks to more and more people dying from TSEs, wastewater treatment systems are more contaminated with prions than ever. Wastewater treatment plants are now prion incubators and distributors. The prion problem is getting worse every day.
The U.S. Environmental Protection Agency (EPA) has confirmed that prions are in sewage and that there has been no way to detect them or stop them. As such, the EPA has never issued guidance on prion management within wastewater treatment plants. Unfortunately, the EPA’s risk assessment on sewage sludge and biosolids were prepared before the world of science knew about prions. The agency continues to cling to its antiquated sludge rule crafted back in the dark ages. It does, however, consider prions a “contaminant of emerging concern.” Meanwhile, its outdated risk assessments are promoting a public health disaster.
“Since it’s unlikely that the sewage treatment process can effectively deactivate prions, adopting measures to prevent the entry of prions into the sewer system is advisable,” said the Toronto Department of Health, November 2004.
Exposing crops and livestock to prions is a very bad idea. Plants absorb prions from the soil along with water and nutrient uptake, which makes the prions even more bioavailable and infectious to humans, wildlife and livestock.
Unfortunately, the damage is real. Deer, elk, moose and reindeer are contracting an unstoppable prion disease now. In deer, the government calls prion disease chronic wasting disease. In cattle, prion disease is called bovine spongiform encephalopathy (they might as well call it what it is—transmissible spongiform encephalopathy). Mad cow disease is the term that most of us know. The government pretends that there is a specific prion responsible for each of these diseases. The fact is that there are thousands of mutations of prions spreading in the environment and food chain now. Some kill quickly, while some are less lethal. The only thing that we need to know is that a deadly prion is a deadly prion. There is no species barrier.
If prion disease is killing these animals, livestock are not immune. Beef and dairy cattle are consuming these infected crops and the infected water supplies, too. Since humans are at the top of the food chain, and since we are often downstream from these infected farms, ranches and forests, our food and water supplies are being compromised. Wind and tornadoes transport the infectious waste even further.
So, is Alzheimer’s disease transmissible? There is absolutely no evidence to the contrary. The truth is your best defense against neurodegenerative disease. It’s time to demand reforms on many levels to safeguard caregivers, family members and our food and water supplies. Despite all of the warning signs, government and industry are insisting that we waste more time, money and lives studying these issues to death. The infection is real. The body count is real. The denial is disturbing.
Crossbow Communications specializes in issue management and public affairs. Alzheimer’s disease, Creutzfeldt-Jakob disease, chronic wasting disease and the prion disease epidemic is an area of special expertise. Please contact Gary Chandler to join our coalition for reform firstname.lastname@example.org.
Maine Medical Center confirmed Friday that a patient treated at the hospital carried a rare, dangerous brain illness to which a “small number” of other patients may have been exposed, though the hospital called that risk “exceedingly low.”
The patient has Creutzfeldt-Jakob disease, or CJD, a degenerative brain disorder caused by an infectious type of protein, the hospital said in a statement. CJD is a form of prion disease, which is fatal.
Hospital officials suspected earlier this week that the patient, who was not identified for privacy reasons, carried the pathogen, based on an initial biopsy result. The National Prion Disease Pathology Surveillance Center at Case Western Reserve University in Cleveland confirmed the diagnosis on Friday, according to the statement.
“We are in the process of reaching out to the small number of patients who we think should be notified based on the details of their specific case,” Dr. Joel Botler, chief medical officer at MMC, said in the statement. “Our staff members have been fielding calls from patients who have legitimate concerns and questions about their care. Let me be clear, only a small number of patients who have had surgery at MMC have been exposed to any degree of risk, and that risk is exceedingly low approaching zero.”
Transmission of the disease in a hospital setting is “extremely rare,” with no confirmed cases in more than 20 years, the statement said.
Humans can contract prion disease from medical procedures, as the pathogen can survive on surgical tools and other equipment even after standard sterilization. Brain tissue from an infected patient potentially can infect subsequent patients before doctors know it’s there.
MMC is determining which patients were treated before the initial pathology report showing Creutzfeldt-Jakob disease and should be notified.
“While the hospital does track surgical equipment used in each case, the decision was made not to rely on tracking and instead make sure that any piece of equipment that could potentially be affected was treated,” Botler said in the statement. “Now that we know this case is confirmed, we can see that our response was 100 percent appropriate and that patients should feel confident in the safety of their care at Maine Medical Center.”
As a precaution, the hospital rescheduled approximately 150 elective surgeries Wednesday and Thursday while staff decontaminated surgical equipment and facilities in accordance with guidelines set by the U.S. Centers for Disease Control and Prevention, the hospital said.
In the meantime, other Maine hospitals loaned equipment so MMC could perform emergency surgeries.
To treat metal instruments contaminated with prions, hospitals have to put them in an autoclave and heat the tools to 121 degrees Celsius for 30 minutes, according to CDC protocols. That’s much more than is required to kill bacteria and viruses.
But even that doesn’t always work. Prions can survive the superheating, though it does weaken them, according to a report in Scientific American.
Another reason why prion disease poses such a risk is that it has a long incubation period. The time between when a person is exposed to when they start feeling symptoms can range from months to years. That means a patient with the disease can arrive at the hospital and show no symptoms. It may not be until they’re on the operating table for another reason that doctors spot signs of trouble. Or the medical staff may spot no red flags at all, only to discover later that the patient was infected. In the meantime, other patients can be exposed to the contaminated tools and more.
Prion disease is distinct from other infectious diseases in that it’s not caused by a bacteria, virus or fungus but by abnormal proteins called prions. They can cause other proteins in the brain to fold abnormally, essentially leaving the organ full of holes like a sponge. That brain damage leads to memory impairment, dementia, personality changes and difficulty moving, among other symptoms. The incurable disease usually progresses very quickly and is always fatal, according to the CDC.
Prion disease refers to a family of progressive disorders that affect humans and animals. The most common form of it among humans is Creutzfeldt-Jakob disease, which can arise spontaneously, for no known reason. A variant form of it is caused by eating meat from cattle infected with another prion disease, bovine spongiform encephalopathy, also known as mad cow disease. (Editor’s Note: In deer, elk, moose and reindeer, prion disease has been dubbed chronic wasting disease. It’s time to put the species-specific names aside. A deadly prion is a deadly prion.)
CJD is rare, estimated to affect about one out of every million people worldwide each year, according to the World Health Organization. About 250 cases are diagnosed each year in the U.S. but thousands of other cases are suspected to go undiagnosed and misdiagnosed.
In 2014, a Kennebunk woman who worked as a nurse at Maine Medical Center died from Creutzfeldt-Jakob disease, according her family.
And in 2013, 15 people in New Hampshire, Massachusetts and Connecticut were warned that they may have been exposed to the disease through potentially contaminated medical equipment.
Editor’s Note: The most common forms of neurodegenerative disease include Alzheimer’s disease, Parkinson’s disease, ALS and Creutzfeldt-Jakob disease–the most aggressive and infectious of them all. According to Nobel Prize Laureate Stanley Prusiner, these brain diseases are on the same disease spectrum—prion disease. It’s also known as transmissible spongiform encephalopathy (TSE). The bodily fluids of TSE victims are infectious and deadly. This infectious waste is now an environmental nightmare.
Prion disease is a spectrum disease that varies in severity. It also varies depending on which region of the brain is impacted first. It affects most, if not all, mammals. Prion disease causes memory loss, impaired coordination, and abnormal movements. It’s not known which patients with brain disease become infectious or when, but both CJD and Alzheimer’s patients are being mismanaged. The most savvy neurologists won’t touch patients with these symptoms because of the risks. They are making diagnoses from across the room. Unfortunately, caregivers aren’t warned accordingly.
CJD behaves like Alzheimer’s disease on steroids,” said Dr. Jennifer Majersik, an associate professor of neurology at the University of Utah.
Experts claim that at least 25 percent of Alzheimer’s diagnoses are not Alzheimer’s disease. Millions of misdiagnoses are actually CJD, which is further up the prion spectrum. Millions of patients and caregivers are being misinformed, misguided and exposed to an aggressive prion disease. Misdiagnosis and misinformation regarding prion disease is a matter of life and death.
Urine can be used to test for Creutzfeldt-Jakob disease. Unfortunately, it also is a pathway that spreads prion disease among mammals.
The Medical Research Council team is working on a simple test. They claim that their prototype test still needs honing before it could be used routinely. Currently there is no easy test available for this rare but fatal brain condition. Instead, doctors have to take a sample of spinal fluid or brain tissue, or wait for a post-mortem after death. What they look for is tell-tale deposits of abnormal proteins called prions, which cause the brain damage.
Building on earlier US work, Dr. Graham Jackson and colleagues, from University College London, have now found it is also possible to detect prions in urine. This might offer a way to diagnose CJD rapidly and earlier, they say, although there is no cure.
CJD is a rare, but fatal degenerative brain disorder caused by abnormal proteins called prions that damage brain cells. In the 1990s it became clear that a brain disease could be passed from cows to humans (it can also be passed from humans to other mammals). Since then, officials have kept a close check on how many people have become sick or died from CJD. There is no known cure.
The study looked at urine samples from 162 people. Of these:
91 were healthy controls
34 had neurological disease that was not thought to be caused by CJD
37 had a diagnosis of CJD (20 of these were sporadic CJD)
The urine test gave no “false-positive” results – meaning it did not falsely suggest there was CJD in any of the patients known not to have the disease. But it was less reliable when it came to detecting actual cases. It accurately detected just under half of the sporadic CJD patients and even fewer of the vCJD patients. The researchers hope they will be able to improve the test further so it can reliably detect all types of CJD.
“Although there is currently no cure for this disease, an accurate and early diagnosis is extremely important for patients and their families, said Dr. Jackson. “In the future, as trials of potential therapies become available, the earlier a patient can be diagnosed the more effective any treatment is likely to be. This test could be a critical step forward.”
Editor’s Note: Prion disease is a spectrum disease that includes Alzheimer’s disease, Creutzfeldt-Jakob disease, Parkinson’s disease, Huntington’s disease, mad cow disease, chronic wasting disease and is likely a contributing factor in the global rise in autism. Victims are infectious long before they exhibit symptoms. Misinformation and mismanagement of sewage and wastewater are contributing to the global epidemic in neurodegenerative disease. As more people get the disease, the waste stream becomes even deadler. It’s time to regulate wastewater streams, including biosolids, as infectious waste and it’s time to enforce the Bioterrorism Preparedness and Response Act of 2002.
Alzheimer’s disease is the fastest-growing cause of death in the world. It’s killing more than 50 million people now. The count is likely much higher. Millions more will be diagnosed this year, while millions more will go undiagnosed and misdiagnosed.Adding to the madness is the fact that millions of other diagnoses are being withheld by physicians. Most of these deaths could have been prevented.
Although there are many factors contributing to the global Alzheimer’s disease epidemic, most of these deaths could have been prevented. In addition to dietary risks, it appears that Alzheimer’s disease is just as infectious as Creutzfeldt-Jakob disease. There is no evidence to the contrary.
The most common forms of neurodegenerative disease include Alzheimer’s disease, Parkinson’s disease and Creutzfeldt-Jakob disease. According to Nobel Prize Laureate Stanley Prusiner, they’re all part of the same disease spectrum—prion disease. It’s also known as transmissible spongiform encephalopathy (TSE). The operative word is transmissible.
Women contract the disease at twice the rate of men.
Caregivers are six times more likely to contract neurodegenerative disease.
People from Finland, Iceland, Sweden and the United States have the highest death rates from Alzheimer’s in the world.
Food is the best strategy to avoid the disease and treat it.
Death rates from heart disease, cancer and other leading causes of death are dropping thanks to advances in nutrition, medicine and disease management. Unfortunately, Alzheimer’s disease is the one glaring exception. It’s spreading exponentially. If we had accurate mortality statistics, we would likely find that neurodegenerative disease is already the leading cause of death around the world.
There are many more questions than answers regarding neurodegenerative disease. Most diagnoses are just a process of elimination and an educated guess. Informed doctors won’t touch these patients. They are making life-changing diagnoses and prescribing meds from across the room. If the patient has a memory disorder, it’s Alzheimer’s disease. If it’s a movement disorder, it’s Parkinson’s disease. If the patient exhibits both symptoms, flip a coin. If the person is incapacitated, it’s Creutzfeldt-Jakob disease (CJD). Confirmation requires an autopsy—which rarely happens due to concerns about the contagion.
Most doctors are unable to distinguish between advanced forms of Alzheimer’s disease and the highly aggressive and contagious version known as CJD. Experts suggest that Alzheimer’s diagnoses are wrong at least 25 percent of the time, which means that at least 25 percent of Alzheimer’s cases are highly contagious cases of CJD. Millions of caregivers around the world are taking care of people with CJD without warning. Given the imprecise diagnostics, all cases of neurodegenerative disease should be considered infectious.
Misdiagnoses and suppressed diagnoses represent a nightmare for caregivers and the public at large. It’s just the tip of an iceberg regarding misinformation and mismanagement that is fueling this devastating global epidemic. As we will discuss, there is no evidence to suggest that Alzheimer’s and Parkinson’s disease are not infectious.
Prion disease also kills wildlife, sea mammals and livestock. It’s known as mad cow disease and chronic wasting disease (deer). There is no species barrier against most prions.
There are many factors contributing to the global epidemic. Age and genetics are not the dominant factors for most people any longer. Navigating our toxic world is getting more difficult by the day. Some foods and water sources are contributing to our demise. Others are the best medicines on earth.
For example, there are three big reasons that organic foods can protect you from neurodegenerative disease. We discuss several foods and factors in our upcoming documentary that can help you and your family avert Alzheimer’s, Parkinson’s and Creutzfeldt-Jakob disease. We also will explain which foods help treat the symptoms of the disease.
Despite billions of dollars spent on research, the FDA has only approved six drugs to treat Alzheimer’s disease. Their benefit is questionable at best.
We offer hope, help and empowerment, but we are challenging reckless policies that are fueling this transmissible epidemic around the globe. There are many steps that you can take to help avoid neurodegenerative disease.
According to the Mayo Clinic, Alzheimer’s disease is largely preventable. They claim that the risk for cognitive impairment is 42 percent lower in elderly individuals who consume healthy fats and fewer carbohydrates. Up to half of those who have Alzheimer’s disease could have prevented it with a smarter diet and exercise. Smart food is our best hope for both prevention and treatment.
As we explain in the documentary, the nutritional insight that promotes brain health promotes our overall health. The foods that benefit our brains often benefit our hearts. They also help us avoid obesity, diabetes and cancer.
We will examine several issues, including the toxic role of glucose and carbohydrates in our diet. We also will discuss how gluten sensitivity is involved in most chronic disease, including those affecting the brain. We offer dozens of strategies and tips that can help you beat and treat neurodegenerative disease and others. This information will empower you with the knowledge to make smarter food choices, while empowering you to seek out more answers and find new hope on your own.
Crossbow Communications, one of the leading public affairs firms in the world, will produce the documentary. Sponsorship and investment opportunities are available. For more information, please contact Gary Chandler email@example.com
Alzheimer’s, Creutzfeldt-Jakobs, Parkinson’s Disease All Part Of Prion Spectrum
Editor’s Note: On September 9, 2015 additional research adds to the evidence that suggests that Alzheimer’s disease is a transmissible disease. Scientists have shown that tissues can transmit symptoms of the disease between animals. A new study published in the journal Nature raises additional concern about the transmissibility of Alzheimer’s disease between people and between species.
A scientific truth triumphs not by convincing its opponents but because its opponents eventually die, said influential physicist Max Planck. For Nobel prize-winning neurologist Stanley Prusiner, the quotation is “so mean” that he doesn’t like to use it. “But it is absolutely true,” he says.
Prusiner won the Nobel prize in 1997 for his discovery of prions – infectious proteins that cause fatal neurodegenerative diseases in people and animals, the most famous of which is BSE or mad cow disease and its human form, variant CJD. But his claim to have found an entirely new type of disease-causing agent, which he first termed a prion in 1982, was treated as heretical by many of his peers and the media for years. Bacteria, viruses, fungi and parasites are the only known infectious agents – a mere protein, with its lack of genetic material, is not alive so can’t transmit disease – so an army of naysayers maintained. Even his Nobel prize in physiology or medicine, for which he was the sole winner, didn’t silence all the critics.
“I understood the skepticism,” says Prusiner. “When there is a really new idea in science, most of the time it’s wrong, so for scientists to be skeptical is perfectly reasonable…[But] it didn’t make it any easier.”
Prusiner tells the story of his discovery in a new autobiographical book, Madness and Memory. He wrote the book, he says, both to ensure that the story was recorded in his own words and the science was properly described.
Prusiner was born in Des Moines, Iowa, in 1942. As a youngster, he had no interest in science and was happy to get Bs in school with little effort. When, later, he wanted to take advanced chemistry, a subject he liked because he didn’t have to memorize anything, the school said he wouldn’t be able to comprehend the science. He took a lower course, but went on to major in the subject at the University of Pennsylvania, following it up with a medical doctorate received in 1968.
It was during his chemistry degree that he got his first taste of research – a summer project to help boost his application to medical school. He found the project, studying hypothermia in rats, fascinating and by the end of medical school had become excited about the possibility of pursuing biomedical research as a career.
After completing a grueling internship in medicine that was required for the post, he took a research job at the US National Institutes of Health. He remained at the NIH for three years, studying enzymes in bacteria, before deciding it was time to move on and build his own laboratory.
Prusiner found his scientific destiny after an encounter with a patient with a rare brain disorder in San Francisco in 1972. He had recently begun a clinical residency in neurology at the University of California, San Francisco (UCSF), with the goal of identifying a big problem to investigate, when a patient dying of Creutzfeldt-Jakob disease (CJD) was placed under his care.
The disease was thought to be caused by a “slow virus” that took many months or years to produce symptoms and, intrigued, Prusiner began reading up. “The more I read, the more fascinated I became,” he says.
Other seemingly related slow virus diseases included scrapie (which occurs in sheep) and kuru (found in the Fore people of Papua New Guinea and spread by cannibalism), all three causing a spongy degeneration of the brain and being transmissible to similar species via injection of infected brain tissue. Yet no actual viruses had ever been isolated and previous work by British scientists on the scrapie agent had even found it had some strange properties, including being resistant to killing by radiation.
They had raised the controversial prospect that it may not even contain DNA or RNA. Prusiner had his problem: he would isolate and characterize the elusive infectious agent responsible for scrapie, which could be studied with rodents, and in so doing shed light on these so-called slow virus diseases.
He began work in 1974 having accepted an academic position at UCSF and despite colleges’ warnings that the problem would be too difficult to crack. It was tough going. He lacked funds to pay for the upkeep of the thousands of laboratory animals he needed and the work was slow because the disease took so long to manifest (he found crucial private funding and sped up the work by moving from mice to hamsters and redesigning his measurement method). “I could now do in one year what would have taken me 80,” he says.
As experimental data began to accumulate, Prusiner grew puzzled. He had anticipated that the scrapie agent he was enriching and purifying from brain material would turn out to be a different and interesting virus. Yet his preparations lacked any genetic material that would indicate one. All he found was a protein. He summarized the work in a journal article in Science in 1982, introducing the term “prion” to denote such a particle.
“I just thought it was really counterproductive to keep calling it a virus when it wasn’t,” says Prusiner. “If you call it that and you believe it at some level, then you miss the next set of experiments.”
The word came from Prusiner’s pondering how “protein” and “infectious” might fit together. When “proin” didn’t sound quite right, he flipped two letters. “What else was I going to do?” he laughs. “I couldn’t come up with some clever Greek words because I don’t know any Greek.” (He pronounces it “pree-on“.)
The word and the concept elicited what he describes as a “firestorm” of criticism and skeptics began staking careers on hunting down the scrapie virus (it has never been found). One particularly low moment he recalls was a 1986 article in the science magazine Discover, which accused him of being more interested in fame than science. He adopted a policy, which he maintained for years, of not speaking to the press.
Prusiner’s answer to his scientific doubters was to keep producing data. Among his contributions, he characterized the scrapie prion and added CJD and other diseases to the list caused by prions. He also showed how prions replicate. They come in two forms, he found, with different shapes: a normal uninfectious form that all animals and people have that is particularly abundant in the brain (it is encoded by a prion protein gene) and a more stable disease-causing form. The disease-causing form can act like a template to guide the normal form to refold into the disease-causing one.
In the late 1980s, as scientific data converged, the tide began to turn on the acceptance of the work. He was elected to various professional bodies and began winning awards. Soon afterwards, so-called knockout mouse studies (which abolished the prion gene in mice making them resistant to prion infection) added further evidence.
Then, in 1996, the first cases in Britain of the human form of mad cow disease were reported and prions were implicated. Variant CJD, it was suspected, had arisen from the consumption of beef infected with BSE, which had been identified as a prion disease using Prusiner’s methods after it was first reported in Britain a decade earlier. A year later, Prusiner won the Nobel prize.
Did the spotlight on prions influence the Nobel committee’s decision?
“It didn’t hurt,” he says.
At the press conference that followed, he faced incredulous journalists still insisting prions were an impossibility. “A Nobel prize doesn’t wipe the scepticism away for some people,” he says.
Prusiner attributes his tenacity in the face of years of doubt to the nature of the problem itself. He would have quit, he says, except there was no alternative that excited or captivated him more. But good scientist, he adds, also stay focused on the problem, going deeper and deeper trying to understand it. That is where the “real opportunity to discover something lies”, he says.
Prusiner is now looking for ways to stop prion diseases (which he believes includes Alzheimer’s and Parkinson’s – though the science of this is not yet settled). For despite all that has been revealed about the strange world of prions, they remain a death sentence to those infected. “We don’t have a single therapy,” he says.
Alzheimer’s disease is the fastest-growing cause of death in the world. People living across Scandinavia have the highest prevalence of the disease in the world.
At least 50 million people already have Alzheimer’s disease and other forms of dementia. It’s vastly undiagnosed and misdiagnosed. According to the Alzheimer’s Association, doctors are withholding millions of additional diagnoses in the United States, so we don’t know the extent of the epidemic in America, but the incidence likely rivals Finland.
According to recent studies, Finland has the highest incidence of Alzheimer’s disease in the world. Iceland and Sweden aren’t far behind. It could be that Finland is doing a better job of screening, diagnosing and offering honest assessments.
What can we learn from these regional variations? What are the common threads that can help us unravel the causes of neurological disease?
1. Finland 34.9
2. Iceland 25.1
3. United States 24.8
4. Sweden 21.5
5. Netherlands 21.4
6. Switzerland 20.0
7. Cuba 19.6
8. Chile 19.6
9. Andorra 19.4
10. Spain 18.7
11. Norway 18.6
12. Uruguay 17.5
13. Denmark 17.4
14. United Kingdom 17.1
15. France 16.6
Although there are many causes of Alzheimer’s disease and related neurological diseases, the Baltic Sea region is a microcosm worth studying. The Baltic Sea is one of the most polluted bodies of water on the planet. Much of the pollution originates upstream and on land, but tons of it are dumped directly in the sea.
It’s infectious waste. Raw sewage and sewage sludge. Waste from morgues, hospitals, nursing homes, slaughter houses, veterinarians and the homes of millions of people who have brain disease and other infectious diseases. This infectious waste is being dumped on open land as fertilizer. It’s contaminating food, water, air and more in most countries.
The Problem With Prions
In order to understand the threat, one must understand the dynamics of this neurological disease. Alzheimer’s disease, for example, is a member of an aggressive family (spectrum) of neurodegenerative diseases known asTransmissible Spongiform Encephalopathy(TSE). The operative word is “transmissible.”
TSEs include Alzheimer’s disease, Creutzfeldt-Jakob disease, Parkinson’s, Huntington’s, mad cow disease and chronic wasting disease in deer. Few, if any, mammals are immune. There is no cure. There is no species barrier.
TSEs are caused by a deadly protein called a prion (PREE-on). Prion disease is unstoppable and the pathogen spreads through the bodily fluids and cell tissue of its victims. Prions are in the blood, saliva, urine, feces, mucus, and bodily tissue of its victims.
“There is now real evidence of the potential transmissibility of Alzheimer’s,” says Thomas Wiesniewski M.D. a prion and Alzheimer’s researcher at New York University School of Medicine. “In fact, this ability to transmit an abnormal conformation is probably a universal property of amyloid-forming proteins (prions).”
Prions linger in the environment infinitely because they defy all attempts at sterilization and inactivation. They spread uncontrollably within victims and within the environment. They know no borders. Unlike radiation, however, prions do not deplete themselves. Unlike cancer, there is no cure. Prions migrate, mutate, multiply and kill with unparalleled efficiency. Each victim becomes an incubator and a distributor of the unstoppable pathogen.
“The (human) brain diseases caused by prions include Alzheimer’s, Parkinson’s, Huntington’s, amyotrophic lateral sclerosis (Lou Gehrig’s disease), and other disorders known as frontotemporal dementias,” said Nobel Laureate Stanley Prusiner, who earned a Nobel Prize in Physiology in 1997 for discovering deadly prions.
Prion disease is a spectrum disease because of its many mutations and genetic resistance. Some prions can kill people within weeks of exhibiting clinical symptoms, while others can take years. Others may not fall victim to the disease, but can still carry the pathogen internally and externally. Victims become infectious long before they appear sick. Their bodily fluids proceed to contaminate the world around them.
Since prion disease is a spectrum disease, doctors can’t tell the difference between Alzheimer’s disease and CJD. It’s a process of elimination and a shot in the dark.
“Creutzfeldt-Jakob disease behaves like Alzheimer’s disease on steroids,” said Dr. Jennifer Majersik, an associate professor of neurology at the University of Utah.
According to neuroscientists Dr. Laura Manuelidis, at least 25 percent of Alzheimer’s diagnoses are not Alzheimer’s disease. These misdiagnoses are actually CJD, which is further up the prion spectrum. CJD, without dispute, is extremely infectious to caregivers and loved ones. Millions of cases of deadly CJD are being misdiagnosed as Alzheimer’s disease. Millions of patients and caregivers are being misinformed, misguided and exposed to an aggressive disease. Misdiagnosis and misinformation regarding prion disease is a matter of life and death. The mismanagement doesn’t end here.
The only definitive diagnosis comes with an autopsy, which rarely happens with neurological disease (concerns over deadly contamination). All doctors are guessing with each diagnosis based on the severity of the symptoms. This problem also complicates the search for accurate statistics about the size and scope of the epidemic.
Unfortunately for caregivers and family members, the protocol for patient care and caregiver safety are vastly different for Alzheimer’s patients and CJD patients. The double standards put many stakeholders at risk. It’s reckless to try to distinguish between prion diseases on the spectrum. In other words, treat people with Alzheimer’s disease as though they have CJD. Assume the worst and hope for the best. A deadly prion is a deadly prion.
The Sewage Tsunami
Although there are many causes and pathways contributing to the prion disease epidemic, many pathways are being mismanaged. Thanks to sewage, biosolids, and reclaimed sewage water, we’re recycling the prion pathogen that causes Alzheimer’s and CJD right back into our food and water. Every sewage system in the world has been used by someone, if not millions, of people with Alzheimer’s disease and Creutzfeldt-Jakob disease. Sewage systems are now prion incubators and distributors. Sewage sludge, wastewater, biosolids and other byproducts are highly lethal.
Thanks to more and more people dying from TSEs, and thanks to more and more sewage mismanagement, we’re dumping deadly pathogens on farms, parks, golf courses and school grounds. Rain and irrigation spread the prions throughout our communities, watersheds and into our oceans. Winds carries prion-laced dust into our communities, schools, offices and homes.
Dumping tons of sewage from millions of people on land and at sea spreads the prion pathogen far and wide. It’s a case of Pandora’s lunchbox. We’re contaminating our food and water supplies with our own sewage.
Now, back to our Baltic story. The Baltic Sea is positioned in Northern Europe and bordered by Sweden, Finland, Russia, Estonia, Latvia, Lithuania, Poland, northeastern Germany, and eastern Denmark and its numerous islands. It’s the source of food for millions of people. Its watersheds provide drinking water for hundreds of communities, not to mention livestock, throughout the region. Unfortunately, pollution is killing the Baltic Sea and residents of the region.
“This is one of the world’s most polluted oceans,” said Fredrik Wulff, a professor of marine systems ecology at Stockholm University. “Because it’s an almost closed body of water, everything that’s dumped here stays for decades.”
The untreated waste from the Russian city of Kaliningrad is part of the problem. Kaliningrad dumps about 150,000 cubic meters of raw sewage from 450,000 people into the sea every day. Most other coastal cities throughout the region dump even higher quantities of sewage, although it’s treated slightly. These treated wastewater facilities might help reduce solids and nitrogen, but nothing stops a prion in sewage.
“Kaliningrad is a medieval city that pours its waste into the gutter,” said Aleksandra Korolyova, a Kaliningrad-based activist with the Russian group Ekozashchita (Environmental Protection). “It’s just a black torrent that pours out of the pipe directly into the lagoon, and the lagoon is part of the sea.”
Poland’s waste compounds the problem. It accounts for 30 percent of emissions into the Baltic Sea. Sweden and Russia each dump in about 12 percent. The sewage pollution impacts everything between the point of dumping and the sea, including codfish, herring, shellfish and the people who eat them. The streams, rivers and groundwater are likely contaminated forever with sewage and prions, not to mention other toxins and carcinogens.
The entire region is swimming in sewage. Prion pollution from sewage also impacts the beaches and the people who play on them. It contaminates clothing and shoes. It contaminates boats of all sizes. Prions don’t need the help of mismanaged sewage to find pathways back to humans. Toxins in mismanaged sewage are contributing to cancer, endocrine system disruption and many other health issues.
Leaders in Alzheimer’s disease, Finland and Sweden dump their sewage into rivers and lakes, which is contaminating waterways and communities, while exposing families to various toxins and pathogens, including Pandora-like prions. This mismanagement is exposing millions of people, wildlife and livestock to the prion epidemic.
Towns and cities across the European Union are required to collect and treat their urban wastewater under the Urban Wastewater Treatment Directive. In 2006, the European Commission took Finland and Sweden to the European Court of Justice for failing to ensure proper treatment of urban wastewater in a significant number of towns and cities. In 2010, Finland and Sweden again were cited for failing to install the proper infrastructure for collecting and treating urban wastewater. Unfortunately, sewage treatment of any sort doesn’t stop a prion, but sewage mismanagement is obviously an issue in the region and in these two countries, which are afflicted with abnormally high rates of neurodegenerative disorders.
“Finland and Sweden are rightly concerned about the state of the Baltic Sea. They can help make it healthier by improving their own wastewater treatment,” said EU Environment Commissioner Stavros Dimas.
Cruise ships in the region also dump their sewage in the Baltic Sea. Last year, 261 international cruise ships pulled to port just in Helsinki. It’s legal to discharge untreated wastewater in international waters, as long as it is done at least twelve kilometers from the nearest coast. Finnish cruise lines stopped dumping wastewater in the Baltic in 2007.
In addition, Baltic countries generate about 3.5 million tons of dry sewage sludge every year. In the past, it was dumped in a variety of ways, including at sea. Sludge dumped into the Baltic has polluted the sea forever. Additional wastewater and sewage runoff just adds fuel to the fire.
Adding to the insanity, sewage sludge has been used in agriculture throughout the Baltic Sea Region for at least 40 years. It is used as a fertilizer. Unfortunately, crops and grass uptake prions and become infectious. The Netherlands, Belgium and Switzerland have forbidden or restricted the agricultural disposal of sewage sludge. They incinerate it. Finland and Norway, however, dump sludge on green areas of all sorts.
Europe alone spends more than 2.2 billion euros every year getting rid of sewage sludge. About 60 percent of it goes toward agriculture and landscaping applications. Disposing of it safely would cost billions more. The same goes for every nation on the planet. It’s better to protect corporate profits than people or the planet?
Sewage mismanagement is not limited to the Baltic Sea region. Virtually every coastal city in the world dumps sewage in the sea. Boston, for example, dumps about 500 million gallons of sewage off the coast of Cape Cod every day. Many more cities dump it in rivers, streams and on crops. Cattle graze on it. Thanks to the creative marketing of biosolids, kids play on it and gardeners are using this death dust at home.
People, wildlife, marine life and livestock around the world are caught in the crossfire. Failure to address these issues will cost billions of lives. The body count is already in the millions.
Whales Are Bioindicators Of Neurological Disease In Iceland
Iceland is a different case study in sewage management and diet. It’s obviously not impacted by the problems of the Baltic Sea, but it could still serve as a canary in a coal mine.
First of all, Iceland is smart enough to not put sewage sludge on its farmlands. It disposes of it in landfills. Unfortunately, if these landfills aren’t capped and lined like a nuclear waste dump, water will leach through the prion pathogens and contaminate groundwater.
The main sources of sewage in Iceland are residential areas, fish processing, livestock, slaughtering, dairy industries, aquaculture, textile industries, tanning plants and some heavy industries. Both the industrial and domestic sewage is usually disposed through the same drainage into the sea. The majority of sewage in Iceland is released untreated into the ocean where it impacts coastal waters, fish, shellfish and waterfowl. It also could be impacting whales and dolphins. Even if the sewage were treated, the deadly prions would survive the process.
Hafnarfjordur, for example, is located on the coast just southwest of Reykjavik on the southwest coast of Iceland. The city of about 21,000 people has four sewage outlets that discharge directly into the bay where people fish, boat, golf and swim. Any sewage that escapes the bay is then driven up the western coast by the currents of the North Atlantic. Pardon my French, but it’s the equivalent of pissing into the wind. The damage done by sewage to Iceland’s coastal waters are well documented. Do you think that it’s contributing to the nation’s high rate of Alzheimer’s deaths? Do you think it’s a good idea to dump sewage where you eat and drink?
Neurological Disease In Whales
Whale meat also is a likely pathway that could be contributing to high rates of neurological disease in Nordic and Baltic nations. Whales and dolphins are vulnerable to prion disease. At least one dolphin has been found with prion disease, but testing is severely lacking. Since dietary factors are clearly linked to neurological disease, studying the correlation between diet and disease can help illuminate the prion problem.
As stated before, Alzheimer’s (and other diseases on the prion spectrum) are extremely high in the region. Pioneering research found that Parkinson’s patients on the Faroe Islands have consumed about six times more whale meat and blubber than their neighbors who don’t have the disease.
Maria Skaalum Petersen is working to shed light on the connection between sick seas, sick whales and the people who consume them. Petersen is a researcher in the Department of Occupational and Public Health in the Faroe Islands health service. One of her projects has included a comparison of the prevalence of Parkinson’s disease (part of the TSE spectrum) in the Nordic countries.
She found that Parkinson’s disease is twice as prevalent on the Faroe Islands as in Norway and other Nordic countries. A traditional diet on the Faroe Islands typically includes pilot whale meat.
Predators, including some whales, are high on the food chain. Animals that consume predators are consuming the toxic build-up from every animal ever consumed. Therefore, these predators (and the people who consume them) often serve as an excellent indicator of the health of an entire ecosystem, including prion contamination.
Not all whales are created equal, though. The whale meat sold in Norway and Iceland is mostly from minke whales, a species that has a diet much lower in the food chain. This means they do not accumulate as many contaminants or prions as pilot whales. This means that the risks associated with whale meat is slightly less for the people in Norway. However, as you recall from the chart above, Norway still has a fairly high rate of neurological disease.
“The Faroe Islanders eat pilot whales, while Norwegians eat baleen whales. Pilot whales have teeth and primarily eat fish and squid, which puts them higher on the food chain,” Petersen says.
Baleen whales feed by filtering zooplankton and krill into their mouths as they swim. Eating lower on the food chain lowers their prion exposure, but it doesn’t make them immune to the prion problem. More importantly, this study indicates that there is prion accumulation in whales–some more than others. It indicates that prions are in our oceans and onward upstream. It indicates that prions are in our food and water supplies and reckless sewage management is contributing to the problem. It reminds us of the hazards associated with wastewater reuse, sewage sludge disposal and biosolids in our communities and watersheds.
Prions have already left Pandora’s box. It’s easy to spot areas of mismanagement. If we fail to connect the dots and react soon enough, it won’t matter. What can we learn from the Baltic Sea, Iceland, the Faroe Islands and whales? Prions are building up in the environment and in mammals now. Eating infected mammals spreads the disease up the food chain.
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Withholding Alzheimer’s Diagnosis Raises Concerns Over Malpractice, Collusion
More than 50 million people around the world have a terminal diagnosis of Alzheimer’s disease. Alzheimer’s and related neurological disease is rapidly becoming the leading cause of death around the globe. Thanks to a new report from the Alzheimer’s Association, those numbers grew exploded overnight.
The Alzheimer’s Association’s new report raises many scathing questions over ethics, treatment, malpractice, denial of care and mismanagement. The report found that just 45 percent of Medicare patients diagnosed with Alzheimer’s disease were informed of the diagnosis by their physician. By contrast, more than 90 percent of Medicare patients with cancer said they were informed by their doctor.
“What we found is really shocking,” says Beth Kallmyer, vice president of constituent services for the Alzheimer’s Association. “This is reminiscent of what happened in the 1960s and 1970s with cancer. But that’s changed now, and it really needs to change for Alzheimer’s disease as well.”
For years, the association received complaints from family members who say that doctors are reluctant to reveal an Alzheimer’s diagnosis, Kallmyer says. So the association decided to investigate by studying medical records and survey results from Medicare recipients.
To make sure that Alzheimer’s patients hadn’t simply forgotten, the group also looked at Medicare survey responses from family members and other caregivers. The result wasn’t much better: Just 53 percent said a doctor told them of the patient’s diagnosis.
The report also found that patients with advanced Alzheimer’s disease were more likely to receive the diagnosis than people in the early stages of the disease. Doctors often blame the time constraints of short appointments. Or, it could be part of a culture of cost containment, risk management and denial in care.
“It’s difficult to disclose a diagnosis of a fatal brain disease in just a few minutes,” said Keith Fargo, director of scientific programs at the Alzheimer’s Association. “It’s also hard for doctors to tell patients they have a fatal disease that can’t be cured. And doctors often fear the emotional reaction an Alzheimer’s diagnosis can cause. By the time people are diagnosed with Alzheimer’s disease they are already losing cognitive functions. That’s distressing. Not knowing why is confusing and frightening.”
Alzheimer’s Disease Diagnosis Not A Precise Science
Let’s refresh our memories on some critical facts about Alzheimer’s disease diagnoses. It’s far from precise. In fact, it’s impossible to diagnose Alzheimer’s disease without an autopsy (which doesn’t happen). After the process of elimination, doctors can only guess at which neurological disease to diagnose.
This is where it gets complicated. Unfortunately, Alzheimer’s disease is a member of an aggressive family of neurodegenerative diseases known asTransmissible Spongiform Encephalopathy(TSE). Again, the operative word is “transmissible.” Related diseases are killing wildlife and livestock. Unfortunately, the TSE epidemic represents an environmental nightmare. The outbreak threatens every mammal on Earth.
TSEs include Alzheimer’s disease, Creutzfeldt-Jakob disease, Huntington’s disease, and Parkinson’s disease. TSEs also include mad cow disease and chronic wasting disease in deer. Few, if any, mammals are immune. There is no cure and there is no species barrier.
TSEs are caused by a deadly proteins called prions (PREE-on). Prion disease is unstoppable and the pathogen spreads through bodily fluids and cell tissue. Prions linger in the environment, homes, hospitals, nursing homes, dental offices, restaurants and many other places infinitely. They migrate, mutate, multiply and kill with unparalleled efficiency. Prions defy all attempts at sterilization and inactivation. Victims of the disease can spread the disease even further via bodily fluids and cell tissue. Victims often are contagious long before they appear sick.
What does all of this background have to do with an Alzheimer’s disease diagnosis? Doctors can’t tell the difference between any of the human forms of prion disease. They basically read the wind, flip a coin and diagnose the patient’s symptoms as Alzheimer’s disease, Creutzfeldt-Jakob disease (CJD) or Parkinson’s disease. It would better serve the public to stop the name game and use the most common term–prion disease. All patients should trigger the same protocol in care and safeguards to the public.
“The (human) brain diseases caused by prions includes Alzheimer’s, Parkinson’s, Huntington’s, amyotrophic lateral sclerosis (Lou Gehrig’s disease), and other disorders known as frontotemporal dementias,” said Nobel Laureate Stanley Prusiner, who earned a Nobel Prize in Physiology in 1997 for discovering deadly prions.
Safeguard Protocols For Prion Disease Not Uniform
Unfortunately, the protocol for patient care is vastly different for CJD and related prion diseases. That’s a mistake. CJD is handled with the respect that a prion disease demands. Alzheimer’s disease is not. Hospitals, doctors and even coroners handle CJD with a wide berth, if at all. Unfortunately, they fail to warn family members. Meanwhile, no one is talking about the transmissible aspect of Alzheimer’s disease. That’s another mistake.
With this background in mind, let’s get back to the issue of doctors withholding information about patients. What does this pattern of activity suggest:
The size of the epidemic is much larger than estimates, which means that it will spread even faster. The latest estimates claim about 45 million people globally who are battling Alzheimer’s disease today. It’s been commonly estimated that two-thirds of cases are undiagnosed. This new report suggests that it could be much higher. Alzheimer’s was already the fifth-highest cause of death in the world. If more than half of the cases are going undiagnosed, neurological disease could already top the list.
Ethical issues abound. Withholding information, even if only suspicions, can delay treatment and humane care. It also can put caregivers in harms way with a sense of false security (given the transmissibility of the disease and the precautions that should be given to caregivers).
Malpractice issues abound. This knife cuts both ways. Doctors could be withholding opinions to avoid malpractice issues over misdiagnosis. Plus, the protocols for patient care and caregiver precautions are vastly different between Alzheimer’s disease and CJD. Since the diseases are handled differently, malpractice issues over misdiagnosis face doctors and hospitals.
Many health experts have predicted that the global surge in dementia cases will bankrupt nations, states and insurance carriers that can’t dodge the bullet. What type of industry guidance is shaping this wave of denial in care? Are insurance companies urging doctors and hospitals to avoid the dicey waters of prion disease? Do insurance companies hope to avoid the murky waters and severe costs associated with patient care? Are governments trying to dilute the true size of the largest health threat on the planet today?
Isn’t it time to offer safeguards and guidance to caregivers and family members to minimize the risk of exposure to deadly prions from patients fighting Alzheimer’s disease, CJD, Huntington’s, ALS and Parkinson’s diseases?
Given the size and speed of this epidemic, isn’t it time to reconsider what we are doing with the infectious waste from millions of infected people around the world? Is it really a good idea to reuse their wastewater and sewage sludge (biosolids)? Is it a good idea to dump their sewage on our crops, golf courses, playgrounds and lawns or in our rivers and oceans? Hospitals dispose of anything that might have possibly been infected by prions. Sterilization is impossible. Therefore, prions in sewage cannot be stopped with wishful thinking. Prions migrate, mutate and multiply. Prions are an environmental nightmare that make radiation look like candy.
As you can see, the new report from the Alzheimer’s Association sparks more questions than it answers. We seek allies in pursuit of truth and reforms. Please join us.
There might not be a difference between Alzheimer’s disease and the more-feared Creutzfeldt-Jakob disease (CJD) at all. That is very bad news for millions of caregivers and community members around the world.
Alzheimer’s disease and CJD are both members of an aggressive family of neurodegenerative diseases known asTransmissible Spongiform Encephalopathy (TSE). The operative word is “transmissible.”
CJD is without question the most infectious and aggressive form of prion disease in humans. Unfortunately, doctors cannot distinguish between the two diseases and neither can anyone else. Meanwhile, the protocol for patient care and hazardous waste is vastly different. I argue that the protocols should be identical for many reasons.
Scenario One: When a person with CJD is diagnosed, they are walking disasters because they contaminate everything in their path. Everything in their wake is exposed. Hospitals will take great precautions when handling a confirmed CJD patient. All exposed equipment becomes disposable. Unfortunately, they don’t pass along this advice to family members and caregivers. These patients proceed to contaminate their homes, communities, sewers and beyond.
Scenario Two: When a person with CJD is misdiagnosed with Alzheimer’s disease, caregivers and the community at large put their guard down because transmission has never been discussed with Alzheimer’s disease. The patient continues to visit restaurants and dentists. They donate blood. They can donate organs in many countries. They discharge sewage. The contamination spreads.
Scenario Three: If there is no difference between CJD and Alzheimer’s disease, we are making many mistakes on many levels. I argue that a deadly prion is a deadly prion and there is no difference between any prion disease in any mammal. Any difference in symptoms and speed of decline is due to the mutation of the prion involved, diet and genetics of the victim. Therefore, it’s time to reform many protocols to safeguard health facilities, communities, caregivers and entire watersheds.
To make a complex story short, prion disease is unstoppable and the pathogen spreads through bodily fluids and cell tissue. Prions linger in the environment, homes, hospitals, nursing homes, dental offices and many other places infinitely. They migrate, mutate and multiply with unparalleled efficiency. Prions defy all attempts at sterilization and inactivation. People and animals with prion disease represent an environmental nightmare.
Prions mutate as they move through the food chain, which puts animals at the top of the food chain, including humans, at greater risk. In fact, prions discharged from humans are much more voracious than those discharged from other animals. As such, we are recycling the pathogen that causes Alzheimer’s right back into our food and water via biosolids and reused water. We’re dumping these killer proteins on parks, golf courses, ski areas and school grounds.
Although there are many causes of Alzheimer’s disease and other forms of prion diseases, the epidemic is being mismanaged on many levels around the globe. This mismanagement is contributing to the epidemic.
There is definitely a connection between sewage and prion diseases. Deadly prions are in the blood, urine, feces, saliva and tissue of millions of infected people and animals. Sewage treatment cannot stop the prions discharged by these people every day, which means that deadly prions survive the sewage treatment process. They are pumped and dumped on golf courses and farms through reclaimed water and biosolids (sludge). This foolish practice also could be contributing to the spread of prion disease in wild and farmed deer–known as chronic wasting disease. It also could contribute to prion disease in livestock–known as mad cow disease.
New research confirms that plants exposed to prions become contaminated and deadly carriers of the disease. Crops grown in sewage sludge and irrigation water that flows over these fields becomes contaminated. So does surface water runoff after rains and snows. That runoff carries deadly prions into streams, rivers, ponds, lakes and oceans. prions now threaten our drinking waters and much much more thanks to the surface applications of biosolids and reclaimed sewage water.
Adding to the insanity, deadly prions are destined for more and more taps around the world through reclaimed water and toilet to tap programs. By recycling disease with sludge and wastewater, the prion pathogen is making its way into drinking water and into food products. We have created Pandora’s Lunchbox with our sewage disposal practices alone. It’s time to reform these practices before the contamination spreads even further. Read more in the book and please advocate for the reform of sewage disposal practices to help stop the Alzheimer’s epidemic.