Science for Patients: Dr. Byron Hyde (of Nightingale Research Foundation) 2016 interview with the Dutch ME/cfs Association
Introduction, history, and definition of M.E. (also known as Enteroviral Encephalomyelitis)
In this lecture (10:21), Dr. Byron Hyde covers the following questions/topics:
My name is Byron Hyde. I am a doctor in Canada. But before I became a doctor, I worked as a geophysical engineer at the Mining Inspectorate. After that, I became a chemist and worked in transplantation biochemistry. Then I moved to the Children's Hospital in Toronto, where I was the chief technician of the electron microscopy unit. Only then did I become a doctor. This gives a pretty good picture of who I am.
How did you get involved in M.E. (also known as Enteroviral Encephalomyelitis) ?
By chance. I became involved with M.E. in a special way. I had a very good friend, and he and his wife were both doctors. She was the admissions physician at McMaster University, and he was a general practitioner. They had rafted down the Ottawa River and came to see me the next day. They asked if I would join them for a party at a hospital in Montreal. I didn't go. And in a sense, that was my good fortune.
At that party, there were doctors with their spouses and a few nurses. Three days later, my friend called me to tell me that almost all twenty doctors at this party had gotten food poisoning in the hospital. They all had headaches and stomach problems. And I said: “You’ll get better, of course, but when did this actually start?” He said: “Just the last few days.” I said: “Well, if it were food poisoning, you would have gotten sick immediately, but it took two or three days for you to develop all the symptoms?” He said: “No, three or four days.”
About a week later, he called me again and said, “We know now what we have, we have M.E.” And I said, “What in heaven’s name is M.E.?” I had never heard that term before. He said, “Myalgic encephalomyelitis. It is an encephalopathy, a brain infection.” And I said, “Remarkable, I have never heard of this.”
After that, I more or less forgot about it until a week later when I got a patient who was also a doctor, and who had been on a house call to a newborn twin and a two-year-old child. The woman had been addicted to heroin, but had been clean for a few years now. He couldn't get an ambulance to take the children to the hospital, so he drove them himself. Meanwhile, the mother and the three children were coughing constantly. They admitted the children to the hospital, as well as the mother. The diagnosis was Coxsackie - an enterovirus infection. At the time, I knew very little about Coxsackie or enteroviruses.
Three days after he had taken those sick children and their mother to the hospital, who all had pneumonia caused by this Coxsackie virus, he fell ill himself. We admitted him to the Civic Hospital. He was diagnosed with a brain tumor.
But the first thing we discovered was that it was not a brain tumor, but that the entire left hemisphere, particularly the posterior frontal lobe and the temporal lobe, was so dark due to inflammation that we initially thought it was a brain tumor.
It turned out to be a viral infection. So we knew that the incubation period was three days and that we were dealing with an enterovirus.
M.E. can be simply defined by two things: It is an enteroviral infection with an incubation period of 3-5 days; that is one. If you cannot detect enterovirus at the start and also do not find it in the gastric mucosa of chronic patients, then there is no enteroviral infection.
The second diagnostic criterion for M.E. is diagnosable inflammation of the brain. This involves microvascular inflammation. This can be detected using a brain SPECT with suitable software or a brain PET with suitable software.
SPECT is much less expensive and emits no radiation of any significance. When using a CT scan, for example, you receive an enormous dose of gamma radiation. With SPECT and PET, there is virtually no radiation. The radiation involved in a PET scan is of a type that gives you a million times more radiation from the sun just by walking outside than from a PET scan. So, radiation is not a problem with SPECT or PET.
So, you need two things to define M.E., and it is very simple. The first is identifying an enterovirus right at the start, which is very difficult because no one expects it, or, in the case of chronic disease, checking the gastric mucosa for the capsid protein. This is quite simple using a gastric biopsy, which many patients undergo anyway, because they have stomach problems right at the onset of the disease that often become chronic. The second is demonstrating via brain SPECT's that the brain regions are affected.
Definition of M.E. (also known as Enteroviral Encephalomyelitis)
The original definition of M.E. is quite surprising, because it originated during a polio epidemic. Probably the third known polio epidemic. It took place in Sweden in 1895, in the Stockholm region.
During this polio epidemic, something else also happened. Ivar Wickman, a twenty-three-year-old doctor who described the epidemic, said: “There is something unusual going on. Some of these patients do not die, and do not become paralyzed, but they do have pain all over their bodies.” And he called it a neuralgic encephalopathy, which closely resembles myalgic encephalomyelitis.
But the real historical breakthrough came in the first massive epidemic of paralytic polio. There had never been a major polio epidemic. There had never been a polio epidemic before the one in Sweden that I just mentioned.
But in 1905, 1,300 patients in the Stockholm area and 800 people in the Oslo area (Norway) fell ill in the same week, and they died or became paralyzed by four or five different forms of polio. Ivar Wickman described them as follows: he distinguished spinal polio, which usually paralyzed the legs, but sometimes the legs and the arms.
Then bulbar polio, which affected the lower brainstem. And because the ability to breathe was affected, almost all patients died, usually within hours or days.
Then there was Landry's polio, the name was changed later. You became increasingly paralyzed, and a large number of these patients also died.
But the fourth form of polio, which he called Superior polio or Medin's polio (after his boss), was the most interesting because all these forms of polio occurred simultaneously.
The other two forms of polio that he also described, because he visited the patients and examined them, were polio in which people picked up the virus but did not become ill, but did transmit that poliovirus to other people. And the second was polio in which patients had the symptoms of the early stage of polio, the same as the early stage of M.E., and recovered within a week or two.
And that was the moment the first major epidemic of M.E. occurred. Simultaneously with the polio epidemic.
On Wednesday, October 5th, the eighty-third broadcast of Science for Patients, initiated by the ME/cfs Association and featuring Dr. Byron Hyde, was available to watch with the theme:
M.E. (also known as Enteroviral Encephalomyelitis) symptoms
In this lecture (10:08), Dr. Byron Hyde covers the following questions/topics:
The core symptoms of M.E. (also known as Enteroviral Encephalomyelitis) in 1905
The core symptoms of the 1905 epidemic described in Ivar Wickman's 1907 (1913 English Translation) book - which I am reading because they are so interesting - are transient paralysis or weakness, sometimes with shaking or tremors, and pain syndromes and malaise, including headaches. Nausea and stomach problems are his third category, the fourth is sore muscles like with the flu, and the fifth is cognitive or psychological disorders.
The sixth category is a low body temperature and reduced sensitivity to cold and heat, transient aphasia - difficulty finding words - and bladder complaints, particularly what we would now describe as interstitial cystitis or painful sex. And this is a question that few doctors ask women with M.E.: what is your sex life like? They don't; they are afraid to ask. And many of these women have interstitial cystitis, which is not an infection, but a viral injury to the bladder wall.
The others are hypotonia, loss of elasticity in the muscles and blood vessels; paresthesia, or abnormal, burning, or stinging sensations; and sweating.
And this is probably the best description of any contemporary M.E. patient. Not all patients have all these symptoms, but they can occur in one or in several patients. It is therefore significant that Wickman described it this way as early as 1907 in his book.
Shifts in insight in M.E. (also known as Enteroviral Encephalomyelitis) and CFS
The shifts in understanding of M.E. and CFS are of great importance to patients' health. The first major shift occurred during the 1932 epidemic at the County General Hospital in Los Angeles. At that time, a battle was raging between the doctor who wrote about it and said it was polio, and the head of the Health Institute in Washington who said it was not polio. And they fought over this like cat and dog.
But the biggest battle at the time was fought by the insurance industry, which, if it turned out that this disease was caused by the immunization they had given doctors and nurses during that epidemic in 1932, would ultimately have to pay millions of dollars. In 1938, a settlement was reached for the 192 people who had fallen ill during that M.E. epidemic. The amount of the settlement was so large that two houses in Hollywood could be bought with it today. So, translated to today's value, it concerns a settlement of about five million dollars. And from that moment on, the insurance industry has caused the biggest shift in the interpretation of M.E. and CFS.
And this happened again during the epidemic in the 1950's at the Royal Free Hospital in London. At that time, a doctor conducted research on these patients for half a day for his doctorate in Oxford and then wrote his dissertation in another half day. Within one or two days of the publication of this dissertation, it appeared on the front page of Time Magazine in the United States, something that had never happened before. He called the disease 'mass hysteria'. And that is probably the most tragic thing that has happened to M.E. and CFS patients: that article on the front page of Time Magazine.
Doctors read Time Magazine back then. They sometimes wanted something to laugh about, and this was mass hysteria at its finest. And this was the biggest and worst shift in understanding regarding M.E.. Especially because most doctors, if they even knew the name, thought it was mass hysteria. It is impossible to publish a dissertation as an unknown writer and have it appear on the front page of Time Magazine just two days later, unless the insurance industry is behind it.
Exclusion disorders and their importance
The exclusion diseases of chronic fatigue syndrome, even more so than those of M.E., are really important. For example, over the past two days I have seen seven patients for the ME/CFS Association. The very first patient had neither M.E. nor CFS, but Ehlers-Danlos syndrome, a remarkable and nasty disease.
There are currently at least 11 variants of Ehlers-Danlos. With some of them, death at birth occurs. Other variants of Ehlers-Danlos occur in patients between the ages of 16 and 22, often immediately after a viral infection or immunization. Sometimes it appears out of the blue, but usually it follows a viral infection.
Ehlers-Danlos is very easy to diagnose. You only have to ask these patients to stick out their tongue and try to touch their nose with it. Most people cannot do that. Most adults cannot do that anyway. Some children can, but adults cannot. Another way is to grab your little finger and be able to twist it straight up without hurting yourself, which I cannot do. Or to grab your thumb and be able to push it backwards towards your forearm. Or extend your arms; instead of a sort of angle like with most people, the arm really bends backwards at the elbow. Or if you look at the knuckles, they are larger because their fingers keep bending in the wrong direction. So this is Ehlers-Danlos syndrome.
It is a fascinating abnormality of the collagen fibers in the body, which give the body, muscles, and blood vessels their elasticity and longevity. And these are affected. You can view them under an electron microscope, and they are called collagen flowers. That is just one of approximately 20 misdiagnoses in CFS, and they are all fascinating.
Other diseases confused with M.E. (also known as Enteroviral Encephalomyelitis)
Are there other diseases that you can easily confuse with M.E. or CFS? Yes, unfortunately there are many. One of the first things you can do quite easily is realize that the primary symptom of M.E. and CFS patients is the deregulation of the central nervous system. This literally causes all the symptoms of these patients.
Now, one of the easiest things is clotting disorders. Many people have a clotting disorder, which increases with age. This can be easily detected by testing for venous and arterial clotting factors. And if the result is positive, you know that these people will regularly develop small clots in their brains that will gradually begin to deregulate the central nervous system.
Another common misdiagnosis is rheumatism and arthritis in those variants where the central nervous system is disrupted. And once again, you only need to test for ANA, which is quite easy to do, or draw up a rheumatology profile, which you can do cheaply, and then you have the correct diagnosis. But there are many others.
If you look at the medications that many patients take, for example. The side effects of many medications can cause typical M.E. and CFS symptoms. You have to look at the side effects of all medications. Some patients take prescription medications without knowing the side effects. Side effects are a very big problem.
And I think these are just three of the things that can be easily looked at or checked, and you could go on like this for a while.
CFS, M.E. (also known as Enteroviral Encephalomyelitis) & SEID
In this lecture (9:40), Dr. Byron Hyde covers the following questions/topics:
What is Chronic Fatigue Syndrome (CFS) ?
CFS is an idiotic definition orchestrated by a doctor, Stephen Straus, who for a long time managed the funds of the American National Institutes of Health. He provided 15 million dollars for research into CFS, which he claimed was caused by the Epstein-Barr virus. Now, every good doctor knows that the Epstein-Barr virus has an incubation period of 40 days and cannot cause an epidemic. He described the epidemic at Lake Tahoe in Nevada, on the border with California, in August 1984, which broke out among a group of high school basketball students traveling together by bus. Literally all definitions of CFS stem from that. And it was a misdiagnosis, because if you really look at the symptoms from 1984 that he mentioned, they are Epstein-Barr-like symptoms. He did not examine the patients who became ill.
The city council members of Lake Tahoe, a tourist town, were so angry that they told their representative that if the NIH and the CDC (Centers for Disease Control) continued to investigate these patients, he would never win another seat. So the investigation was stopped. No one paid any attention to these people anymore, and so the disease was invented based on chronic Epstein-Barr, epidemic Epstein-Barr, which does not exist. And this has caused enormous problems, because they then tried to twist the epidemic to make it seem true, but that doesn't work. That is like trying to turn a rat into a racehorse. You cannot start with a wrong premise and then try to straighten it out.
Why seperate M.E. (also known as Enteroviral Encephalomyelitis) from the term ME/CFS ?
CFS is a misdiagnosis. It can be all kinds of diseases. These people do not have an enterovirus infection. They may have a brain disorder, but that can also have completely different causes, including psychiatric illnesses. And this makes it very difficult for M.E. patients and CFS patients who receive an incorrect diagnosis. Because too many doctors now believe that we are dealing with a psychiatric disorder, while in reality, it is a misdiagnosis of one of many other diseases. So it is very important to look at the tests.
Today, for example, I had a little girl of 11 who had been sick for two years. She had been to as many as six or seven doctors in the past two years, and what they had done was very interesting. They performed the same tests, a whole series of 30 to 40 tests, 10 to 15 times in those two years. They did not examine her, but only repeated the same mistakes. And yet they said: the mother has Munchausen syndrome by proxy. This implies that the mother is the person who has a psychiatric disorder and is pretending that her daughter is sick.
But what she probably had was a simple streptococcal infection, which resulted in a scarlet fever-like illness that became chronic. There was enough documentation, which they hadn't looked at, to take a throat and nasal swab from the parents and the daughter to test for a chronic streptococcal infection or another bacterial infection. And also to perform a blood test on the child to see if that diagnosis was correct. It might not have been, but the point is that there were enough clues in the examination that they should have followed up on. Nobody saw it. So that is very important, otherwise you start thinking that there is nothing wrong with the child and place the blame on her.
Oh yes, she was admitted to a psychiatric hospital for five months, that poor child, because she wasn't really sick. Of course she was sick. She slept through the entire appointment. Sweet child. Clearly still sick. And certainly not mentally ill.
What is Systemic Exertion Intolerance Disease (SEID) ?
The question is what I think of SEID. It is yet another worthless definition of chronic fatigue syndrome by Straus from 1988, which he said
was the same as M.E., but with a different name. But it isn't.
The most important thing in that SEID definition that I get quite worked up about is that they say you cannot see what is wrong with these patients with a brain scan. Of course you can. If the scan is normal, then they do not have M.E.. If the scan shows no abnormality in the limbic system, an essential part of the brain that is affected in all M.E. patients, then the patient does not have M.E. So to me, it is clear that once again a group of experts who have never seen an M.E. patient are defining the disease.
This also happened with the 1988 definition. Of the 13 doctors involved in that definition, 10 or 11 had never published anything about M.E. or CFS before or after that time. And I do not think that any of those doctors, with the exception of two or three, had ever even seen an M.E. or CFS patient. And yet they were allowed to divide about 30 million dollars in research funds among themselves. I inquired with the NIH accountants about what they actually received the money for: approximately 10 million went to fatigue in alcoholism, 10 million to fatigue in cancer, and 10 million to fatigue in depression.
This was not M.E. (also known as Enteroviral Encephalomyelitis), this was not CFS.
M.E., myalgic encephalopathy or enteroviral encephalomyelitis ?
What is the difference between myalgic encephalomyelitis and those other forms of the disease? First of all, I would like to reiterate that in the 1895 definition, Ivar Wickman was the first to mention, during that polio epidemic, the fact that some of these patients had neuralgic encephalopathy, the precursor to myalgic encephalomyelitis. The term myalgic encephalomyelitis originates from the epidemic in the 1950s at the Royal Free Hospital in London.
And what you must remember is that most of these patients start with severe muscle pain, like with the flu. They feel as if they have been beaten, as if someone has battered them all over their body. It is terrible. But after a period of a year or two, these pains usually go away. They do keep coming back, but they are not chronic, not in the way they were in the first weeks or months. And every patient is different.
Many patients overcome these pain syndromes, but what does not go away are the changes in the brain that cause dysregulation of the central nervous system, which in turn give rise to all the other problems these patients have.
On Wednesday, November 2nd, the eighty-fifth broadcast of Wetenschap voor Patiënten, initiated by the ME/cfs Association and featuring Dr. Byron Hyde, can be viewed with the theme:
M.E. (also known as Enteroviral Encephalomyelitis), viruses and bacteria
In this lecture (9:15), Dr. Byron Hyde covers the following questions/topics:
Epstein Barr Virus (EBV) & Borrelia
Let us now discuss all viral and bacterial infections, and other microbial infections associated with M.E. and CFS. First, Epstein-Barr. We have already covered that in detail. Epstein-Barr has an incubation period of 40 days. An infectious disease can only cause an epidemic if this is less than five or six days. Otherwise, it does not happen.
The other is Borrelia. Borrelia is a serious threat. Borrelia started in Scotland and then came to America, to the town of Lyme in Connecticut. The deer in that area became infected, and from there, Borrelia has spread across the entire US and two parts of Canada over the past 50 years. It causes a chronic disease.
Unfortunately, there is a laboratory in California that consistently tests positive for Borrelia. But Borrelia shows the same pattern as a standard streptococcal infection. In many patients, the test will give a positive result for streptococci, which they may have had ten or twenty years earlier but are no longer bothered by. Yet the result looks like Borrelia. Borrelia is real and causes serious problems, but we do not yet know enough to treat it. One of my patients from last week clearly had Borrelia. He had only been treated for two weeks and then they said they could do nothing more. Treating Borrelia properly is a problem. It is a real, serious disease and it closely resembles CFS.
Other Human Herpes Viruses (e.g. HHV-6A)
The various herpesviruses, and I don't know how many there are - at least 6 and perhaps as many as 12 - can cause chronic infections in some people. In theory, they could cause CFS. But again, I have never seen that in the 30 years that I have been conducting research on these patients.
Why is it so difficult to define M.E. (also known as Enteroviral Encephalomyelitis) ?
The fact that it is difficult to understand viral infections and their causes is mainly related to identifying the virus in acute and chronic disease. I can best illustrate this by discussing the problems with polio.
The poliovirus, paralytic polio, was first described very well by Dr. Ivar Wickman in 1907, as mentioned earlier. In December 1907, two German scientists succeeded in grinding a boy's spinal cord and passing it through a ceramic filter, and injecting this filtrate into guinea pigs, rabbits, mice, and two monkeys. None of the animals became ill except for one of the monkeys. That monkey became paralyzed.
They saw that as definitive proof that they had isolated the poliovirus and transmitted it to a human-like animal, and could therefore truly cause polio. And they were right. That was in December 1907. What happened afterward: people became increasingly afraid because the epidemics were growing. There was an epidemic in Brooklyn, New York. I don't remember exactly how many people got sick, but you have to think of about twenty thousand. They were unable to isolate the viruses, even though these people were dying.
It wasn't until the 1932 epidemic, a mixed epidemic of polio and M.E. at the County General Hospital in Los Angeles, that this happened. They took serum from what they thought were recovered patients and injected it into the 192 doctors and nurses so that they would not contract polio. But what they did get was M E.. They did not realize at the time that they had actually conducted the first human trials with M.E. by injecting a virus into people that caused M.E..
The first polio vaccination was introduced in 1935. However, it was based on the incorrect theory that polio was caused by only one virus. They injected this into about a hundred people, and a number of them died. Why? Because it was 1935, and the first poliovirus had not been discovered until 1907, and doctors up until 1935 believed that there was only one poliovirus that caused serious illness or death.
Around 1940, two Australian doctors said: “This isn't right, we haven't found another serious poliovirus like this.” But the American doctors didn't believe them. It wasn't until the 1950s that Salk, with the help of a lot of money, was able to demonstrate that there were three types of poliovirus that caused epidemic poliomyelitis, paralytic polio, which can be fatal or cause disfigurement.
Together with a large group of great scientists from Concordia University, he designed a fantastic vaccine containing all three viruses. It put an end to paralytic polio in the United States almost immediately. Very soon after that, shortly after Sabin appeared in 1949 - or was it '59? - they were able to put a stop to global polio. But they made a mistake. This year, in the Netherlands, Germany, Denmark, Canada, and the US, many children who had been vaccinated became paralyzed again. I believe that 7,000 people in China also contracted a paralytic disease around the time the Olympic Games were held in Shanghai.
What was it? Because it wasn't polio 1, 2, or 3. It was the other enteroviruses. There are at least four or five other enteroviruses that are now causing paralytic diseases. I suspect that M.E. could be completely stopped if all enteroviruses had been included in that vaccination. What I believe is going to happen in the next ten years is that there will be increasingly more cases of paralytic polio-like diseases caused by enteroviruses rearing their heads again. Doctors will receive more and more funding, and they will develop a new polio vaccine containing not only polio 1, 2, and 3, but all enteroviruses. And when that happens, I think M.E. can be stopped. We are not there yet, but it will happen.
On Wednesday, November 16th, the eighty-sixth broadcast of Science for Patients, initiated by the ME/cfs Association and featuring Dr. Byron Hyde, was available to watch with the theme:
M.E. (also known as Enteroviral Encephalomyelitis) and the role of enteroviruses
In this lecture (3:03), Dr. Byron Hyde covers the following questions/topics:
What is an enterovirus? An enterovirus is a virus with an incubation period of 3-5 days. At least a hundred are now known. They are all
identical; they differ in only about 1% of the capsid protein. The capsid protein is just one part of the virus. So, polio is an enterovirus.
Coxsackie, ECHO, and the numbered enteroviruses are all enteroviruses. And they all have one or two peculiarities.
First of all, they mutate constantly. They mutate outside the body, and once they have infected the body, they continue to mutate. They keep changing. The immune system therefore has a tremendous amount of trouble destroying that virus. And this has caused major problems with polio, and it causes major problems with all enteroviruses.
Which enteroviruses play a role in M.E. (also known as Enteroviral Encephalomyelitis) ?
Which enteroviruses cause M.E. or play a role? That is an impossible question to answer. The reason for this is very simple. We know that
Coxsackie, especially Coxsackie B, can cause M.E.. We know that the ECHO viruses can cause M.E.. And we know that a few numbered enteroviruses can cause M.E.. But because they are so difficult to detect unless the patient dies, it is almost impossible to know what is going on.
The fact that we sometimes discover what is going on is due to the detection system that most children's hospitals have. Specifically, they look for rising titers in acute infections in children.
Unfortunately, adults are not believed; they wait until they become chronically ill. Doctors say: “You just have a cold, you’ll get better in a few days, don’t worry.” So they are never tested. But they do test the children who come in and could easily die for these viruses. So we learn more from children than from adults.
On Wednesday, November 30, the eighty-seventh broadcast of Science for Patients , initiated by the ME/cfs Association and featuring Dr. Byron Hyde, was available to watch with the theme:
M.E. (also known as Enteroviral Encephalomyelitis) and poliomyelitis
In this lecture (8:16), Dr. Byron Hyde covers the following questions/topics:
How are M E. (also known as Enteroviral Encephalomyelitis) and polio intertwined ?
How are M E. and polio intertwined? This is extremely interesting. Up until the introduction of Salk and Sabin's great polio vaccination, every major polio epidemic from 1895, and especially from the Stockholm epidemic of 1905, was well documented. Most were well documented, particularly the larger epidemics. In an epidemic, multiple diseases were involved simultaneously, and M.E. always occurred at the same time as the polio epidemics.
Unfortunately, or perhaps fortunately, once they were able to cure polio - well, truly curing it once you had the disease was not possible - when the disease came to an end with Salk and Sabin's vaccination, there were, of course, no more polio epidemics. But there were M.E. epidemics, and there were many of them. They started in 1932, but they still occur today.
M.E. (also known as Enteroviral Encephalomyelitis) after the spresd of poliomyelitis epidemics
What happened to M.E. after the end of the polio epidemics? It actually really started in 1934, when nearly a hundred thousand people between San Francisco and the Mexican border fell ill. Most contracted M.E., but about five percent got polio. This was concentrated at the County General Hospital in Los Angeles, where the doctors, as I mentioned earlier, were vaccinated with the serum of cured M.E. patients. In effect, they gave these doctors M.E..
Since then, there have been several epidemics. Like the major epidemic that followed, in Akureyri. I went there and examined thirty patients. That was in 1946, 1947, and 1948; it lasted about three years. It was very interesting, because only about five percent of the patients actually had polio. And something very remarkable happened. Three children, all three younger than twelve - I believe between eight and twelve - developed M.E. and also Parkinson's disease. Children do not get this disease. But those three children all died of Parkinson's disease within two years of developing M.E..
Something else amazing happened during that epidemic, and I say amazing from a scientific point of view, because it was of course terrible, since all these patients were laughed at. When I examined thirty patients in the late eighties, early nineties, it was still wrongly claimed that these were not M.E. patients, because everyone said it was hysteria.
Many of them still had problems walking, thinking, really big problems. One of those patients was the mayor of the capital of Iceland. He still carried the stigma of the disease. When you realize that these people were considered hysterical, it is very tragic; they were very sick.
And then something amazing happened regarding the knowledge about M.E.. Three years after the end of that epidemic, there was a major polio epidemic in Iceland. And everywhere, people were getting sick; they were dying or becoming paralyzed by polio. But in the entire area around Akureyri in northern Iceland, where the same group of viruses, enteroviruses, was prevalent, no one contracted polio. So whatever it was, the people who had contracted M.E. were now immune to polio. Thus, the virus that had caused M.E. in Akureyri was so closely related to polio that it protected these people.
Recent outbreaks of M.E. (also known as Enteroviral Encephalomyelitis)
The next question is to talk about the recent M.E. epidemics. This is extremely interesting. These occurred simultaneously throughout North America. It began, and this is the best known, in Lake Tahoe, where a girls' basketball team traveling by bus contracted the disease. It subsequently spread to their teachers and the residents of Lake Tahoe. During that same period, the North Carolina Symphony Orchestra in North Carolina, a touring orchestra that traveled through the state by bus, also fell ill with that same M.E.. The same thing happened in Toronto, Montreal, and Ottawa. We did not know about those other epidemics until two to three years later.
But they all started around the same time: late July, August, September. It began to decline in October. And this is very typical of enteroviruses. Enteroviruses and polioviruses peak in the Northern Hemisphere in July, August, September, and October. In the Southern Hemisphere, it is the other way around. So, in these countries, a disease with two phases occurred, just like polio.
As I mentioned earlier, following criticism of the NIH, the investigation into the Lake Tahoe epidemic was halted. However, the Ontario government did conduct an investigation, and we were able to demonstrate not only that this epidemic was caused by an enterovirus, but also that Epstein-Barr virus was almost non-existent at that time. But in the following few months of this epidemic, the enterovirus changed. It spread via two or three different types of enteroviruses. Was this because the enterovirus changed, or did it constantly mutate into subtypes that are considered distinct groups of enteroviruses? We do not know.
It is also fascinating that this epidemic occurred simultaneously throughout North America. In the cases we knew of, the incubation period was the same. And in Canada and Scotland, it was identified as belonging to the same group of viruses. That epidemic moved to Scotland and England the following year, and enteroviruses were found there as well. So we know for certain that it was an enteroviral infection.
Friday, December 16th, the eighty-eighth broadcast of Science for Patients, initiated by the ME/cfs Association and featuring Dr. Byron Hyde, was available to watch with the theme:
Clinical practice and hope for the future
In this lecture (8:41), Dr. Byron Hyde covers the following questions/topics:
The different possibilities in clinical practice
What are the various options in clinical practice for approaching the treatment and research of M.E. and CFS patients? First of all, doctors must understand that they are dealing with a serious chronic illness. And it is not psychiatric. So that is one thing.
But the second point is that doctors in the Netherlands, Canada, and the US simply do not get paid enough by the government or insurance companies to really dedicate time to it. I have seen seven patients in the past two days. Yesterday I started at eight in the morning and worked until six in the evening, and in that time I only had six patients. That is ten hours, with a 15-minute lunch break. Ten hours just to briefly examine six patients. Doctors are underpaid. Whether they spend five minutes on those patients or three hours, the insurance pays the same amount. So doctors are not going to spend time on it.
What one must realize regarding chronically ill patients is that the government receives no tax money from them. A working person generates between ten and fifty thousand euros per year for the government, whereas a chronically ill patient costs them ten to twenty thousand euros per year. Wouldn't it be best, then, to set up a system to properly examine these patients? General practitioners and internists are not capable of doing this well. Until we know more about the disease, we need at least one central clinic in every country. Preferably more, but at least one where you can conduct a thorough examination of the various aspects of this disease over a period of several days. You cannot diagnose and treat these patients in five minutes or in an hour. Because we understand so little about it, you must conduct a very thorough examination of chronically ill patients. And this requires a health system that no country in the world currently has.
Then the next question: is there really no hope for M.E. and CFS patients? The answer is yes. For of the seven patients I have seen over the last two days, at least six had a completely different medical history. With proper investigation, many of these issues are treatable. These are not just enteroviral dysregulations of the central nervous system. They also involve chronic infections. Such as something as simple as Epstein-Barr. Most people, in fact almost everyone, gets Epstein-Barr once in their lifetime. If you get it as a child, you don't really get sick. If you get it as a teenager, you often don't even have to miss a day of school.
After puberty, it becomes a problem. We have had patients, women in their thirties who were pregnant, who contracted Epstein-Barr for the first time and died. So, the older you are, the worse it is with this viral infection. There is no vaccine against Epstein-Barr, and it is very easy to test young people to see if they have had it. It would be an easy vaccine to administer if it existed. But no one has even thought about developing one, because it is not taken very seriously.
This is just one thing. For example, doctors generally think that the Epstein-Barr patient has chronic fatigue syndrome. In England, they call it glandular fever. It has different names everywhere. But they do a blood test, and that shows whether you have an early or a late infection with the virus, and that gives a picture. But this picture is often wrong.
If someone has chronic Epstein-Barr, a throat rinse is sufficient. You have the patient gargle with plain water - and spit into a glass - and then you examine that sputum for enteroviruses. Then you only have to say: you have chronic Epstein-Barr and you will get better. If this does not happen within six months, it can take two years. But it will almost never be longer. So don't worry anymore, don't do any further tests, you will get better. But you must perform the throat rinse to find live viruses that indicate whether someone really has a chronic Epstein-Barr virus infection. Very easy to do and very cheap.
CFS, M.E. (also known as Enteroviral Encephalomyelitis) and psychiatry
I would like to briefly discuss CFS, M.E., and psychiatry, and what is actually going on here. First of all, what happens is that doctors cannot afford to spend time examining M.E. and CFS patients because it is complex and difficult. And then, very quickly, after patients have seen one or two doctors, they say: “Look, I can’t afford this anymore; I’m referring you to a psychiatrist, and he can listen to you for an hour.”
Thus, adults in particular are constantly referred to psychiatrists who say: “Oh, you just think you are sick.” And they prescribe antipsychotic medication. In most cases, this causes massive weight gain in these patients. Many of these antipsychotics cause weight gain; others cause liver disorders, which in turn can lead to CFS. This is a problem because general practitioners and internists are not paid to conduct thorough examinations of these patients – they do not even know how. Patients are referred to a psychiatrist, and this can have very harmful consequences.
What happens when children get sick? Like the child I saw today, who spent five months in a psychiatric hospital. The mother was said to have Munchausen syndrome by proxy. This means that the child is not sick at all, but the mother is just pretending. These children are admitted to the hospital, taken away from their parents, and sometimes die.
Why do they die? Because they are unintentionally mistreated, contract an infection in the hospital, and are not treated as seriously chronically ill patients. Because doctors do not have the time and are not paid for it. This brings us back to the system. A central system is needed, certainly in smaller countries, which could set this up quite easily for chronically ill children and adolescents.
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