Science for Patients: Professor Leonard Jason (Psychologist) 2014 interview with the Dutch ME/cfs Association
My name is Lenny Jason and I am a professor of psychology at DePaul University in Chicago.
I’m also the director of the Center for Community Research. I’ve been at DePaul University for the past 39 years.
How did you get involved in M.E. (also known as Enteroviral Encephalomyelitis) ?
I initially got involved in M.E. (also known as Enteroviral Encephalomyelitis) Research in the early nineteen nineties. At that time people
were talking about this disease as the ‘yuppie flu’.
What I found was that the CDC had done
some prevalence research, called the four-city study. And they had estimated that fewer
than 20,000 people had this illness.
I was very skeptical of that research, and when I looked at their methodology as a research psychologist, it was significantly flawed.
For example, they had referred people into their study who had been identified by doctors as having M.E.. And yet as we know lots of physicians don’t even think this illness exists.
So how can they refer such people into their catchment prevalence study? So basically looking at that research I was skeptical, realizing the CDC at that time was getting several thousand phone calls every month about severe fatigue and possibly M.E.. And I decided that I would try to work with some colleagues on a prevalence epidemiology study with adults.
What kind of research did you do regarding M.E. (also known as Enteroviral Encephalomyelitis) ?
After looking at the research literature, we found that basically there were better ways of
estimating prevalence than through ascertainment methods by physicians. So myself, Judy Richman and several other colleagues wrote a NIH grant. We were able to get funding to actually sample 26,000 people. And in that large sample, a community-based sample, we tried to find out how many people might have M.E..
What we found was that the rates were much higher than what the CDC had estimated. So by the mid-late 1990's we were able to
make projections that approximately a million people had this illness.
That was one of the first large studies our group did. But it took us ten years to work on that basic epidemiology, from writing grants, getting it funded, doing the research, to publishing it. So it is a long term commitment to do this type of research.
What are the most important discoveries you made?
I think one of the important things that we learned was that not less than a million people
had this illness, rather than the 20,000 which were estimated. So it wasn’t really a rare
disorder, but the ‘yuppie flu’ was really a myth.
The people we found having this illness did
not tend to be yuppies. In fact we found people who had lower incomes had more likely to
have this illness. So folks belonging to minorities, colored people, were more likely to have this illness.
Those were important findings, both the prevalence as well as the numbers. And
that led us ultimately to make statements about this illness that we really needed to have
more public resources devoted to it. In part because it wasn’t a rare disorder, just affecting a bunch of middle-class individuals who were possibly lingering or doing something else. This was a serious illness, affecting a lot of people, many of them not having resources and suffering other disadvantages besides this illness.
What research are you into currently?
In terms of the work we’re doing currently, certainly we thought that in terms of
epidemiology it was important to find out the prevalence rates for adults. We’re now in a
way trying to do some community-based prevalence studies with young people, with
pediatric M.E..
And that work we’re going to be doing for the next five years. We’re also going to be doing research on college students who have mononucleosis and will test them when
they’re healthy.
Looking at what happens when they develop mono, and trying to follow them as to which ones recover and which ones don’t. So with Ben Katz at Children’s Hospital in Chicago I’ll be doing this work on those two very large projects over the next five years.
Is your research psychological or also physiological?
The current research that we’re doing implies that we want to get a look at all the different
parameters. In terms of what are risk factors for those who end up getting this illness versus those who don’t. And particularly looking at them before they get ill. That’s a very important factor.
Some research that we’re just publishing for example looked at mononucleosis in
youth.
We basically found that there were no psychological factors predicting as to which
ones would get more severe M.E. in the future.
What we found was that the severity of the
illness they got actually was the only thing that was a significant predictor. So that’s an
important factor suggesting that there might be more biological factors that involve both the initiation of this illness as well of its maintenance.
Prof. Leonard Jason. Broadcast September 2th 2014
What would you call this disease and why?
The British started calling this illness M.E. many years ago and there’s been a regression back to CFS in 1988 through the CDC in the USA.
(This would assume, they mean the same thing, THEY DO NOT)
I think there’s been a movement to change that, and actually some people are calling it "ME/CFS" as a transition term.
But I ultimately think this illness should be called M.E., for Myalgic Encephalomyelitis.
I think that’s the legitimate name for this illness. In a sense it got hijacked thirty years ago and it needs to revert back to that original name.
Does the name CFS trivialize this illness and why?
The name CFS is a terrible term with which the CDC came up many years ago, in 1988. If you
think about someone who is coughing and you would say he suffers from ‘chronic cough
syndrome’, people would say ‘who cares, everybody coughs. It just isn’t a big thing’.
However if we call it bronchitis or emphysema, people would say ‘that really sounds as a
significant issue’.
So the name counts. And you can’t use a name for an illness that trivializes a condition.
Chronic Fatigue Syndrome is one of those names that ultimately has to change.
Our group actually did some research looking at attributions.
We called it M.E. and we gave a case description.
Then we gave it the name CFS and after that we attached the term Florence Nightingale Disease.
We did the same case study and we found that names do make attributions and they do significantly make a difference in how one thinks about those cases. We did this research with medical interns as well as psychology undergraduates and we found, attributions undergo changes, based on the terms that are used to describe cases.
What is wrong with the CDC-criteria?
The CDC-criteria are often considered to be the same as the Fukuda 1994-criteria. They were
assembled by consensus of a group of people.
I think consensus based case definitions
contain problems, specifically with four symptoms required out of eight possible ones.
You can miss some of the cardinal symptoms of this illness.
For example, three cardinal symptoms are post-exertional malaise, memory and concentration problems and
unrefreshing sleep.
However if a person has four other symptoms and not these three cardinal symptoms, he can still get the diagnosis CFS.
That’s the major problem with an illness category when the cardinal features of the illness are not required to be diagnosed.
What criteria do you use in your current research?
Our group actually looks at several criteria and tries to have people fill out a questionnaire.
And then we actually look at how a person meets the 1994 Fukuda-criteria, how they meet the new 2011 ICC-criteria for M.E., as well as the Canadian ME/CFS criteria.
So we try to compare and contrast those three. But I must say, there’s limitations with all three. And consensus based efforts are probably not really the best way for us of characterizing this
illness.
What’s the difference between your primer of 2013 and the ICC/ICP of 2011-2012?
The IACFS/ME put out a primer that uses the Canadian Consensus Criteria of 2003.
We found that there had been a good amount of research that at least had suggested that this particular case definition selected a smaller group of patients that had more functional impairment.
So we decided to focus our primer around the case definition that had been around for ten years. It most importantly specified the core cardinal symptoms of post-exertional malaise, memory- and concentration problems as well as sleep difficulties.
So that’s why we decided to kind of write a primer and focus it around a case definition that we thought was an improvement of the Fukuda 1994-criteria.
In fact there was another case definition, the ICC, that did come out in 2011 and 2012, but there hasn’t been as much research done at that particular case definition.
So we decided to use the one that had a little bit more been used by the research community.
Web lecture by Prof. Leonard Jason, broadcast on September 9, 2014
What do you think is the cause of M.E. (also known as Enteroviral Encephalomyelitis) ?
There are many different opinions regarding the cause of M.E.. For some people, it certainly started with a viral infection, sometimes with glandular fever. Others had some kind of accident after which they contracted the disease. Still others suffered some kind of poisoning from their environment or were exposed to mold.
There are actually quite a few different things that can lead to this disease. It is entirely possible that these people have a genetic predisposition to M.E.. Just as with other chronic diseases, it has been discovered that there can be a genetic predisposition. But in my opinion, it certainly seems at the moment that there are a number of triggers that cause some people to develop M.E..
Where does the stigma surrounding M.E. (also known as Enteroviral Encephalomyelitis) come from?
There is a terrible stigma attached to people with M.E.. Many people wonder why this is the case.
Our group at DePaul University has developed a scale to measure stigmas, so that we can get some idea of what is going on. After all, we live in a society where more value is placed on energy, stamina, and perseverance than on anything else. It is probably even more important than money.
Unbelievable, but true. And if you don't have that energy, you are probably discriminated against more than any other group in our society. Because energy makes the American Dream possible. People who are tired are looked upon as if they are somehow falling short.
That is because everyone gets tired sometimes. Sometimes it is caused by running a marathon, and sometimes by having multiple jobs.
The ordinary fatigue that most people experience probably goes away when they go on vacation. Or when they are not stressed by too many responsibilities. Most people think about fatigue completely differently than patients with M.E..
When an M.E. patient says that he has no energy or stamina, other people say: “Geez, I have a lot of things to do and I just keep going, why can't you do that?” And even worse: “You don't look sick.”
The combination of these various value judgments leads to an incredibly negative societal attitude towards patients, making them almost the lepers of the 21st century. As it probably was for people with that disease up to two hundred years ago.
Do you diagnose M.E. (also known as Enteroviral Encephalomyelitis) by exclusion? What is included?
I think it is important to diagnose M.E. not only by exclusion, but also by inclusion. We must understand that someone has the main symptoms of this disease, such as deterioration after exertion. These must be present; without them, the disease does not exist.
And yet, some questionnaires state: “Do you experience any symptoms, including fatigue, 24 hours after exertion?” These questionnaires cause problems, and I will tell you why.
This is because many people do not push themselves that far, precisely because they are so ill. As a result, they do not have to experience deterioration after exertion, because they have learned to hold back in a certain way. They are in a kind of energy bubble, a shell, which I will talk about another time. So, in a sense, it is possible that some people would indeed experience deterioration after exertion if they were forced to do something. If they had to exert themselves or if they had to do the daily things that most people do. But because they do not do those things, they do not experience that deterioration either. So if they are asked if they have it, they will answer no. But the reality is that they do, if they were to do daily things.
What I want to say is that we must be careful in formulating the questions correctly to gain insight into these various complex symptoms. And if you put someone on an exercise bike and really challenge them, you will find deterioration after exertion. Remarkably, not after one day, but after two days. Because after one day they are still able to force themselves to look good and maintain good oxygen exchange. But on the second day after the test, you see the deterioration after exertion. So, regarding exertion, challenges, and self-report questionnaires, one must be very careful about how the questions are phrased. So that we identify the people who truly have the main symptoms.
Naturally, you do not want people in your research or practice who have another disease. So, if they have M.S., if they have fatigue due to cancer, or if they have other diseases that cause fatigue as a result of medication, then you want to exclude those people. If they have psychological reasons for their fatigue, such as a depressive disorder with melancholic features, then you actually want to exclude them as well.
You want to find people with M.E., exclusively M.E. and not something else. To receive an M.E. diagnosis, I think you need to have three main symptoms: deterioration after exertion, neurocognitive problems such as memory and concentration issues, and unrefreshing sleep. In my view, those symptoms must be present. I am not saying that there cannot be other symptoms, such as immunological, neuroendocrine, and autonomic. But I believe the first three I mentioned are of crucial importance.
What is the DePaul Symptoms Questionnaire? What is it aimed at?
Over the past fifteen years, our group at DePaul University has been working on ways to use self-report questionnaires to assess a patient's symptoms. Our latest work is called the 'DePaul Symptom Questionnaire'. We have placed this in a database called 'red camp', and it can now be downloaded by anyone around the world. This is essentially a list of 54 questions that, in our opinion, measures the current symptoms of many patients who have these types of diseases.
We have rated each symptom on frequency and severity on a five-point scale. We have conducted some basic research on this questionnaire to ensure that it is reliable and suitable. We are quite confident that this scale can be used in clinical practice and for research. And there are a number of researchers from different continents currently using our scale.
Can the DePaul symptoms questionnaire be used by everyone?
This questionnaire, the DePaul symptoms questionnaire, can truly be used by anyone. It can be administered to patients in a clinic, and researchers can give it to participants in studies where patients can fill it out. What is great about the questionnaire is that we have built in an algorithm that looks for a pattern in the answers. After someone has completed this questionnaire, we can see which criteria they fall under. This allows us to use the questionnaire to specifically look at how many necessary criteria people meet with their symptoms.
Web lecture by Prof. Leonard Jason, broadcast September 23, 2014
1. There is confusion between M.E. (also known as Enteroviral Encephalomyelitis) and (major) depression. How can you distinguish between them?
(I don't believe its possible to confuse a brain and spinal cord infection by an enterovirus with major depressive disorder)
Our group has spent a number of years trying to map out the differences between depression and M.E..
In short: if you ask someone with major depression, “What would you do if you were better tomorrow?”, they would answer: “I don't know.”
If you ask the same question of someone suffering from M.E., they would give you a long list of all the things they would like to do, but have been unable to do because they are too ill.
Self-blame is therefore an important factor here. People with M.E. do not have such negative feelings about themselves. People with major depression do have these kinds of negative feelings.
So self-blame, expectations for the future, and also exertion play a role. People with major depression often feel better after exertion. We know that people with M.E. often experience deterioration after exertion.
There are therefore clear differences between these two illnesses, and they must be kept separate.
2. Are there biological differences between depressive disorder and M.E. (also known as Enteroviral Encephalomyelitis) ?
A number of studies have actually found physical, biological differences between people with depression and people with M.E..
Cortisol levels, for example, are generally reduced in people with M.E. and elevated in people with major depression.
If you simply ask the right questions, such as through self-reports, one of our doctoral students was able to distinguish the two groups from each other with 100% accuracy. If you do it properly.
That is why designing questionnaires is so important. Because if you ask the right questions, you can distinguish people with these two different illnesses really well. This is of crucial importance in the research that we and others conduct.
The best research looks at things from multiple perspectives, using multiple disciplines. For example, you want to keep self-reports brief so that you can determine which symptoms someone has.
Then you want to conduct a physical examination in order to exclude other illnesses. If someone has lupus or M.S., you want to exclude them.
But you also want to perform tests. For example, you might have someone perform an exercise test using a maximal or submaximal test. From this, in principle, certain genetic markers might emerge that could distinguish patients from healthy people.
So, in a sense, we want the best sources for our data, so that we can comprehensively assess both patients' own reports and the medical aspects. This allows us to better characterize this illness.
If you miss one aspect, you miss an important tool for truly understanding these people.
3. Are other psychiatric disorders confused with M.E. (also known as Enteroviral Encephalomyelitis) ?
Besides depression, with which M.E. can be confused—and which, in my opinion, it often is—there are other psychiatric disorders with which this can also happen.
For example, a somatization disorder is sometimes confused with M.E..
There are also anxiety disorders that are sometimes confused with M.E..
What I am trying to say, therefore, is that when you go to a general practitioner for a medical examination, there really needs to be a structured psychiatric interview to make sure that someone is not suffering from certain disorders. Because you want to distinguish these people from one another.
Unfortunately, general practitioners are not trained to make such a psychiatric assessment. As a result, they often do not know whether someone is suffering from depression. Or from a somatization disorder.
So you really want to carry out a comprehensive psychiatric and medical examination before you can determine whether someone has M.E., because you want to exclude other causes of their illness.
4. What role does depression play in M.E. (also known as Enteroviral Encephalomyelitis), and how can it be treated?
With every chronic illness, the percentage of patients with depression is increased. Why should that not also be the case for people with M.E.?
Not all M.E. patients will be depressed, but some will be.
Just think about it. You have an illness that many people do not understand, that many people do not believe in. The condition is extremely debilitating, and you are frequently questioned about it. All of these are reasons to become discouraged.
So it can be discouraging, and at times you can feel almost hopeless. That happens.
I think we need to understand that this also happens to people with other kinds of chronic illness.
The depression that arises with any chronic illness basically begins with the people surrounding the sick person responding to what they see. The support network surrounding someone needs to be examined.
If there are situations where parents do not believe their child is ill, or nurses do not believe that someone is ill, and there is discouragement and skepticism, then that becomes a deadly influence.
That must first be removed before you begin treating someone's sense of helplessness, or their despair at being afflicted by an illness that society understands so little about.
If someone has M.E., I think it is important that you treat all of their symptoms. If, for example, they experience pain, certain medications can be used for that. If someone develops other types of symptoms, different medications should be considered.
What the patient needs is the best possible team working on the different aspects. That could include a nutritionist or a physiotherapist.
The patient may need different disciplines. We need to enable patients to assemble a treatment team to meet their needs, and those needs often change.
That is the key to success: employing both pharmacological and non-pharmacological disciplines to arrive at a treatment program tailored to the individual.
5. Similarities between M.E. (also known as Enteroviral Encephalomyelitis) and M.S., Parkinson's and Alzheimer's
There has not yet been much research comparing M.E. with many other illnesses. I think that kind of research is necessary because it will help us understand something about the similarities and differences.
Regarding M.S., my colleague Matthew Sorensen and I are just putting the finishing touches on a publication examining proteins in the brain in M.S..
For example, we have discovered that individuals with M.E. tend to have similarly low levels of a cerebral protein called BDNF as people with M.S.. This is one of the principal biological markers of M.S..
And what produces that BDNF protein? The myelin sheath, which allows electrical impulses to travel to the brain.
So, once again, it is possible that there are some similarities between M.S. and M.E. that we do not yet know very much about.
But I think that in the future we will conduct more comparative biological research to understand this better.
Web lecture by Prof. Leonard Jason, broadcast October 7, 2014
1. What role does a psychologist play in treating M.E. (also known as Enteroviral Encephalomyelitis) ?
Psychologists and mental-health professionals play an important role in the treatment of every patient with a chronic illness, including M.E.
What we in mental healthcare must do first is take the patient's experience seriously. We need to listen to them and become their ally. And really try to understand what they have been through, in order to build an empathetic relationship.
That is so important because patients with M.E., in particular, have been victimized, often by the medical profession and others. This relationship is therefore especially important in letting that person know that we believe them. And that we care about them.
I think that without that basic trust, you can make very little difference, and that as a mental-health professional you can actually be harmful to the patient if you do not build a relationship of trust.
2. How can we prevent the psychological approach from becoming dominant?
Patients with M.E. need the best possible team involving multiple disciplines in order to have a good chance of receiving high-quality care.
You cannot simply send a person with M.E. to a psychologist or psychiatrist, because they probably need much more additional care to help them deal with the many different symptoms of this illness.
Imagine a doctor saying to someone with cancer: “Just go to the psychologist or psychiatrist; that's all you need.”
That cancer patient would become extremely upset. And that is exactly what is happening to M.E. patients around the world.
3. What treatments do you consider useful for M.E. (also known as Enteroviral Encephalomyelitis) ?
There are various treatments for M.E. I am going to talk a little more about lifestyle because I am a psychologist. But in the medical field there are also many good treatments for things such as pain and sleep problems.
Regarding lifestyle, patients often feel that they may have only 10 or 20 percent of the energy they had previously. So their battery, their store of vital energy, has deteriorated.
But they often have obligations requiring them to do twice as much work as they have the energy for. And that is a problem.
So how can we adjust their lifestyle so that patients do not do too much, exhausting themselves and potentially deteriorating after exertion?
Learning to stay within the energy envelope, as we call it, is, in my opinion, essential to ensure that the battery does not become further depleted. That is what I think we need to do.
Many patients are like a yo-yo. When they are very ill, they do little and are very careful. But when they feel a little better, they do too much.
Then they crash. That is the yo-yo effect.
Anything we can do to prevent that is, in my opinion, of crucial importance in the lifestyle of patients with M.E..
4. What are the advantages and disadvantages of CBT and GET?
Cognitive behavioral therapy is used for all kinds of illnesses, with some very positive results.
Why is it so controversial among patients with M.E. (also known as Enteroviral Encephalomyelitis) ?
That is because it is often offered as the only treatment.
If, for example, someone with epilepsy who needs medication were told:
“We're only going to do cognitive behavioral therapy,” that patient would become furious.
But that does happen to M.E. patients.
What they need goes far beyond psychological aspects. They have physical problems. They have physical dysfunctions. They have abnormalities of biological origin.
They need the best medical care and treatment.
Instead, they receive only a very limited approach. That is why they are upset: because they are not receiving the appropriate medical care.
They receive inadequate care that does not meet their needs.
5. What is pacing, what is enveloping, and what are the differences?
A number of people have talked about pacing. There have been some developments that Ellen Goudsmit in Great Britain has written about.
Here in the United States, we use the term “energy envelope.”
I think there are more similarities than differences between these approaches.
Basically, they both say that we need to help patients manage their energy in a very carefully calibrated way.
For example, if someone has a battery that is only 20 or 30 percent full, whereas they once had a battery at 100 percent, they now have only a fraction of their previous energy.
How do you do all the things in life with such a small amount of available energy?
What we are essentially saying is that pacing, or staying within the energy envelope, means trying to remain within the energy that is available and not exceeding your limits or pushing yourself.
Because if someone does that, I think they will crash more frequently and their symptoms will worsen after exertion, which ultimately leads to more oxidative stress in the brain.
And I think that has some very negative consequences for the patient.
So pacing or the energy envelope are appropriate lifestyle changes that can lead to improvement.
Not a cure, but improvement for many patients.
Web lecture by Prof. Leonard Jason, broadcast October 21, 2014
1. What role does the nervous system play in M.E. (also known as Enteroviral Encephalomyelitis) ?
I think there is evidence that the nervous system does not function normally in patients with this illness. The work of Alan Light and Kathy Light at the University of Utah suggests that when patients undergo a submaximal exercise test, a number of types of genetic indicators can be observed.
So I do indeed think that patients can have significant problems in parts of the nervous system. And I believe these play a direct role in this particular illness.
I think that in most patients we see sympathetic dominance over the parasympathetic system. In a sense, their body is “revved up.” We often see the symptom that we call “wired.” That is a very common description from patients. They are exhausted, but their minds are still extremely active.
So, in a sense, their nervous system is too active, and I think anything we can do to calm this system down is good.
It is very interesting that many medications that patients sometimes try, such as Klonopin and similar drugs, seem to help calm the system down.
So I think many patients have an overactive nervous system.
2. What role does the circulation play in M.E.?
Many patients with M.E. have a lower blood volume than healthy people.
When they stand up, “orthostatic stress” occurs, which means they often do not have enough blood flow to the brain. A person may sometimes feel as though they are going to faint or they may feel unwell.
That is because they are not getting enough blood to their brain when they are standing.
So there appear to be major problems with circulation in patients, and orthostatic intolerance is one manifestation of this.
3. How do you measure PEM (post-exertional malaise)?
Post-exertional malaise can be measured by asking the right questions in self-reports and by means of exercise tests, such as a bicycle test lasting ten or eleven minutes, or through twenty minutes of submaximal exertion.
So it is important to look both at what people say and at what people do in a testing situation, and to combine these in order to understand the complex syndrome called “post-exertional malaise.”
4. What role do infections play in M.E. (also known as Enteroviral Encephalomyelitis) ?
Many patients develop their first symptoms after a viral infection.
That therefore seems quite likely, because in some samples as many as 70% report having had a viral infection.
The best way for us to understand the role of these viral infections is through longitudinal prospective studies.
For example, in Chicago we are working with Ben Katz from Children's Northwestern. We are going to follow thousands of healthy students over a period of time to see who develops mononucleosis, who among them recovers, and who does not.
That is the best way for us to determine whether a specific virus or other factors might be involved in the cause as well as the persistence of an illness.
5. Are there markers for M.E. (also known as Enteroviral Encephalomyelitis) ?
Markers for M.E.... We can say that we have begun to identify some, and I think there will be many others in the future.
For example, cortisol problems. It appears that people who have a reduced cortisol increase in the morning could provide a very good indicator.
A number of publications have discussed natural killer cell activity.
But there may also be subgroups of individuals who have other types of markers, and I hope that the future will enable us to discover many more of them and that we will be able to have them processed through laboratories.
But again, you will only find markers if you have the same types of patients under different circumstances, and that is why the case definition is so important.
We need to arrive at the same group of people under different circumstances if we are ever going to find the same consistent markers.
That is so important because if you do not find consistent biological markers, it becomes very easy for people to assume that it is a psychogenic, psychological illness rather than a biological illness.
Web lecture by Prof. Leonard Jason, broadcast November 4, 2014
1. Is the risk of M.E. (also known as Enteroviral Encephalomyelitis) greater because of gender, race, genes, or occupation?
It has been asked whether M.E. differs in different parts of the world. It began with the myth that M.E. occurred more frequently among yuppies, among people with higher incomes. That myth is not true.
We know that M.E. occurs more frequently among people with lower incomes. That is something important. We have also discovered in the United States that M.E. occurs more frequently among minorities or people of color. We also conducted a study among a group of people in Nigeria, and we discovered that M.E. occurred more frequently there than in the United States.
So we think that M.E. occurs in many different places around the world. We are not certain among which particular groups it occurs more frequently, but in the United States we have definitely found some differences. In particular, people with a lower socioeconomic status are more likely to have this illness.
Whether M.E. is related to race is something that we do not really understand very well. Some of the symptoms of M.E., such as orthostatic intolerance, appear to be different in African Americans than in white people. Whether we will ever definitively understand some of these factors, we do not know.
For example, we have discovered that Latinos in the United States are the population group in which M.E. occurs most frequently. Particularly more among female than male Latinos. That was interesting. We have also discovered that its prevalence among Latinos who are more assimilated into American society differed from those who are not.
Genetically, we think that certain people have a greater predisposition to many chronic illnesses, and M.E. is probably a good example of this. We still need to do a great deal of research on this, but I expect that we really will be able to reach that conclusion.
Whether the likelihood of M.E. is somehow greater in certain groups than in others is something that future research will probably help us understand better.
We are still trying to understand some of the risk factors. The best research that will help us understand some of the genetic markers involves looking at the genes of healthy people and observing who develops M.E. over time and who does not.
Then we can look at certain risk factors, such as environmental and biological factors. That is the way in which we can separate the role of genes from the role of the environment and determine both.
2. What are your findings regarding recovery in long-term studies?
Only a few long-term studies have been conducted on people with M.E.
It appears that those who have had the illness for longer have more cognitive difficulties and more symptoms.
We are currently working on a publication in which we are trying to look at people who have had the illness for a longer period of time.
There really have not been many studies published on this subject, but it appears that the duration of some symptoms increases their severity.
3. What physical impairments do you see in people with M.E. (also known as Enteroviral Encephalomyelitis) ? How severe can they be?
In patients with M.E., you find functional impairments just as severe as in some of the most serious illnesses, including cancer and other severe chronic illnesses.
So these are seriously ill patients. Patients who need the best medical care, but who often receive the worst.
We see that one of the greatest functional problems for patients is the lack of physical capacity to do things. They probably experience their greatest limitations in terms of endurance.
Sometimes there is cognitive confusion, where they cannot remember things or cannot remember why they are doing something. This often makes it extremely difficult for them to work.
There is a physical limitation in being able to do things consistently for a period of time and then continue doing them the following day.
You find many limitations, particularly in tests of deterioration following exertion.
With cognitive challenges, they also appear to have great difficulty thinking, remembering things, or concentrating.
We see neurocognitive and functional deterioration following exertion in patients.
4. What does M.E. cost the individual and society?
Economic analyses have occasionally been conducted, and in America our group has estimated that the costs associated with the problems faced by M.E. patients could be as much as $20 billion per year.
But the patients pay the real price, because they are in a situation where they have one of the most serious illnesses we know of and yet receive the least comprehensive care.
These are people facing some of the most difficult problems imaginable, and yet whether they are genuinely ill is still questioned.
Can you imagine a greater personal price than being so ill while people ask you whether you are really sick?
Government funding is at a very low level. What is needed are places where you can go to be diagnosed and treated. In the United States, these generally do not exist.
If you have cancer or MS, you can go to specialist clinics and receive the best diagnosis and treatment.
For example, I live in Chicago, but there are no appropriately knowledgeable physicians here who treat M.E. patients. And that is a problem.
We need a healthcare system that provides facilities accessible to patients.
At present, those facilities do not exist, nor do they have research funding available to provide us with the necessary data for potential pharmacological treatments.
In both research and service provision, we have very few financial resources available relative to the seriousness of the problem affecting our population.
5. What can be done about the terrible situation in which M.E. (also known as Enteroviral Encephalomyelitis) patients find themselves?
What can be done for M.E. (also known as Enteroviral Encephalomyelitis) patients?
Over the past year, I have been working on a book called Principles of Social Change, which was published by Oxford University Press.
In that book, I seriously try to describe what other social movements have done to bring about change, such as the civil rights movement and other groups such as the women's movement.
Ultimately, it comes down to persistence, to being committed to a cause over a long period of time.
Social coalitions are needed that are committed to exposing the injustices that have occurred. We need to look for a number of other structural problems that we need to address.
We need to organize. We need to become more effective. We need to change the status quo, because it is not working for patients with M.E.
Only if we collectively become involved in action will the situation truly change, just as it has changed and can change for many other groups of seriously ill people.
Look particularly at people with HIV/AIDS, who have truly demonstrated that it is possible to bring about a transformation in the treatment of and attitudes toward people with that illness.
6. What societal support can help?
We need societal support for patients, including their families: parents who protect their children, guardians, spouses, parents who can stand up for the rights of those who are ill.
We need people in education and social services, in the medical profession, and also in the workplace, who can meet the specific needs of patients.
First of all, we all need to recognize that this is a real illness, and we need to be willing to accept some of the patients' limitations.
We must also acknowledge their experiences and work together with them on what they need.
An individualized approach is of crucial importance.
The entire social network needs to be mobilized. That could include someone's brother or sister, father or mother, grandparents, people from their religious community, and healthcare professionals involved in their care.
Everyone needs to work together as a team that makes their life more manageable and provides the patient with the respect and services that give them some quality of life.
Change does not require only M.E. patients, because many of them are too ill. Healthy people also need to become involved, as well as caregivers and partners.
There needs to be a social movement of people who say that they are no longer going to accept this and that they are going to change things.
And that needs to involve thousands of people working together, saying with one voice:
“Things cannot continue the way they are now.”
That will be the beginning of a movement for social change.
That is about to happen not in one country, but in many countries simultaneously.
Web lecture by Prof. Leonard Jason, broadcast November 18, 2014
1. You published research on education about ME/CFS in medical schools in the United States. What were your findings?
We conducted an initial study of medical textbooks. And we discovered that in the textbooks used to educate future physicians, M.E. and CFS were rarely mentioned.
Even worse, when they were mentioned, the information provided was often not up to date.
So the basic educational materials used in our medical schools are seriously inadequate and often inaccurate. That needs to improve.
Recently, we also conducted a study examining what takes place in medical-school classrooms in the United States, and there too we discovered that these subjects are underrepresented. That needs to change.
There needs to be greater attention to educational material about M.E. and the application of research in medical education.
Until that changes, there will not be adequately trained medical professionals capable of providing the care patients need.
Therefore, this must be one of the highest priorities in our work.
2. You also conducted this type of research a number of years ago. Has anything changed since then?
We think that the research we are doing now increasingly makes use of lessons from the past.
For example, we are trying to combine all kinds of work involving computers and experts in artificial intelligence.
That means, for example, that we do not have to rely solely on a consensus approach to arrive at a case definition. We can also use the best scientific capabilities, such as data storage and artificial intelligence, to arrive at case definitions that are more specific, accurate and sensitive.
That is what we are doing at the moment.
We are also looking again from different perspectives at how we can apply multidimensional and complex models, in order to reach empirical conclusions so that we can understand how body systems work—instead of arriving at case definitions or making scientific statements through consensus.
We believe our research has made some difference.
In the 1990's, M.E. was regarded as a relatively rare condition, a kind of “yuppie flu.”
When we presented our data in the late 1990s and early 2000s, the federal government's estimates of the prevalence of M.E. changed, and they are now closer to our estimates of approximately one million people with this illness.
So we succeeded in fighting against the misconception and myth that this was a rare “yuppie flu.”
It is now regarded as a very important illness, rather than a yuppie flu, and many more people suffer from it than we previously thought.
In addition, our research has challenged the term CFS, and we have been advocates in the effort to move toward a different term.
A number of organizations now use both M.E./CFS and M.E., and I think our research has contributed to that shift.
Finally, there is our case-definition research, in which we compare the different case definitions and use empirical methods rather than consensus methods.
This allows us to think about what the most important characteristics are and how they can be measured.
We think we are continuing to make important contributions to the ongoing debate about case definitions.
3. Are medical students at DePaul University/Rosalind Franklin University taught about M.E. (also known as Enteroviral Encephalomyelitis) ?
DePaul University does not have a medical school.
There have been some discussions about a possible form of collaboration with Rosalind Franklin, but this is at an early stage.
We have made some attempts to begin working with people at Rosalind Franklin, but again, at the moment these are preliminary efforts.
We do believe that multidisciplinary efforts are important, so we work with an epigeneticist in Iowa, an immunologist in DePaul's nursing department, an expert in computer technology in DePaul's computer-science department, and people at various universities.
It is crucial for us to think about multidisciplinary research extending across the laboratories of our respective institutions.
That will be the research of the future, whether or not we have our own medical school.
4. What research are you currently conducting?
We are concentrating on several lines of research.
In one of them, we are compiling large databases using our DePaul Symptom Questionnaire.
We believe that with these large databases of patients versus controls, we will be better able to understand which symptoms distinguish these groups from one another.
We are using very sophisticated techniques, as well as artificial intelligence, that are empirical rather than consensus-based. They help us formulate conclusions regarding the case definition.
In addition, we are not interested only in issues arising from our questionnaires. We are also looking at data from physical and biological measurements.
For example, we are currently trying to determine which students develop mononucleosis over time and which do not, and who recovers and who does not.
We take blood samples from all of those students so that we can see what they were like while they were still healthy and what happened after they became ill.
This kind of prospective longitudinal research is of crucial importance.
In addition, we are conducting an epidemiological study of M.E. in children.
That will also provide us with important lessons, allowing us to examine both biological and other aspects so that we gain a better understanding of the risk factors and how many of our young people have this illness.
That is something we will continue working on in the future.
5. Which research do you think can give us hope in the near future?
I think the most important research of the future will take place through multidisciplinary efforts involving people from different disciplines.
That includes computer scientists who, with their mathematical abilities, can help us understand decision trees so that we can determine which symptoms are the best predictors of illness.
Hopefully, we can involve the best scientists, such as top virologists, top epidemiologists and leading experts in the autonomic nervous system.
It means finding genetic experts, environmental specialists and public-health specialists and bringing all of them into these kinds of rich multidisciplinary efforts to understand what we believe is the greatest contemporary medical challenge.
Medicine knows how to heal a broken bone, how to treat people with influenza, and how many different illnesses can be treated.
But these complex illnesses remain a major question mark.
If we gain insights into the mechanisms involved in complex illnesses such as M.E., a new understanding will emerge of what people endure and of how we can better understand the human condition.
This kind of research requires adequate funding.
One day, we will be able to reinterpret various illnesses based on what we learned from M.E. patients.
At the moment, countries face many economic challenges. These are difficult times for both basic researchers and patients.
But I trust and hope that, over time, we will discover that patients with the most complex bodily problems, such as those found in M.E., played a role in some of the greatest medical insights we achieve.
As more scientists and researchers begin to recognize this fundamental fact, I believe we will bring together the best scientists in the world to conduct research into what I consider the most neglected but most important illness facing our world.
Q&A Session 1 - September 5th, 2014
Prof. Leonard Jason - Wetenschap voor Patiënten
1. What do you think of a new name: Viral Mitochondrial Syndrome?
Jason: I think that is an interesting name, but part of the problem is that there are already dozens of possible names.
It would be a good idea to hold an international poll, but my guess is that M.E. would be the clear winner, given the historical issues surrounding it.
Questioner: But that only relates to the brain, and perhaps partly to the spinal cord, and I think the same problem occurs in all sorts of places.
2. You propose going back to the original name M.E. (also known as Enteroviral Encephalomyelitis) ? What justifies using that name?
Jason: There is currently growing evidence of inflammation, and that is part of the name.
Just as the name is important, it is also important that we are able to determine who has this illness.
That is a critical issue for all of us.
3. You have researched the prevalence of M.E. (also known as Enteroviral Encephalomyelitis) ? Are there large percentage differences between countries, continents and climates?
Jason: I like research that is conducted within communities, and I regret that only a handful of such studies have been conducted.
A study in Africa showed rates comparable to those in the United States. That study was conducted in Nigeria.
4. Does it occur more frequently in places where everyone is vaccinated?
Jason: I wish I could answer that question, but, as I said, only a few good epidemiological studies based on community data have been conducted.
Therefore, I have to be cautious about what we know regarding your question.
5. Has any research you know of demonstrated an association between ME/CFS and spinal disorders, such as degenerative disc disease?
The questioner explains that both illnesses developed at around the same time, although the spinal problems probably began earlier.
Jason: The two illnesses could have been related, and it is clear that people with M.E. can also have other illnesses.
Those illnesses may be related to M.E., or they may exist independently.
6. How many patients with severe mononucleosis develop severe M.E. (also known as Enteroviral Encephalomyelitis) ? And what is the risk of developing M.E. (also known as Enteroviral Encephalomyelitis) after mononucleosis?
Jason: Very good question.
We are currently literally recruiting thousands of healthy research participants to follow over a longer period of time, to investigate who develops mononucleosis and recovers and who does not.
Hopefully, I will be able to answer this question better in a few years.
7. You said your interest in M.E. (also known as Enteroviral Encephalomyelitis) began when you saw a very poor CDC report in the early 1990's. Had somebody asked you to comment on that report?
Jason: Yes. Many patients were quite angry about the stigma of the “yuppie flu” and everything associated with it.
We began discussions with several parties in the Chicago area and throughout the United States.
We even received some financial support from the large national M.E./CFS Association of America.
That helped us refine our methods so that we could successfully compete for an NIH grant, which we ultimately received.
8. A doctor once told me that mononucleosis absolutely cannot be a cause of M.E. (also known as Enteroviral Encephalomyelitis) because so many people would test positive for it. What can I tell this doctor?
Jason: We know that many people develop mononucleosis and subsequently recover.
But when we ask M.E. patients about their illness, they say that they first had mononucleosis.
A new study is needed, and that is what we are currently doing.
9. You are currently studying students with Epstein-Barr virus (EBV). How strong is the evidence that EBV can trigger M.E. (also known as Enteroviral Encephalomyelitis) ?
Jason: We are currently recruiting thousands of students in order to determine the relationship between EBV and M.E.
Questioner: Only EBV, or other herpesviruses as well?
Jason: We are studying EBV.
Questioner: Do you ultimately expect to find EBV in the blood of those you are following who currently have mononucleosis and later develop M.E., or somewhere else? And how?
Jason: The EBV study among students is funded by the NIH.
We will have to wait and see what the results are, and that will take another few years.
10. None of the criteria for ME/CFS are suitable. Which criteria would you recommend, and why?
Jason: There are currently several case definitions - for CFS, M.E./CFS and M.E.
Each has different criteria.
More than 20 have been developed, but rarely on the basis of a scientific method.
That is a major problem.
11. Which criterion do you consider most characteristic of M.E. (also known as Enteroviral Encephalomyelitis) ? And do you distinguish between M.E. (also known as Enteroviral Encephalomyelitis) and CFS?
Jason: I certainly distinguish between M.E. and CFS.
The Fukuda criteria are broad and do not require core symptoms such as post-exertional malaise.
M.E., however, requires specific symptoms, such as neurocognitive symptoms and post-exertional malaise.
12. Would it help scientists, doctors and patients if everyone used a single set of criteria?
Jason: Three things are needed:
First, explicit criteria that can be applied - in other words, consensus within the scientific community regarding a specific case definition.
Second, rules determining the threshold at which a symptom is considered problematic.
Third, structured interview schedules to ensure that the necessary information is obtained from an interview.
Case definitions are a set of rules that allow researchers and clinicians to determine who does and does not have the illness.
It is crucial that the scientific community reaches consensus on this issue.
13. Do you think M.E. (also known as Enteroviral Encephalomyelitis) is contagious, or could it be hereditary?
Jason: Some people are genetically at risk when they are exposed to certain viruses or environmental factors.
They have a greater chance of developing M.E.
We have done some work among families of M.E. patients and discovered that certain illnesses occurred within those families.
Questioner: But that genetic predisposition has not yet been established?
Jason: I agree that more research is needed to establish the genetic predisposition to M.E.
I think more good research will be conducted in this area in the future.
Questioner: By the Lights, or by others as well?
Jason: The Lights are doing excellent work. They are true pioneers in this field.
14. Can you name a scientist or group of scientists who could take a leading role and bring large numbers of scientists together to achieve the consensus that is so badly needed?
Jason: I think we need an international movement that brings the patient community and government officials together to bring about change.
Scientists need to provide compelling information for that.
I think we are now at a point where that is possible.
When the questioner says this is encouraging, Jason adds:
Real progress often takes time.
Change can occur gradually and unevenly, and there will also be setbacks along the way.
Patience and long-term commitment are essential elements of movements seeking to bring about social change.
15. Many M.E. (also known as Enteroviral Encephalomyelitis) ? patients with depressive feelings are given antidepressants. Are there treatments other than antidepressants for dealing with depression?
Jason: There are probably several things that could help someone with depression, but I would rather not go into that further without knowing more about that particular person and their symptoms.
16. Should treatment assessment consider not only whether symptoms are present, but also their severity and frequency?
Jason: We certainly believe that it is crucial to use validated measures that indicate the frequency and severity of symptoms.
Someone can have a very severe symptom that occurs so infrequently that it does not create major problems for that person.
Likewise, some symptoms can occur frequently without being severe.
As a result, they may not meet the threshold for a serious problem.
17. How common do you think M.E. (also known as Enteroviral Encephalomyelitis) is?
Jason: My best estimate is that approximately 4–5% of the population is fatigued for six months or longer.
For approximately half of those individuals, there is a clear medical explanation, such as cancer.
If you use the Reeves data from 2007, more than 2% of the population has CFS.
If more specific criteria are used, such as the Canadian criteria, far fewer people have M.E.
18. Could there be similarities between M.E.
(also known as Enteroviral Encephalomyelitis) and the fatigue experienced with cancer?
Jason: One of my colleagues in DePaul's nursing department is currently researching fatigue following cancer treatment.
We need to learn more about this, and I hope he receives funding to continue his research in this area.
Then we may better understand the differences in fatigue between M.E. and cancer.
We now hope to investigate the differences between M.E. and several other illnesses, such as lupus and M.S..
19. Do you know of another condition in which people experience post-exertional malaise (PEM)? Is it unique to M.E. (also known as Enteroviral Encephalomyelitis) ?
Jason: There are other conditions that can cause PEM.
That is why we ask patients about 54 symptoms.
We hope this larger group of symptoms will help us discover clusters of symptoms that reveal the difference between other medical conditions and M.E..
20. Do your colleagues take M.E. (also known as Enteroviral Encephalomyelitis) seriously?
Jason: Yes, my colleagues take M.E. seriously, although I know that many people are still very skeptical.
Those people generally do not associate with me because they know how I feel about this subject.
21. Can you provide a link to the DePaul Questionnaire?
Jason provides the link to the DePaul questionnaire.
Q&A Session 2 - September 26th, 2014
1. In College 53 you say M.E. (also known as Enteroviral Encephalomyelitis) patients have lower cortisol while people with depression have higher cortisol. Can you explain this difference?
Jason: Low cortisol levels lead to an overactive immune response, so this is consistent with what we see in the patient data.
More specifically, these findings can probably be applied to a reduced cortisol awakening response, from waking until half an hour after waking.
2. Have you made further progress in finding medication for M.E. (also known as Enteroviral Encephalomyelitis), apart from painkillers or antidepressants?
Jason: Lily Chu published some results for the FDA last year concerning the effects of various medications.
3. Has your group discovered more biological differences between M.E. (also known as Enteroviral Encephalomyelitis) and depression?
Jason: Our group has found self-reported differences between patients with major depressive disorder and M.E.
For example, M.E. patients experience severe post-exertional malaise (PEM) and other core symptoms.
Patients with major depressive disorder frequently blame themselves, which generally does not occur in M.E.
What is sometimes found among M.E. patients is discouragement.
That can occur when many other people question the legitimacy of their illness.
4. Why do people with depressive disorder have high cortisol levels?
Jason: There are several theories concerning low cortisol levels in M.E. patients.
It probably has something to do with the HPA axis, which is presumably dysregulated.
I think this is centrally controlled, and we would like to better understand why it occurs.
5. You say M.E. (also known as Enteroviral Encephalomyelitis) can be distinguished from depression if the right questions are asked. What questions?
Jason: Yes, it is important to develop reliable and adequate surveys so that we can ask questions that distinguish M.E. from other illnesses.
Our group developed a tool called the DePaul Symptom Questionnaire. We have made it available to researchers around the world.
It is psychometrically sound, and we now have a database of approximately 1,000 people who have completed it.
That is the kind of sample required to conduct the necessary statistical analyses.
Regarding the questions, we now have a detailed questionnaire assessing 54 symptoms.
For every symptom, we try to determine both its severity and frequency, because we believe both are necessary.
6. Is frustration at being unable to do what you want different from depression and lack of self-confidence?
Jason: Yes.
Frustrations and disappointments because you are unable to do everything due to lack of energy can leave you somewhat discouraged.
But that is different from the feelings of someone with depression who does not want to do anything even though they have the energy.
7. Is the DePaul questionnaire being used internationally?
Jason: Yes. Our questionnaire is now being used from Japan to Norway, and even in Iran.
Several large projects are also using it.
If we can encourage researchers to use comparable, reliable tools, we can do a great deal to reduce some of the confusion within this field.
8. What advice would you give pregnant M.E (also known as Enteroviral Encephalomyelitis) patients?
Jason: Some reports indicate that some pregnant women experience fewer symptoms.
The cause could be reduced immune-system activity so that the fetus is not attacked.
This is a very preliminary conclusion, and it is important that scientists understand this better.
9. How can M.E. (also known as Enteroviral Encephalomyelitis) be distinguished from somatization disorder and anxiety disorders?
Jason: There are many psychiatric disorders that can cause fatigue.
The best known is substance abuse, but other important disorders include depression and anxiety disorders.
Just as we expect a thorough medical investigation to determine whether someone has M.E., we must also ensure that a proper psychiatric screening is performed so that we know patients have M.E. and not a psychiatric disorder.
10. You call PEM one of the three main symptoms of M.E. (also known as Enteroviral Encephalomyelitis) What exactly do you mean by the “malaise” in PEM?
Jason: Malaise is not a great word, because it can be misinterpreted.
What happens is that following exertion, someone experiences severe symptoms in multiple areas, including physical, cognitive and others.
But the term PEM has been used for so long that it has become very common in the literature.
The International Consensus Criteria for M.E. instead use Post-Exertional Neuroimmune Exhaustion (PENE).
11. My neurocognitive problems are getting worse. What can I do to prevent deterioration or improve them?
Jason: I am sorry to hear that your symptoms are worsening.
A long-term follow-up study indicated that cognitive symptoms can worsen over time.
The IACFS/ME guide contains some useful material that you may wish to look at.
12. If M.E. (also known as Enteroviral Encephalomyelitis) patients become depressed partly because of reactions from people around them, are you developing education to address this?
Jason: For years, we worked with a buddy program to try to support M.E. patients.
There is a need for more information and education about how patients can best deal with people in their social environment who often do not understand their illness.
13. My condition continues to deteriorate. How can I improve without exceeding my limits?
Jason: Our group works with the energy envelope.
It is a concept developed by a patient years ago.
In our view, this method can be compared with pacing, although there are some differences.
Our approach clearly focuses on helping people monitor their energy and remain within the energy available to them.
I notice that patients often undertake more activity than their energy level permits.
That is understandable because, when they develop M.E., they suddenly have so much less energy available.
Several of our studies have demonstrated positive outcomes from remaining within your energy envelope.
When asked where the research can be found, Jason provides a study on the energy-envelope approach.
14. Do M.E. (also known as Enteroviral Encephalomyelitis) patients respond poorly to antidepressants?
Jason: As a psychologist, I do not prescribe medication.
But from the research I have read, there is no clear evidence demonstrating whether antidepressants are or are not appropriate.
Some people say they help; some say they do not.
15. Can ME/CFS negatively affect or accelerate osteoarthritis?
Jason: Someone with M.E. can certainly suffer from other illnesses, such as osteoarthritis, just as someone with heart disease or cancer can have osteoarthritis.
So it is possible for someone with M.E. to have osteoarthritis or other illnesses.
The tragedy for many M.E. patients is that once healthcare professionals discover that the patient has M.E., they stop considering all the other possible illnesses that the patient may also have alongside M.E. and that may also need treatment.
That too is part of the stigma attached to people with M.E..
When asked specifically whether M.E./CFS could worsen osteoarthritis, Jason continues:
M.E. can certainly lead to multiple conditions in the body. It is logical that this could lead to other illnesses.
One of my graduate students is trying, for her thesis, to determine what happens to people who die after having M.E.
It is clear that many people develop a number of illnesses after developing M.E., including cancer and heart disease.
16. Is that the main reason M.E. (also known as Enteroviral Encephalomyelitis) patients have a lower life expectancy?
Jason: In a study we published, we found that approximately one-third of people who died after having M.E. died of heart disease, and one-third died from cancer.
They died much younger than would be expected according to national mortality figures for these diseases.
We now want to investigate this more precisely.
17. Which risk factors do you expect to play a role in developing M.E. (also known as Enteroviral Encephalomyelitis) ?
Jason: One risk factor could be exposure to mold.
Another risk factor is developing mononucleosis.
Those are just a couple of the important risk factors that require further research.
18. Can you donate your body somewhere for scientific research into M.E. (also known as Enteroviral Encephalomyelitis) ?
Jason: I hope there will be places where patients can donate their bodies, because this research is essential for the future.
Comments
Post a Comment