Dr. Andreas Kogelnik’s Talk on Re-Evaluating Chronic Fatigue Syndrome and Immunology

This is a summary of Dr. Andreas Kogelnik’s Lunch N Learn talk “Re-Evaluating Chronic Fatigue Syndrome and Immunology” at El Camino Hospital in Mountain View on April 19, 2011. This summary mostly follows the chronological order of issues as discussed by Dr. K., but a few times I moved things around a bit to help understand the issues better, I hope. Here is a video of the lecture, which also includes the slides.

The talk was set up in a small conference room with chairs and tables for about 30 people.  The hospital staff kept bringing in additional chairs when more and more people showed up.  All in all, I would guess that there were about 60 to 70 people in attendance.  Dr. K. was pleased by the good turnout and expressed his hope that the hospital would schedule more CFS events in the future with a bigger venue next time.

Dr. K. talked for about 45 minutes and answered questions for another 10 minutes. He stayed for 30 minutes or so afterwards to answer one-on-one questions, but eventually had to leave because he had patients waiting for him at his clinic.  Some of his talk was merely an overview of CFS, but later he talked about new findings from the last 5 years as well ongoing or upcoming studies.

Dr. K. started out saying that CFS is a misperceived and poorly defined syndrome.  He then talked a bit about his clinic/research institute, the Open Medicine Institute.  He said that it was created about 2 years ago as an offshoot of what he and others had been doing at Stanford and to enable physicians to do research and avail themselves of a network for specialists, including immunology-based research.  He said that the Open Medicine Institute has a strong network of CFS patients and physicians throughout the US, but that they are also involved in some other areas, which helps bolster the infrastructure of the institute.

He then started talking about the disease by saying that the ratio of women to men affected by CFS is 6 to 1, partly because of thyroid issues.  CFS affects patients of all ethnicities.  The number of children unable to go to school because of CFS is increasing, particularly in the San Francisco Bay Area.  There are no socio-economic patterns; it can affect people in all walks of life.

The latest CDC estimate of the number of CFS patients is between four and eight million people affected in the US.  Dr. K. suspects that the numbers are even higher than this.  Most of the patients that Dr. K has seen over the years have been to an average of 20 to 40 doctors.

Dr. K. briefly talked about the definition of CFS as a diagnosis of exclusion and that the existence of multiple definitions creates issues, but he didn’t elaborate on that.

In terms of the clinical course, CFS often starts with a very acute infection (e.g., routine EBV or Lyme disease) that the patient doesn’t recover from or only partially recovers from and continues to relapse.  This often means a fluctuating course of the illness and varying severity.  The disease involves multi-systemic symptoms.  He briefly touched on neurologic, endocrinological, rheumatologic, sleep, cardiac and dermatological abnormalities as well as general symptoms, such as fatigue, nausea, headaches, etc.  What stood out for me here was that he said that 40 % of his patients progress to diabetes (I didn’t catch whether type 1 or type 2.) and that 60% of patients will have some level of gut dysfunction.  An abnormally large number of CFS patients have thyroid disease, which was one of the ties to the autoimmune theory for CFS.  Some patients have severe cognitive impairment.  Others “only” have physical impairment and no cognitive problems.  Some Olympic-level athletes are all of a sudden unable to complete even a short, easy bike ride.  There is a big overlap with fibromyalgia, but not all patients have pain.

Dr. K. is not sure that that CFS is just one single illness because he is seeing clusters of symptoms, such as sleep disruptions. In his mind, CFS represents a number of different, but related, diseases that overlap with respect to the immunologic pathways that they are affecting.

He also doesn’t think that there is just one etiologic agent for CFS.  He said that most likely there are various pathogenic or immunological triggers that are setting off different immunologic responses. So, most likely the same treatment will not work for all patients.  However, later, when he took questions, Dr. K. said that it is also possible that CFS is caused by one single virus similar to how HIV causes the initial immune problem, which then leads to other opportunistic infections causing the clinical problems of AIDS patients.  In fact, later during the talk, Dr. K. did say that he thinks a retrovirus may very well be responsible (for more on that and XMRV, see below).

Dr. K thinks that one of the reasons that CFS has been ignored by the medical community for so long is that the often very general, non-specific symptoms, such as fatigue or sleep disruptions, are very difficult for doctors to get a handle on.  A patient with any one of those symptoms just by itself probably wouldn’t get treated or just get treated with medication for insomnia, for example.  But when you look at CFS patients who have a number of those symptoms, some other patterns emerge that are not even listed in the CDC definition of CFS, such as cardiac abnormalities.

He said that because there is no clear definition for CFS, the CFS medical community, over the last 5 years, has been working towards letting go of the clinical criteria and trying to establish some molecular criteria.  There are some new immunological tests that can identify specific deficits and correlate those with some of the other abnormalities in CFS.

Dr. K attributed the fact that there haven’t been many if any treatment successes to the fact that the few trials that have been done were not well controlled.  The placebo-controlled Valcyte trial at Stanford about 5 years ago was the first placebo-controlled CFS trial in more than a decade.  He said this was an indicator that the disease hadn’t been taken seriously, but he thinks this is starting to change.  There have been some treatment successes on the viral side and the immunological side and in the Lyme area.  He feels that CFS has been getting more people’s attention as it has been becoming clear that it’s a multisystem disease.

Dr. K then talked about testing of objective markers:

Neurological Testing:  Improved MRI technology has shown that about 60% of patients with severe cognitive impairment had white-matter changes (spots/lesions on the white matter) in their brains that correlate with cognitive flare-ups.  The lesions resolve as the severe cognitive-impairment flares resolve. This does not correspond to anything that is known in medicine.  Radiologists have compared these changes to those happening in HIV patients with encephalitis, but Dr. K. stressed that CFS is a different disease than HIV.

Functional MRIs are making it possible to document decreased ability to process in terms of cognitive tasks. He didn’t say more.

Endocrine testing: Dr. K mentioned (but didn’t elaborate on) testing for adrenal dysfunction, hypocortisolism, disruption of cortisol rhythms, disruption of growth hormones, thyroid abnormalities (particularly in women, but also in men), increase in cytokines and different patterns of TNF, IL1, IL6, IL8 and IL12 in CFS.

Cognitive testing:  Dr. K said he is particularly interested in cognitive testing, but not particularly good at it. Some patients have severe disruption of short-term memory and information processing ability.   Some patients are not able to count anymore after a flare.  Many patients have word-finding difficulties, concentration issues, even in the absence of headaches.  Those are testable things.

Cardiac testing:  Some patients have clear cardiac changes, which can be tested.   A lot of work has been done, especially on the East Coast, but also by, e.g., Dr. Lerner, looking at cardiomyopathies.  Dr. Lerner and others feel very strongly that all CFS patients will eventually progress to cardiomyopathies, but Dr. K. is not sure he fully agrees with that.

Tilt-table testing can test for POTS syndrome, which is an abnormal sensing of the vascular state.  Patients feel like they are constantly in a low blood-volume state and their bodies react inappropriately by increasing the heart rate.  As a result, they feel dizziness, nausea, fainting.  Ninety-five percent of patients who have those symptoms will have an abnormal tilt-table test.

Other testing:  Some patients have EEG changes that are distinct and different from depression.  This is where Dr. K. mentioned “some studies” (I am sure he meant the PACE study, but didn’t use the name.) in the last year that claimed that people who have their depression treated or who exercise will get better.  Dr. K. said that therapy and exercise may help somewhat, but generally only to a small degree.  He said that a patient who went from 100% to 40% functionality because of CFS might get a boost of four to eight percent by treating depression or by exercising, which will really not help them very much.  He said that most of his patients had no history of mental-health issues prior to getting sick with CFS.  Yes, CFS patients are often depressed, but that is to be expected given the impact the illness has on their lives.  He made it clear several times during his talk that he definitely doesn’t believe that this is a psychological disease.  He also briefly mentioned that he has seen abnormal levels of anxiety in CFS patients, particularly while treated with antiviral medication.

Dr. K. then shifted gears to talk about immunology, which he said was one of the most exciting pieces for him.  In the last 5 years, (in addition to the new findings regarding cytokines), some specific areas of the immune system were found that are not functioning correctly in CFS patients.  That opens up a new path to diagnosing and treating the illness.  In terms of treatment, Dr. K believes that this is the most promising path.

Regarding natural killer cells functional impairment, he has lots of patients with natural killer cells in the single digits and recently saw his first patient with a natural-killer cell number of one, which he called a “horrible” number because it means that the natural killer cells basically aren’t working at all.  Natural killer cells are involved in viral defense and help the body destroy infected cells.  Most physicians test for natural killer cell counts because they don’t know better, which often come back normal or slightly increased, but the functional tests are the relevant ones.

CD 8 and CD 4 cells and the ratios between them are helpful to look at, which was one of the key areas for HIV.

Dr. K. talked a little bit about cytokines.  CFS patients often have abnormal IgG levels for antibodies that are produced by various B cells and monocytes.  The antibody levels can be both excessively low or excessively high. Subsets of patients with these abnormalities cluster with similar issues. IVIG treatment with these patients have been effective only short-term, but not in the long run.  Given the issues with IVIG production, Dr. K. recommended to be careful with IVIG treatments. He didn’t elaborate on that.

Dr. K. often sees patients reporting decreased levels of immunity.  There is an increase in the number of patients with recurring strep infections.

Dr. K. moved on to talk about putative etiology.  Dr. K. is a firm believer that genetics contribute to one’s susceptibility to CFS, which can get triggered by many environmental factors. Toxins (he mentioned mercury and arsenic) have direct adverse impact on the immune system.  Even though vaccines have no proven direct tie to CFS, they are immunologic stimulants and may play a role.

A stressor on the immune system, such as a vaccine, another illness (viral, bacterial, fungal infection) or toxins have an impact on the immune system and that can become the precipitating factor for CFS.  He doesn’t know whether one of these stressors is enough to tip over the immune system.  Maybe patients who are susceptible to infections get set up by one or more stressors and eventually, when exposed to the right agent, become ill with CFS.  There are plenty of precedents for that mechanism in the infectious-diseases area.

Dr. K. then talked about etiologies.  He talked about the focus on the human herpes viruses, which are very present in the environment. Almost everybody is exposed to them at some point in our life.  Ninety-five percent of people are exposed to HHV-6 by the age of 5 and to CMV and EBV by the age of 20.

He just mentioned enteroviruses, parvovirus, bacteria, Lyme, parasites, and other pathogens and then talked about Lyme disease, which overlaps with CFS.  There is an immunologic issue regardless of the pathogen triggering the disease.  Therefore, treatments could be immunologically-based or pathogen-based.  Dr. K. proposed that one possible reason for the failures on the treatment side might be that treatments for both CFS and Lyme disease have been focused on specific pathogens, which may not work if the underlying problem is an immunological one.

No clear link between EBV and CFS has been established, but EVB can cause a lot of other problems, many of which are related to immunology, such as B cell lymphomas and other issues that are typically only present in patients with immune suppression or dysfunction, but not in healthy people.  This points to an immune system problem.

Many viruses “like” nerve and lymph cells and, in CFS patients, there often is specific dysfunction within those cells.  One problem in the CFS arena is that one of the markers used for viruses are antibodies, both to EBV and HHV-6.  While antibodies are very useful to determine whether somebody has been exposed to a virus, there is a lot of controversy as to how useful they are for diagnosing chronic infections.  Chronic infections were accepted slowly in the infectious diseases area, but now there are more and more precedents, most notably HIV, but also, e.g., Tb.  The question is whether the virus triggers a continued, but fluctuating immune response or whether we are dealing with a continued viral infection and continued seeding. There is reasonable data for both theories.  Of course, there are also non-viral potential causes, which are probably largely affecting the same pathways.

Dr. K. then talked a bit about the placebo-controlled Valcyte study at Stanford.  Valcyte is a relatively new antiviral, but it’s about to go off patent.  There have been some “good treatment successes” in treating CFS with it.  It targets largely the herpes virus family.  According to Dr. K., the initial data from the Stanford trial was underwhelming.  But over time, it turned out that there were some consistent changes across the patients.  Most of the patients continued to improve after the range of the study period.  Patients were taking Valcyte for six months.  They were evaluated at six months and one year.  Many of them reported that they had gotten back, or close, to their healthy levels only after the one-year mark.  A lot of them are not tracked anymore because Stanford lost touch with them.

Dr. K. thinks that several hundred if not several thousand of CFS patients have been trying Valcyte in the US and that nobody has been tracking those patients.  He said tongue in cheek that Roche must be very happy that Stanford did that trial because it probably prompted many CFS patients to try it.

Dr. K. said that there is a possibility that the very strong patient-reporting outcomes of the initial (uncontrolled) Stanford study were the result of a selection bias because patients were not selected at random.  Self-reported pre-treatment activity levels were at an average of 10%, which Dr. K. called “pretty lousy.”  Those patients reported that they were at 90 % after 6 months of Valcyte.  Dr. K. called this outcome “pretty amazing.”

This first, uncontrolled trial was followed up with the placebo-controlled trial of Valcyte.  Some people didn’t respond to Valcyte at all.  It seems that people are either going to respond to it or not.  According to Dr. K., the duration of the treatment was and still is in question.  How long do patients need for their immune systems to recover?  He likened it to cardiac surgery after which you wouldn’t expect the patient to get off the operating table and go jog.  He said that there is a long rehab process, the duration of which depends on the health of the patient before the surgery, comorbidities and the level of support and stress after the surgery.

In terms of antibody levels, some of the patients in the trial had some really high HHV-6 and EBV numbers. One of the patient’s EBV VCA IgG was 10,240, which is something you would never see in the general population where you normally see numbers between 140 and 180.  A year after the six-month treatment with Valcyte, only half of the patients dropped their antibody levels.

Dr. K. didn’t say anything about some patients actually feeling worse in the long run after taking Valcyte.

At this point, Dr. K. said that CFS almost certainly has an infectious component (although there may be variants that are purely immune), but because the etiologic agent hasn’t been identified, he called it probably infectious.

He then talked a little bit about XMRV.  He said that the most likely outcome is that XMRV will not pan out in CFS.  He explained that XMRV is a retrovirus that was discovered and reported in a group of patients (66% out of 100 patients).  It had also been found in prostate cancer a few years earlier and there was a question of whether prostate cancer is caused by XMRV.  In terms of CFS, more and more studies are coming back negative and there is some concern of possible contamination in the original studies.  But he said that the idea of a retrovirus being implicated in CFS is a viable one.  He followed that up by saying that any number of other agents might be capable of triggering CFS symptoms, such as the herpes viruses.  He said that if he cultured the throats of the people in the room for viral cultures he would probably find EVB in most of the people.  The problem is that nobody has ever done a study to quantify EBV in CFS patients’ throats and that we don’t know whether the virus seeds from the throat or whether it seeds from some of the immune cells.  All of this is actively being looked at right now because of concerns over the integrity of the blood supply and possible XMRV and other infections.

When asked, after the talk, for some more details on why he doesn’t believe that XMRV is the cause of CFS, Dr. K. referred to a paper that he, as part of a team with many collaborators, submitted to a major medical journal and that he hopes to get published next month.

Lastly, Dr. K. talked about some ongoing and future studies.

The clinic at Open Medicine Institute is using various antiviral protocols depending on a patient’s profile.  They mostly look at a patient’s antibodies, but also at direct PCR positivity and sometimes antigen testing.

They are also testing for non-viral causes, such various environmental abnormalities like mercury and arsenic levels, etc.  Instead of the traditional blood testing, they are using a new test that was developed for the EPA and that is more sensitive.  A larger study is planned for that.

Somebody in the field (I think he meant Open Medicine Institute, but that wasn’t clear.) is also completing some genomic and proteomic expression studies where they looked at actual genes that are up-regulated or down-regulated in some patients.  They are attempting to cluster patients differently using molecular criteria instead of the clinical definition.  Dr. K. said that this is very promising, but that they have to increase their numbers a little bit.  I assume that means that they need more trial participants.

Open Medicine Institute will soon make a registry available to the public that allows patients to quantify their disease and to potentially tie that back to their own biologic samples.

Within the next two weeks, Open Medicine Institute will start immune-modulator trials.  There’s been some researech in Norway with Rituxan.  Rituxan is a B cell agent that wipes out B cells, which is one of the potential reservoirs especially for EBV or HHV-6, but also for other pathogens.  There has been some great clinical success with Rituxan on a short-term basis, but there is no long-term data yet.  Patients on Rituxan have had almost complete resolution of their symptoms within 24 hours.  Unfortunately, after the drug wears off, the symptoms return.  So the question to look at is what Rituxan is doing immunologically and how that can be sustained long term.

In order for patients to be prescribed Rituxan, they have to have one of three main indications for it: (1) cancer, (2) RA or (3) immunoglobulin abnormalities, which is the group of patients looked at for the initial trial of Rituxan in CFS.

Several regimens for oxidated boosting of the immune system’s ability to fight infections are being considered (I couldn’t tell whether that was done by Open Medicine Institute or somebody else.), e.g., by improving natural killer cell functioning.  There are also things that can be done to help with the mitochondria, which has been implicated in CFS.  Dr. K. also mentioned co-enzyme Q and dietary changes as an alternative route.  This is similar to boosting the immune system of HIV patients who don’t respond well to anti-retrovirals.  When their immune system gets boosted, many of them start responding to anti-retrovirals.  A similar approach is being considered for CFS patients who don’t respond well to anti-virals.

For some time in the future, a study is planned on using hyperthermia with CFS patients.  I couldn’t tell whether that would be done at Open Medicine Institute or somewhere else.  The goal is to tweak the body metabolically and to periodically create an environment that’s hostile to viruses and bacteria. There has been some really good response with regional hyperthermia in various cancers, which seem to be potentially virus-driven or immune-system-driven.

Dr. K. wrapped up his talk with a shout-out to Dan Peterson who, he said, is one of the people who started this office (I assume he meant Open Medicine Institute, but I am not certain) and has been a great mentor to him. He has also worked very closely with Jay Levy at UC and a couple of people at Wisconsin Viral (didn’t catch their names) as well as Dr. Ron Davis at the Stanford Genome Technology Center.

In answering one of the questions at the end, Dr. K. said that some patients are light and/or noise sensitive and that a more stimulating environment can affect how they feel on a day-to-day or even minute-to-minute basis.  A lot of patients are also reporting an inability to process when they are in large crowds or noisy places.

 *****

I am not in the habit of speaking highly or even well of medical doctors; I usually have no reason to.  But I am convinced that Dr. Kogelnik couldn’t be more committed to finding a treatment for CFS.  He is tirelessly working to that end.  I know that many CFS patients will be upset about his stance on XMRV. I am reserving judgment until I see his reasons in his soon to be published paper.  But even if it turns out that he is misguided on the XMRV issue, I know that he will do everything he can to try and help CFS patients and that is much more than I can say about almost every other medical doctor.

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41 Responses to Dr. Andreas Kogelnik’s Talk on Re-Evaluating Chronic Fatigue Syndrome and Immunology

  1. wally says:

    Excellent recap! Thanks for all the time and effort you put into this write up. Sorry I did not get a chance to meet you on Tuesday. Hopefully the videotape of this talk will be made available on-line for viewing. Well worth the time for people to view this talk.

  2. Xpoz says:

    Thank you for the summary. I was too ill to attend.

    This part made my day:

    “Improved MRI technology has shown that about 60% of patients with severe cognitive impairment had white-matter changes (spots/lesions on the white matter) in their brains that correlate with cognitive flare-ups. The lesions resolve as the severe cognitive-impairment flare resolve.”

  3. lisa says:

    great recap. thank you very much. i agree that dr. kogelnik is very committed to me/cfs patients and finding a treatment. i think we are lucky that such a bright young dr. has decided to put his brain power and energy into the me/cfs field. hopefully more and more young drs. will follow his lead; and the next time, someone who first becomes ill with this horrific disease, goes to a doctor they will not be told they are depressed and need a vacation.

    thanks to you and dr. K.

    i too hope others won’t b too harsh of dr. K for his views on xmrv….we all have the right to agree or disagree with him, but it does not take away from the good hard work he is doing.

    regards, lisa

  4. amberlin says:

    This is a fantastic summary of the talk. Thank you so much for taking the time to do this. As a patient of Dr. Kogelnik’s I can tell you that I have never met a doctor that was so committed to his patients and his work. I did a 9 week in patient antiviral/anti-retroviral treatment under Kogelnik in the hospitalk, and he came and saw me EVERY day. He would come on Saturday nights at 10pm, after putting his children to bed. His commitment to helping our community towards a cure is unwavering.

  5. Terri says:

    Thanks for the great write up! You’ve convinced me to go see Dr. Kogelnik. He is the type of MD that I’ve been looking for.

    BTW I’m also looking for a ME/CFS support group. I moved from an area that had a support group to an area where I can’t find anyone who has this disease so that I can start one.

    Feel free to contact me at my email address.

    Thanks again!

  6. Erik Johnson says:

    “No clear link between EBV and CFS has been established, but EBV can cause a lot of other problems, many of which are related to immunology, such as B cell lymphomas and other issues that are typically only present in patients with immune suppression or dysfunction, but not in healthy people. This points to an immune system problem.”
    ———————————————————————————

    The main point of “CFS” was that “CEBV Syndrome” could not possibly apply to patients who had no EBV at all. It was only reactivated or enabled in those people who had it, which comprise the vast majority since EBV is so common, but it was not inherent to the illness.
    This necessitated the creation of a paradigm that could address this situation.

    In terms of considering causation for “CFS”, EBV can be disregarded, for the very act of creating CFS was based on the finding that it was only an opportunistic infection due to an immune system problem.

    • I am no scientist or medical doctor, but it seems to me that, if even the leading experts in this field, such as Dr. Montoya and Dr. Kogelnik, can’t rule out that EBV is causing CFS in some CFS patients, then I certainly wouldn’t go out a limb and claim that. It is true that not every CFS patient has high EBV titers and that goes to the fact that there seem to be different sub-groups of patients with CFS. Some have high herpes virus titers, some have high parvovirus titers, others have high chlamydia pneumoniae titers, etc. But again, I am no expert. Just reporting what one of them said. You may very well be right. I just don’t know.

  7. Erik Johnson says:

    The reason I know this for certain is that CDC had absolutely no intention of altering “CEBV Syndrome” until Dr Cheney placed them in an untenable position by locating a small group of patients who might have otherwise qualified for a CEBV Syndrome diagnosis, but for being EBV negative.

    This left the CDC little choice but to abandon CEBV Syndrome and replace it with a descriptive paradigm that was congruent with the evidence.

    At its very core, “CFS” was based on an illness-entity that was devoid of EBV.

    • I have to confess that I know little about CEBV since I came to this after that debate I think. But I am not convinced just by the fact that not every CFS patient is EBV positive. What if different pathogens (one of them being EBV) affect the same immunologic pathways, as Dr. Kogelnik was suggesting, all of them causing CFS as the end result? The fact that not all CFS patients have high EBV titers doesn’t mean that EBV doesn’t play a role in cases of patients with high EBV titers. I also wouldn’t draw any conclusions based on what the CDC did or didn’t do. I think we need to look at scientific evidence here and there is none proving that EBV has no link to CFS (just like there is none proving that it does).

  8. Erik Johnson says:

    http://articles.latimes.com/1986-06-07/news/mn-9956_1_lake-tahoe
    160 Victims at Lake Tahoe
    Chronic Flu-Like Illness a Medical Mystery Story
    June 07, 1986|ROBERT STEINBROOK
    INCLINE VILLAGE, Nev. — Sandy Schmidt, 42, came down with the mysterious illness soon after she ran a marathon in San Francisco last July. She got better before becoming sick again this spring, forcing her to quit her job as a business office manager. Running even one mile now would “put me in bed for a day and a half,” she said.

    Schmidt is among 160 residents of Lake Tahoe’s North Shore who have been diagnosed by two local physicians since the winter of 1985 as having a chronic flu-like illness in a medical puzzle that has assumed national proportions.
    Most of the victims are well-educated, previously healthy, about 40 years old and are more likely to be women than men. Their complaints also are similar: severe fatigue, recurrent colds and difficulties with memory and concentration. About half of them have enlarged lymph nodes in their neck and almost all have abnormal blood tests, suggesting that a common viral infection may be involved.
    Drs. Peter R. Cheney and Daniel L. Peterson believe the explanation may be a chronic version of the familiar Epstein-Barr virus, which causes mononucleosis. But the so-called “kissing disease” affects primarily children and young adults, albeit the short-lived symptoms are not unlike those being seen here.
    If they are right, solving the puzzle of this cluster of illnesses may have wide repercussions. Perhaps tens of thousands of Americans throughout the country with chronic lethargy have been similarly diagnosed in recent years as suffering from chronic infection with the Epstein-Barr virus. And many of them have joined support groups or sought unproven treatments with antiviral or other drugs.
    But there is sharp disagreement over whether the Epstein-Barr virus explains more than a handful of cases of chronic illness nationwide–or any of the cases in this area. Indeed one Incline Village physician has accused the two doctors who have been making the local diagnoses of “perpetrating a hoax.”
    And last fall, two investigators from the federal Centers for Disease Control spent several weeks here looking into the mystery. They concluded last week that they could “neither prove nor disprove” the relationship between the Tahoe illnesses and the Epstein-Barr virus.

    Finding Challenged!

    That finding was immediately questioned by Dr. Paul R. Cheney, one of the two doctors who has been treating the patients. He said the investigation was too narrow and has been overtaken by subsequent developments.

    ———————————————————–

    The “subsequent developments” was evidence that EBV was not even present.

    So, in essence, “CFS” was created specifically to address an illness that defied any possibility of being CEBV Syndrome.
    -Erik

  9. Pingback: Referat fra Dr. Andreas Kogelniks foredrag 19. april på El Camino Hospital « Rutts tankespinn og ME-nyheter

  10. Allison says:

    Thanks for the great info! Anyone know how hard it is to get into see him or how much it costs? He sounds like an amazing doctor and I’m just a little south of the area.

    • He is indeed a great doctor. I think it doesn’t usually take more than 2 weeks to see him. I don’t remember the exact amount for the first visit, but I think it was somewhere around $400 or maybe a bit more. That first visit is an hour long. Follow-up visits are usually half an hour, but can be longer depending on how much you want/need to discuss with him. He doesn’t take insurance, so you have to pay him at the end of the visit and then get reimbursed for (parts of) it from your insurance company.

  11. Sara says:

    I was at Dr. Kogelnik’s presentation and can’t imagine a better write-up of his talk. Thanks for taking such great notes.
    Since you are a patient of his, I was curious if you are planning to participate in the rituximab trial? No worries if you would rather not reveal your treatment plan.

    • I don’t mind sharing my treatment plan, but I just don’t know yet what I am going to do. I was planning on starting Valcyte and Rituxan some time this summer, but I have read several patient accounts that said that they are feeling much worse after taking Valcyte and that really scared me because as limited as I am right now, I am definitely grateful that I am not worse as so many others who can never leave the house. What they were talking about wasn’t just the initial Herxheimer effect of things getting worse before they got better; they are feeling worse long after they stopped Valcyte.
      (As far as I know, the Rituxan trial will be only in conjunction with Valcyte, but maybe I am wrong about that so, don’t rely on that! It could very well be that the idea of taking Valcyte in addition to Rituxan has to do with my particular situation.)

  12. Barry Shurtz says:

    Thanks, great info. I’m going to look into going to see Dr. K.

    Barry

    P.s, as you probably guessed my Dad sent me the URL to your blog. Nice work!

  13. Erik Johnson says:

    The irony is that although the creation of the new syndrome of “CFS” was to insert a conceptual separation between the reactivated EBV and an illness entity that could operate without it, patients themselves didn’t understand that the separation is only to mean that EBV is not inherent to the underlying process, and fought to have “CFS” conceived of as being an aftermath of EBV.
    In effect, “educating” people that CFS no different that it was before CEBV syndrome was abandoned.
    The point of “CFS” was lost, and people continued to think of the illness as being a form of EBV for decades afterward.
    As the authority on ME Dr Byron Hyde said, “Such is the perseverence of error”.

    • I hear you, Erik.

      But I am just wondering if it has been scientifically proven that no cases of CFS are caused by EBV. One problem with CFS is that it’s impossible to define it correctly until we know what causes it, but without a name change, nobody who’s not affected takes it seriously and we are not getting any meaningful amount of money for research to try and find the cause. Changing the name, however, (to something that does the disease justice) without knowing what’s causing it is tricky because we don’t want to have to change it again once science catches up. And on and on it goes …

      I am not saying that EBV is the cause (or one of several) of CFS in some patients. I just don’t know. It may be in patients with high EBV titers or it may not be, even in those patients. My point is that we need to rely on science here and I don’t think the science is there yet. The mere fact that not every CFS patients has high EBV titers does not convince me, as there seems to be a number of subsets of patients with different symptoms and potentially different causative agents. Of course, I would agree that patients who do not have high EBV titers wouldn’t have gotten CFS from EBV.

  14. Erik Johnson says:

    There is one small group for whom defining CFS is irrelevant.

    It is the group of prototypes upon whose evidence CFS was based.
    The concept of “What CFS is” must conform to the prototypes, or whatever is being considered is rendered speculative, as to whether it matches the syndrome.

    In an attempt to ensure that the parameters of the new syndrome did not revert back to a conceptual framework of CEBV Syndrome (EBV plus stress), Dr Cheney selected a small group called “the pristine cases”, who were entirely EBV negative.
    Although the Holmes CFS definition study group also included patients who had reactivated-EBV, it was the evidence from the pristine-cases which slammed the lid on CEBV Syndrome, since the others could conceivably have fit into the old paradigm.
    Their illness did not sufficiently defy the “chronic mononucleosis” concept sufficiently to cause its abandonment.

    Above all, the creation of the new syndrome was to address the evidence which defied the old one, and brought it to a close.
    And since it pushes the bounds of science and semantics to call an illness CEBV syndrome, when there is no EBV, that is the main reason that something had to be done to address it.
    That “something” was “CFS”.

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  17. Erik Johnson says:

    Here’s the citation explaining how the mixup happened.
    -Erik

    s presented at the Invest in ME
    London Conference of May 12, 2006
    by Dr. Byron Hyde MD

    Extracts from
    A New and Simple Definition of Myalgic Encephalomyelitis
    and a
    New Simple Definition of Chronic FtiSd

    This is an abridged version of Dr. Byron Hyde’s booklet entitled

    A New and Simple Definition of Myalgic Encephalomyelitis and a New Simple Definition of Chronic Fatigue Syndrome
    &
    A Brief History of Myalgic Encephalomyelitis & An Irreverent History of Chronic Fatigue Syndrome
    Which is available from the Nightingale Foundation at http://www.nightingale.ca

    The Lake Tahoe Epidemic
    The Lake Tahoe epidemic that started in August 1984 also started amongst students. In this case the epidemic began in a high school girls’ basketball team that was travelling in a bus to play various other teams. The epidemic spread rapidly with an incubation period of approximately a week. As in many of the other epidemics, it then spread to the general community. After the epidemic started it then involved three high schools, both students and teachers and ultimately spread to the community. For some reason it was considered to be an epidemic of infectious mononucleosis. This is an illness caused by a virus Epstein Barr Syndrome. Associating the Lake Tahoe epidemic with Epstein Barr Syndrome was frankly ridiculous and you will see why almost immediately.
    Dr Paul Cheney and Dr Daniel Peterson were inundated by the number of rapidly developing cases of seriously ill patients and called the Centre for Disease Control (CDC) in Atlanta for back up.
    First International Symposium on Immunology and Pathogenesis of Persistent Virus Infections
    Fast-forward to April 1987 and the First International Symposium on Immunology and Pathogenesis of Persistent Virus Infections held in Atlanta Georgia. This was a symposium hosted by the CDC and Dr Carlos Lopez. At this meeting Dr Gary Holmes gave out his new paper, “A cluster of patients with a chronic mononucleosis-like syndrome,” that had just been published in JAMA. (See Holmes, Kaplan, Stewart et al: JAMA 1987:287:2297-2302)
    The publication essentially stated that Epstein Barr Virus was not the apparent cause of this illness in the 130 patients from which they took blood samples. But they weren’t sure and suggested that further study be done.
    Epstein Barr Virus (EBV)
    Now anyone who realizes that infectious mononucleosis is caused by the herpes family virus, Epstein Barr Virus (EBV), and that the incubation period of this illness is approximately 40 days, should have realized that you simply cannot have a rapidly spreading viral epidemic with a virus with a latent period of 40 days.
    Neither Dr Straus nor Dr Holmes, senior government physicians, should have fallen into such a trap. They only had to go to the excellent CDC library to realize that rather than spending half a million dollars or so on a publication that they should have known would not have incriminated EBV.
    Yet this epidemic somehow spread the myth that this illness was caused by EBV. Today, as I write this short history of M.E. and CFS the vast majority of physicians and the public still associate Epstein Barr Virus with CFS.
    Such is the perseverance of error.

  18. Erik Johnson says:

    For nearly a quarter century now, people hear the story of how CFS came to be.

    It makes them angry that it doesn’t agree with what they thought, so they turn around and walk away.

    Simply “decline” to reconsider anything. That’s innocent enough, isn’t it?

    And by doing nothing, become part of the reason why things never changed from CEBV Syndrome.

  19. T says:

    I just wanted to report back that I saw Dr. Kogelnik. I’m so glad I did. I feel hopeful about the research going on, the treatment planning, and he is kind and empathic. I think he’s going to be one of the top cfs doctors in the field.

    I’m wondering about starting an online group that consists of his patients. That way we can compare our progress on various protocols?

    Thanks again for the write up…

  20. I am glad you had a good experience with Dr. Kogelnik. Yes, he is very kind and empathic. We are very lucky to have him.

    The online group is a great idea!

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  22. ryan says:

    Does Dr. Kogelnik ever recommend treatments? I’ve talked to several people who’ve seen him and they never went back because he didn’t have any treatment to offer. All 3 had been on av’s and he didn’t have anything else to suggest.

    Based on their experience he doesn’t sound worth the money.

    • He is about to start (or maybe is already in the middle of–not sure) a trial with Valcyte plus Rituxan, which looks promising. He talked about Rituxan a bit in his lecture.

      He is also hoping to become an Ampligen site.

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  24. M says:

    I was wondering how much difficulty you have with getting a hold of Dr. K. I am a relatively new patient of his.

    While i am generally pleased with the treatment plan he has come up with for me, i have a very difficult time getting a hold of him in order to have follow up conversations as i move from one phase to treatment to the next. This has become such a problem that i often go weeks at a time waiting for a reply from him.

    I was just wondering if you have had the same difficultly or if i have just become a patient of his at a unfortunately busy period for him.

    • I am so sorry, M, that is has been difficult for you to get in touch with Dr. K. Pursuing any kind of treatment is stressful enough without the added problem of not being able to get a hold of your doctor.

      I have not done any kind of treatment with him, so I haven’t been in your position of really needing to talk to him. Having said that, he has always been fairly responsive to my emails and I have heard the same from other patients.

      I do hope that this is just an unusually busy time for him that has contributed to your situation, but I would very much encourage you to talk to him about this if you feel comfortable.

      Good luck, M.

    • Anonymous says:

      I don’t know if you’ll get this but I and several others have had a similar experience. He is more interested in research than providing good patient care.

      I found a different doctor. There are quite a few doc’s here in the bay area that are really good and have excellent follow up.

      Feel free to email me for more info: thomasryan41@gmail.com

      Personally, if I were in your shoes I would find another doctor. You need to have a doc with good follow up if you go on a medication that needs close follow up.

  25. WDN says:

    I flew to CA for an appt with dr kogelnik. I felt very good about the visit but then no one contacted me afterwards with blood test results and treatment recommendation. I had to contact them for copies of the test results and then Dr Kogelnik still did not email as promised to give his interpretation & recommendation. I had to contact the office again and then the dr sent a very brief and incomplete email. I then called to ask if I could set up a phone consultation–it went pretty well. Later though, when I was ready to start the medication, I used the email address I was given to contact the dr. I wanted to ask a couple questions and then get the prescription. The email was never answered so I called the office a couple weeks later. They said he would respond within a couple days. I still got no response until over a week later when the office contacted me to get the pharmacy #. There has been no mention at all about the blood tests I was told I would have to get every three weeks while on the meds (learned this during the phone consult).

    I still have hope that he’s a very knowledgeable doctor, but all of this does give reason for concern. And it really doesn’t make sense that he’s just too busy because when you call for an appointment he’s not booked out far at all.

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  27. Deborah Waroff says:

    Excellent write-up. Thank you so much. Regarding Erik’s comments, I want to add that molds, via the toxins they produce, are well known as factors that destroy immune systems. The molds I have in residence cause liver and kidney cancer in India and China, via grain contamination. At Tahoe, the water was exceptionally just before the epidemic started, which adds to suspicions. That said, the Herpes clan of viruses cause damage to the immune system, and for those of us who had mono it seems likely the EBV helped set us up for ME/CFS. We would have a clear picture of the phases of responsibility and the division of responsibility among pathogens and toxins if the NIH were to research for us. Please keep in mind that your suffering could be alleviated by your government funding research in line with funding for other diseases.

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