Report From the 7th Annual AACFS ConferenceIn Madison, Wisconsin Oct 8-10th, 2004’Byron Hyde’s Talk’by Rich Van Konyenburg


Report From the 7th Annual AACFS ConferenceIn Madison, Wisconsin Oct 8-10th, 2004’Byron Hyde’s Talk’by Rich Van Konyenburg

This is my review of the third talk presented at the pre-AACFS conference session on Effective Therapies for Chronic Fatigue Syndrome (CFS) and Fibromyalgia (FM), sponsored by the Wisconsin CFS Association. VHS video tapes and DVDs of these talks are offered by this group at their website,

Biographical Information on Dr. Byron Hyde, M.D. (taken from his website,

Dr. Byron M. Hyde attended the Haileybury School of Mines and worked as a geophysicist. He then did premedicine in the Faculty of Medicine and University College, University of Toronto, obtaining a degree in chemistry and nutrition. He graduated in medicine from the University of Ottawa, where he was the Director and Chief of the International Exchange Program for the Canadian Association of Medical Students and Interns (CAMSI). Dr. Hyde founded the International Summer School in Tropical Medicine. He interned at Hotel Dieu in Montreal, was a resident at St. Justine Hospital in Montreal and at the Ottawa Civic Hospital. He also studied in Munich at the University Kinderklinik and in Paris at the Necker Hospital for Children.

He was a research chemist at the Roscoe B. Jackson Laboratory at Bar Harbour, Maine, a leading world laboratory in immunological research. Following this, he was Chief Technician in charge of the Electron Microscope Laboratory in Toronto at the Hospital for Sick Children, followed by a similar post at the University of British Columbia.

Dr. Hyde has authored a book on electron microscopy and two non- medical books. Dr. Hyde has been a physician for 25 years and has performed charitable work as a physician in Laos and the Caribbean. He held the position of Chairman of the Ottawa Community Health Services Association, and is presently Chairman of The Nightingale Research Foundation.

In 1984, Dr. Hyde began full-time study of the disease process then known as Myalgic Encephalomyelitis (ME)(renamed in 1986 by Dr. Gary Holmes in the USA as Chronic Fatigue Syndrome). He has worked exclusively with ME/CFS patients since 1985. In 1988, Dr. Hyde organized an association and founded The Nightingale Research Foundation, dedicated to the study of Myalgic Encephalomyelitis / Chronic Fatigue Syndrome. He also acted as Chairman of the 1990 Cambridge Easter Symposium, and of the Workshop on Canadian Research Directions for Myalgic Encephalomyelitis / Chronic Fatigue Syndrome in May, 1991, at the University of British Columbia.

How Dr. Hyde Became Involved in ME/CFS Work

In his talk, Dr. Hyde described the circumstances that caused him to become interested in studying ME/CFS. A friend invited him to come to a party in Montreal, which he did. About ten other physicians, two social workers, nurses, wives and girlfriends also came. Three days after the party, about half the people who had come fell ill with a severe brain dysfunction and seizure syndrome. It was obvious to him that this was an infectious disease because of the circumstances.

Somewhat later, his daughter, who was then eight years old, also fell ill, with considerable pain. She recovered after three months, and has not had any relapses since,though she has worked in Baghdad and, as he put it, some fairly “nasty” places in the world.

Studying the Epidemics, and Studying Non-epidemic Patients in Canada

In response to these events, Dr. Hyde traveled to all the places where there had been ME/CFS illness epidemics reported, including Los Angeles (where a 1934 epidemic occurred at Los Angeles County General Hospital), Australia, New Zealand, England, Scotland, Switzerland, Denmark and Iceland (1946-47 epidemic). In most cases he was able to find and speak to physicians who had been involved in dealing with these epidemics. In Iceland he examined over 50 patients who were still ill almost 40 years later, including the mayor of Reykjavik. Some were working, some were not, but all were still disabled.

Generally speaking, Dr. Hyde found that the epidemics occurred in hospitals, schools or military barracks. In the case of students, all were on sports teams, such as the girls’ basketball team near Lake Tahoe. In North Carolina, there was a symphony orchestra that had an epidemic in 1984. In the cases involving hospitals, an infection either went through the community, bringing a lot of sick people into the hospital, and then the hospital staff became ill also, or as in the case of the Mercy Hospital in California in the 1980s, people in the hospital fell ill first, and then it spread to the community from there.

He said that there have been over 50 epidemics, and in 90% of these cases an incubation period of three to five or six days has been observed, making it clear that an infectious disease was involved. In 1992, he studied 2,000 patients in Canada who had become ill with ME/CFS sporadically (in other words, not as part of epidemic outbreaks) between 1984 and 1992, and he found that the group most injured, in terms of the highest fraction of their total population, were respiratory technologists. These people worked with patients who had longstanding lung infections, of months to years duration. He concluded that this suggests that a chronic viral infection must have been involved.

The highest absolute numbers of people who became ill in terms of occupation were among primary school teachers, followed by other teachers, and then hospital workers in general who had contact with patients. Among the teachers and healthcare workers, the top group as a proportion of their total population were those who worked with physically or mentally challenged people, such as deaf, blind, or psychiatric patients. Dr. Hyde suggested that these people might have had more stressful jobs, but also that the state of cleanliness is usually not as high in these situations, again suggesting infectious disease.

Dr. Hyde’s Current Clinical Approach

Dr. Hyde currently sees only 35 patients per year, but he examines, tests, and studies each patient very thoroughly. He refers to his testing protocol as a “total body assessment.” He said that his experience as a geophysicist contributed to his development of this approach. In geophysical exploration for ore bodies that can be profitably mined, a number of different techniques are used to measure various characteristics of the subsurface and to plot them on maps. When anomalies in the different measured parameters intersect on the maps, these intersections suggest the location of ore bodies. In the same way, he has found that much can be learned about the human body by conducting many different kinds of tests and combining the results in an overall analysis.

The total testing program that he orders for each patient costs about $5,000 (Canadian) and takes about six months. He justifies this cost on the basis that it is a small figure in comparison to the income loss of an individual who remains ill for many years, and in comparison to the consequent tax loss to the government. The tests fall into the following categories: brain and vascular survey, sleep study, dental and mandibular survey, vertebral survey, cardiac survey, chest and pulmonary survey, abdomen and pelvic tests, thyroid and endocrine survey, arthritic and autoimmune survey, blood tests, general tests (including mammogram and pap smear), metals and toxin tests, infectious disease survey, and psychiatric assessment. In addition, he asks patients to report their medications, surgeries, allergies and sensitivities, and a complete personal and family medical history, and he performs a physical examination.

One of the main techniques that he relies upon is high-resolution SPECT scanning of the brain. SPECT stands for “single photon emission computed tomography.” In this technique, the patient is injected intravenously with a substance that incorporates a radioactive gamma ray emitter. After a short period of time to allow the substance to bed distributed within the brain, emitted gamma rays are tallied by a special detector system (gamma camera) coupled to a computer. This system pinpoints the locations of the gamma ray emitters and is able to produce a three-dimensional image of the brain that reflects how well blood flows throughout the brain
and how metabolic activity is distributed within the brain.

The use of SPECT in ME/CFS was pioneered in 1990 by Dr. Jay Goldstein and Dr. Ismael Mena, who found certain abnormalities. Others have reported later SPECT studies with varying results. Dr. Hyde suggested that the reason for these different results may be that the various groups of patients who were studied did not all have ME. He emphasized the complexity of diagnosis and the need for a total body assessment. He also emphasized the importance of using a machine with high spatial resolution.

His patients are scanned with a dedicated-head Picker 3000 gamma camera system, which he noted is no longer manufactured, but that used units are still available on the market. He has scanned over 500 ME patients with this machine, which achieves a spatial resolution of 1 to 1.5 centimeters. This will not resolve the pituitary gland because it is too small, but it will resolve the thalamus and hypothalamus.

Comments on the Development of the Case Definitions

Dr. Hyde emphasized that his findings about ME/CFS patients have been very different from the case definitions that were promulgated by the U.S. National Institutes of Health (NIH) and the Centers for Disease Control (CDC. [Rich–I might mention here that Dr. Hyde is on record several times as having been a persistent and severe critic of these case definitions from their beginnings.]

He said that in his view, these definitions have totally failed us. His view of one of the reasons these definitions are so far off the mark is as follows: In the United States, there are many poor people without adequate health insurance. Up until a few years ago, these people could go to any of the CDC clinics that formerly existed, “whether they were alcoholics or psychiatric patients or whatever, and they could say that they were chronically tired or had muscle pain, and this may or may not have been true.” Dr. Hyde believes that these indigent patients had an effect on the attitudes of the CDC researchers, because the latter concluded that “there was really nothing physically wrong with these patients; they were alcoholics or major depressives, or whatever.” On the other hand, when Dr. Hyde examined the ME/CFS patients who came to his practice in Canada, he didn’t find any of these things.

When the original board met at the CDC in 1988 to establish a case definition for CFS, Dr. Hyde was in attendance, because those interested in this type of diseases were invited to come. He said that “it was obvious to those who had actually seen ME/CFS patients that the vast majority of the people on the board were researchers who had never seen an ME patient clinically.”

Dr. Hyde said that the definition this board developed totally warped the whole concept of ME/CFS-type disease, because the authors introduced the word “fatigue” into the name. Fatigue can be produced by many things, and it is a totally undefinable term in his view. Furthermore, in the 50 epidemics up to that time, fatigue had only occurred in one. What actually did occur in these epidemics again and again was central nervous system (CNS) derangement: sleep dysfunction, cognitive problems, and in general, difficulties with any tasks the brain is required to perform.

According to Dr. Hyde, the second factor that came into the picture in 1988 and was perpetuated as well in the development of the revised 1994 Fukuda et al. case definition process as well those carried out in other countries, was that they brought in more psychiatrists. The overall result was that the definitions were developed primarily either by epidemiologists who were in his view forced by the government to go and start looking at these patients and produce a definition, or by people who did not believe that there was any physical thing wrong with any of the people who had what they called CFS.

Dr. Hyde said that at a meeting initiating the development of the 1994 definition there was not a single clinician on the entire board, with one exception, and he therefore got up and said, “Why don’t you put some people on this board who have actually seen patients?” He said they accommodated by adding one more who had. Dr. Hyde said the people on the board were brilliant, but they had never seen a case of CFS. According to Dr. Hyde, bringing in so many physicians who had never actually seen CFS patients, and particularly psychiatrists, who wanted to say that these patients had depression or anxiety or some other psychiatric problem, and
trying to accommodate these extremes in the definitions destroyed the reality in the definitions that resulted.

Dr. Hyde quoted a 1993 paper by Dr. William Reeves of the CDC, to wit, “Chronic fatigue syndrome has no confirmatory physical signs or characteristic laboratory abnormalities, and the etiology and pathophysiology remain unknown.” In Dr. Hyde’s view, any reasonable physician who did not actually deal with CFS would conclude from reading this that CFS had to be a form of psychiatric or somatizing illness. He said that we need to redefine what is going on, and that there is a lot of good evidence with which to do so. He said that a good part of the 1994 CDC definition would just as well describe someone who had just finished climbing Mount Everest. He noted that this definition paper contains over 15,000 words, and suggested that those writing it could not have been very clear on what they were defining, to have to use so many words.

[Note by Rich: In the light of these comments by Dr. Hyde, I found it very interesting the next day at the open session of the AACFS conference to hear Dr. Reeves make some remarks about the history of the development of the 1994 case definition. He had just finished reporting that the CDC plans to develop an empirical case definition from its epidemiological studies on actual people who have CFS, which sounded to me like a very positive step forward. Then he contrasted this with what had been done in the past (and I am able to present this verbatim, because I had a tape recorder running), “The current case definition is what we have. It was basically–uh, being an author I can do this in the crudest terms–a bunch of old cronies in a cigar-filled room writing on their favorite symptoms. Now those old cronies in this–we weren’t smoking cigars because this was at the CDC. There were people in fact who deal with CFSpatients for a living, but the definition was not based on empiric data. It was based on impressions of patients.”

These two testimonies are also in substantial agreement with the account given by Hillary Johnson in her book about the history of CFS, Osler’s Web (see pages 636 and 670).]

Dr. Hyde’s Definition of Myalgic Encephalomyelitis (ME)

Dr. Hyde stated that he believes that “If a disease cannot be scientifically measured or appropriate tests made to confirm its presence, it cannot be defined or treated with any assurance of success. Without the ability to measure or test for a disease, most physicians will reject the concept entirely or state that the illness is psychiatric, psychological, or social in nature.”

He went on to set forth his definition of ME: “ME is a measurable, diffuse post-encephalitic illness. The illness is characterized by (1) its acute onset, (2) the diffuse, non-focal persisting nature of the encephalopathy, and (3) the chronicity of the resulting symptoms. These symptoms consist of the rapid exhaustion or loss of stamina of motor, sensory, intellectual, cognitive and emotional abilities. ME is of infectious/autoimmune origin and less commonly, a toxic/autoimmune origin. ME occurs in epidemics and sporadic cases.” He further noted that in the case of epidemics, the observed incubation time of 3 to 6 days rules out both Epstein–Barr virus and HHV-6 as causes, because they have incubation times of approximately 40 and 12 days, respectively.

[Note by Rich–Basically, what he’s saying here is that ME starts with an inflammation of the brain that occurs rather suddenly. This initial inflammation usually results from an infectious/autoimmune process, but it can also be caused by a toxic/autoimmune process. This sudden, short-term inflammation is followed by a disorder of the brain that continues over time. This chronic disorder of the brain is not localized to a small part of the brain, but is spread out over large regions of the brain, and it leads to chronic symptoms that can involve essentially all the normal functions of the brain. ME occurs both in epidemic-type clusters of cases as
well as cases that are occasional and isolated.]

Dr. Hyde said that though the primary injury in ME is the diffuse CNS encephalopathy, the illness may cause or be associated with measurable dysfunction in end organs and various body systems. The most commonly injured end organs and systems are (1) the thyroid gland, (2) the cardiovascular system and (3) the immune system. The CNS dysfunctions are caused by widespread, measurable, diffuse micro- vasculitis affecting normal cell operation and maintenance. [Micro- vasculitis means inflammation of small blood vessels.]

He went on to say that in ME, “the brain changes are not progressive but of acute onset and relatively stable over a period of years.” The evidence would suggest that ME is caused primarily by a diverse group of viral infections that have neurotrophic [Note by Rich–I think he meant neurotropic] characteristics and that appear to exert their influence primarily on the CNS arterial bed. The available brain technology limits the viral site of action to the capillaries and microarterial CNS bed. This diffuse vascular site of injury rather than a neurological cellular site of injury explains the natural history of ME-type illness.”

[Note by Rich–What he is saying here is that there is evidence that the causes of ME are any of a group of viruses that are able to infect the brain. By means of high-resolution SPECT scanning, he can tell that they mainly affect the small arteries and capillaries in the brain.]

“It is also noted that many ME patients also have generalized arterial pathophysiology [Note by Rich–In other words, there are problems with the arteries all over their bodies.], causing various vascular problems that include in numerous patients: (1)insufficient blood pressure increase on exertion, (2) hyperelasticity and hyper-contractibility of arterial blood vessels, (3) various forms of arterial mediated vascular orthostatic pathophysiology

[Note by Rich--In other words, they have difficulty standing up because of problems with their arteries as demonstrated by Drs. David Streeten, David Bell, and Peter Rowe, and (4) cholinesterase dysfunction in the arterial wall, causing arterial elasticity dysfunction as demonstrated by Dr. Vance Spence at Dundee University, Scotland."

(Note by Cort - its interesting that POTS - the form of orthostatic intolerance most commonly experienced by CFS patients often has an infectious onset - as, of course, does CFS.)

[Note by Rich–Dr. Spence and his group have found that when they inject acetylcholine into the forearms of CFS patients using a special electrochemical technique, the arteries dilate more than normal, and stay dilated longer than normal.]

Dr. Hyde noted that Dr. Erich Ryll had described the 1975 epidemic at the Mercy San Juan Hospital in Sacramento, California as epidemic vasculitis.

Dr. Hyde also mentioned that as part of his testing protocol, he runs a Persantine (dipyridamole) stress test. This agent dilates the arteries and causes an increase in the heart rate. He finds that if a patient has acute onset ME, or sometimes gradual onset CFS, and particularly if they also have FM, this agent will instantly cause intolerable pain all over their body, which is eliminated right away with an antidote, but he believes that this is another indication that there is a problem with the arteries in this disorder.

He believes that another indication is that if a cardiac stress test is run on one of these patients, the heart rate and blood pressure will often decrease, rather than increasing as they do in a person who is a “couch potato” (i.e. out of condition) but otherwise healthy. He also mentioned observations of low total circulating blood volume in these patients, sometimes as low as 40% of normal, as another problem involving the vascular system. An additional test he runs that points toward vascular problems is a Doppler ultrasound examination of the transcranial arteries at the back of the head. These arteries are found to be in spasm in these patients.

He reported his finding that “Depending upon (1) the severity and persistence of the initial encephalopathy, (2) the locations and extent of the brain areas affected, and (3) the initial and consequent organ and system injuries, the severity of the patient’s clinical illness and disability generally increased with increased central nervous system SPECT changes.”

Dr. Hyde’s Definition of Chronic Fatigue Syndrome (CFS)

Dr. Hyde stated that in his view that “CFS comprises two systemic illness variations: (1) an acute onset central nervous system disabling illness that he believes should be referred to as ME rather than CFS, and (2) a cyclical or gradual onset disabling illness consistent with any of the increasing number of ponderous CFS definitions in use at the present time.”

He went on as follows: “Gradual or cyclical onset CFS illness can be subdivided into three principal categories:

(1) Acute onset ME that has been misinterpreted as a gradual onset disease.

(2) A single disease or illness state causing a fatigue and cognitive illness and frequently a pain and sleep dysfunction. This may be due to any number of recognized diseases or injuries whose diagnosis has been missed due to inadequate investigation. Routinely in the examination of reputed CFS patients I find missed myocardial infarcts (at least 5 to 10 % of patients), missed cerebral-arterial obstructions, multiple sclerosis (perhaps 5 % of patients) and genetic diseases.

(3) Perhaps the most interesting type of illness of the CFS group is when the patient has a large number of recognized illnesses or pathologies or injuries that have not been diagnosed. Individually, many of these pathologies might not be disabling, but cumulatively they will cause the patient’s overall disability. The insurance physician will latch onto one disease entity and make statements such as: ‘There are many people with this condition, and they seem to be able to work.’ The point is that an individual can sustain a large number of injuries and pathologies and still be capable of going on. But there reaches a point when the organism can no longer tolerate the number of disabilities without being chronically exhausted. It is a case of the straw that broke the camel’s back.”

Dr. Hyde went on to explain his view of why group (3) is present: “Since Osler [Note by Rich–Sir William Osler (1849-1919) was a Canadian-born physician who became a professor of medicine at McGill, Johns Hopkins and Oxford Universities. He wrote an influential textbook of medicine and had a major impact on the teaching and practice of medicine] physicians have attempted to find one disease underlying a patient’s illness, with the concept that once found this identified disease can be potentially treated and the patient made better. This is a very efficient concept and solves the problem of most illnesses, if there is a cure.”

However, he says, “the theory doesn’t consider the possibility that an individual may have a large number of pathophysiological conditions, and that it is the significant number of illnesses that causes patients to be chronically exhausted. In some extreme conditions I have found patients with as many as 20 disabling diseases. Commonly, I find in excess of eight or nine. The body and brain of the individual can only tolerate a certain degree of pathophysiological weight.

Unfortunately, when a physician finds one disease state and treats it, and the patient does not improve, rarely does the physician investigate the possibility that there are multiple causes to explain the patient’s illnesses. When this happens, the patient may be blamed for not getting better. Worse, the patient may be told that their problem is psychological or social. When multiple diseases are the cause of a fatigue state, sometimes some of these diseases may be treatable. When a sufficient number of these problems can be treated, the patient sometimes will show dramatic improvement.”

Results of Dr. Hyde’s Clinical Examinations

Dr. Hyde reports the following: “There are times that the discoveries made using this investigation protocol has saved the lives of patients.

“There are times when we find a large number of pathologies, some that are treatable and some that are not treatable. Often when we treat those that physicians know how to treat, the patient improves to the point that they can return to work.

“There are times when we find a large number of medical problems that we cannot treat, and yet this is almost always sufficient to win a disability pension for these patients.

“There are times when I cannot help the patient except to explain to them the actual cause or the many causes of their illness. This is of enormous emotional benefit to the patient, and opens much better channels for future treatment, since the patient and I both know why they are ill and what has to be treated when a treatment becomes available.

“When I find a pathological subsection I usually do more in-depth testing in that particular area, so that when I send the patient to the appropriate specialist, the specialists do not have to waste their time repeating obvious tests.”

Recovery of ME Patients

Specifically concerning patients that he has diagnosed as having ME using the SPECT scan, he made the following observations:

“Recovery depends largely upon the extent and severity of the initial measurable SPECT brain changes. The ME patients most likely to recover were those patients who had the least SPECT CNS involvement.” Dr. Hyde distinguished the following three types of ME, based on his SPECT observations:

“Type I ME: Patients who demonstrate primarily a mild persisting encephalopathy of only one of the brain hemispheres are most likely
to have some chance of recovery.

“Type II ME: Patients who demonstrate an encephalopathy involving both cerebral hemispheres rarely or never recover.

“Type III ME: These patients have both a bilateral cortical hemisphere and a subcortical encephalopathy. Type III patients have the most severe and most chronic form of illness and demonstrate the largest degree of increased end-organ pathophysiology.”

Dr. Hyde emphasized that the changes he observes on the SPECT scan in ME patients are not found in healthy people, and that they are clear evidence of disease.

He believes that the causes of these changes could be viral, chemical, or autoimmune agents.

He further believes that “These central nervous system changes can potentially affect other body organs and systems that are controlled by the specific CNS areas injured, and that these organ and system changes are also measurable.”

[Rich’s comment–I suggested to him that perhaps these organ and system changes are not caused by the CNS changes, but instead that both result from a common cause, namely glutathione depletion. I made this argument on the basis that glutathione is responsible for protection of all the body’s organs, including the brain, from damage by reactive oxygen species, certain toxins, and (by its participation in the immune system) pathogens, including viruses. It remains to be seen whether this will turn out to be true.]

Dr. Hyde’s Observations of Thyroid Cancer in ME/CFS Patients

Dr. Hyde made the startling announcement that in the past 100 patients whom he has investigated for ME/CFS with or without FM, he has found that 7% of these patients had thyroid cancer. This is surprising, in that thyroid cancer is usually found in 0.5 to 1 patient per 100,000, which is a prevalence that is a factor of 7,000 to 14,000 lower than he has observed in his patients!

In each of these patients, the diagnosis was made by ultrasonography and needle biopsy under ultrasonography, This was followed by surgical removal of the thyroid, and in each case the malignancy was confirmed. Each of these patients had a history of acute onset of their illness, and significant ME/CFS and/or FM for 5 to 7 years prior to the discovery of the thyroid malignancy, including significant brain dysfunction. Each had Type III ME, based on the SPECT scans. The pathology reports on the first six of these patients indicated that they also had Hashimoto’s thyroiditis. Five of these six had normal serum levels of TSH, free T3, free T4 and microsomal antibodies. The other showed elevated microsomal antibodies, but normal TSH, free T3 and free T4.

Dr. Hyde reported that 25% of the rest of his patients who do not have thyroid cancer do show ultrasound evidence of Hashimoto’s thyroiditis or other thyroid injury, many without abnormal TSH, free T3 or free T4, but a “modest number of these with antibody signs of thyroid disease.”

Another very interesting thing that Dr. Hyde reported was that after these patients with thyroid cancers had had their thyroids removed, they were given thyroid replacement hormones and were closely supervised by good endocrinologists, but there was nevertheless no improvement in their fatigue syndrome.

He also noted that five of these six patients had cervical disc disease, but only one had a history of neck trauma.

Dr. Hyde recommended that all ME/CFS patients should be evaluated by thyroid ultrasound and, where appropriate, needle biopsy to rule out thyroid malignancy and other thyroid pathology. The fact that ME/CFS patients may have normal blood serum values of TSH, free T3, free T4 and normal microsomal and thyroglobulin antibodies does not eliminate thyroid disease

[Note by Rich: Wikland (2001) reported that about 40% of patients suffering from “chronic fatigue” showed evidence of chronic autoimmune thyroiditis by fine needle aspiration cytology, even though TSH levels were in the normal range in many of them.]

Dr. Hyde also concluded that “A chronic Hashimoto’s Encephalopathy- like syndrome may be concurrent with ME/CFS patients who have thyroid malignancy or multinodular thyroid disease or other thyroid pathology and chronic subcortical and cortical brain SPECT changes. Non-recovery after thyroid malignancy surgery and adequate thyroid hormone replacement may be related to this chronic ME/CFS encephalopathy. ME/CFS patients without thyroid malignancy yet with treated thyroid pathology, and who have not recovered from their fatigue syndrome, may also have a similar NeuroSPECT brain dysfunction.”

[Concluding comments by Rich–Dr. Hyde is one of those few physicians who has been in the ME/CFS field continuously since the early days when CFS began to receive official recognition in the mid- 80s. He has clearly done important investigations of the history of this disorder. He is coeditor of a major textbook in this field, published in 1992 (available from He probably does the most detailed testing of his patients of any physician in this field. He calls things as he sees them.

I found this talk extremely interesting, though somewhat foreboding in the prognoses it suggests. His observations of vasculitis in the brain and of thyroid cancer in ME patients seem to me to be very profound and significant. While the pathogenetic origin of these features remains to be scientifically established, my current hypothesis, which I have shared with Dr. Hyde, is that glutathione depletion lies at the basis of both, as I believe it lies at the basis of many other features of the pathogenesis of these disorders, as I have explained in my recent AACFS paper.]

Rich Van Konynenburg, Ph.D.


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