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Chronic Fatigue Syndrome and Non-HIV AIDS

 

 

 

 

Making LemonAIDS Foundation
CFS Straight Talk


2012

 

I have Chronic Fatigue Immune Dysfunction Syndrome (CFS/CFIDS/ME) and NON-HIV AIDS, idiopathic CD lymphocytopenia. With these two clinical diagnoses, I believe that makes me living proof that the AIDS-like CFS/ME is transmissible, something that the medical establishment seems unable to admit or to acknowledge. I also believe it makes me living proof that CFS and NON-HIV AIDS are the same mysterious immune disorder.

Three years ago, after a heterosexual sexual encounter, I became seriously ill with what looks like the natural disease progression of AIDS. After an "acute infection" and a "period of asymptomatic health," I have fallen extremely ill to an unrelenting, progressively-worsening AIDS-like demise. I can pinpoint exactly when I was infected with my "chronic viral syndrome of unknown etiology" and because the "acute infection" stage was so distinguishable, I can also pinpoint exactly when my undiagnosed pathogen left my body and infected yet another host.

Increasingly, I have become concerned that my systemic diagnosis is caught up in the treacherous politics of CFS/ME and AIDS. Most people with CFS/ME do not like to talk about the many symptoms and immune abnormalities that they share with AIDS patients. I also suspect that most ailing patients would rather be told that they have the very mysterious CFS than to be told that they have AIDS.

I have a Master's degree. I am a director at my firm. I used to be a triathlete. I have never used IV drugs. I have never traveled abroad. I can count my sexual partners on two hands. Statistically speaking, I know that my undiagnosed infectious and communicable disease is not rare...so, you tell me, if they are not in the miscellaneous CFS/ME category, where are all these other immunosuppressed people?

Anyone with CFIDS, who does not consider the possibility that CFS/ME will eventually progress to a NON-HIV AIDS diagnosis, is very well trumping their own ability to diagnosis the root cause of their illness.

Why isn't CFS/ME a reportable disease overseen by our public health department? Why are CFS and ME (i.e., the same exact disorder) suspiciously categorized as two separate illnesses on a worldwide level (i.e., by ICD codes)? Doesn't anyone else but me, very clearly see, the catastrophic cover-up going on here?

Why are we not reading about NON-HIV AIDS cases (and/or the AIDS-like nature of CFIDS) on the front pages of every newspaper in the world? And if CFS/ME is NON-HIV AIDS, then, depending on who you believe, there are anywhere between 500,000 - 14,000,000 Americans out there with a transmissible illness. If that is what it truly is, our new form of AIDS dwarfs the ‘original’ AIDS epidemic ---> TENFOLD.

I am not afraid to say that I have AIDS without HIV -- idiopathic CD lymphocytopenia.  I am equally as unafraid of saying the most obvious thing about CFS/ME: IT SURE DOES LOOK LIKE AIDS TO ME.

If it takes courage to think and to say the things that I do, I hope that there will be a miraculous outbreak of bravery from coast-to-coast. I stopped fighting for myself a long, long time ago. I fight for humanity.

I demand a CFS/HIV revolution.  Vive La Revolución‏.

To learn more about NON-HIV AIDS, and to see the *new* face of AIDS, please visit: CFS Straight Talk

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  • Guest - OM

    IS CFIDS RELATED TO AIDS?
    America's Biggest Cover-Up: 50 More Things Everyone Should Know About The Chronic Fatigue Syndrome Epidemic And Its Link To AIDS
    by Neenyah Ostrom

    Table of Contents

    Foreword

    1. Some CFS Patients May Be "Non-HIV AIDS" Cases

    2. A Virus Found In AIDS Patients Is Found In CFS Patients With Brain Lesions And May Be The Primary Attacker Of The Immune System

    3. HHV-6 Kills An Important Immune System Cell In AIDS And CFS Patients

    4. HHV-6 Seems To Be Causing Lung Disease In Immunosuppressed Individuals

    5. A Virus Found Growing In CFS Patients Has Been Linked To Miscarriage

    6. HHV-6 Infections Can Be Fatal

    7. A New Virus, HHV-7, Has Also Been Found In CFS Patients

    8. A Natural Immune System Anti-Viral Pathway Doesn't Work In CFS

    9. A Mysterious Organism Called A Mycoplasma May Be Peripherally Involved In CFS

    10. Just As In AIDS, Immune System Cells Called Monocytes Do Not Work Properly In CFS Patients

    11. As In AIDS, The Immune System Is Both Over-Stimulated And Depressed In CFS

    12. One Researcher Thinks That CFS Should Be Called "Lymphokine Overdose Disease"

    13. CFS, Like AIDS, May Be Primarily A Tumor Necrosis Factor Disease

    14. Zinc Deficiency May Contribute To CFS

    15. Magnesium Can Be A Missing Element In CFS

    16. There Is A Hormonal Imbalance In CFS Similar To The One In AIDS

    17. CFS Patients' "Crimson Crescents" May Be Diagnostic Of The Syndrome

    18. CFS Patients May Develop A Cancer Similar To One Found In AIDS

    19. Like AIDS Patients, CFS Patients May Be Especially Susceptible To Tuberculosis

    20. CFS Patients Have A Brain Defect Similar To That Found In AIDS Dementia

    21. There Can Be A Significant Weight Fluctuation In CFS

    22. Dizziness Can Be A Severe Problem In CFS

    23. As In AIDS, Sinusitis Can Become Chronic In CFS

    24. A Recent Rise In Childhood Asthma May Be An Effect Of The CFS Epidemic

    25. Endometriosis Seems To Be Common In Women With CFS

    26. Pregnancy Can Be A Disaster For A CFS Patient

    27. Men With CFS Can Develop Chronic Prostate Infections

    28. CFS Can Cause A Particular Type Of Heart Murmur

    29. Like AIDS Patients, CFS Patients May Bruise More Easily Than Healthy People

    30. CFS Can Lead To Serious Diseases Of The Mouth and Gums

    31. CFS Can Cause Perception Problems For Drivers

    32. People With CFS Often Have Bizarre Sleep Problems

    33. CFS Is Often Characterized By Nausea

    34. CFS Patients Can Develop Serious Bladder Problems

    35. Fingers Can Become Swollen In CFS

    36. CFS Patients Can Develop Skin Rashes And Other Disorders, Especially Acne And Shingles

    37. The Hair Can Be Severely Affected By CFS

    38. CFS Patients Can Have False Positive Tests For Syphilis

    39. In CFS Patients, As In AIDS Patients, The T4 Cells May Be Sequestered In The Lymph Nodes

    40. Sunbathing May Make CFS Symptoms Worse

    41. As It Progresses, CFS Can Be Measured In "Stages"

    42. Some CFS Patients Become Suicidal

    43. Health Care Workers May Be At Increased Risk For CFS

    44. CFS Can Result In Financial Disaster

    45. A Drug Made From Pig Liver Appears To Help Some CFS Patients

    46. An Experimental Drug That Appears Promising For CFS And AIDS Is Being Evaluated By The FDA

    47. Nothing Is Being Done To Protect The Blood Supply From CFS- Infected Blood

    48. CFS Has Spawned A Powerful Patient Movement That Has Become Mired In Denial

    49. The Two "Variants" Of HHV-6 Appear To Act Very Differently

    50. A Virus That Causes An "Acquired Immune Deficiency Syndrome" In Pigs May Be The Real Cause of CFS And AIDS

    References

    Foreword

    Chronic Fatigue Syndrome is not the only illness that is frustrating contemporary medical science. Gloom pervaded the Ninth International AIDS Meeting (held in Berlin in June 1993), as clinicians and researchers acknowledged that little progress was being made in fighting the illness. The drug that has been touted for years by the U.S. government as stopping the progression of AIDS and extending patients' lives, AZT, does neither. In fact, researchers revealed, AZT is so toxic that it may actually hurt AIDS patients more than it helps. And the immune system marker used to evaluate AIDS patients' health (and AZT's action), T4 cell counts, it was admitted in Berlin, has essentially no correlation with patients' health.

    Although uneasiness and distress permeated news reports during and following the Berlin meeting, no reporter asked the obvious question: Is it possible that so little progress has been made in combating AIDS because a mistake has been made in the definition of the epidemic?

    This book will attempt to answer not only that question, but also other, potentially even more alarming, ones: Is CFS actually part of the AIDS epidemic? Are CFS and AIDS, in fact, the same illness?

    Since the Berlin conference, for anyone interested in observing it, evidence linking these two refractory epidemics, AIDS and Chronic Fatigue Syndrome, has continued to accumulate.

    Anxiety about the direction of AIDS research had really begun at the previous international AIDS conference, held in Amsterdam in 1992.

    The bombshell of 1992's AIDS conference was the announcement that some researchers had identified cases of AIDS without evidence of infection with the "AIDS virus," HIV.

    These "non-HIV AIDS cases" had severely depleted T4 (or CD4) cells, like AIDS patients; they also developed life-threatening opportunistic infections.

    What wasn't known to most observers was that one of the researchers who had first publicly identified some of the non-HIV AIDS cases, Dr. Sidhur Gupta of the University of California, Irvine, is a Chronic Fatigue Syndrome researcher.

    And some of the non-HIV AIDS cases, it was soon revealed, were actually CFS patients.

    Shortly after the June 1992 AIDS conference in Amsterdam, Chronic Fatigue Syndrome researcher Dr. Paul Cheney announced that he had 20 CFS patients in his practice who had the same immune system deficiencies as the non-HIV AIDS cases.

    The hallmark of the HIV-negative AIDS cases, as defined by the Centers for Disease Control and Prevention, is a depletion of the T4 (or CD4) cells.

    Therefore, the CDC decided to call the HIV-negative, AIDS-like disease "ICL" (an abbreviation of the tongue twisting "idiopathic CD4-positive T-lymphocytopenia," which means, simply, an unexplained loss of T4 cells).

    Most healthy people have a T4 cell count of approximately 1,000; a T4 cell count below 800 is considered abnormal. In order to be diagnosed with ICL, a person must have a T4 cell count of less than 300.

    One of the most puzzling things about the ICL cases to AIDS researchers -- other than the fact that they don't have HIV -- is that most of the patients do not fit into recognized AIDS "risk behavior" categories; that is, they are not gay men, IV drug users, or the sexual partners of people in those risk groups.

    How can AIDS exist in the absence of the virus that causes it? None of the AIDS researchers gathered in Amsterdam in June 1992 seemed able to answer that question.

    The mystery of what role HIV plays in causing the immune system deterioration and symptoms seen in AIDS deepened in early October 1992 when a British medical journal carried a report about a strain of HIV that does not appear to cause any kind of illness.

    An Australian research team wrote to The Lancet to report on five people who had received blood from a man later found to be infected with HIV. However, ten years following the transfusions, the five blood recipients, as well as the original, HIV-positive donor, remained free of AIDS symptoms and were apparently healthy. The Australian researchers concluded that all six people were infected with a non-disease-causing strain, or type, of HIV.

    Studies have shown that HIV is spread only through blood products (i.e., in transfusions), or through exchange of bodily fluids, such as during sex. AIDS is considered to be primarily a sexually-transmitted disease, but one that requires many exposures -- some estimates run as high as 500 exposures -- to catch.

    CFS appears to be transmitted much more easily; some researchers have guessed that it might be spread by saliva, as when people share eating utensils. Dr. Cheney, in fact, has reported that as many as 40 percent of his CFS patients also have a close associate -- not a sexual partner -- who has an illness similar to CFS.

    Dr. Cheney's statistic -- along with the mystery of why AIDS could develop without HIV infection and why HIV infection does not always lead to AIDS -- raises the possibility that a virus or bacteria that spreads more easily than HIV could be attacking people's immune systems.

    Dr. Cheney described the immune system damage seen in CFS patients for the Food and Drug Administration in May 1993. Dr. Cheney told the FDA that five of his CFS patients had died during the preceding six months. Two of these patients committed suicide, which is all too common among CFS patients. But three of Dr. Cheney's patients who died, like AIDS patients, succumbed to overwhelming infections that their damaged immune systems just couldn't fight off.

    But Dr. Cheney's CFS patients, like the ICL patients, appeared not to be infected with HIV, even though they developed AIDS-like immunodeficiencies and, in some cases, life-threatening opportunistic infections.

    One of the AIDS-like immunodeficiencies seen in CFS involves cells in the immune system that are important in fighting infections: natural killer cells. Natural killer cells are the scavengers of the immune system; they attack and kill anything that appears to be foreign, including the body's own cells that are infected with viruses or other disease-causing agents. Because of that activity, natural killer cells are considered to be part of the immune system's front line of defense against both viruses and cancer.

    Natural killer cells are also essential in protecting against tuberculosis, but at the same time, they are disabled by the TB germ. If a person's natural killer cells are not working properly, they are at much increased risk for developing active tuberculosis.

    In both AIDS and Chronic Fatigue Syndrome patients, natural killer cells are almost completely disabled. One study of CFS patients found that their natural killer cells' functioning was decreased by 86 percent.

    In other words, if a healthy person's natural killer cells worked at 100 percent capacity, a CFS patient's natural killer cells are working at only 14 percent.

    Of all the conditions in which natural killer cell activity has been studied, only AIDS patients have been found to have natural killer cells as disabled as those of CFS patients.

    However, most AIDS researchers have concentrated on studying the immune system cells implicated in the non-HIV AIDS cases, the T4 (or CD4) cells. T4 cells have been thought to be a good indicator of failing or improving health in AIDS patients; when their numbers decreased, patients were thought to be at higher risk of developing serious infections. Conversely, rising numbers of T4 cells were seen as proof that therapies, such as AZT, were improving patients' health.

    As a result of this belief that T4 cell numbers correlated well with health status, very few scientists have studied the natural killer cells and how they fit into the puzzle of AIDS.

    In early 1993, however, a study was published in the prestigious British medical journal Nature which not only forged several more links between the AIDS and Chronic Fatigue Syndrome epidemics, but also went a long way toward explaining why natural killer cells stop working in both syndromes.

    National Cancer Institute researcher Dr. Robert C. Gallo and his colleagues made an astonishing assertion in the Nature study: They reported that a virus found to be actively growing in both AIDS and Chronic Fatigue Syndrome patients, Human Herpes Virus 6 (HHV-6), infects and kills natural killer cells. Moreover, according to the report from the Gallo laboratory, HHV-6 is the only virus known to be able to do that.

    This landmark study answered two previously unanswered questions: It explains at least part of what the actively growing (or "replicating") HHV-6 is doing in AIDS and Chronic Fatigue Syndrome patients, and it partly explains why natural killer cells don't work in those patients.

    In fact, Dr. Gallo and his co-workers suggested that HHV-6 "may contribute to the immune dysfunctions associated with CFS and AIDS."

    Even studies of T4 cells published in early 1993 inadvertently linked the AIDS and Chronic Fatigue Syndrome epidemics.

    The government scientist responsible for Chronic Fatigue Syndrome research at the National Institutes of Health, Dr. Stephen Straus, finally admitted in early 1993 -- after 13 years of trying to prove that Chronic Fatigue Syndrome is a type of depression -- that immune system deficiencies are part of the illness. Dr. Straus and his colleagues published data showing that CFS patients, like AIDS patients, experience a drop in the number of T4 cells in their blood.

    Dr. Straus proposed a novel mechanism to explain the loss of T4 cells in CFS patients: The T4 cells of CFS patients are not destroyed, as they are in AIDS patients, according to Dr. Straus; the T4 cells are just hiding in the lymph nodes where they cannot be detected by blood tests.

    Therefore, according to Dr. Straus, the T4 cell depletion observed in CFS patients is completely different from the T4 cell depletion seen in AIDS patients.

    Unfortunately, Dr. Straus was unable to produce any evidence to support this theory (and still has not). Dr. Straus did not suggest, in contradiction to what Dr. Cheney has found, that any of his CFS patients had T4 cell counts so low they could be identified as ICL patients.

    Almost simultaneously, Dr. Yvonne Rosenberg, a scientist working at the Henry M. Jackson Foundation Research Laboratory in Rockville, Maryland, announced that her studies had indicated that T4 cells in AIDS patients are not as decimated as they might appear to be. Instead, Rosenberg suggested, at the prestigious Keystone Conference held the last week of March, 1993, that AIDS patients' T4 cells are sequestered in the lymph nodes where they remain unmeasured by blood tests.

    Although Dr. Anthony Fauci, the man in charge of AIDS research in the United States, attended the conference and presented the work his research group had performed on the lymph nodes of AIDS patients, neither he nor any other government scientist chose to comment about the parallel finding about T4 cells in the lymph nodes of AIDS and CFS patients.

    And, as the Centers for Disease Control and Prevention (CDC) lurches toward finishing its several-year-long surveillance study to estimate how many people in the U.S. have Chronic Fatigue Syndrome, new information on that subject has come from a surprising source. A group of researchers at the New England Medical Center (in Boston) studying Lyme disease discovered that up to 50 percent of people diagnosed with Lyme disease actually have Chronic Fatigue Syndrome.

    The Lyme disease researchers set out to answer another question altogether. They were trying to figure out why Lyme disease treatment is unsuccessful in so many cases.

    Lyme disease is caused by a bacterium similar to the one that causes syphilis; it is treated with antibiotics. But a large percentage of people diagnosed as having Lyme disease didn't improve when treated with antibiotics, and the Boston researchers were trying to find out why.

    They discovered that the patients whose Lyme disease didn't respond to antibiotics didn't have Lyme disease.

    Even more surprisingly, they found that almost 50 percent of those wrongly diagnosed with Lyme disease had, instead, a putatively viral illness: Chronic Fatigue Syndrome.

    In addition to its importance to people with Lyme disease and their physicians, this study potentially has enormous importance for the CDC surveillance study. The CDC study is examining people diagnosed with CFS, to see how many of them fit the very strict CDC definition. From those numbers, CDC investigators will extrapolate to the rest of the population and attempt to estimate how many Americans have CFS.

    But they are not examining people who have been diagnosed with other, more accepted illnesses, like Lyme disease.

    As the New England Medical Center study showed, there could be thousands -- or hundreds of thousands -- of people who have Chronic Fatigue Syndrome who have been diagnosed as having some other disease. Those people are quite unlikely to be counted by the CDC.

    The CDC's estimate of how many Americans have CFS could, therefore, be terribly wrong unless this type of misdiagnosis is taken into consideration.

    And this kind of misdiagnosis is likely to continue until there is a diagnostic test available for CFS.

    Many researchers are attempting to create such a test for CFS. One line of research that originally appeared to be promising involved finding a retrovirus, like the virus that supposedly causes AIDS, in CFS patients. Some researchers had believed that finding such a retrovirus, and proving that it causes CFS, would result in a definitive way to diagnose the syndrome, as the HIV antibody test has done for AIDS.

    But the "CFS retrovirus" research apparently ran into some roadblocks, and little progress has been made since the single report describing the retrovirus was published in early 1991.

    Meanwhile, HIV has come under intensified scrutiny as a disease-causing organism.

    Although the controversy over whether HIV causes AIDS -- with or without the help of "co-factors" -- has continued, few attacks on the retrovirus have appeared in the medical literature. In June 1993, however, an Australian research team published a devastating attack on the HIV antibody test, often called the "AIDS test."

    The Australian research team, in fact, raised serious questions not only about whether HIV causes AIDS, but even about its existence as a distinct, infectious retrovirus.

    Writing in the June 11, 1993, issue of the journal Bio/Technology, Eleni Papadopoulos-Eleopulos and her colleagues examined the HIV antibody test and found that it had many problems.

    Eleopulos and her co-workers found that the HIV antibody test is not consistent; that is, the same blood sample tested in several laboratories does not give the same results in every test performed. They suggest that some of the biological molecules that the HIV antibody test is measuring may be just background junk, cell proteins that are contaminating the test.

    Even more disturbing, through an extensive study of the HIV literature, Eleopulos and her colleagues raised the question of whether HIV has ever really been isolated as a discrete entity. The answer they reached is that it has not.

    This research caused Eleopulos and her co-workers to conclude that, not only is the HIV antibody test extremely unreliable and perhaps not at all useful, but that it may be a test for something that does not cause AIDS.

    This takes us back to the original questions: Is it possible that a mistake has been made in formulating the definition of AIDS? Is Chronic Fatigue Syndrome actually part of the AIDS epidemic?

    If this is even a remote possibility, why haven't other books been written about it? Why isn't every health reporter in the country writing about it, every investigative reporter investigating?

    The answer, I believe, is pretty simple, and it is a problem that has dogged the AIDS epidemic from the beginning: denial.

    From the very beginning of the AIDS epidemic, the syndrome has been characterized as affecting "the other": Haitians (i.e., blacks), gay men, IV drug users, and these groups' sexual partners. These individuals have been contrasted -- and still are -- with the "innocent victims" of the AIDS epidemic: the unknowing wives, and their babies.

    AIDS patients, and people who test HIV-positive (whatever that actually turns out to mean), have been so badly treated, so discriminated against, so scapegoated and demonized that it is not surprising that there is an almost reflexive recoiling from the possibility that AIDS is not the narrowly-defined illness that it has been portrayed as being.

    People have been murdered for testing HIV-positive; they have been accused of murder; they have been driven to suicide; they have been jailed; they have been denied jobs and health insurance and places to live.

    Given all this, denial that AIDS could be even more widespread than government officials admit is not too surprising. What rational person would want to be diagnosed with an illness that could produce such terrible repercussions in every area of life?

    Oddly enough, this denial appears to be most fiercely concentrated among medical researchers, and not among the patients themselves.

    Chronic Fatigue Syndrome patients, in fact, know they suffer from a profoundly debilitating, life-altering illness that is destroying their immune systems.

    Until the denial among medical professionals about the relationship between the AIDS and Chronic Fatigue Syndrome epidemics is overcome, however, it is difficult to imagine how either epidemic can be ended.

    Chapter One

    Some CFS Patients May Be "Non-HIV AIDS" Cases

    A disturbing announcement was made at the July 1992 international AIDS conference held in Amsterdam: Several people with symptoms of AIDS, but who had no evidence of infection with either HIV-1 or HIV-

    2 (the viruses generally believed, at the time, to cause AIDS), had been identified by the U.S. Centers for Disease Control. A few weeks later, in early September, Newsweek made an even more shocking announcement: that Chronic Fatigue Syndrome researcher Dr. Paul Cheney had in his practice 20 CFS patients who had the same immune system deficiencies as the non-HIV AIDS cases revealed at the Amsterdam conference.

    What wasn't known to most observers was that one of the researchers who had first said publicly that he was aware of such cases, Dr. Sidhur Gupta of the University of California, Irvine, is himself a Chronic Fatigue Syndrome researcher.

    The fact that some CFS patients were developing exactly the same immune system problems as AIDS patients, however, raised the questions not only of what was causing that immune system destruction but also of the relationship that exists between the two syndromes.

    The hallmark of the HIV-negative AIDS cases, as established by the Centers for Disease Control, is a depletion of a type of immune system cell called T4 (or CD4) cells. The T4 cells of AIDS patients can fall to very low levels and, although recent studies have suggested that there is no real correlation with health status, a decreasing T4 cell count is generally viewed as a sign of worsening disease.

    The CDC decided to call the HIV-negative, AIDS-like disease "ICL" (an abbreviation for "idiopathic CD4-positive T-lymphocytopenia," which simply means an unexplained depletion of T4 cells).

    Most healthy people have a T4 cell count of approximately 1,000; a T4 cell count below 800 is considered abnormal. In order to be diagnosed with ICL, a person must have a T4 cell count of less than 300.

    One of the most puzzling things about the ICL cases to AIDS researchers -- other than the fact that they didn't have HIV -- is that most of the patients do not fit into recognized AIDS "risk behavior" categories; that is, they were not gay men, IV drug users, or the sexual partners of people in those risk groups. These cases may, in fact, be dramatic evidence that federal officials have not told the public the whole truth about the nature and the full scope of the AIDS epidemic.

    The mystery of what role HIV actually plays in causing the immune system deterioration and symptoms seen in AIDS deepened in early October 1992. The British medical journal The Lancet reported that five people had received blood from a man later found to be infected with HIV; however, ten years later, the five transfusion recipients as well as the original, HIV-positive blood donor remained free of AIDS symptoms and were apparently healthy. The Australian researchers who reported those cases concluded that these six people were infected with a non-disease-causing strain, or type, of HIV.

    The link between the immune system dysfunction seen in AIDS and in CFS was made explicit in early 1993 when government scientists admitted that CFS patients, like AIDS patients, suffer a decline in T4 cells. The government's leading CFS researcher, Dr. Stephen Straus at the National Institute of Allergy and Infectious Diseases, published a research paper in The Journal of Clinical Immunology in which a decrease in the number of T4 cells in CFS patients was documented.

    Dr. Straus proposed a novel mechanism to explain the loss of T4 cells in CFS patients: The T4 cells of CFS patients were not depleted, as they were in AIDS patients, according to Dr. Straus; they were just hiding in organ tissues. Unfortunately, Dr. Straus was unable to produce any evidence to support this theory (and still has not done so). Dr. Straus did not suggest that any of his CFS patients had T4 cell counts so low that they could be identified as ICL patients.

    Meanwhile, Dr. Cheney, in addition to announcing that some of his CFS patients had low enough T4 cell counts to be considered non-

    HIV AIDS cases, reported that as many as 40 percent of his CFS patients also had a close associate with an illness similar to CFS. This information -- along with the mystery of why AIDS could develop without HIV infection and why HIV infection does not always lead to AIDS -- raised the possibility that a virus or bacteria that spreads more easily than HIV could be attacking people's immune systems.

    Chapter Two

    A Virus Found In AIDS Patients Is Also Found in CFS Patients With Brain Lesions And May Be The Primary Attacker Of The Immune System

    A virus that has been considered for several years a possible cause of Chronic Fatigue Syndrome is Human Herpes Virus 6 (HHV-6). This virus was first discovered in AIDS and cancer patients in the mid-1980s at the National Cancer Institute. It was subsequently found that people with Chronic Fatigue Syndrome, like people with AIDS, can have extremely high levels of antibodies to HHV-6.

    As more is learned about HHV-6, its ability to attack the immune system -- and perhaps other parts of the body, like the nervous system -- has been documented in more and more frightening ways. Even more alarmingly, the most recent research on HHV-6 suggests that it, and not HIV, is the primary infection that destroys an important part of the immune system in AIDS.

    That part of the immune system is the natural killer (NK) cells. NK cells are crucial to the immune system's front-line defense against both viruses and cancer, because they attack and kill any cells they perceive to be foreign. If the NK cells aren't working properly -- which they aren't, in both AIDS and CFS -- this very important protection is knocked out.

    The research team that discovered the existence of HHV-6, working with Dr. Robert C. Gallo at the National Cancer Institute, announced in early April 1993 that HHV-6 is the only virus known to be able to infect and kill NK cells.

    Furthermore, Dr. Gallo and his colleagues asserted, HHV-6 infection allows the AIDS virus, HIV, to invade NK cells and kill them.

    The question of how many other kinds of cells require HHV-6 to be present before HIV can invade them remains, at this time, unanswered.

    HHV-6 is capable of wreaking all kinds of havoc, not all of which is confined to the immune system. In January 1992, a study was published showing that a large percentage of CFS patients who had HHV-6 actively growing in their blood streams also showed evidence of organic brain disease.

    When CFS patients from the first detected outbreak of CFS in the U.S. -- which occurred in Incline Village, Nevada, in the mid-1980s -- were studied, brain scans showed that 80 percent of those infected with actively growing HHV-6 had (several years after the initial outbreak) developed brain lesions.

    No one knows what the lesions mean or are doing to the patients, or whether HHV-6 is actively growing at the site of the brain damage.

    But the Incline Village CFS patients were also found to have NK cells that weren't functioning properly. Now, we know that HHV-6 is, most likely, directly responsible for the dysfunction in the CFS patients' NK cells, but the virus' involvement in causing the brain lesions has yet to be proven conclusively.

    The scientists studying the Incline Village patients concluded that there was an infectious agent, capable of being spread from person to person, in the CFS patients: HHV-6.

    This very important study of CFS patients not only indicates that CFS is a contagious illness, but also suggests that HHV-6 is its cause.

    Chapter Three

    HHV-6 Kills An Important Immune System Cell In AIDS And CFS Patients

    Human Herpes Virus 6 (HHV-6) was first discovered in people with damaged immune systems who had cancer or AIDS. However, when studies showed that it seemed to infect about 90 percent of the world's population by age three, HHV-6 was generally portrayed by scientists as a fairly harmless virus.

    More recent research, however, has thrown the supposition about HHV-6 being harmless into doubt. For one thing, there are two different types of HHV-6; one is isolated from infants, and seems to cause only a mild childhood illness, with fever and rash, called roseola.

    The other type of HHV-6, however, is found in very sick adults who have AIDS, cancer, Chronic Fatigue Syndrome, or other immune system abnormalities. And the newest research on this type of HHV-6 suggests that it may be the cause of the immune system deficiencies seen in both AIDS and CFS.

    National Cancer Institute researcher Robert Gallo and his co-workers are generally credited with the discovery of HHV-6, and Dr. Gallo and his lab workers have continued to study the virus intensively. (Dr. Gallo's claims to virus discovery have to be taken with a grain of salt, however. He also claimed, for a number of years, to have discovered HIV, the "AIDS virus." After a lengthy investigation and charges of virus-lifting by other scientists, however, Dr. Gallo admitted that he had simply "discovered" a virus that had been sent to him by Pasteur Institute scientist Luc Montagnier and his research group. For having made false claims about discovering the "AIDS virus," Dr. Gallo was judged guilty of scientific misconduct by the National Institutes of Health in December 1992.)

    The HHV-6 that Dr. Gallo and his colleagues are studying at the National Cancer Institute is the type that infects adults who have AIDS, cancer, or Chronic Fatigue Syndrome.

    In April 1993, Dr. Gallo and his colleagues published an astonishing report in the prestigious British medical journal Nature. They reported that HHV-6 was able to infect and kill the natural killer cells, which are an important part of the immune system, and that it was the only virus ever found to do so.

    Natural killer cells are the body's front-line defense against viruses and some kinds of cancer. When natural killer cells encounter a cell that is "foreign" -- either because it is infected with a virus or because it has become cancerous -- they engulf and destroy it. Unlike other types of immune system cells, natural killer cells do not require any type of priming or activating by another part of the immune system; that is why they are considered to be the first line of defense in protecting the body against certain invaders.

    In both AIDS and Chronic Fatigue Syndrome patients, the natural killer cells just don't work the way they do in healthy people. One researcher found a natural killer cell activity deficit of 86 percent in the Chronic Fatigue Syndrome patients she studied. AIDS patients have similar deficits in natural killer cell activity. Before Dr. Gallo's study linking HHV-6 and natural killer cell destruction, no one had been able to explain why natural killer cells stopped working in AIDS and CFS patients.

    Dr. Gallo and his colleagues, however, not only showed that HHV-6 can infect and kill natural killer cells, but actually suggested that the virus "may play a role in the acquired immunodeficiency syndrome (AIDS) and in the chronic fatigue syndrome, two disorders associated with a defective NK cell activity."

    They are also the first researchers to confirm that the immune system abnormalities seen in AIDS and CFS are actually the same.

    In fact, in the conclusion of their research report, Dr. Gallo and co-workers stated that their results "elucidate a novel mechanism whereby HHV-6 may contribute to the immune dysfunction associated with CFS and AIDS."

    Further studies of HHV-6 in AIDS and CFS patients may provide even more examples of how this virus causes the immune system abnormalities the two syndromes share and may even suggest even more strongly that CFS and AIDS are simply different manifestations of the same illness.

    Chapter Four

    HHV-6 Seems To Be Causing Lung Disease In Immunosuppressed Individuals

    People who receive organ transplants are given drugs that suppress their immune systems so that they do not reject the transplanted organs, thus placing them in a state that is similar to AIDS or CFS. While they are in that immunosuppressed state, they are especially vulnerable to infections, just like CFS and AIDS patients are. Now it appears that an often-fatal lung illness that can occur following bone marrow transplantation may be caused by a virus that infects AIDS and CFS patients, Human Herpesvirus 6 (HHV-6).

    If HHV-6 is causing lung disease in bone marrow transplant recipients, that raises the question: Is HHV-6 also causing lung disease in CFS and AIDS patients?

    Another extremely serious immunological complication that occurs after bone marrow transplantation, Graft-Versus-Host Disease (GVHD), may also be caused by HHV-6. Both of these findings were published in the New England Journal of Medicine in July 1993.

    The lung illness caused by HHV-6 is pneumonitis, which is inflammation of the lung (basically, a type of pneumonia). When lung tissues from patients who'd had bone marrow transplants and subsequently developed pneumonitis of unknown cause were examined by a research group in Seattle, the tissues were found to contain considerable amounts of HHV-6.

    That led the researchers to conclude that HHV-6 was probably causing some cases of the often-fatal pneumonitis in bone marrow transplant patients.

    This is the first time that HHV-6 has been implicated in causing a lung illness.

    Graft-Versus-Host Disease (GVHD) is another potentially life-threatening illness that strikes bone marrow transplant recipients. In GVHD, the donor's healthy T-cells (which are impaired in AIDS and CFS) attack the recipient's tissues; GVHD is a form of organ rejection. The symptoms of GVHD include fever, rash, hepatitis, diarrhea or abdominal pain, vomiting, and weight loss.

    Some of the bone marrow transplant patients studied by the Seattle researchers who developed pneumonitis caused by HHV-6 also developed severe GVHD.

    Those patients were also found to have very high levels of HHV-6, particularly in their lungs.

    That is to say, three conditions occurred together in the patients: high levels of HHV-6, pneumonitis, and severe GVHD.

    This led the Seattle researchers to suggest that HHV-6 is the likely cause of both the pneumonitis and the GVHD seen in some bone marrow transplant recipients.

    Another report about HHV-6 also appeared in the same issue of the New England Journal of Medicine. This report was from Japan, where researchers had observed a ""mononucleosis-like illness'' they believed to be caused by HHV-6.

    The 43-year-old man described by the Japanese research team was admitted to the hospital with a high fever, rash, swollen lymph nodes, a swollen spleen, and inflamed tonsils; he was also suffering from liver dysfunction.

    This man, too, had high levels of HHV-6 during his illness, leading the Japanese researchers to conclude that the man's ""mononucleosis-like illness'' had been caused by HHV-6.

    Although some researchers have suggested that HHV-6 is a basically harmless virus that infects approximately 90 percent of the world's population by the age of three, new information being published about the virus indicates that some varieties, or strains, are capable of causing profound immune dysfunction and serious illness. These three problems may be just the tip of the iceberg in terms of the damage that HHV-6 is able to inflict on the immune system.

    Chapter Five

    A Virus Found Growing In CFS Patients Has Been Linked To Miscarriage

    One of the viruses that has been found to be active in both CFS and AIDS patients, Human Herpes Virus 6 (HHV-6), has been linked by Japanese scientists to miscarriage.

    HHV-6 is a virus that primarily invades the T-cells of the immune system (though it can also live in other immune system cells). T-cells are critical in regulating immune responses -- both in getting an immune response started, and in shutting it down. When the T-cells don't work because a virus is attacking them, the immune response can be severely affected, as is seen in both CFS and AIDS.

    Very recently, HHV-6 has been found to be the only virus that is capable of invading and killing natural killer (NK) cells. NK cells don't work properly in both CFS and AIDS; a deficiency of NK cell activity, in fact, has been cited by numerous researchers to be the most consistent immune system abnormality found in CFS patients. If the NK cell activity of AIDS patients is examined, it, too, is found to be consistently abnormal. HHV-6, which is known to be actively growing in both AIDS and CFS patients, has been identified as the only virus known to be able to infect and kill NK cells. It is reasonable to assume that it is causing the abnormal NK cell activity seen in both sets of patients.

    HHV-6 has also been linked, in CFS patients, to the development of brain lesions (areas of dead or damaged brain tissue). A recent study found that CFS patients with a lot of active HHV-6 also had developed brain lesions that are visible on specialized brain scans; patients without active HHV-6 did not have brain lesions.

    A Japanese research team from the Nara Medical University studied 30 patients who'd had miscarriages early in pregnancy (at 6-12 weeks). When tissue from the miscarriages was examined, they were found to contain HHV-6 antibodies that were four times higher than those found in pregnant women who did not miscarry. In a report published in the British medical journal The Lancet in November 1992, the Japanese research team suggested that active HHV-6 "may predispose" to miscarriage in pregnant women.

    Chapter Six

    HHV-6 Infections Can Be Fatal

    Human Herpes Virus 6, HHV-6, has been presented to the world as rather a Dr. Jekyll-Mr. Hyde kind of a virus: On the one hand, researchers like Dr. Jay Levy at the University of California-San Francisco point out that HHV-6 infects so large a percentage of people world-wide that it must be essentially harmless. On the other hand, some pediatricians have reported that HHV-6 infections have been fatal.

    It is possible, given that more than 10 different strains, or types, of HHV-6 have been identified, that different strains of the virus cause different levels of illness, ranging from almost unnoticeable (a "silent" infection) to deadly.

    High levels of antibodies to HHV-6 have been found in several groups of very sick patients, including AIDS and CFS patients.

    No one knows for sure what damage HHV-6 is doing in those patients. In the laboratory, however, it has been demonstrated that at least some strains of HHV-6 are very efficient killers of immune system cells -- especially T4 (or CD4) and natural killer cells, the two types of cells most affected in both CFS and AIDS.

    And HHV-6 has recently been found in more than one-third of a group of Kaposi's sarcoma tumor biopsies, suggesting that it may play a role in causing this unusual cancer seen in AIDS patients.

    Recently, the HHV-6 strains have been divided by researchers into two groups, or variants: Variant A, viruses which have been isolated from sick adults (those with CFS, AIDS, or cancer); and Variant B, which has been found in relatively healthy babies.

    Most of the fatal HHV-6 infections identified in the medical literature, however, have occurred in very young children. Cases of fatal hepatitis, or liver disease, caused by HHV-6 in children were reported in the medical literature in 1990 and 1991. HHV-6 infection was localized, not surprisingly, primarily in the children's livers.

    In summer 1992, however, a group of New York University re searchers reported a fatal, systemic -- that is, spread throughout many different organs and tissues -- HHV-6 infection in a 13-month-old girl.

    The child's illness began with a fever and lack of appetite; soon, however, she began to show evidence of hemorrhaging -- uncontrolled bleeding or leaking of blood vessels -- on her face, trunk, arms, legs, and around her lips. This child also developed liver disease. She died from congestive heart failure on the fifth day after being hospitalized.

    When an autopsy was performed on the child, HHV-6 infected white blood cells were found in numerous internal organs: heart, lungs, liver, spleen, thymus, kidney, and bladder, as well as in the gastrointestinal tract, salivary glands, bone marrow, lymph nodes, middle ear, peripheral nerves, and skeletal muscle.

    Not too surprisingly, the physicians concluded that this disseminated, or very widespread, HHV-6 infection had killed the little girl.

    If certain strains of HHV-6 are capable of causing fatal illnesses -- assuming that this is a strain-dependent phenomenon, which it may not be -- it seems that a reasonable next step in HHV-6 research would be to identify the most deadly strains.

    Chapter Seven

    A New Virus, HHV-7, Has Also Been Found In CFS Patients

    A new virus, called Human Herpes Virus 7 (HHV-7), was isolated from a CFS patient in 1992. This virus was found in the National Cancer Institute; it has been studied most intensively in the laboratory of Dr. Robert C. Gallo.

    Whenever Dr. Gallo and his colleagues claim to be studying a new virus it should again be noted that he, and certain colleagues, have been under investigation for several years because of allegedly fraudulent claims that the Gallo lab isolated the AIDS virus (HIV) in 1983. In fact, on December 31, 1992, Dr. Gallo and one of his colleagues involved in the isolation of HIV were found by the National Institutes of Health (only one of the regulatory bodies investigating Dr. Gallo and his colleagues) to be guilty of scientific misconduct.

    The other virus found actively growing in both AIDS and CFS patients, Human Herpes Virus 6 (HHV-6), was also isolated in the Gallo laboratory in the mid-1980s; Dr. Gallo's account of the discovery of that virus, like his account of the discovery of the AIDS virus, has been challenged by other scientists.

    It is not known whether HHV-6 -- which is closely related to HHV-7 -- contributes to causing CFS, or AIDS. It is known that HHV-6 infects and kills not only T4 cells, one of the major cells that is affected in AIDS, but also infects and kills natural killer cells, which are dysfunctional in both AIDS and CFS.

    Like HHV-6, HHV-7 is believed to infect T-cells.

    And also like HHV-6, HHV-7 is quite similar to cytomegalovirus (CMV), which can cause blindness and other serious illnesses in AIDS patients. However, HHV-7 is different enough from both HHV-6 and CMV to be declared by Dr. Gallo's research team to be an entirely new human virus.

    An important question not posed by these investigators is: Where are these "new" viruses, found to be infecting both AIDS and CFS patients, coming from?

    Chapter Eight

    A Natural Immune System Anti-Viral Pathway Doesn't Work In CFS

    The immune system has evolved many different mechanisms to fight invaders: viruses, bacteria, parasites, and anything perceived as "non-self," such as defective or cancerous cells. Some of those mechanisms are incredibly specific, like antibodies; others are pretty general, like natural killer cells. One of the continuing mysteries of the immune system is how all of these mechanisms interact, overlap, and appear to compensate for each other to protect against infectious agents.

    One way the immune system protects against viruses is through a biochemical pathway with the name "2'-5'A synthetase/RNase L pathway." This pathway's anti-viral effects are turned on by interferon, one of the chemicals (called cytokines) produced by T-cells and other cells of the immune system.

    Although this sounds rather technical -- and it is -- the most important fact about the pathway is very simple: It malfunctions in both CFS and AIDS patients.

    Basically, the pathway works like this: When a virus is detected by the immune system, interferon is produced. Interferon stimulates the inactive chemical 2'5'A synthetase; it interacts with other chemicals and produces a biologically active substance called 2'-5'A. "Biologically active" means that the 2'-5'A is capable of acting on other molecules and making them active, too.

    And that is what 2'-5'A does; it activates another immune system substance, RNase L. Activated RNase L is then able to stop the invading virus from reproducing itself and spreading the infection.

    When this pathway works correctly, interferon production results, through the steps outlined, in stopping viruses from spreading throughout the body. But in CFS patients -- and AIDS patients -- the pathway doesn't work properly.

    Dr. Robert Suhadolnik, working at Temple University in Philadelphia, has discovered that CFS patients have too much of both active substances in the pathway, 2'-5'A and RNase L.

    As a result, not only viral reproduction, but also much of the cell's own internal activity, is halted. That means that the cells of the immune system are unable to react properly to invaders.

    The failure of this pathway is another example of how an overreaction by a portion of the immune system in a person with CFS can actually result in decreased immunity.

    The defect in the anti-viral pathway also suggests that CFS patients, like AIDS patients, are vulnerable to opportunistic infections that can make them very sick.

    Interestingly, one of the experimental treatments for CFS (and one which has also shown promise in treating AIDS) is Ampligen, a chemical that is structurally similar to interferon. It appears to correct the defect seen in the 2'-5'A Synthetase/RNase L pathway. Studies using Ampligen to treat CFS are currently being reviewed by the Food and Drug Administration.

    Another interesting observation made by Dr. Suhadolnik demonstrates how a malfunction in the immune system in CFS can result in either up- or down-regulation. While most CFS patients studied by Dr. Suhadolnik have increased amounts of RNase L, he has also reported that he has seen some CFS patients in whom there is virtually no detectable RNase L -- which is exactly what is found in AIDS patients.

    That finding has led some researchers to speculate that a retrovirus -- like HIV, the "AIDS virus" -- may be involved in causing CFS.

    This natural anti-viral pathway may provide not only an understanding of what goes wrong in CFS, but also a way to diagnose the syndrome. In July 1992, a research firm in Houston, Texas, announced that the firm had developed a diagnostic test for CFS. The company is Oncore Analytics, Inc., and the test measures the anti-viral pathway. The Oncore test is performed on a blood sample.

    The virus that causes CFS has not yet been identified and, in fact, there are still researchers and clinicians who do not believe that a virus -- or any infectious agent -- causes CFS. If the Oncore test, which measures a defect in an anti-viral pathway, is capable of reliably separating CFS patients from healthy people, that would be another piece of evidence suggesting that CFS is caused by a virus.

    Chapter Nine

    A Mysterious Organism Called A Mycoplasma May Be Peripherally Involved In CFS

    Mycoplasmas are extremely small bacteria, and are perhaps the smallest self-sufficient organisms that exist. Mycoplasmas can cause human disease -- particularly pneumonia and a type of urinary tract infection -- but have not been considered to be major human pathogens. Since 1986, however, there has been speculation that a newly-discovered type of mycoplasma may be involved as a co-factor in causing AIDS and, perhaps, even CFS.

    The new mycoplasma was discovered in AIDS patients by Dr. Shyh-Ching Lo at the Armed Forces Institute of Pathology. The mycoplasma appears to invade many internal organs -- kidneys, spleen, brain, liver -- and causes the organ tissue to die.

    While Dr. Lo's suggestion that the mycoplasma might play some role in causing AIDS is controversial, Dr. Luc Montagnier, the Pasteur Institute researcher who discovered HIV, the "AIDS virus," has found the same kind of mycoplasma infecting French AIDS patients. Dr. Montagnier, like Dr. Lo, believes that this mycoplasma may play an important role in causing AIDS.

    And Dr. Lo has been able to accomplish with the mycoplasma what no scientist has been able to do using HIV: Dr. Lo has taken mycoplasma from AIDS patients' tissues, injected them into animals, watched the animals die of a wasting illness that resembles AIDS, and then re-isolated the mycoplasma from the animals' tissues.

    In other words, Dr. Lo has created a classical animal model for the mycoplasma-caused illness. Such an animal model does not exist for HIV and AIDS; no animal has ever been made to develop an AIDS-like illness after being infected with HIV.

    Dr. Lo also found the new mycoplasma in a number of non-AIDS patients -- previously healthy people who died very suddenly following a flu-like illness. These cases prove that this particular mycoplasma can infect people who do not have AIDS.

    Fortunately, mycoplasma can be controlled by readily-available antibiotics such as doxycycline or tetracycline. The fact that many CFS patients report that their symptoms improve when they take doxycycline causes Dr. Lo to suspect that the mycoplasma may be involved in causing some cases or symptoms of CFS.

    Unfortunately, Dr. Lo's work is still very much in the research stage, and a diagnostic test for the mycoplasma is not readily available. But if a physician suspects a CFS patient may be infected with the mycoplasma, it is safe to treat the patient with an anti-mycoplasma antibiotic, just in case, according to Dr. Lo.

    Some CFS patients report considerable improvement in their symptoms when they take antibiotics. "The burning feeling in my spine and head disappear," CFS patient "Ruth" told me, when she takes ciprofloxacin, an antibiotic. She added, "The joint pain -- especially the neck pain -- goes away, and I am able to think clearly when I take ciprofloxacin."

    Chapter Ten

    Just As In AIDS, Immune System Cells Called Monocytes Do Not Work Properly In CFS Patients

    Cells called monocytes are an essential part of the immune system. Monocytes are found in the circulating blood, and they perform a variety of functions: They ingest and kill invaders, they communicate with other immune system cells to indicate when an immune response should be mounted, and they make a number of enzymes that are essential to properly functioning immunity.

    Monocytes are the precursor cells to another very important type of immune system cell called macrophages. Macrophages are essentially the mature forms of monocytes; they are found situated in organ tissues (rather than in the blood, like monocytes). Macrophages perform basically the same functions as monocytes.

    Like just about every other cell in the immune system, monocytes do not work properly in CFS patients. Some research teams have found that about half of CFS patients have monocytosis, in which too many monocytes are produced. When there is an excess of monocytes, there can be an excess of the lymphokines that the monocytes produce; these lymphokines can make patients feel very sick.

    Additionally, a Spanish research team from the University of Navarra, in Pamplona, studied monocyte function in CFS patients and found it to be disturbed in a large percentage of patients. The Spanish researchers examined the delicate fibers on the surfaces of monocytes and macrophages, called "vimentin filaments," that are thought to help the cells move about in the body and to play a role in immune responses.

    When the monocytes and macrophages of CFS patients were compared to those of healthy people, the Spanish scientists found a "marked reduction" in the vimentin filaments. Consequently, they found, the monocytes and macrophages of CFS patients are quite dysfunctional.

    In fact, 30 of 35 people who fit the U.S. CDC criteria for CFS (six men and 29 women who ranged in age from 19 to 51) had, according to the Spanish research team, "monocyte dysfunction."

    Chapter Eleven

    As In AIDS, The Immune System Is Both Over-Stimulated And Depressed In CFS

    The balance maintained between the interacting parts of the immune system appears to be extraordinarily delicate, we are learning as scientists unravel more and more of its mystery. What is becoming clear is that it's possible for one part of the immune system to be over-stimulated at the same time as other parts are depressed.

    In CFS, the immune system cells called T-cells are often over-stimulated; this state is called "T-cell activation." Research has shown that, when T-cells are activated, they make immune system chemicals called cytokines; interleukin and interferon are examples of cytokines. When the T-cells make excessive amounts of cytokines, they can actually cause symptoms similar to those seen in CFS.

    Fever, swollen glands, sore throat, aching muscles and joints, sleep disturbance, and even psychological symptoms can be caused by excessive amounts of cytokines.

    Dr. Paul Cheney, who was one of the first physicians to recognize CFS in the U.S. -- and who has a number of CFS patients who can be designated "non-HIV AIDS cases" because they have very low T4 cell counts -- explains it this way: The sicker his patients feel, the more T4 cells (which are also called CD4 cells) they have. The less sick the patients feel, the lower their CD4 cell counts are.

    Dr. Cheney says that the notion of "sick" is used differently with respect to AIDS and CFS patients.

    "Sick is a semantic term in the sense that it implies different meaning in CFS than it does in AIDS," Dr. Cheney says. "We have sort of defined AIDS patients as what happens to them, and when bad things happen to them, they have low CD4 counts. CFS patients feel bad all the time, and their CD4 counts are actually high."

    Dr. Cheney blames his sickest patients' symptoms on having activated T-cells. "It will make you royally sick" to have activated T-cells, he points out. "And, I'll tell you, the sickest people I have, the people who come in here who are really, really, sick, they'll have CD4 counts of 2,000," which is about twice as high as normal. "And the cytokines that are being expressed, of course, typically cause CD4 cell proliferation" -- so the T-cells, which are already too high, increase even more. This is the type of T-cell malfunction that can occur when the immune system is over-stimulated.

    But Dr. Cheney also has CFS patients with very low CD4 cells counts; so low, in fact, that they can be diagnosed as being "non-HIV AIDS," or ICL, cases. Dr. Cheney believes that both sets of patients -- those with high CD4 cell counts and those with low CD4 cell counts -- have CFS. He thinks that the patients with the low T4 cell counts, however, are in "a different state" from other CFS patients.

    Dr. Cheney says that his CFS patients who have fewer than 200 CD4 cells -- a level that is considered very dangerous for AIDS patients -- are "not feeling so good." He also points out, however, that those patients who have CD4 counts between 300 and 500 typically don't feel too bad, even though 1000 T4 cells is considered "normal."

    "Looking at this group as a whole, the patients with low CD4 counts are relatively less sick -- less symptomatic, I should say," Dr. Cheney says. "Their symptoms aren't as severe. They seem to be more stable. If I had to guess what is happening, I think what is happening is that you are looking at the same disease in two different states."

    One of those states is "up-regulated," in which the T-cells are activated and producing large amounts of cytokines; the other is a state of down-regulation, in which even the numbers of immune system cells drop.

    Sometimes increased amounts of certain cytokines can cause the depression of some types of immune system cells. One of the cytokines that is elevated in CFS, for instance, is interleukin 1 (abbreviated IL-1). IL-1 has been shown to cause other parts of the immune system -- like natural killer cell activity -- to be suppressed. This is only one example of how an elevation in one part of the immune system can cause the depression of another part.

    Chapter Twelve

    One Researcher Thinks That CFS Should Be Called "Lymphokine Overdose Disease"

    Dr. William A. Carter is a Professor of Oncology and Hematology at Hahnemann University in Philadelphia. He is also the co-developer of an experimental drug called Ampligen, which has shown promise in treating both Chronic Fatigue Syndrome and AIDS, and is currently under review by the Food and Drug Administration. At a conference held in late 1991, Dr. Carter discussed a clinical trial of Ampligen and explained that he thinks CFS could be called "lymphokine overdose disease."

    Lymphokines are substances produced by white blood cells (also called lymphocytes) when the immune system encounters an invader. They include the interferons (alpha-, beta-, and gamma-interferon), the interleukins (there are at least 12 interleukins), tumor necrosis factor, and others. Most lymphokines stimulate cells to do something: either to reproduce themselves (interleukin-2 used to be called "T-cell growth factor," for instance), or to interact with other components of the immune system (gamma-interferon works in this way).

    When Dr. Carter made his 1991 presentation at the 31st Interscience Conference on Antimicrobial Agents and Chemotherapy, he was also interviewed by the on-site Conference Journal. The lymphokine that Dr. Carter spoke about in his interview was interleukin-1 (IL-1), the primary action of which is to stimulate cells to produce interleukin-2 (IL-2).

    Dr. Carter told the Conference Journal that his research group had determined that more than two-thirds of CFS patients have abnormally high levels of lymphokines; because of that, he suggested that CFS might more appropriately be named "lymphokine overdose disease."

    According to Dr. Carter, many of the symptoms of CFS -- such as fatigue, memory loss, and other problems with thinking -- are probably caused by the high levels of lymphokines that patients are making in their own bodies.

    CFS patients who have very high levels of IL-1 responded well to Ampligen treatment, Dr. Carter told the Conference Journal. Just as importantly, the patients in Dr. Carter's study who had high levels of IL-1 and who received a placebo (inert, or phony) substance instead of Ampligen got progressively worse.

    One of the most disturbing findings made by Dr. Carter and his research team was that CFS patients with abnormally high levels of IL-1 had "anatomic holes" in their brains that were detected by using brain scans. It was not clear to the research team whether the holes were reversible or permanent.

    From this information, Dr. Carter and his colleagues concluded that IL-1 is important in causing the symptoms of CFS, particularly the mental symptoms. Dr. Carter said that increased IL-1 could be used as a "footprint" to help diagnose severe CFS.

    Chapter Thirteen

    CFS, Like AIDS, May Be Primarily A Tumor Necrosis Factor Disease

    Tumor Necrosis Factor, TNF, was one of the first lymphokines to be discovered. Lymphokines -- also called cytokines -- are chemicals that are produced by immune system cells; they help different kinds of cells to communicate with each other in mounting immune responses.

    TNF is produced by the immune system cells called macrophages, and was named "Tumor Necrosis Factor" because it was observed to make cancer cells die. TNF is also primarily responsible for causing the extreme weight loss observed in people with cancer and AIDS.

    TNF has been found by some researchers to be increased in CFS patients. Other lymphokines -- gamma-interferon, interleukin-2, and interleukin-6, for example -- have also found to be increased in CFS. But some researchers have found these same lymphokines to be decreased in CFS, pointing out once again that a malfunctioning of the immune system can result in contradictory information being gathered.

    Whether these cytokines are produced at increased or decreased levels in CFS, it is clear that their normal production is disturbed in these patients. Also, because different lymphokines and various types of immune system cells interact with each other in not-yet-understood ways, it's not clear exactly why CFS patients have abnormal amounts of TNF and other cytokines.

    TNF has also been observed to cause HIV to reproduce at higher levels than it normally does. For that reason, Dr. Jay A. Levy, a prominent AIDS researcher in California, has suggested that AIDS is primarily a TNF disease. Dr. Levy has also suggested that, if TNF levels were decreased, a lot of the symptoms and illnesses seen in AIDS patients would disappear.

    Interestingly, an experimental drug that has shown promise in treating both AIDS and CFS, Ampligen, has been shown to lower TNF levels, as well as improving symptoms.

    Chapter Fourteen

    Zinc Deficiency Can Contribute To CFS

    Zinc is a trace mineral that is very important in maintaining a healthy immune system. But as many as 85 percent of CFS patients may have a serious zinc deficiency, which is extremely common among AIDS patients as well.

    Zinc is perhaps the most important "growth factor" in the human body; any cells that are rapidly reproducing -- such as those involved in healing wounds, immune system cells that are actively fighting infections, and growing fetuses -- require a steady supply of zinc. Zinc deficiency in a pregnant woman can cause very serious birth defects in her child. The most dramatic birth defect caused by zinc is an encephaly, in which a child is born with only part of a brain, or actually no brain at all.

    Zinc deficiency can also cause stunted growth (in children), skin lesions, hair loss, and increased susceptibility to infections because of impaired immunity.

    A physical sign of zinc deficiency -- which is, according to some researchers, found in a large number of CFS patients -- is white spots on the finger nails, a condition called "leukonychia." Some CFS researchers have reported that a large majority of their CFS patients exhibit the white spots on their fingernails that are indicative of zinc deficiency.

    Zinc deficiency may be responsible for another symptom of CFS -- alcohol intolerance. Many CFS patients are unable to tolerate alcohol. Zinc is responsible for helping to form the enzyme that breaks down alcohol, called alcohol dehydrogenase. Too little zinc may lead to insufficient production of alcohol dehydrogenase and, therefore, to alcohol intolerance.

    Zinc deficiency, then, may not only contribute to lowered immunity and birth defects among CFS patients and their children, but also to the alcohol intolerance that is often a symptom of the disease.

    Chapter Fifteen

    Magnesium Can Be A Missing Element In CFS

    Magnesium is a trace element that is necessary for the activities of many enzymes; serious deficiency can cause vascular problems, convulsions, tremors, depression, and psychotic behavior. In 1990, a British research team discovered that not only did CFS patients have a deficiency of magnesium in their red blood cells, but that magnesium injections actually helped some symptoms to improve.

    In the British study, 35 CFS patients were divided into two groups. One group received a magnesium injection once a week for six weeks; the other group received a placebo injection (in this case, sterile water) once a week for six weeks.

    At the end of the study, the patients who were treated with magnesium had much greater improvement in energy, pain, and emotional reactions than the placebo group did.

    The British investigators concluded that, while magnesium may not be a cure for CFS, it could prove to be helpful in treating some symptoms of the syndrome.

    Chapter Sixteen

    There Is A Hormonal Imbalance In CFS Similar To The One In AIDS

    The U.S. government's leading Chronic Fatigue Syndrome researcher, Dr. Stephen Straus at the National Institute of Allergy and Infectious Diseases, has for several years wasted a great deal of the government's resources by attempting to prove that CFS is a psychiatric illness, similar to depression. In one recent study in which he compared certain hormonal levels in CFS patients to those in people with depression, however, Dr. Straus uncovered a hormonal abnormality that contradicted his own theory.

    Dr. Straus, working with researchers at the National Institute of Mental Health and the National Instit

  • What is Adrenal relief exactly?
    Is it used for treating Chronic fatigue syndrome or HIV ?

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    Adam Young Why isn't CFS/ME a reportable disease overseen by our public health department? Why are CFS and ME (i.e., the same exact disorder) suspiciously categorized as two separate illnesses on a worldwide level (i.e., by ICD codes)? Doesn't anyone else but me, very clearly see, the catastrophic cover-up going on here?
    27 minutes ago · Like
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    Adam Young I can answer this above question
    27 minutes ago · Like

    Adam Young Why isn't CFS/ME a reportable disease overseen by our public health department? Because it costs thousands to treat a patient; thus a burden to the health industry financially.
    24 minutes ago · Like
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    Adam Young Why are CFS and ME (i.e., the same exact disorder) suspiciously categorized as two separate illnesses on a worldwide level (i.e., by ICD codes)?
    24 minutes ago · Like
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    Adam Young I can answer the above question also.
    24 minutes ago · Like
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    Adam Young Because no one really knows what causes the symptoms of the disorders (CFS / ME); and these 2 disorders are just a suggestion of what the diagnosis / doctor is looking at. Like a guestimate or a suggestion. My doctor said 'it COULD be M.E. or it could be CFS. But she couldn't be certain; or she couldn't confirm it.' Maybe it's a new way / softer way of telling someone they have hiv or aids (so not to shock them), plus, it could be a new way of treating the symptoms of AIDS, because it isn't absolute. Meaning it is a tamer way of telling some one, there IS a chance you will survive with these symptoms, a pose to. 'No that's it, you have aids and you are definitely going to die.'
    7 minutes ago · Like
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    Adam Young Doesn't anyone else but me, very clearly see, the catastrophic cover-up going on here?
    7 minutes ago · Like
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    Adam Young I can answer the above question also
    7 minutes ago · Like
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    Adam Young Yes I see it, but not as a cover up. I see it as a way of DIAGNOSIS. For example: One patient, and Two different doctors; giving Two different suggestions to what the illness (disorder) may be. And having Two different schools of thought on how to treat the patient; depending on the Doctors experience/ knowledge and personal out look on treating AIDS / ME or CFS.
    A few seconds ago · Like

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