"The most extensive of all the morbid mental conditions which reflect themselves so disastrously in the human system is the state of fear. It has many degrees of gradation, from the state of extreme alarm, fright, and terror, down to the slightest shade of apprehension of intending evil. But all along the line it is the same thing -- a paralyzing impression upon the centers of life which can produce, through the agency of the nervous system, a vast variety of morbid symptoms in every tissue of the body."
-Dr. William H. Holcomb (Omkar 1998)
"Fear is like carbonic acid gas pumped into one's atmosphere.
It causes mental, moral and spiritual asphyxiation and sometimes
death to energy, death to tissue and death to all growth."
- Horace Fletcher (Omkar 1998)
The Buddha said, in Kalama Sutra: "Do not believe in
what ye have heard. Do not believe in the traditions because they
have been passed down for many generations. Do not believe in
anything because it is rumoured and spoken by many. Do not believe
merely because a written statement of some old sage is produced.
Do not believe in conjectures; do not believe in that as truth
to which you have become attached by habit. Do not believe merely
in the authority of your teachers and elders. After observation
and analysis, when it agrees with reason and is conducive to the
good and gain of one and all, then accept it and live up to it."
- Posted outside the Blue Ridge Zen Group's Zendo
"Look, Mom, the emperor isn't wearing any clothes!"
Author's Note :
The "positive" and the "negative" aspects of a given topic
are two sides of the same coin. This book focuses on the "dark side"
of the mind-body-spirit continuum, and uses AIDS as a contemporary example of
how negative beliefs, social isolation, and severe, chronic, psychological stress
may bring about serious and fatal illnesses which may then be blamed on more
conventional "physical" causes. Many of these negative effects may
often be brought about, inadvertently, by the diagnosis, itself, creating a
kind of self-fulfilling prophecy. Although this is likely to be true of a variety
of illnesses, AIDS is an easily recognized example, partly because the science
behind AIDS suffers from a number of obvious inconsistencies and contradictions.
The "bright side" of the mind-body-spirit continuum has also been well described and documented by a number of researchers. Two recent books, Love and Survival: the Scientific Basis for the Healing Power of Intimacy, by Dean Ornish M.D., and Timeless healing: the Power and Biology of Belief, by Herbert Benson M.D., provide excellent discussions and research reviews that describe the power of positive beliefs, love, and intimacy to create and maintain health.
In truth, however, each side depends on the other for existence. To truly undertstand a subject like this one, I like to consider as many sides of the issue as possible. Otherwise, one may run from one witch doctor who has cast a "voodoo hex" on them straight into the office of another witch doctor to beg for healing.
I do not claim that the thesis of this book has been "proven", nor do I think anyone should try to "prove" it, as such attempts would involve extremely cruel experiments on animals and, ultimately, humans. I think there is enough available evidence for people to make an informed decision, and I have tried to present a great deal of it in this book. I also do not intend readers to use this book as their only source of medical advice. There are resources provided at the end of this book, such as the "Long-term surivivor's network", based in London, England (Walton 1999), to help people who want more information or contacts.
If you have been diagnosed "HIV positive" or diagnosed with "AIDS", you may benefit a great deal from reading this book. Ultimately, however, you will have to decide for yourself what arguments make the most sense to you, and what course to follow for your own health.
In the fall of 1987 a guest lecturer came to speak to a class that I was attending
at the University of Virginia. The topic was AIDS. He told us that it was caused
by HIV, the "human immunodeficiency virus", which was a special kind
of virus called a "retrovirus". He told us about how it was transmitted,
via blood to blood contact or sexual contact, about the agonizing, slow death
that it produced as it ate away at your immune system. He told us that it only
took one HIV to infect someone, and that once infected the end result was always
fatal. It was a terrifying prospect, and one that I silently prayed would never
happen to me.
The first person I knew who was diagnosed HIV positive was a good friend from high school. He committed suicide shortly after his diagnosis. Based on what I had heard in the fall of 1987, suicide almost seemed preferable to the slow wasting death that I HIV would apparently cause. Although I would have encouraged him to struggle to maintain his health as best he could, I could at least understand his motives given the future that was believed to await him. The second person I have known who was diagnosed HIV positive is still alive. She told me how she experienced prolonged and uncontrolled vomiting in the doctor's office immediately after she was told of her diagnosis. She then spent three years in a state of depression in which she tried to drown herself in alcohol and marijuana. Her health improved, acccording to her, when she began to learn that HIV was not as dangerous as she had previously believed.
The guest lecturer also told us something that has stuck in my mind over the years, because it didn't seem to make sense. He said that it took, on average, five or six years after becoming HIV positive ("seroconverting") before people would progress to AIDS. A few years later this estimate was pushed upwards to "10 to 11 years". I remember thinking at the time: "how do they know it takes, on average, five or six years for AIDS to develop, when HIV was only discovered a few years ago?" Looking back, I have realized that HIV, then called "HTLV-3" or "LAV" was first reported as the "probable cause of AIDS" in the spring of 1984, three years before the lecturer came to speak to my class. An "average" of five to six years means that only about half of people testing positive on the HIV antibody test will be diagnosed with AIDS after that time, and yet HIV had been discovered only three years before. Furthermore, this five to six year latency period was only concerning the diagnosis of "AIDS", which is not the same as mortality, and yet they were stating unequivicably that HIV was a universally fatal infection.
That sounded to me like a mathematical impossibility. If HIV tests had only been around for three years, it would be impossible to know that it took, on average, five to six years for people to "progress to AIDS". Although these questions bothered me, I quickly shrugged them off. I was sure that there must be a reasonable explanation. Little did I know that this small, nagging question, would be but a drop in the bucket of contradictions that infuse the science surrounding AIDS.
The Power of Belief
There have been a few groundbreaking studies that suggest just how powerful beliefs can be in causing or healing illness. Many were performed several decades ago. The two studies to be reviewed here were never followed up, to my knowledge, in spite of their potential implications. The first was published in 1962 by two Japanese researchers, Dr.'s Ikemi and Nakagawa (Ikemi 1962). In Japan there is a tree whose leaves produce a rash like poison ivy when touched. These researchers had noticed that some people developed a rash if they thought they had touched the tree, even when no such contact had occurred. They thought that maybe the power of suggestion was at work, and decided to test this hypothesis with a controlled study. They took 57 school boys, and selected only the ones who reported being allergic to the trees in question. They then performed a simple experiment. On each boy, they brushed one arm with harmless chestnut leaves, and the other with poisonous leaves. They told the boys that they had done just the opposite, however, so that the boys thought the benign leaves were poisonous and vice-a-versa. To their amazement, within minutes the "placebo" arm reacted in many cases with a bright red rash with bumps, while in most cases the arm brushed with the poisonous leaves did not react at all. Thus it was shown that a perfectly harmless substance could produce a specific physical reaction through the power of suggestion, and that the physical symptoms produced would match perfectly with the symptoms that were suggested. It was also shown that the reaction to a toxic substance could be prevented, even in highly susceptible individuals, if they were convinced that the toxic substance was actually a harmless one.
The second study to be reviewed was performed in the United States in 1950, about ten years prior to the Japanese study. In this study a bold experiment was performed, one that might not be allowed today for ethical reasons. The author of the study, Dr Wolf, gave a group of women a toxic substance called syrup of ipecac that causes nausea and vomiting. He essentially lied to the women, however, telling them it was actually a drug that would cure nausea and vomiting, since the women were already suffering from chronic nausea and vomiting of pregnancy. In most cases their symptoms ceased entirely when they were given the syrup of ipecac while being told it was an anti-nausea drug. The results were more than just the marked subjective improvement, because Dr. Wolf had the patients swallow small tubes that measured the amount of contractions in the stomach which are associated with nausea and vomiting. After taking the toxin, the contractions subsided. This second study shows that, at least in the short term, a drug that is highly toxic can actually cure the very subjective and objective symptoms that it normally causes - if the power of belief is working in it's favor.
Many other studies showing the power of "placebo" or positive beliefs have been performed, and are summarized in Herbert Benson's book (mentioned above). The concept of relying exclusively on "placebo controlled, randomized, double-blind" studies evolved from evidence like this. This type of study design is supposed to eliminate the potential for placebo-like effects, and distill out the "truly effective" drugs from those that have no physiological benefit. Unfortunately, it is often easy to tell who is getting placebo and who is not, which ruins attempts at blinding. This is due to specific "side effects" and other physiological effects that the drugs being tested usually have. Studies have found that patients and physicians involved in "double blind" studies can correctly guess who is getting placebo and who is not about 70% to 80% of the time (Greenberg and Fisher 1997), which opens up a Pandora's box of questions regarding the effectiveness of most drug treatments. It is this "Pandora's box" that may explain why studies like these have not been followed up, because it is a frightening prospect to consider that it is impossible to know which drugs in use today are truly effective.
Can AIDS Be Caused By Stress, Social Isolation, and Negative
A large portion of this book reviews research showing that severe stress, social isolation, and negative beliefs can cause a syndrome very similar to AIDS, characterizedby immune suppression of exactly the same type seen in AIDS, opportunistic infections, dementia, muscle wasting, and death.
But how much can the power of suggestion influence viral illness, a type of illness that is described in such physical terms? Perhaps the war metaphors used to describe viral infections, in which viruses "invade" our bodies and our bodies send out troops to defend against the attack, are not as appropriate as many people like to think. To begin with, we are "infected" by millions of viruses and microorganisms all the time, with no ill effects. The medical definition of infection shows that physicians are very aware of this, which is that a tissue can only be diagnosed "infected" if it has more than 100,000 microorganisms per gram of tissue. Since the human body weighs, on average, about 70,000 grams, it is obvious that a few thousand microorganisms here and there are totally harmless, in people with healthy immune systems. There are also at least fifty retroviruses (the family of viruses to which HIV belongs) which commonly live peacefully in people, in large numbers, with no resulting illness. These are often referred to as "passenger viruses", and are another indication that attempts to "prove" that a virus causes a disease must meet strict scientific criteria. Just finding a virus in some people who are sick is hardly sufficient, since the virus could be completely harmless.
In a syndrome like AIDS which is characterized by such a devastating and fatal course, claims of causality require the highest standards of proof, especially in light of the millions of benign organisms that exist in apparent harmony with our bodies. This high standard is also required because the specter of such a terrifying infectious disease can result in severe stigmas, social isolation, despair, and deep-seated fear in those diagnosed. It can also result in the use of very toxic medications in high doses, for years on end, as now done with people diagnosed HIV-positive. The argument used to justify such aggressive drug regimens is that the disease itself is much worse than the serious adverse effects of the drugs. This is one of the reasons why it is necessary to be absolutely sure that the natural course of the disease is well established before drug treatments are put in place.
A "scientific" proof that a given microbe is the cause of an illness would require careful application of the scientific method. While anecdotes, conjectures, and associations are useful, they are limited in their ability to rule out alternative explanations. A more scientific approach would involve purifying the agent to remove contaminants, injecting it into animals and observe that the exact same illness results. In addition, one would have to find the agent in nearly every case of the disease, and it would have to be multiplying in the host in sufficient quantities to cause the illness in question. Alternative explanations should be carefully considered, and accounted for as well as possible both in study design as well as in the analysis of data.
The person who performed such a proof with HIV should be famous, perhaps even a candidate for a Nobel Prize, but I have since learned that this person does not exist, and that no one performed a careful, rigorous scientific proof. Instead the evidence supporting a role of HIV relies almost entirely on correlations, conjectures, and anecdotes. Many of the correlations are artificially produced. For instance, someone with symptoms of AIDS can only be diagnosed with AIDS if they test HIV positive on the HIV antibody tests.
Questions, but no Answers
When I first heard these kinds of arguments, I went to my medical library and began looking things up. I began thinking about the question that had nagged me back in the fall of 1987 - what scientific evidence is there to justify the terrifying descriptions of deterioration and death told to people diagnosed HIV positive, especially given the mathematical conundrum of a latency period reaching back much farther than the discovery of HIV?
Through conversations with people diagnosed HIV positive, as well as through searches of the medical literature, I began trying to understand AIDS, and to try to understand how best to help people cursed with this disease. Far from getting answers, what I found was confusion. The state of unknowing that has resulted is a very uncomfortable feeling. I have not found anyone who knows how it was decided, and can provide references from the medical literature, that HIV can cause the state of immune suppression called "AIDS". There have been some attempts, but they gloss over obvious flaws and were not published until the latter half of the 1990's. Thus the contradictions, which are readily available in the medical literature, have gone largely unanswered. For example:
* The search for a mechanism continues to be controversial, with top scientists in disagreement and researching completely different, competing hypotheses. To their credit, many scientists in the field have the courage to openly admit that we do not know what the mechanism is, even after more than 50 billion dollars of research funding over the past fifteen years.
* No one seems to know how it was proven, with any semblance of scientific rigor, that HIV is transmitted sexually, something that every school-child is now being taught in elementary school. I had hoped to find some animal models showing sexual transmission; instead, I found that the best available studies actually found that HIV was not transmitted sexually between monogamous partners of people diagnosed HIV-positive. This study was published in 1997 in the Amercian Journal of Epidemiology, a prestigious medical journal that focuses directly on how diseases are caused and transmitted.
* I found that the evidence for blood to blood transmission is also questionable, since it would take over 300 needle sticks, on average, before a person would become HIV positive, and this rate is within the error of the studies and antibody tests. Also, studies of IV drug users find that those who exclusively use clean needle exchange programs to reduce their risk are at much greater risk than IV drug users who do not use such programs, even after other "risk factors" are controlled for in the statistical analysis.
* I found that the tests used to diagnose HIV positive status suffer from many inconsistencies and false positives, making it difficult to assess who really is "HIV positive", and what it means exactly to be "HIV positive".
I provide detailed descriptions of studies like these in the pages that follow, with extensive quotes to show that I am not making things up or quoting out of context. I hope you will read them, and I hope you will have the courage to try to find answers to the contradictions they pose. This description of contradictions in the science behind HIV makes up the first part of the book. The rest deals with evidence suggesting that many of the symptoms of AIDS can result from the extremely negative beliefs created by the diagnosis, together with social isolation, psychological stress, and adverse effects of medications.
Questions and Answers
Others undoubtedly have explanations that I do not provide which will fit better with the prevailing hypothesis. I hope that you will ask for their explanations, but please do not be convinced by convenient explanations with no references, or explanations based primarily or solely on retrospective studies. Because of the the societal effects and implications that AIDS has had, please demand a high standard of proof that addresses the issues raised here. You may meet with resistance or anger, but please do not let charged emotions convince you, either.
People who defend the hypothesis that HIV causes AIDS need to address the contradictions discussed here, not with denial and hostility, but with clear, well-controlled studies that provide irrefutable evidence. If these studies have not been performed, they should be performed immediately and people diagnosed HIV positive should be informed about them and why they are being undertaken. Unfortunately, with so many egos, careers, and beliefs hanging in the balance, there is a strong risk of researcher bias. For this reason, any new studies should be co-designed and co-administered by scientists from both sides of the debate.
Perhaps even more significantly than careers, people's egos and self-identities would also have to be reconstructed, something that many people hold dearer than life, itself. The state of unknowing is an incredibly frightening place to be.
Over 700 M.D.'s and/or Ph.D.'s Have Signed a Statement Calling
for a Reappraisal of the Causes of AIDS
During my search for answers, I learned of a large group of scientists who had doubts about whether HIV could do all the damage for which it was being given credit. There is a statement signed by about 700 M.D.'s and/or Ph.D.'s that calls for a scientific reappraisal of the causes of AIDS, although very few people are aware of it (Philpott 1999). This statement and the list of signatories is posted on the internet (see the reference, Philpott 1999).
The idea that the HIV hypothesis is wrong may be labelled "dangerous", and people spreading such ideas are often accused of homophobia. Alternatively, they may be called "crazy" or referred to as "followers" of something resembling a cult. Many of the 700 scientists in question, however, are at the top of their fields, including two winners of the Nobel Prize in chemistry. The most well-known critic of the HIV hypothesis is Peter Duesberg, a professor of virology at the University of California at Berkeley who received world wide acclaim for his work on retroviruses (the family of viruses to which HIV belongs) in the 1960's and 1970's. Because of his stance on HIV, his very name has come to inspire anger or ridicule, his research funding has been cut off, and he now has to rely on donations from alumni to keep his laboratory open.
Certainly, it is possible that these scientists, including the 700 or so who have signed the statement that no one seems to know about, are wrong. But how does one decide who is right and who is wrong? Normally, one is supposed to turn to the medical literature to answer these questions, which is what I attempted to do. This book is a record of what I have found. It began as a research paper designed to document that CD4 counts are selectively depleted in people experiencing severe stress and social isolation, and to look at how this might apply to claims that HIV selectively depletes CD4 counts. The paper quickly began writing itself, however, as more and more lines of evidence presented themselves.
I do not claim to be an "expert" on this subject, nor do I claim to have "proven" anything except, perhaps, that the science behind AIDS is a confusing jumble of contradictions. The burden of proof does not lie with me, however, but rather with those who make bold claims about a new super-virus which is like no other virus in history.
Maybe This Book Is Not for You
If you are comfortable with the answers to the following two questions, you may not be interested in reading furthur:
1) What researcher or group of researchers proved that HIV was the "probable" cause of AIDS, and how did they prove it?
2) Who proved that HIV could be transmitted through sexual or blood to blood contact, and how did they prove it?
Surely these people should be easy to locate with a few questions
to professors, scientists, and health professionals, and these
people should be proud to share how their proof was performed.
They should be able to quickly point out research that is readily
available in the medical literature. The proof should have been
performed in the early eighties, since by 1987 the belief in HIV
as the cause of AIDS was firmly established, and highly toxic
therapies had been introduced.
To my knowledge, this proof was never carried out by any group of researchers. The idea that HIV was the cause of AIDS and that AIDS was infectious was presented and accepted without any supporting peer-reviewed literature, and attempts to prove it in a controlled way have resulted in numerous contradictions and outright failures.
What if a debilitating "syndrome" closely resembling AIDS were found in people who were not "HIV positive"? What if the tests used to diagnose people as "HIV positive" give more false positives than true positives, and several groups of researchers say that the tests are so inaccurate that they may be meaningless for all practical purposes? What if the best studies available found that people did not become infected by HIV after multiple unprotected sexual contacts? What if the best available study of HIV transmission among IV drug users found that people who only used clean needles from needle exchange programs were at much greater risk of seroconversion to "HIV positive" status than people who used did not participate in such programs, even after controlling for other variables claimed to be risk factors for HIV seroconversion. What if the scientific community still has no idea how HIV supposedly kills CD4 T-cells, even after over $50 billion worth of research? What if CD4 cells become depleted by a variety of conditions and infections, all of which commonly occur in people, whether or not they are "HIV positive"? What if the drugs used aggressively, for years on end, in people diagnosed "HIV positive" caused symptoms "similar" or "indistinguishable" from those attributed to HIV, according to studies in the medical literature? What if severe and chronic stress, deeply held negative beliefs about one's own health and well-being, and social isolation, all of which are created by the diagnosis, itself, have been found in both animals and humans to cause a fatal wasting syndrome that resembles AIDS, to cause dementia that resembles "HIV dementia", and to cause immune deficiency with the same reduction in CD4 T-cells claimed to be the "hallmark" of HIV infection?
This book will provide a review of studies in the medical literature that strongly support all of these "what ifs". It will be made clear that these studies are not exceptions or isolated cases, but are representative of typical results and often are from the largest and most well-controlled studies available. The thesis of this book applies not only to AIDS, but to any prediction, medical or otherwise. Predictions and prophecies have the potential of changing people's behavior in a way that can create what was predicted, and the beliefs engendered can have direct effects on a person's physiology. This is true of "positive" as well as "negative" beliefs. The effects are exponentially more powerful when one's friends, family, coworkers, and everyone in their society all reinforce the beliefs in question.
The prospect that AIDS is a self-fulfilling prophecy eventually began to torment me, as it does to this day. Writing this book became, for me, a way of coping. A way that I can face my children some day and say that I did what I could to try to help people diagnosed "HIV positive", and to try to understand what the diagnosis means, as well as its implications for general health and well-being. I would like to tell them that I did not stand by, waiting for someone else to raise a red flag.
In the beginning, there was a press conference...
In 1984 Robert Gallo and Margaret Heckler, the Secretary of Health and Human Services under the Reagan administration, held a press conference in which they claimed that Dr. Gallo had found the "probable cause of AIDS". This pronouncement was unleashed into an electrified atmosphere that had been building in intensity for several years. Front page media reports had been proclaiming a steadily rising death toll caused by the modern "gay plague", originally called "Gay Related Immune Deficiency", or "GRID". This constant stream of high profile media stories, fed by reports from the Centers for Disease Control (CDC) had created an atmosphere of fear and hysteria, especially in the gay community, since the assumption had been accepted that the deaths were due to an infectious epidemic. This assumption was accepted even thought several years of searching had not revealed a common pathogen, and even though people often presented different clinical pictures. The gay community had become more and more active in their demands that the microbe be found. The entire country had been primed for an announcement, but after four years of such stories, some people were becoming dubious of the claims made.
Many scientists had argued from the beginning that AIDS was not caused by an infectious agent, but their voices were virtually ignored by the media and the CDC, who had a much more interesting story of a modern day plague spreading out from gay men. These reports were especially electrifying to the gay community, where the infection was believed to be spreading. Gay activists were demonstrating in front of the white house, accusing the government of standing idle while their lives were at risk from the mystery microbe that their community was believed to be infected with. Everyone wanted an answer, and on April 24th, 1984, Robert Gallo and Margeret Heckler stepped in to provide them with one. "HIV is the probable cause of AIDS".
The Voodoo Hex Is Given a Name
The message emanated from that press conference and quickly swept the country. It went something like this:
"You might look healthy now, but if you test positive on the HIV antibody test, your immune system is already beginning to crumble and ebb away which will lead inevitably to a series of debilitating infections as the virus in you eats away at your life force. You will be "infected", and there is no way to alter your status. There is no way to become "uninfected" as happens with other viral illnesses like the flu and the common cold. You must take great care not to infect others with your infected state. You are, in many ways, an "untouchable". You cannot under any circumstances engage in sexual intercourse unless people are protected from you. If you are a mother, you cannot even breastfeed your own children since you might also infect them. A slow, painful, inexorable decline, and an agonizing loss of dignity awaits you, and only with death will the curse be lifted".
When such a curse is laid, what is the risk of a self-fulfilling
prophecy? This paper suggests that the risk is significant. Much
of the strongest evidence for this argument comes directly from
the medical literature, since virtually every claim ever made
about HIV has been repeatedly contradicted. Usually, these contradictions
have not been countered by other studies showing results that
agree with the prevailing hypothesis. Instead, the authors of
the studies either minimize their findings, or ask pointed questions
that gather dust in medical libraries around the world.
Evidence will be presented which suggests that many of the symptoms of AIDS are either directly caused, or made much worse, by the severe, chronic psychological stress, social isolation, and negative beliefs created by the diagnosis. Although this claim may sound implausible at first glance, a deeper look, combined with a review of the literature, reveals that severe, chronic stress has been observed in animals, humans, and non-human primates to cause a fatal wasting syndrome very similar to AIDS, and to cause immunodeficiency that is also very similar to that seen in AIDS, including selective depletion of CD4 T-lymphocytes.
The most direct, and controversial, example of this in humans is the phenomenon of Voodoo Hexing, in which people from some traditional societies have been observed by Western physicians to contract chronic and often fatal illnesses after being "hexed" by a local "witch doctor". A number of reports of this phenomenon have been published in the medical literature by some of medicine's most distinguished researchers, and the similarities between this syndrome and AIDS are striking. Similar events also occur in modern medical settings where, for example, a cancer patient dies, but autopsies reveal that their disease has not spread enough to cause their death. The literature on these topics will be reviewed in detail.
The situation in AIDS is further complicated by other immunosuppressive factors present in many people diagnosed HIV positive, including IV drug use, recreational drugs, factor VIII transfusions, and malnutrition. Malnutrition occurs both in Western nations and in Africa, and is made worse by the medications used to treat people diagnosed HIV positive.
One of the most frightening and disturbing possibilities is that the very drugs used to treat people diagnosed HIV+ can cause immunosuppression and other toxic effects which can easily be mistakenly blamed on HIV. The makers of these drugs have placed strongly worded warnings in their reference materials stating that the side effects of their drugs are often indistinguishable from the symptoms of AIDS. These effects include immunodeficiency of various types, muscle wasting, neuropathy, and other symptoms often seen in AIDS patients. Broad spectrum antibiotics, DNA chain terminators, and protease inhibitors, are just a few of the many drugs taken in large quantities by people diagnosed HIV positive.
Health and Well Being
The proposal that much of the suffering associated with being HIV+ may be the result of a self-fulfilling prophecy created by chronic and severe stress, social isolation, and overmedication, rather than a result of any HIV-induced damage, is a sobering one which may provoke a variety of strong emotional reactions. However, it also presents the possibility of much better long-term health than is currently believed possible for people who are diagnosed HIV+. As a result, a change in current practices regarding HIV diagnosis and treatment is urged. Clinicians should avoid fatalistic predictions, and exercise a great deal of caution when prescribing drugs that can have immunosuppressive side effects. The value of antiretroviral therapy has not been established in controlled trials because they have focused exclusively on biochemical markers that may be of questionable value. These treatments should be avoided until a reassessment of the causes of AIDS, that focuses on the issues presented here, is carried out by a suitable, independent body of scientists, with members from both sides of the debate.
CHAPTER 1: In a Nutshell
Disagreement about HIV's role in causing AIDS has been curiously
absent from public and scientific debate, even though many of
the previously mentioned 700 M.D.'s and/or Ph.D.'s who have signed
a statement calling for a reappraisal of the causes of AIDS have
published their reasons for their concern (Philpott 1999). Members
of this group include current and former professors of molecular
and cell biology at Harvard, Berkeley, and other prestigious universities,
as well as two Nobel Prize winners in chemistry, Walter Gilbert
and Kary Mullis. HIV is a "retrovirus", and Peter Duesberg,
one of the earliest people to call for reappraisal, has been called
the "father of retrovirology". David Rasnick, the president
of the Society for the Scientific Reappraisal of AIDS, holds nine
patents on protease inhibitors, the drugs claimed to have saved
many people from the brink of death. And yet, Dr. Rasnick admantly
maintains that these drugs are contributing to, or directly causing
their deaths rather than helping them. For a topic which has become
so entrenched in the national and world-wide mindset, such a large
number of dissenting voices among people with the highest credentials
in their fields is unusual, to say the least, and yet researchers,
health professionals, and the public have not been informed about
the magnitude of the debate, or about the reasons why these dissenting
scientists are questioning conventional dogma.
HIV is claimed to cause a wide variety of symptoms in people who test positive on the HIV antibody test, but even for the most common symptoms, like immunosuppression and low CD4 T-cells, there is continued difficulty and disagreement in understanding the mechanism involved (Balter 1997), a fact that has led the original discoverer of HIV, Luc Montagnier, to state that he does not think HIV can cause AIDS without other unidentified cofactors (Balter, 1991).
Studies of both animals and humans have shown that severe, chronic stress results in a syndrome remarkably similar to AIDS, and some of the proposed mechanisms are easily reproduced in animal and test tube models (Benson 1997, Binik 1985, Campinha 1992, Cannon 1957, Cecchi 1984, Cohen 1988, Eastwell 1987, Golden 1977, Kaada 1989, Meador 1992, Milton 1973, Uno 1994). The effects of stress are mediated at least in part by the hormones cortisol and epinephrine, which cause a state of immunodeficiency characterized by a reduction of the number of T-cells. The CD4, helper T-cells are selectively depleted, exactly as is seen in people diagnosed HIV+ (Antoni 1990, Castle 1995, Herbert 1993, Kennedy 1988, Kiecolt-Glaser 1991, Laudenslager 1983, Kiecolt-Glaser 1988, Pariante 1997, Stefanski 1998).
Severe stress has also been linked to increased incidences of specific illnesses and symptoms that are officially considered "AIDS defining conditions", including pneumonia, tuberculosis, dementia, wasting, and death. Stress has been demonstrated in both animals and humans to cause brain damage and neuronal atrophy, resulting in a dementia that mirrors "HIV dementia", with the same changes in the brain that are often observed in people who die of AIDS (Axelson 1993, Berent 1992, Brooke 1994, Frol'kis 1994, Gold 1984, Jensen 1982, Lopez 1998, Magarinos 1997, Momose 1971, Sasuga 1997, Sapolsky 1990, 1996, Starkman 1992, Uno 1989,1994). Severe, chronic psychological and social stress has also been linked to increased death rates due to illnesses like pneumonia and tuberculosis (Kennedy 1988, Luecken 1997, Russek 1997), and has been found, in animals, humans, and non-human primates, to cause a fatal wasting syndrome that is remarkably similar to AIDS. Although these studies will be reviewed later in this paper, here is an introductory quote from one study of captured wild monkeys:
"Wild-caught vervet monkeys... occasionally showed a syndrome of cachexia associated with persistent diarrhea, anorexia, and dehydration that usually proved fatal. Those animals appeared to be socially subordinate and to have suffered an atypically high rate of social harrassment and attack from their peers. Two animals died as early as one month under such conditions, and others died after six months to 4 years in captivity... The fatal outcome, caused by severe prolonged social stress, induced classic pathology associated with stress, including gastric ulcers and adrenal hyperplasia. In these animals we also found unique insidious degeneration and resultant depletion of neurons in the hippocampus (the area of the brain that controls learning and memory)... Similar degeneration was also found in cortical neurons." (Uno 1994, page 339)
Most people have heard of Voodoo hexing, where a hexed individual
succombs to a chronic illness that often results in death, exactly
as predicted. Most people are not aware, however, that some of
medicine's leading researchers and physicians have studied this
phenomenon. In addition, most people have not considered how this
might relate to AIDS.
A number of reports, mostly by Western physicians working in traditional societies, have appeared in medical journals over the years. The phenomenon has been called "Voodoo death", "root work" and "bone pointing" (Benson 1997, Binik 1985, Campinha 1992, Cannon 1957, Cecchi 1984, Cohen 1988, Eastwell 1987, Golden 1977, Kaada 1989, Meador 1992, Milton 1973). A similar phenomenon occurring in modern, "developed" societies has also been described, where people have died after receiving terminal diagnoses from their physicians, but before the pathology has spread enough to cause death. This has been called "unexplained death", "self-willed death", "the given-up-giving-up complex", and "the nocebo effect" (Benson 1997, Engel 1968, Milton 1973). As one small example of what will be presented in that section of this book, Meador (1992) reported on two men given voodoo hexes by very different medicine men, one modern, and one traditional.
The first patient, a poorly educated man near death after a hex pronounced by a local voodoo priest, rapidly recovered after ingenious words and actions by his family physician. The second, who had a diagnosis of metastatic carcinoma of the esophagus, died believing he was dying of widespread cancer, as did his family and his physicians. At autopsy, only a 2 cm nodule of cancer in his liver was found. (page 244)
Another comparison between these two phenomena had been provided twenty years before by the Australian physician G.W. Milton (1973) in a special article to the Lancet, a top medical journal.
There is a small group of patients in whom the realisation of impending death is a blow so terrible that they are quite unable to adjust to it, and they die rapidly before the malignancy seems to have developed enough to cause death. This problem of self-willed death is in some ways analogous to the death produced in primitive peoples by witchcraft ("pointing the bone"). (page 1435)
Because of the controversy surrounding this topic, as well
as its possible significance in AIDS, this subject will be reviewed
with extensive quotes in the final portion of this paper.
In addition to the severe stress of living with such a devastating prognosis, people diagnosed HIV+ also often face severe social rejection and isolation. The groups of people primarily affected by AIDS, male homosexuals and IV drug users, already experience this kind of rejection, often by members of their own families. This isolation is made much worse by being diagnosed HIV positive, in spite of efforts by caring family, friends and health care workers. Tragically, these same friends and loved ones may unintentionally perpetuate the social isolation because of fear of infection. Social isolation has been shown to be an independent risk factor for immunosuppression and to lead to low levels of CD4 T-lymphocytes. Socially isolated people, when compared to people with high levels of social support, have been found in over eight studies to have between double and triple the death rates (Berkman 1979, House 1988, Ornish 1997). A recent study found that people diagnosed HIV positive were two to three times more likely to "progress to AIDS" if they were socially isolated and under high levels of stress (Leserman 1999). Here are some quotes from the abstract of their paper:
Faster progression to AIDS was associated with more cumulative
stressful life events (p<0.002), more cumulative depressive
symptoms (p<0.008), and less cumulative social support (p<0.0002).
... At 5.5 years, the probability of getting AIDS was about two
to three times as high on those above the median on stress or
below the median on social support. ... (page 397)
Other studies have looked at this question, but every one, including this one, suffers from a fundamental oversight which is critical to the argument of this book. None of them take into account the severe stress and feelings of isolation associated with being diagnosed "HIV positive", but instead only examine other major stressors. Such a study would be challenging to design, or perhaps even impossible, without breaking people's right to be fully informed about their own medical diagnoses, but this does not solve the quandary. Similar problems exist with a number of other studies of HIV that would shed light on this issue, which is why I recommend that people simply be allowed to make up their own minds. To satisfy their right to informed consent, however, the large number of inconsistencies in HIV science must be fully disclosed, as well. In the chapter that follows I will try to outline some of the most obvious problems, with a number of direct quotes that may prove especially revealing.
CHAPTER 2. Problems With HIV Science:
Mechanism of Action
An article in the journal, Science by Balter (1997) gives a description of the ongoing state of confusion and disagreement among the leading scientists regarding HIV's proposed mechanisms of action. This article by Balter describes a conference in the fall of 1997 that focused specifically on the disagreement and conflicting reports regarding how HIV supposedly kills CD4 T-cells. Here is an introductory comment from the article that summarizes the problem:
"It might be said that AIDS researchers know the virus that causes the disease, HIV, inside and out. They have isolated its proteins, sequenced its genome, and identified the receptors it uses to dock onto the CD4 T lymphocytes that are the viruses primary target. Yet the central mystery of AIDS remains unresolved: How does the virus cause the severe loss of CD4 T-cells, which wrecks the immune system, that is the hallmark of the disease?" (p.1399)
The article also quotes Harvard Medical School professor of immunology Paul Johnson, who is one of the leading figures in this area of research:
"We are still very confused about the mechanisms that lead to CD4 depletion, but at least now we are confused at a higher level of understanding." (Balter 1997, page 1400).
The reasons for this confusion, as outlined in the article,
stem primarily from competing hypotheses, none of which has held
up under scrutiny. This situation is not at all new to HIV, but
has plagued it since Bob Gallo first claimed that it killed CD4
T-cells. Since that time, a number of hypotheses have come and
gone, leading some of the top researchers in the field to question
whether HIV is really capable of killing CD4 T-cells, at all.
The mechanisms proposed originally by Robert Gallo have had to be abandoned, only to be replaced by new theories which are now in the process of being abandoned, as well (Balter 1997, Gorochov 1998, Grossman 1997, Pakker 1998, Roederer 1998). Robert Gallo claimed in 1984 that HIV probably killed CD4 T-cells as other viruses do, by direct rupturing of the cell. It quickly became clear that this was not possible, however, as researchers discovered that this did not occur in test tubes. Also, there were extremely low levels of HIV in people's blood which were insufficient to explain any lowering of CD4 counts, let alone the dramatic lowering observed in people diagnosed with AIDS.
The "Viral Load" Hypothesis
Two papers published in 1995 in the journal, Nature, appeared to resolve this dilemma of extremely small quantities of HIV (Ho 1995, Wei 1995). They used a new genetic detection system, called "quantitative PCR", which relies on a complex mathematical formula to quantify the amount of virus in people's blood. PCR does not actually directly detect any intact viral particles, but instead is entirely based on the detection of tiny fragments of HIV's genetic material. This abstract quantification system is what is still used today to find what is called a person's "viral load", and has become a major method used by clinicians to determine the health status of people diagnosed HIV-positive. Thus, "viral load" is not found by counting even one single intact particle of HIV, but rather by a using complex mathematical system of estimation. This quantification system has serious problems that have been largely ignored, in spite of being clearly reported in the medical literature, and yet it has become the sole marker of health in research as well as the primary tool used in treatment decisions with people diagnosed HIV positive.
How many HIV particles are there, really?
Viruses can only cause damage if they are infectious. Researchers attempting to see what proportion of the huge numbers of HIV reported by quantitative PCR represent active, infectious viruses, have found that as few as 1 in 10 million are actually infectious. This is done by "culturing" the virus, which usually means trying to infect other cells with it. A virus that cannot infect another cell is essentially sterile, since it cannot harm any cells if it cannot infect them. Here are some comments on the results from one such study published in Science in 1993 (Piatak 1993).
Circulating levels of plasma virus determined by (quantitative) PCR correlated with, but exceeded by an average of 60,000-fold, numbers of infectious HIV-1 that were determined by quantitative culture of identical portions of plasma... Total virions have been reported (in other studies) to exceed culturable infectious units by factors of 1000 to 10,000,000, ratios similar to those we observed in plasma. (page 1752)
This means that these researchers estimated that about 1 in
60,000 copies were infectious, and that other studies also find
gross exaggerations of the number of viral particles when using
PCR. They also admit in a footnote that the actual amount in their
study is likely to be even lower than 60,000.
Even more surprising, they were not able to culture any virus at all in more than half (35 of 66) patients, even though all the patients studied had relatively large "viral loads". the study subjects were also HIV-positive by the ELISA and Western Blot antibody tests, the two tests used to diagnose people as "HIV-positive". People with no infectious virus at all had "viral loads" as high as 815,000 "copies per milliliter". This difficulty in finding active HIV particles is not surprising to those familiar with the literature on this topic, however, as similar results have been found by many researchers who have tried to confirm the presence of HIV in people's blood (Chiodi 1988, Gallo 1984, Learmont 1992, Popovic 1984, Sarngadharan 1984, Schupbach 1984). Based on these results, the abstract system used by "quantitative PCR technology", in which tiny bits of genetic material are amplified by a complex set of mathematical equations into frighteningly large numbers, is highly questionable. Even more significant, most people diagnosed HIV positive may have no infectious virus in them, at all.
It was after reading this study that I started putting quotes around the words "viral load", since I am very unsure what it means, exactly. As mentioned before, "viral load" has become the only measure of health in clinical trials of new drugs. News reports about people "doing well" on the new anti-retroviral cocktails often speak about people whose disease is controlled, or whose disease came "roaring back" after stopping the drugs, but what they are referring to is not clinical health, at all. Careful reading of such news articles reveals that the person in question often feels much better off of the drugs, due to their often extremely high toxicity. The description of their health "poor responses" is solely because their "viral loads" have risen.
As often occurs in studies like this one that fundamentally challenge HIV science, however, the authors appear unphased by their results, and focus completely in the discussion section of their paper on other aspects of their study that fit better with conventional views about what it means to be "HIV-positive" and to have a high "viral load". While it is of questionable significance to have such high numbers if only a tiny minority, or none of the particles is actually infectious, it can still be terrifying to be told that one has several million copies of HIV in every milliliter of blood. This type of news has a powerful symbolic meaning to clinicians and patients, even if the biological meaning is questionable. This can result in profound immunosuppression whether HIV is causing damage, or not.
High Viral Loads in People Who Are "HIV-Negative"
Adding furthur confusion to the issue, PCR technology has found extremely high "viral loads" in people who are HIV negative by the antibody tests. For instance, Schwartz et al. (1997) found a person with a viral load of 100,000 who was negative on the ELISA and Western Blot antibody tests. the authors concluded that lab error had led to this reading. this would be a reasonable explanation but for the presence of other studies finding similar results. Another study, for example examined the blood of health care workers who accidentally received needle sticks of HIV-infected blood. As will be seen shortly, only a very tiny risk existed that any of them would seroconvert to HIV-positive status. They found that false positives occurred in about one of every thirty people (Gerberding 1994). This study also found that it would take 333 needle sticks, on average, before someone seroconverts to being "HIV positive" on the antibody tests. These results will be reviewed in detail later in this paper.
More Questions About David Ho's Hypothesis
David Ho's hypthesis did not stop with PCR and "viral load", however. He also proposed that the immune system was waged in a life-and-death struggle, with the person's own CD8/ cytotoxic T-cells killing CD4 T-cells because they were infected with these huge quantities of HIV. This is how Ho et al believed that CD4 T-cell depletion was occuring, and it also explains the elevated CD8 cells often observed in AIDS since lots of CD8-cells would be needed. He claimed that that billions of CD4 cells were being produced daily in a desperate attempt to replace the infected ones which were being killed. This would explain why CD4 cells in test tubes do not die when infected with HIV, since the entire process must take place inside a human body where CD8 cells can be programmed to attack.
While aesthetically appealing to many people, this theory has also proved fundamentally unsound. An article by Roederer (1998) gives a good overview of the reasons why David Ho's theory is no longer considered viable.
These reports (Ho 1995, Wei 1995) received enormous publicity in the popular press, with vivid portrayals of a "massive immunological war" in which billions of CD4 T cells were produced and destroyed daily. However, there has been considerable debate about this simple hypothesis. The Nature papers ignited a heated controversy that resulted in publication of several well-designed studies which raised serious doubts about this "war". In this issue of Nature Medicine, reports by Pakker et al (1997) and Gorochov et al (1997) provide the final nails in the coffin for models of T-cell dynamics in which a major reason for changes in T cell numbers is the death HIV-infected cells. (page 145)
Roederer does not question the hypothesis that HIV is causing
the damage, however, which he accepts without question. He goes
on to discuss new mechanisms proposed by a different set of researchers,
which he thinks are more plausible.
It seems impossible that fifteen years of research with so many billions of dollars devoted to it would not reveal a more clearly delineated mechanism of action. As will be outlined later in this paper, however, the mechanisms by which chronic stress affects the immune system, are much better understood, as are the mechanisms of toxicities from AZT and other drugs used to treat people diagnosed HIV positive.
HIV Rates Do Not Reflect an Infectious Epidemic
Another major problem with AIDS science is that the official estimates for the number of people in the United States who are HIV positive have never actually resembled an epidemic. One of the first estimates of HIV prevalence in the US was published in the New England Journal of Medicine in 1985. Sivak and Wormser (1985) estimated that about 1,765,470 people in the United States were infected at that time. A few years later the Centers for Disease Control in Atlanta, Georgia estimated only about 1,500,000, a drop of nearly 300,000 cases. Today the estimates hover around 750,000 to 1,000,000, representing a furthur drop of at least 30%. An article in the Washington Post on September 2, 1997 commented on these confusing figures:
"The most recent estimate of the number of Americans infected (with HIV), 750,000, is only half the total that government officials used to cite over a decade ago, at a time when experts believed that as many as 1.5 million people carried the virus. They later revised that figure, saying that in the mid-1980's only about 450,000 people were infected." (Okie 1997).
Similar results were reported by Katz et al (1997) for HIV
infection rates in San Francisco, supposedly the "epicenter
of the epidemic". They found that the rates of new HIV infections
peaked in 1982 at 7500, long before the introduction of any safe
sex campaign and even longer before the introduction of anti-HIV
drugs. The rates dropped quickly, finally plateauing at only 500
new infections every year from 1988 through 1997.
Another study found that HIV rates among applicants to a government youth social service program, Job Core, were dropping steadily during the 1990's (Valleroy 1998). All 357,443 applicants over the seven year period from 1990, to 1996 were tested for HIV antibodies. The rates for both female and male applicants in 1996 were half the rates found in 1990. Curiously, the authors still refer in their opening line to HIV as an "epidemic among youth in the United States", even though the rates of HIV positives had been cut in half in only six years.
Africa is commonly pointed to as an example of rampant spread of HIV. Since African AIDS is not the focus of this paper, a few comments here will have to suffice. The widely believed stories about Africa are also not well-supported. The statistics for African AIDS are even more tenuous than those in the United States, because the HIV antibody tests are rarely used there. They are simply too expensive to use on any kind of regular basis, so HIV prevalence rates are based on loose estimates. Since Africa was thought to have infection rates as high as 25% over ten years ago, one would expect that about quarter of the population would have died by now, something that is very far from the truth.
Finally, AIDS deaths and new AIDS cases in the United States have been dropping for years. The CDC 1998 year-end HIV/AIDS Surveillance report clearly indicates that new AIDS cases started a steady decline beginning in 1993, which completely explains the declining death rates that began in the fall of 1994. This decline began several years before the introduction of protease inhibitor combination therapies, which were introduced starting in 1995, so it is unlikely that they deserve the widely publicized credit for the decline. If the definition of AIDS had not been continually updated to include people with formerly non-AIDS defining conditions like low CD4 T-cell counts, the number of new AIDS cases would have started declining years before 1993.
After reading these studies and CDC reports, I began putting the word, "epidemic", in quotation marks when describing HIV and AIDS.
Can HIV Really Be Transmitted Sexually?
Another aspect that does not fit the predictions made over a decade ago is the fact that HIV remains confined primarily to the original risk groups, unlike what would be expected from an infectious epidemic. This lack of epidemic behavior may be explained by studies questioning whether the virus can really be spread from one person to another via sexual or blood to blood contacts.
Perhaps the most well-controlled study to date on this topic was published in the American Journal of Epidemiology in 1997 (Padian 1997). A group of researchers decided to follow a large number of HIV positive people involved in monogamous sexual relationships, and to attempt to count how many acts of intercourse were needed, on average, before a partner would become HIV positive. This is one of the very few studies that followed people over time, giving it a better chance of accurately documenting seroconversion. Their abstract is confusing, or perhaps even misleading, because they claim that they did a "prospective study" and determined that it would take slightly over 1000 sexual contacts, on average, before a partner seroconverted. This is an extremely small risk, especially given the "AIDS education" that is provided to the public, but even this amount of risk is exaggerated. When one reads the text of the article, however, one finds that actually there was not even a single seroconversion in the couples followed prospectively, even though the majority of the couples (75%) were not using condoms at entry to the study. While some couples changed their behavior and started using condoms, fully 25% continued to practice "unsafe sex" for the duration of the study. The "1 in 1000" sexual contact risk was based entirely on finding a small minority of couples who were already both HIV positive at the outset of the study, and ASSUMING that they must have transmitted it from one to another. Here are the author's own comments on their data:
We followed 175 HIV-discordant couples (couples where one member was positive and one negative) over time for a total of approximately 282 couple-years of follow up (table 3)... The longest range of follow-up was 12 visits (6 years). We observed no seroconversions after entry into the study... To our knowledge, our study is the largest and longest study of the heterosexual transmission of HIV in the United States. (p. 354)
No transmission occured among the 25% of couples who did not use their condoms consistently, nor among the 47 couples who intermittently practiced unsafe sex during the entire duration of follow-up. This evidence argues for low infectivity in the absence of either needle sharing and/or other cofactors. (page 356)
"Low infectivity" may be a monumental understatement
given the public and scientific stance on how HIV is spread. In
spite of their remarkable findings, and in spite of this being
the "largest and longest" study of its kind, the authors
do not even raise the question of whether HIV can be sexually
If this study stood alone, it might be reasonable to discard the results, even though it is the best available study of the subject. It does not stand alone, however, as the next study to be reviewed shows.
Can HIV Really Be Transmitted By IV Drug Use?
Another way of spreading HIV, according to conventional HIV science, is through the shared needles of intravenous (IV) drug users. This idea, like sexual transmission, is widely believed, but it is uncertain how this belief was established scientifically. It is the reason behind clean needle exchange programs where free needles are given to IV drug users in an attempt to slow the spread of the "epidemic". The largest and best controlled study to date of this issue, however, actually found that people who used only clean needles from needle exchange programs were at a greatly increased risk for seroconversion (Bruneau 1997). In the abstract the authors state that people who use needle exchange program are three times as likely to seroconvert, even after controlling for all known potential confounding variables like "unsafe" sex. It is astounding to find this result of triple risk in users of clean needles, but if one reads the article, not just the abstract, one finds that tha actual increase in risk is many times greater than this.
The authors compared four goups of people based on how consistent they were in using only clean needles from needle exchange programs; the first group used clean needles from the needle exchange program 100% of the time, a second group used them greater than 50% of the time, a third group used them less than 50% of the time, and the final group (the "controls") did not participate at all in clean needle exchange programs. The authors found that people who exclusively used clean needles were nearly 30 times more likely to seroconvert than people who did not participate at all in clean needle exchange programs. This number was reduced after controlling for confounding variables to 10 times increased risk, and after controlling for even more "confounding variables", the risk increased to 13 times. While it is possible that the study subjects, who self-reported their clean needle use, simply lied about their use of clean needles, there are at least two good reasons to doubt this claim. First, the people had no apparent reason to lie. Second, there is evidence that HIV cannot be transmitted sexually, as reported in the previous section, which reduces the chances that it can be transmitted by "dirty" needles. As the next section will indicate, there is also reason doubt whether HIV-infected needle sticks can transmit HIV.
It was couragious of the authors to publish their findings of increased seroconversion in people participating in needle exchange programs, given the controversy the resuts might generate, and it took courage and integrity for the American Journal of Epidemiology to publish them. The most astounding figures, however, which showed a 30-fold increased risk in exclusive users of clean needles, is not presented in the text or in the abstract. The reader has to read Table 5 to see these results (p. 1000). The only discussion of this result states: "As shown in table 5, there was a clear tendency for risks of seroconversion to increase with frequency of needle exchange program use over time. Upon adjustment for cofounders, significant elevations remained among self-reported consistent users for all subjects and for males only." (page 998). Following are some direct quotes from the authors concerning their findings.
Needle exchange programs are designed to prevent HIV transmission among injection drug users. Although most studies report beneficial effects in terms of behavior modification, a direct assessment of the effectiveness of needle exchange programs in preventing HIV infection has been lacking. A cohort study was conducted to assess the association between risk behaviors and seroprevalence and seroincidence among injection drug users in Montreal, Canada. ... In the cohort study, there were 89 incident cases of HIV infection with a cumulative probability of HIV seroconversion of 33% for needle exchange program users and 13% for non-users. (p<0.0001) ... Risk elevations for HIV infection associated with needle exchange program attendance were substantial and consistent in all three risk assessment scenarios in our cohort of injection drug users, despite extensive adjustment for confounders. In summary, in Montreal, needle exchange program users appear to have higher seroconversion rates than non-users. (p. 994)
The authors also provide a research review showing that needle exchange programs are successful in lowering the number of "risk behaviors".
In London, England, and Glasgow, Scotland, a significant reduction in injecting behaviors was observed among recent needle exchange program attenders.. In the UK a prospective survey between 1987 and 1988 reported higher levels of risk behaviors among non-attenders. ... In Tacoma, Washington, in a case control study among injection drug users entering a methadone program, the nonuse of the needle exchange program was associated with a significant risk for hepatitis B (p. 995)
It is curious that hepatitis B, which is supposedly transmitted
the same way as HIV, through sexual contact and blood to blood
contact, shows reduced rates in clean needle exchange program
users, but HIV does not. As will be seen below, this dilemma presents
itself even more clearly in studies of health care workers whose
skin is accidentally pierced by needles contaminated with HIV-infected
Finally, their discussion section has a number of revealing comments. Even though the authors do not openly question the dogma that HIV is transmitted via "dirty" needles, it appears that they are calling for a reappraisal in much the same way as the "Group for the Scientific Reappraisal of AIDS".
Most of the excess risk appeared to be experienced by those
reporting consistent and exclusive attendance at needle exchange
programs, which was their primary source of new intravenous equipment.
We hypothesized initially that the direction of this association represented simply the net confounding effect of behavioral characteristics biasing ... toward an effect that would be opposite from the expected protective one. Interviews conducted at entry and on multiple opportunities during follow-up elicited detailed information on numerous potential confounders... All plausible sociodemographic, behavioral, and drug consumption variables available were examined as potential confounders...
The fact that the association between needle exchange program attendance and HIV infection risk persisted after being scrutinized with such a conservative analytical approach bolsters our conclusion that it is internally valid and merits furthur attention. (pp. 999-1000)
It was after reading these two studies that I began to put the words, "HIV-positive" in quotes, because I no longer knew exactly what they meant.
It is reasonable that while we wait for this "furthur attention" people diagnosed HIV+ should be informed of the results of this study (Bruneau et al 1997) as well as the previous study by Padian et al (1997). As will be seen in the next topic to be reviewed, health care workers should probably also be informed of probable minimal or non-existent risk of infection from their patients, especially since latex-allergy has become rampant among health care workers.
Can HIV Be Transmitted Through Needle Sticks?
Being stuck with a needle that has HIV infected blood, as has happened to thousands of health care workers, very rarely results in HIV infection. Studies of such exposures find that only about 1 in 333 people exposed to HIV-infected needle sticks seroconvert (Cardo 1997, Gerberding 1994, Henderson 1990), and that a total of only about 50 seroconversions have been reported worldwide since the epidemic began. This is an incredibly small number when compared to other blood borne diseases like hepatitis B.
This risk of seroconversion after a needle stick, 1 in 333, is less than the prevalence of HIV in the general population of the United States, which is about 1 in 250 people (Okie 1997). This raises the question whether these people really got HIV from the needle stick, since picking randomly from the population will result in more HIV positive people than picking randomly from people who have been stuck by a needle. One could even argue, somewhat facetiously, that being stuck by a needle is actually protective, just as using "dirty" needles for IV drugs might be protective. The 50 cases of seroconversion that are claimed to have occured in the world were reported in a multitude of small studies, with only one or two seroconversions per study. An in depth analysis of these studies would be quite revealing, but is unfortunately beyond the scope of this book. Instead, two of the largest and best controlled studies will be discussed, to serve as examples.
Gerberding (1994) found one case of seroconversion out of 327 cases of HIV-infected needle sticks. These all occurred over the space of 10 years in a clinic that specialized in HIV and AIDS. This single case of seroconversion was a woman who developed a flu-like illness about two weeks after the needle stick occurred, and then tested HIV positive two weeks after that. Another study by Henderson et al. (1990) reports a similar circumstance, where the HIV positive test occurred two weeks after a "severe mononucleosis-like illness, characterized by persistent fever, malaise, and weight loss". These types of anecdotal cases are what led to the conclusion that, at least in some cases, the initial stages of HIV seroconversion result in flu-like symptoms.
There is a completely different way to view this result, however.
Both the flu and mononucleosis have been found to cause false
positives on HIV antibody tests (Cordes 1995, Challakeree 1993,
MacKenzie 1992). False positives occur for all antibody tests,
and are much more likely to occur after people have had an infectious
illness, at which time there is a high quantity of many different
types of antibodies present in a person's blood. No reports are
made by Gerberding et al or Henderson et al of any repeat tests
in the two health care workers who seroconverted to confirm the
diagnosis, and thus it is not known whether these people may have
converted back to HIV negative status after their levels of antibodies
returned to normal, which can take a number of months. People
who experience a needle stick from HIV infected blood experience
some of the stress and social isolation that people who are HIV
positive experience on a permanent basis, which may have also
weakened their immune system and made them more susceptible to
the flu and other common infections, thus increasing their likelihood
of a false positive result.
A final aspect of Gerberding's findings presents an even more serious question about whether HIV can be transmitted via blood contaminated needle sticks. They compared the extremely low rate of HIV antibody seroconversion to rates of hepatitis B seroconversion among the health care workers at their HIV-AIDS clinic. Hepatitis B is transmitted the same way that HIV is supposedly transmitted, via direct blood to blood contact or by intimate sexual contacts, and yet "the incidence of hepatitis B was 55 times greater than that of HIV, and 38 times greater than hepatitis C" (p. 1415). Since the setting of this study was a clinic specializing in HIV and AIDS, the prevalence of hepatitis B in the patients seen at the clinic was not expected to be much higher than the 25% to 40% prevalence of HIV positivity. Although not the subject of this paper, problems are also revealed with regards to Hepatitis C infectivity, and there are many other inconsistencies with this virus that are reviewed elsewhere (Duesberg 1996).
How Reliable Are HIV Antibody Tests?
Serious challenges of the specificity of the HIV antibody tests have been raised by several researchers (Papadopulos-Eliopulos 1993). Currently the ELISA is used as a screening test and the Western Blot as a confirmatory test. If the rate of HIV seroconversion after a needle stick is truly 1 in 333, then extremely specific tests would be needed, in which false positives would occur in much less than 1 in 333 tests (less than 0.3%). Papadopulos-Eliopulos et al. (1993) argue that since no one has completely isolated the HIV virus, the specificity of these tests is completely unkown. Only by checking the accuracy of the tests against a "gold standard" of purified HIV can specificity be established. All available electron micrographic pictures of HIV show impure solutions in which what is said to be HIV only represents a small minority of the visible elements (Verney-Elliott 1999, de Harven 1998). Even if the tests had been based on such a gold standard, however, false positives would still occur due to antibody cross reactions. False positives are also much more likely if antibodies are present in large quantities, as often occurs when people have suffered from multiple infections or have had foreign agents injected into their bloodstreams, as is true for all the major risk goups, including IV drug users, male homosexuals, and hemopheliacs.
Several reports discussing false positives, by researchers who support the use of these tests, shed light on why such concerns have been raised. MacKenzie et al (1992) found seven people who had repeated false positives on the ELISA test, apparently due to flu vaccination, and estimate that "0.6% to 1.7% of blood donors who received influenza vaccine this season had multiple false positives." This rate is much higher than the prevalence of HIV in the US population, which is about 0.4%, so that people who receive a flu vaccine are much more likely to get a false positive than a true positive. Furthermore, they based their decision that these were false positives on the fact that their Western Blots, used as confirmatory tests, were negative or, in one case, indeterminate, and that about 11 weeks later the six people available for follow up tested negative. The significant question to be asked is, what about people whose Western Blot is positive? How does one know they are not just false positives with more active reactions than the official "false positives"? People with positive Western Blots are not normally retested months later, but even if they were, how is one to know that the repeat test is not also a false positive? As a side note, this study also looked at false positives to hepatitis C virus, and found that after 11 weeks, four of seven false positives remained positive, which indicates that this test is possibly even less reliable for Hepatitis C than it is for HIV.
A letter to the Western Journal of Medicine (Challakere 1993) reported finding 5 false positives in a sample of 127 people, for a false positive rate of 4%. Through careful history taking they determined that the flu vaccine as well as previous viral infections like herpes simplex 2 were the probable causes of these false positives. This rate of false positives would lead to ten times as many false positives as true positives, since only one in 250 people are "HIV positive" according to the most recent CDC estimates. These researchers also relied on negative Western Blots to decide which tests were true positives and which were false. A summary article on the use of HIV antibody tests that appeared in Infectious Disease Clinics of North America (Proffitt 1993) discussed some of the known causes of false positives on the ELISA.
Notable causes of false positives reactions have been antibodies that sometimes occur in multiparous women and in multiply transfused patients. Likewise, antibodies to proteins of other viruses have been reported to cross react with HIV determinants. False positive HIV ELISAS also have been observed recently in persons who received vaccines for influenza and hepatitis B virus. (page 205)
Since such heavy reliance is placed on the Western Blot test,
one rightfully needs to know how specific it is, and how this
specificity was determined. This test's specificity is based on
its high correlation with the ELISA test (Papadopulos-Eliopulos
1993), which presents a classic example of circular reasoning,
and it turns out that false positives for the Western Blot test
are also quite common.
The specificity of the Western Blot is called into question by reports such as one from the journal, Infectious Disease Clinics of North America which describes the inconsistent guidelines for reading of this test, as well as numerous causes of false positives that can occur on the Western Blot (Proffitt 1993).
Indeed, not even the interpretation guidelines in the brochures of each FDA-licensed manufacturer of HIV Western Blots are the same. However, the majority of the laboratories have accepted the recommendations of the ASTPHLD. Following those recommendations, a negative Western Blot would have no bands, a positive would have at least two of the key bands, and an indeterminate would have a single band or a combination that does not fit the interpretation of positive.(page 208)
This comment hardly inspires confidence that these interpretations are based on sound scientific principles. The most disturbing evidence they cite, however, is the rate of indeterminates that appear for Western Blots, even when the ELISA is negative.
Problems may be encountered when an HIV Western Blot is done on someone at no identifiable risk of infection. For example, recent studies of blood donors in whom no risk of HIV infection could be ascertained, who were nonreactive on the ELISA, and for whom all other tests for HIV were negative, revealed that 20% to 40% might have an indeterminate Western Blot... (Proffitt 1993, page 209)
A 20% to 40% rate of indeterminates on a test that supposedly determines life or death issues is outragiously high, to say the least. One wonders how the extremely high specificity claimed for it can possibly be true. A later article from 1995, that also supports the use of these tests, places these two seemingly irreconcilable claims in the very same sentence.
Thus, incidences of inaccurate results (on the Western Blot) vary from a false positive rate of 1 in 20,000 to indeterminate results in 20% to 40% of cases in which the ELISA test was serum negative. (Cordes 1995, page 185)
The only conclusions that the authors draw from this extremely
high "false indeterminate" rate is that the Western
Blot should not be used as an initial screening test, and the
only harm mentioned is that "the anxiety an indeterminate
result creates in a test subject is understandably
intense" (Proffitt 1993, page 209). If an indeterminate result creates intense anxiety, a result considered to be a "true" positive can create levels of anxiety and despair that are many times more intense, and yet the decision about what is "true", "false" or "indeterminate" appears highly arbitrary. It is also notable that here the false positive nature of the Western Blot is established by negative ELISA's, but in the previous one the reverse was true. Thus one does not know which test, if any, can truly be relied upon, a fact that is even more significant when one considers that as many as 40% of people with negative ELISA's will have indeterminate Western Blots.
A very recent study looked at a number of cases of people who had consistently repeated false positives on the Western Blot, along with false positive ELISA's (Sayre 1996). They decided these were false positives based on the fact that only the minimum number of Western Blot bands were positive and that there were no risk factors.
Recently, a group in Australia reported identifying low risk, uninfected blood donors whose sera reacted nonspecifically with gp 41 and gp120/160 (proteins said to be specific to HIV), which resulted in apparently false positive interpretations... We report here on studies on initial donations and follow up samples from four U.S. blood donors with similar reactivity, as well as data documenting the increasing frequency with which these patterns have been observed in the blood donor setting... (page 46)
The four donors were identified by the individual blood centers as having possibly false positive Western Blots, on the basis of the donor's denial of HIV risk factors and the restricted ractivity of the Western Blots performed. (page 48)
Our results document a fourth source of false positive HIV-1 Western Blot results, which is the reproducible but nonspecific reactivity to (proteins from HIV)... Preliminary studies suggest that the basis for this cross reactivity with HIV-1 gp 41 proteins may be infection by paramyxoviruses, carbohydrate antibodies, or autoantibodies against cellular proteins. (page 48-49).
The authors also looked at rates of these types of false positives among all tests performed on blood donors in the U.S., and conclude that 1992 had the highest rates to date of 52 out of 683, or 8% of positives actually being false positives. The question is, how do they know that only these people are false positives? If two bands can represent a false positive, why not three or more bands?
PCR False Positives
Gerberding's study of needle sticks, described above (Gerberding 1994) also uncovered data that call into question the value of PCR testing. They gave PCR tests to 133 healthy workers who had needle sticks but remained HIV negative on the antibody tests. Seven of them had "indeterminate" PCR results, and four others had one or more actual positive results, for a false positive rate of 3%. If the "indeterminate" results are counted as well, the false positive rate is 8%. For a very rare infection like HIV, with an estimated prevalence of only 0.4%, these rates of false positive results in perfectly healthy people are extremely high. The ratio of 3% to 0.4% reveals that for every 30 people with "positive PCR's" only 4 will be actual positives. The decision that these are actual positives is based on the ELISA and Western Blot antibody tests, which also have lots of false positives, as previously shown. Gerberding et al. comment on their findings with PCR as follows:
The failure to demonstrate seroconversion... among those with positive PCR tests suggests that false positives occur even under stringent test conditions. The low predicitive value of a positive or indeterminate PCR test... contraindicates the routine use of gene amplification in this clinical setting. (page 1415)
Other cases of people with positive PCR tests but who were negative on the ELISA test were reported quite recently (Rich 1999). They report on three such cases which occurred over a two month period. The third case has a particularly interesting series of conflicting results:
(Case 3) had a positive result on ELISA and an
indeterminate result on a Western Blot (WB) test... During a four month period after her initial indeterminate result, she had a positive result on ELISA and another indeterminate result on WB test, on separate occasions. Five months later, both ELISA and WB tests yielded negative results, but the patient had a plasma viral load of 1300 copies/mL. (page 38).
Finding viral loads in HIV-negative people should be a major
wake-up call to people people diagnosed "HIV-positive",
their doctors, scientists working in the field, and the public
at large. What makes the results so much more surprising is that
they were never reported in the media, nor were they discussed
in the research community, nor were they presented to physicians
at AIDS conferences, and finally, they were definitely never told
to people diagnosed "HIV-positive".
Perhaps this is why Kary Mullis, the scientists who won the Nobel Prize for inventing the PCR test, agrees with scientists like Peter Duesberg and Eleni Papadopulos-Eliopulos who challenge nearly every aspect of HIV science, including questioning the significance of PCR based viral load measurements (Duesberg 1996). Kary Mullis is one of the signatories of the statement calling for a reappraisal of the causes of AIDS.
Weak Correlation Between HIV and AIDS
The evidence that HIV causes AIDS has been based from the very beginning on correlations between testing positive on the HIV antibody test and later developing AIDS. Even this correlation, however, breaks down under scrutiny.
There is a significant minority of HIV positive patients who have not gotten AIDS, most of whom have never taken any anti-HIV medications. Some of them were diagnosed as far back as 1984, when the virus was first discovered by Robert Gallo and Luc Montaignier. They are often called "long-term non-progressors", and represent from 7% to 10% of all people infected with HIV. Conventional science has focussed narrowly on a search for genetic protective factors to explain them. A group of such non-progressors have organized a "Long-term Survivor's Network". They have concluded that one of the major factors they have in common is that they resist the belief that HIV will kill them. This claim is supported by the fact that they have also refused to take anti-HIV medications, and many of them believe that avoiding these medications is the reason they continue in good health (Walton 1999).
Uncountable numbers of people would have been diagnosed with AIDS, except that a negative HIV test result was used to exclude AIDS as a diagnosis. To clarify, the very definition of AIDS requires a positive HIV antibody test result. This means that people with symptoms of AIDS or "AIDS defining conditions", but who test negative on the HIV antibody tests, are not diagnosed with AIDS. People with the exact same illnesses and symptoms are given different diagnoses based solely on the result of an HIV antibody test, which creates a completely artificial correlation between HIV and AIDS. Tuberculosis with a positive HIV antibody test is AIDS, but tuberculosis with a negative test is just tuberculosis, even if it is occuring in an IV drug user with multiple opportunistic infections.
Even the syndrome of chronic infections and extremely low CD4 T lymphocyte counts turns out to be relatively common in people who are HIV negative. A wave of reports of this syndrome, dubbed "non-HIV AIDS" (Bird 1996) and occurring in IV drug users, male homosexuals, and hemopheliacs, surfaced in the early 1990's. While this represented a major challenge to the correlation between HIV and AIDS a solution was quickly found. This syndrome, which looked just like AIDS, was given a new name. When the syndrome was found in people who were HIV negative, it would be called "Idiopathic CD4 Lymphocytopenia". If they were HIV positive, it would be called "AIDS". This was decided at a conference in 1993, and dramatically reduced the number of HIV-free AIDS cases that were reported. It is interesting that reports of this phenomenon have focussed on how this syndrome differs from AIDS, while the difference may be simply that these people are not engulphed in the death-education that surrounds an HIV positive diagnosis, nor are they treated with powerful and highly toxic medications.
Where Is the Virus?
Finally, and most significantly, it is difficult to find actual HIV viruses in most people who have antibodies to HIV. This includes people who have "full blown AIDS". Robert Gallo only found actual viruses in about 40 to 50% of his patients with AIDS, as reported in his original articles in the journal, Science (Gallo 1984). He claimed in those articles that this low rate was probably due to contamination. Later attempts have only been able to find actual viruses in between 20% and 80% (Chiodi 1988, Learmont 1992). These dismal results are similar to those of Piatak et al who found that most people with high "viral loads" (800,000 was the highest level reported) had no infectious virus at all. Even in people who did have actual HIV in them had tiny amounts, and it starts to appear that HIV antibodies might actually be doind exactly what they are designed to do, which is to clear their targets from the bloodstream. The presence of antibodies to other microbes usually means that the body has cleared the infection, and one wonders why this is also not true in the case of "HIV".
Here is a brief summary of the problems with HIV science covered so far:
- Proposed mechanisms by which HIV supposedly kills CD4 T-cells
have been revised several times, and remain in debate.
- HIV rates in the general population do not reflect an infectious epidemic, and have been declining since 1984 according to all available sources.
- Evidence of infection by unprotected sex or blood to blood contact is weak or non-existent.
- ELISA, Western Blot, and PCR are all prone to false positives, and are used amongst them- selves incestuously to prove each other's validity.
- There are a large number of HIV-free cases of AIDS, so many that a new diagnosis was invented to describe them, "Idiopathic CD4 Lymphocytopenia".
- Researchers only find actual HIV in 20% to 80% of people who test positive on the HIV antibody test, and PCR reports "viral loads" in about one in thirty HIV negative people.
- Even a perfect correlation would not prove causation, and HIV=AIDS is not at all perfect.
Chapter 3: A Brief History of AIDS
Many of the problems with HIV science stem back to the original
claims made in 1984 by Robert Gallo at his infamous press conference.
The first reports of an unusual illness among a handful of gay
males had appeared in 1979, and by 1984 there was an enormous
amount of pressure being put on the government and the scientific
establishment to find the cause of AIDS. The idea that an infectious
epidemic was spreading among gay men had already been widely propogated
by the press and the Centers for Disease Control, but after several
years of searching, no infectious agent could be found. Since
an infectious agent with such devastating effects should be present
in large quantities in the people affected, and the inability
to find such an agent implied that the illnesses observed were
not infectious, an idea which none of the people or organizations
involved were prepared to accept (Duesberg 1996). Since the reported
cases of "AIDS" had different microbes affecting them,
the hypothesis that a microbe was attacking their immune systems
became popular among scientists. The only problem was that no
one could find such a microbe. Then came Bob Gallo to save the
In April of 1984, Robert Gallo convinced Margaret Heckler, who at the time was the Secretary of Health and Human Services under the Reagan administration, that he had finally found the "probable cause of AIDS". They held a joint press conference to announce their findings (Hockenberry 1993, Papadopulos-Eliopulos 1993, Duesberg 1996). In doing this they completely side-stepped the peer review process. None of the claims made at that time about HIV and AIDS have proved to be true, and yet their hypothesis has survived.
The most significant claim made by Robert Gallo at that time was that everyone who tested positive on the HIV antibody test would die, and the decline would begin after a latency period of about ten months to a year, on average, even if they were presently in perfect health. In spite of the seriousness of his claims, he did not present any type of documentation to support them at the press conference, and his papers published in Science later that year also failed to support them. As outlined above, those papers indicate that Gallo and his group of scientists only found actual HIV in 40-50% of patients diagnosed with AIDS. In addition, they only found antibodies to HIV in 88% of AIDS patients (Gallo 1984, Popovic 1984, Sarngadharan 1984, Schupbach 1984). Having antibodies to a virus, with no virus present, usually means that the immune system has successfully cleared the infection, and yet Robert Gallo, without providing any evidence to support his claim, said exactly the opposite. People with HIV antibodies were thus branded with the marker for a long, slow, and painful death. To add to their misery, they were also marked as carriers of a deadly virus that would start the plague of the 20th century and sweep through the population. They must also abstain from any sexual intercourse of any kind, unless it is with another person who is infected. They were now the "untouchables" of the Western world.
This story was immediately given widespread coverage by the media, and was also spread throughout the scientific and medical communities, all of whom received the news with eager belief. At last, the infectious agent had been found! Robert Gallo, himself, patented the HIV antibody test on the day after the press conference, a conflict of interest that few people have noted (Duesberg 1996), and his claims quickly proved to be untrue.
Perhaps the most obvious false claim made by Robert Gallo in 1984, was his claim that it would take about ten months to a year for people to develop AIDS after being infected with HIV. This proved to be wildly off-base. Two studies that were begun in that year quickly refuted these claims completely, because only a small minority of people diagnosed HIV positive developed AIDS in the next year. As these studies continued, the latency period of the virus, also called the incubation period, had to be continually extended, until by 1990 the average latency was estimated to be 10 or 11 years (Bailey 1997, Bacchetti 1989, 1991, Hendriks 1993, Lui 1988, Taylor 1991, Weyer 1987). By 1987, when AZT was introduced as standard therapy after a rushed FDA approval, about 20% of these people had been diagnosed with AIDS. Even the new 10-11 year average latency was suspicious, however, because HIV had only been discovered six years before, and here claims were being made that it took 10 to 11 years to develop AIDS. In spite of this glaring inconsistency, very few people publicly challenged the idea that HIV caused AIDS, let alone that it caused it in 100% of people infected, something that had never been claimed about any previous virus in history. Even the dreaded polio virus only caused paralysis in less than 1% of those infected, and when this happened the virus was present in huge quantities, unlike HIV. By the mid 1990's, claims were made that new drugs were keeping people alive longer, and that certain people had genetic predispositions that resisted the disease.
During this "latency" period, people diagnosed HIV positive are treated with aggressive regimens of broad spectrum antibiotics and antifungals, which are known to promote the development of resistant strains of microorganisms. They also destroy the natural microbial flora that is a major aspect of intestinal health and nutrition intake. AZT, other DNA chain terminators and protease inhibitors are also liberally prescribed in the belief that their toxic effects are less important than lowering "viral load", even though immune suppression is a common adverse effect. When combined with the severe stress associated with the diagnosis, it is clear that one's immune system could become overwhelmed, whether or not HIV is causing any damage.
The prognosis described to the public and to people diagnosed HIV+ continues to be relatively unchanged since 1984. People are told to expect a long and protracted illness, characterized by gradual loss of health, immunity, and dignity, followed by certain death. Because of this dire prognosis, people diagnosed HIV+ live with the constant fear of a terrifying deterioration and death, and are treated with much more aggressive drug regimens than would be used in HIV negative people.
Because they are thought to harbor such a deadly infectious virus, they are also subjected to severe social isolation. Constant reminders of their infected, untouchable state are provided on a daily basis as people use latex gloves when touching them, and wash items they have touched with special soaps. Of course, they are considered far too untouchable for any sexual intimacy of any kind, except perhaps with someone who is also "infected". This social isolation and rejection, combined with the tremendous fear of the inexorably approaching decline and aggressive drug regimens, may be all that is necessary to destroy a persons immune system and create the syndrome called "AIDS".
The Effects of Severe, Chronic, Psychological
A Self-Fulfilling Prophecy
Severe, chronic psychological stress and social isolation can
have health effects that are nearly identical to AIDS, especially
when combined with physical stress or illness. Stress causes a
state of immunodeficiency characterized by a reduction of the
number of T-lymphocytes, with special targeting of CD4, helper
T cells. There is also a reduced CD4:CD8 ratio, with a relative
increase in CD8, suppressor/cytotoxic T cells (Antoni 1990, Bonneau
1993, Castle 1995, Herbert 1993, Kennedy 1988, Kiecolt-Glaser
1988, 1991, Laudenslager 1983, Pariante 1997, Stefanski 1998).
Both of these immunological changes are considered characteristics
specific to AIDS. Since being diagnosed with AIDS carries with
it a high level of psychological stress and social isolation,
the cause of low T-cells are likely caused, at least in part,
A marked increase of the hormone cortisol, which is released during times of stress, appears to be one of the primary causes of these immune changes. Catecholamines like epinephrine, which are also released, have also been implicated but to a lesser degree. Multiple studies have found that people diagnosed HIV positive have chronically elevated cortisol levels (Azar 1993, Christeff 1988, 1992, Coodley 1994, Lewi 1995, Lortholary 1996, Membreno 1987, Norbiato 1996, Norbiato 1997, Nunez 1996, Verges 1989). It is important to note, however, that chronic stress can induce immune suppression even when cortisol and epinephrine are not elevated (Bonneau 1993, Keller 1983), so that the mechanisms by which stress affects health and immunity are not at all completely understood.
Severe stress has also been shown to cause brain damage and neuronal atrophy, especially in the hippocampus, the area of the brain that controls learning and memory (Axelson 1993, Bremner 1995, Brooke 1994, Frol'kis 1994, Gold 1984, Gurvits 1996, Jensen 1982, Lopez 1998, Magarinos 1997, Sapolsky 1990, 1996, Sasuga 1997, Sheline 1996, Starkman 1992, Uno 1989,1994). This results in decreased mental function similar to what is often called "HIV dementia". The most chilling research, however, is research that has demonstrated that severe social and psychological stress can cause a fatal wasting syndrome in animals, humans, and non-human primates that is very similar to AIDS (Benson 1997, Binik 1985, Campinha 1992, Cannon 1957, Cecchi 1984, Cohen 1988, Eastwell 1987, Golden 1977, Kaada 1989, Meador 1992, Milton 1973, Uno 1994), a topic that will be covered in detail.
Being diagnosed HIV-positive is perhaps one of the greatest stressors one can imagine. Not only does it raise the constant and extreme fear of a relentless deterioration and death, but it also creates a social isolation that pervades all aspects of people's lives. To make matters worse, many of the people diagnosed with AIDS already suffer from social isolation and rejection. Social isolation, alone, has been associated with a 100% to 200% increase in mortality in several large prospective studies, and the increase in mortality is equal to the increase associated with smoking (Berkman & Syme 1979, House 1988). The amount of psychological stress in people diagnosed HIV positive is likely to be much greater than the stress in the people in these studies.
The reduction of CD4 cells in people diagnosed HIV+ has been
called the "hallmark of the disease" (Balter 1997), and it has been
claimed since the initial discovery of HIV that it selectively targets these
cells, creating a CD4/CD8 ratio with a value less than one, referred to as an
"inverted" ratio. As reviewed earlier in this paper, the mechanisms
by which it might do this are still in debate, raising doubts about whether
HIV is actually the cause. Research done before and since that time has added
strength to this argument by showing that CD4 cells become depleted in a wide
variety of ways, and that such depletion is an incredibly non-specific finding
which is common in many people suffering from all types of physical and psychological
stress (Bird 1996, Carney 1981, Feeney 1995, Junker 1986, Kennedy 1988, Lotzova
1984, Pariante 1997, Zachar 1998). It is even relatively common in people with
no illness (Bird 1996).
Low CD4 Counts in Chronic Illness
In 1981 a group of researchers looked at CD4 and CD8 counts in ten consecutive patients with acute mononucleosis, and compared their counts with those of ten healthy volunteers (Carney 1981). At this time CD4 counting was a newly discovered technique, as was the idea of looking at CD4/CD8 ratios. The CD4 counts in the healthy volunteers were 73% higher than those found in people with mononucleosis. The CD8 cells in people with mono were increased, resulting in an inverted CD4/CD8 ratio in every single patient. The average ratio was only 0.2, compared to the normal average of 1.7 found in controls. Of the nine patients whose CD4 counts were measured, the three with the lowest CD4 counts had 194, 202 , and 255 cells/mm3. People who are HIV positive with less than 200 CD4 cells are immediately diagnosed with AIDS, and the assumption is made that HIV is attacking their T-cells. This assumption that seems ill-advised in light of findings like this one.
More recently another group of researchers looked at CD4 counts in HIV negative people, this time in 102 consecutive Intensive Care Unit (ICU) patients who were admitted for a variety of reasons (Feeney 1995). Fully 30% of these patients had CD4 counts less than 300. They do not discuss how many were below 200, the level diagnosed as "AIDS" in people with a positive HIV antibody test. They also did not find that low CD4 counts were linked with poor health, nor were they linked with a poor prognosis. Here are the author's comments on their findings.
Our results demonstrate that acute illness alone, in the absence
of HIV infection, can be associated with profoundly depressed
lymphocyte concentrations. Although we hypothesized that this
depression would be directly related to the severity of illness,
this was not seen in our results. The T-cell depression we observed
was unpredictable and did not correlate with severity of illness,
predicted mortality rate, or survival rate. This study was consistent
with prior studies that have shown similar decreases in T-cell
counts in specific subsets of acutely ill patients. These subsets
included patients with bacterial infections, sepsis, septic shock,
multiple organ system failure, tuberculosis, coccidioidomycosis,
viral infections, burns, and trauma patients. Most of these studies
reported decreases in lymphocyte populations, some of which were
severe and included CD4/CD8 ratio inversions...
In the largest study to date of hospitalized patients, Williams et al (1983) evaluated T-cell subsets in 146 febrile patients with serious acute infections... with 19 of 45 patients having a CD4 count of less than 300 per microliter.
We also found that CD4 counts were linearly related to total lymphocyte concentrations, as Blatt et al. (1991) reported in HIV-positive patients. (page 1683)
Curiously, although these researchers did find the low CD4
cell counts as seen in AIDS, they did not find that such counts
were very good measures of immune function. One major double-blind
study of AZT use in over 2000 HIV positive people found the same
result. AZT increased the number of CD4 T-cells, but in spite
of this people who received AZT died at a faster rate (Seligman
1994). This study was the major reason AZT fell out of favor as
the sole drug used on HIV positive people, but it also seriously
questioned the value of CD4 T-cells as a marker for immune health.
This study, called the Concorde Study, will be reviewed in the
appendix discussing anti-HIV medications.
In contrast to the confusion over how HIV affects the immune system, the mechanism for the immunosuppression during during states of chronic physical and psychological stress is comparatively well understood. One of the major changes during times of stress is an outpouring of the hormones epinephrine and cortisol, which lead to a dramatic reduction in the number of T-lymphocytes. The strength of the correlation between decrease in T-cells, also called "lymphocytopenia", and excess cortisol is so strong that low T-cells is one of the diagnostic criteria for identifying excess cortisol.
Here are some quotes on this topic, from a basic textbook which is used in most medical schools to teach physiology (Guyton 1996).
"Almost any type of physical or mental stress can lead within minutes to greatly enhanced secretion of ACTH and consequently cortisol as well, often increasing cortisol secretion as much as 20-fold" (p.966).
"Cortisol suppresses the immune system, causing lymphocyte production to decrease markedly. The T lymphocytes are especially suppressed." (p.964)
"Cortisol decreases the number of eosinophils and lymphocytes in the blood; this effect begins within a few minutes of injection of cortisol and becomes marked within a few hours. Indeed, a finding of lymphocytopenia or eosinopenia is an important diagnostic criterion for overproduction of cortisol by the adrenal gland. Likewise, the administration of large doses of cortisol causes significant atrophy of all the lymphoid tissue throughout the body... This occasionally can lead to fulminating infection and death from diseases that would otherwise not be lethal, such as fulminating tuberculosis in a person whose disease had previously been arrested" (p.965).
This description of death from infections that "would
otherwise not be lethal" sounds identical to a description
of the symptoms usually blamed on HIV.
Many studies have linked cortisol levels with CD4 depletion, and some have linked epinephrine, as well. These are the two major hormones released during times of stress, and when injected into humans and laboratory animals, immune suppression results (Crary 1983a, 1983b, Tornatore 1998). Tornatore (1998), for example, found reductions of 70% in the number of CD4 cells in both young and elderly people after a single injection of a synthetic analogue of cortisol called methylprednisone. After the single injection, it took 8-12 hours for the numbers of lymphocytes to return to normal.
It is important to note that studies have found that these are not the only mechanisms. The adrenal glands are the source of both cortisol and epinephrine, but when rats have their adrenal glands removed they still have reduced T-cell number and function when subjected to stress (Bonneau 1993, Esterling 1987, Keller 1983).
People diagnosed HIV+ have been found in a number of studies to have elevated levels of cortisol, and some have reduced cortisol responses when artificially stimulated, which indicates the presence of chronic stress as well as chronically overactive cortisol production (Membreno 1987, Christeff 1988, 1992, Verges 1989, Azar 1993, Coodley, 1994, Lewi 1995, Lortholary 1996, Nunez 1996, Norbiato 1996, Norbiato 1997). Norbiato et al. (1997), for example, compared patients with AIDS with healthy, HIV negative controls. They placed the AIDS patients into two groups, those with normal cortisol receptor affinity (AIDS-C) and those with low cortisol receptor affinity (AIDS-GR). When comparing urinary free 24 hour cortisol levels, they found that patients with AIDS-GR had 451 micrograms/24hr, while control subjects had only 79 micrograms/24hr. People with AIDS excreted nearly six times as much cortisol as normal controls. AIDS-C patients had levels of 293 micrograms/24hr, 3.7 times higher than normal. Plasma cortisol levels were also increased, with levels nearly three times as high in AIDS-GR patients as in normal controls. Their comments on their findings are revealing:
"In HIV disease, the normal interaction between hypothalamic/pituitary axis is altered, thus producing an oversecretion of cortisol, resulting in immune suppression. In most patients, this trend continues throughout the course of the disease." (page 3262)
These levels are compatible with levels of cortisol commonly
found in patient's with Cushing's Disease, a disease of cortisol
overproduction that results in severe immunosuppression, opportunistic
infections, neuropsychiatric abnormalities, muscle wasting, weakness,
and fat deposits in the upper back, face, and belly (Britton 1975,
Momose 1971, Robbins 1995, Starkman 1992).
Several studies have linked high stress with a selective depletion of CD4 helper T-cells, often with increased CD8 cells. One of the problems in comparing the immunsuppression due to stress with that in people with AIDS, however, is that most researchers do not consider CD4 counts to be a good measure of immune function, and therefore most studies do not measyre CD4 counts. Instead, lymphocyte responsiveness is preferred, which is nearly always reduced in states of chronic psychological stress (Antoni 1990, Kiecolt-Glaser 1988). There are studies that look at T-cells in times of stress, however, and these will be focused upon here. The results to be reviewed first will be from a study of non-human primates, followed by several human studies.
Stress and Lymphocytes in Humans, Non-human Primates, and
A group of researchers led by Robert Sapolsky has done a great deal of work observing the effects of psychological stress on baboons and other primates. Most of their work has focused on neurotoxicity, which will be reviewed in a later section of this paper. In one study, however, they measured total lymphocyte counts and cortisol levels in a group of baboons that were invaded by a highly aggressive young male baboon, whom they named Hobbs (Alberts 1992). Hobbs was particularly threatening to females in the group, and was apparently attempting to use fear, physical intimidation, and abuse to increase his chances of successful mating. Cortisol levels in the group nearly doubled after Hobbs joined the group, with a slightly greater increase among females. T-lymphocytes plummeted in the group, from a pre-Hobbs level of 67 per 10,000 red blood cells (field conditions prevented them from determining the number of lymphocytes per microliter of blood, or from measuring CD4 cells) to a level of about 39, a drop of 42%. When looking at only the levels in baboons who were victims of Hobbs' aggression, the levels fell even more steeply, to only 29 per 10,000 RBC's, a drop of 55%. Interestingly, Hobbs, himself, had the lowest number of lymphocytes in the group, and the highest cortisol level, suggesting that his behavior may have been taking an even greater toll on his system than it did on the victims of his aggression. The authors comment on their use of lymphocyte counts instead of more sophisticated methods:
Whereas most studies of the effects of stress upon immunity examine functional indices of immune competence (e.g. mitogen stimulation tests, antibody generation, cytokine responsiveness), our field conditions limited us to this rather crude quantitative measure of numbers of cells. (Alberts 1992 page 174)
It is notable that these researchers also agree that T-cell
function tests are the best way to measure immune competency,
something supported by earlier reports that question the value
of CD4-cell counting (Feeney 1995, Seligman 1994).
Pariante et al. (1997) measured the CD4 helper T-cells and CD4/CD8 ratio of people who were under chronic stress due to being caregivers of severely handicapped family members. They found that the caregivers had "significantly lower percentages of T cells, a significantly higher percentage of T suppressor/cytotoxic cells, and a significantly lower helper:suppressor (CD4/CD8) ratio." Another study of caregivers, this time of people caring for people with late-stage Alzheimers, also found decreased CD4/CD8 ratios, in addition to impaired T-cell function (Castle 1995).
A study in rats compared the effect of three weeks of chronic stress in rats who either had normal pre-natal experiences, or who were exposed to ethanol in utero. Males were especially affected, and ethanol exposed rats had significantly more lowering of CD4 counts when placed in a stressful environment than non-exposed rats (Giberson 1995). This suggests that chemical insults can increase the susceptibility to stress-induced immunodeficiency, especially if the exposures occur in utero, a finding that is especially significant to childhood AIDS cases as many of them are born to women who are IV drug users.
It is important to note that short-term stress can have very different effects from long-term stress. For instance, one study compared the effects of two hours of social stress in rats with the effects of 48 hours of stress. After two hours, there were decreases in the number of T-cells, but an increase in the CD4/CD8 ratio. After 48 hours of the same social stress, however, the CD4/CD8 ratio had lowered to the normal range, while T-cell numbers remained reduced (Stefanski 1998).
The effects of stress also show a lot of individual variance, which may be due to factors like coping strategies and social support. Several studies have found that isolated people have more immune dysfunction than people with high levels of social support (Kennedy 1988, Kiecolt-Glaser, 1984, 1991). These studies will be reviewed in the next section of this paper. Another mediating factor appears to be the amount of control that one has over the source of stress. Rats who were given some measure of control over the source of stress showed normal lymphocyte responses, while rats who had no control showed impaired responses, even though the amount of external stress producing events (electric shocks) were equal (Laudenslager 1983). A review of relevant studies from 1988 examined some of these variables, with the following comments:
"Data are given which document immunosuppressive effects of commonplace, short-term stressors, as well as more prolonged stressors, such as marital disruption and caregiving for a relative with Alzheimer's disease. Immune changes included both quantitative and qualitative changes in immune cells, including changes in herpes virus latency, decreases in the percentages of T-helper lymphocytes and decreases in the numbers and function of natural killer cells. These effects occurred independently of changes in nutrition. Psychological variables, including loneliness, attachment and depression were related to the immune changes. The data are discussed in a framework in which quality interpersonal relationships may serve to attenuate the adverse immunological changes associated with psychological distress, and may have consequences for disease susceptibility and health." (Kiecolt-Glaser 1988).
Another review article (Antoni 1990) has several discussions of this topic, including some discussion of the effects of stress in people with AIDS. Following are some of the author's statements regarding effects on T-cells:
"Animals subjected to uncontrollable stressors, for instance, have been noted to display... immune system decrements such as thymic involution, decreased NK cell cytotoxicity, suppressed lymphocyte proliferation, and decreased helper/suppressor cell ratios." (page 41)
"In research using naturally occuring uncontrollable stressors in human subjects... (there were) decreases in total T-lymphocyte number, total macrophage number, and total number of CD4 cells." (page 41-42)
"Other recent work has noted that a high stress level, increased depressive symptoms, dissatisfaction with social support, and limited use of coping strategies predicted decreased CD4 cell number and increased CD8 cell number." (page 42).
Several different types of stressors led to these immune system changes, including loneliness, lack of social support, and bereavement, all three of which have a high prevalence in people diagnosed with AIDS. A final quote from this article (Antoni 1990) discusses the impact of HIV diagnosis on immune function.
"Indeed, we have observed discrete and significant psychological and immunological changes among asymptomatic gay men across the anticipatory period preceeding HIV-1 antibody testing and during the impact period following news of diagnosis. Furthermore, we have noted significant benefits of behavioral interventions on psychological and immunological functioning among asymptomatic, HIV-1 seropositive and seronegative gay men." (page 46)
It is notable that these two reviews (Antoni 1990, Kiecolt-Glaser
1988), and also a meta-analysis (Herbert 1993) of studies looking
at the effects of stress on immune function
consistently find CD4 helper T cells selectively reduced in people subjected to chronic stress together with a decrease in CD4/CD8 ratio. If found in someone who is HIV positive, these effects would unquestionably be blamed on HIV, and the effects on immunity of the extreme stress of living with an HIV positive diagnosis would be ignored.
Chapter 2: Stress-Induced Dementia
Multiple studies have found that chronic psychological stress,
and the resultant hypercortisolism, induces brain damage characterized
by atrophy of cortical neurons, especially in the hippocampus,
the region of the brain that controls learning and memory. Another
reported finding is enlargement of the ventricles in the brain
(Axelson 1993, Brooke 1994, Frol'kis 1994, Gold 1984, Jensen 1982,
Lopez 1998, Magarinos 1997, Mimose 1971, Ohl 1999, Sapolsky 1990,
Sasuga 1997, Starkman 1992, Uno 1989,1994). Dementia is a classic
finding in people diagnosed with AIDS, and similar changes in
the brain have been reported.
A commonly recognized example of how severe stress impairs mental function is the gaps in memory that people often have in relation to periods of prolonged trauma, as occurs in many cases of childhood sexual abuse, for example. Most people are not aware, however, that chronic stress actually causes atrophy of the brain tissue.
A quote from Uno et al (1994), in the introduction to this paper, discussed the cases of stress-induced fatal wasting syndrome in monkeys. The authors also indicated that they found atrophy of cortical neurons in the hippocampus, as well as in other areas of cortex. This phenomenon was observed both in wild-caught animals subjected to severe social stress by their peers, as well as in animals injected with synthetic analogues of cortisol.
This phenomenon has also been observed in humans. Jensen et al reported in 1982 that torture victims showed long-term signs of dementia, as well as other problems, and described their findings in five such victims:
"Examination of torture victims throughout the world has
revealed a high incidence of late physical and neuropsychiatric
sequelae. The most prominent mental and neurologic symptoms are
impaired memory and ability to concentrate, headache, anxiety,
depression, asthenia (loss of strength), sleep disturbances, cerebral
asthenopia (aching and burning of the eyes), and sexual dysfunction.
These conditions are present in other conditions in which brain
atrophy or intellectual impairment or both are frequent findings
We recently examined five young men subjected to to various forms of torture years earlier. These previously healthy young men (mean age 31 years) had all been tortured severely for from two to six years. Similar mental and neurologic symptoms developed in all of them immediately or shortly after torture; these symptoms persisted unaltered until examination (an average of four years later)... Computerized axial tomography (CT scans) showed definite cerebral atrophy that was cortical in four men and central in one...
The symptoms and signs in the present cases were in many ways comparable to those seen in survivors of World War Two concentration camps. Although the social and mental complications in concentration camp survivors were initially considered to be transient, later follow-up studies showed that signs of dementia occured in a high proportion of cases 10 to 20 years after detention (Thygesen 1970). The same long-term effects with signs of irreversible brain damage may occur in today's torture victims..." (page 1341).
Alzheimer's patients have also been found to have hippocampal
atrophy whose severity correlated with high cortisol levels (DeLeon
1988), and people with depression have been found to have enlarged
ventricles and greater cognitive impairment if their cortisol
levels were elevated.
Starkman et al (1992) studied the effects of chronic excess cortisol on brain function and hippocampal atrophy. They found hippocampal atrophy that was correlated with the amount of cortisol in the patient's blood, just as was found in Alzheimer's patients (Starkman 1992). In their conclusions they briefly discuss these effects as observed in various studies:
Significant correlations between elevated cortisol levels and severity of hippocampal atrophy have been reported in patients with Alzheimer's disease, as well (De Leon 1988). In a broader context, it should be noted that the role of cortisol in cognitive dysfunction likely extends beyond its specific effects on the hippocampus. For example, CT scans revealed ventricular enlargement and cortical atrophy in patients with yhypercortisolism due to Cushing's disease (Momose 1971). In primary depressive disorder, patients with abnormally high cortisol were more likely to have larger ventricles, as measured by ventricle to brain ratios (VBRs), and those patients with large VBRs demonstrated greater global cognitive impairment. (page 764)
Cortical atrophy and ventricular enlargement are two characteristics
commonly found in what is called "AIDS Dementia Complex"
(Robbins 1996). Patients with Cushing's Disease have also been
found to develop meningitis, due to cortisol-mediated immunosuppression,
which is another common neurological complication in people diagnosed
HIV positive (Britton 1975).
While cortisol has been studied the most, epinephrine, the other major hormone released in times of stress, also causes brain atrophy and impaired brain function, as has been indicated by controlled animal experiments. Gold (1984) performed such an experiment using epinephrine injections:
"a single injection of epinephrine results in long lasting change in brain function... The findings suggest that some hormonal responses may not only regulate neuronal changes responsible for memory storage but may also themselves initiate long-lasting alterations in neuronal function." (p. 379)
There are also likely other mechanisms by which this brain
damage occurs that are not yet understood, but no matter what
the mechanism, the effects appear to be swift and often irreversible.
Robert Sapolsky, whose work has been cited often in this paper, wrote an article published in the journal, Science, that reviewed the literature on the effects of stress in the brain (Sapolsky 1996). His review is of such high quality that a large number of his comments will be included here.
Glucocordicoids (GCs) like cortisol, along with epinephrine
and norepinephrine, are essential for surviving acute physical
stress (evading a predator, for example) but they may cause adverse
effects when secretion is sustained.
Excessive exposure to GCs has adverse effects in the rodent brain, particularly in the hippocampus, a structure vital to learning and memory (McEwen 1992, Sapolsky 1994)... Over the course of weeks, excess GC reversibly causes atrophy of hippocampal dendrites, whereas as GC overexposure for months can cause permanent loss of hippocampal neurons. Although studies suggest that similar effects can occur in the brains of primates (Magarinos 1996, Sapolsky 1990, Uno 1989), until recently there has been no evidence (except perhaps Jensen et al, 1982) for GC induced damage in the human. Some new exciting studies present such evidence.
A first example by Sheline and colleagues concerns major depression (Sheline 1996). Approximately half of depressed patients studied secrete abnormally high amounts of GCs... The authors of the new study report MRIs with far more resolution than in previous studies and have excluded individuals with neurologic, metabolic, or endocrine diseases. They have found significant reductions in the volume of both hippocampi... The authors ruled out alcohol or substance abuse, electrocunvulsive therapy, and current use of antidepressants. Remarkably, there was a significant correlation between the duration of the depression and the extent of atrophy.
A similar relation was seen in patients with Cushing's syndrome (where) there is bilateral hippocampal atrophy (Starkman 1992)... The extent of GC hypersecretion correlated with the extent of hippocampal atrophy, which also correlated with the extent of impairment in hippocampal dependent cognition...
In Vietnam combat veterans with post traumatic stress disorder (PTSD), Bremner et al (1995) found a significant 8% atrophy of the right hippocampus, and near significant atrophy in the left. In (another study) Gurvits et al. (1996) also examined Vietnam veterans with PTSD and found significant 22 and 26% reductions in volumes of the right and left hippocampi. Finally, in another study... Bremner et al (1996) found a 12% atrophy in adults with PTSD due to childhood abuse... These studies controlled for age, gender, education, and alcohol abuse... In the studies by Bremner.. there were nearly as large (but non-significant) reductions in volumes of the amygdala, caudate nucleus, and temporal lobe...
How persistent are these changes? Although the Cushingoid atrophy reverses with correction of the endocrine abnormality (excess cortisol/GC production), in the PTSD and depression studies, the atrophy occurred months to years after the trauma or last depressive episode... Thus, these changes could represent irreversible neuron loss. (pages 749-750)
Chapter 3: Social Isolation, Health, and Immunity
Large, prospective clinical trials of the general population
have found that people with low levels of social support have
between double and triple the death rates of people with the highest
levels of social support (House 1988, Berkman & Syme 1979).
In addition, socially isolated people have reduced numbers of
T-lymphocytes (Kennedy 1988, Kiecolt-Glaser 1984, 1991), as do
socially isolated non-human primates (Sapolsky 1997). These types
of results are extremely consistent and go back for decades in
the medical literature. In 1956, for instance, socially isolated
people were found to have much higher rates of tuberculosis, even
when they lived in wealthy neighborhoods (Holmes 1956). It is
worth noting that tuberculosis is an "AIDS defining illness",
so these people would have been diagnosed with AIDS if they tested
positive on the HIV antibody tests.
The effects of social support on survival of cancer has been examined by many researchers, as well. In all eight prospective studies found by this author in which levels of social support were compared among cancer patients, increased survival was observed in people with higher levels of social support. These increases were statistically significant in seven of the eight studies (Cassileth 1988, Colon 1991, Eli 1992, Goodwin 1987, Maunsell 1995, Reynolds 1990, 1994, Waxler-Morrison 1991). Similar results for heart disease have also been found in a large number of studies (Ornish 1998).
Perhaps the most tragic findings regarding social support and human contact involve childhood development. Infants raised in severely understaffed Romanian orphanages have been found to have extremely high rates of developmental disorders and very high death rates (Carlson & Earls 1997, Rosenberg 1992).
Social isolation and cortisol levels in non-human primates:
A study by Sapolsky et al. (1997) looked at the effects of social isolation and social subordination on cortisol levels in twelve wild baboons. They found basal cortisol levels four times as high in the six more isolated baboons, when compared with the six more socially connected baboons, an astounding and statistically significant difference. Here are some excerpts from their report:
Hypersecretion of glucocordicoids (excess cortisol production)
can have deleterious effects on immune defenses, metabolism, reproductive
physiology, tissue repair, and neurological status...
Detailed data about adult male social behavior were collected by one of us (S.C.A.) during the two months prior to darting for anesthetization. These data were collected as part of a larger multi-year study of adult male baboon social behavior and presented an opportunity to examine social correlates of hypercortisolism (excess cortisol production). (pages 1137-8).
Socially isolated males had significantly higher basal cortisol concentrations than males that were well-connected socially (the six more isolated baboons averaged 850 mmol/L compared to only 213 mmol/L in the six more socially connected baboons). (page 1141, figure 1)
In a previous study with a wild population of baboons, we observed that among dominant males, those with the lowest rates of grooming with females and social interactions with infants had markedly elevated cortisol levels... These studies cannot reveal whether there is any causality to this link. However, studies with rodents and captive primates demonstrate the power of social proximity or affiliation to blunt the cortisol response to various stressors, suggesting that these baboons are hypercortisolemic because they lack the stress-reducing advantages of social affiliation... This association echoes the classic finding in behavioral medicine that social isolation represents a highly notable mortality risk factor across a wide range of maladies in humans (House 1988). A key finding in those studies was that no particular form of social affiliation (spouse, friend, or community group) was more protective than the others, but that the association instead emerged from the aggregate of social connections. Simlarly, we did not observe any 1 of the 8 measurements of social connectedness to predict adrenocortical status; instead, it was their aggregate that was highly predictive. (pages 1141-1142)
Some of the studies mentioned by Sapolsky et al above were
analyzed by Coe (1993). He reviewed the research that examined
the effect of psychosocial factors on the immune systems of non-human
primates. Many studies showed that when young, captive monkeys
were separated from friends or from their mothers, their T-cells
showed markedly impaired function. Researchers also tried to assess
why some monkeys were more affected than others, and found that
many subtle variables such as the timing of the separation, the
age of the monkeys, and the way the separation was created, could
all have a significant effect. Thus measuring the effects of social
support is a complex task, as is measuring psychological stress.
The influence of subtle factors related to the social environment
and to the person's internal coping mechanisms may have significant
A review by Levine et al. (1996) looked at research showing that social relationships significantly buffered the effects of stress in a variety of animal studies. Here are some of the authors' comments.
Our initial studies of squirrel monkey adrenocortical activity
showed that social separations of mother and infants produce striking
increases in cortisol in both mothers and infants... We also showed
that the magnitude of this physiological effect is at least partly
dependent on the degree of social support available to the infants.
In the company of mothers and/or familiar peers, social buffering
of stress-induced increases in cortisol is apparent. Dramatic
increases in cortisol occur during maternal separations when infants
are placed in novel environments... Long-lasting increases in
cortisol also occur in subadults and adults... (page 211)
Social separations can induce long-lasting increases in cortisol, whereas companionship can result in social buffering... From 1 to 21 days post separation, however, cortisol remains elevated above pre-separation controls. (page 216)
One section of this review applies particularly to people diagnosed HIV positive. The authors discuss the effects of creation of newly formed social groups on stress and cortisol levels, along with the effects of major changes.
Novelty, uncertainty, and lack of predictability are all psychogenic factors known to activate the HPA-axis in a variety of animals, and increased cortisol levels have previously been reported in newly formed squirrel monkey groups. Recent evidence suggests, however, that group formation-induced changes probably prbably depend on a monkey's prior social-psychological state.
This applies to the members of the gay community, where AIDS still concentrates, who had recently created a new community in San Francisco as well as a few other cities. It also applies to people for whom many social contacts are disrupted or eliminated as a result of their HIV positive antibody test.
Social support and cancer:
Cancer patients with high levels of social support have as much as double the survival rates as those with low levels of social support (Berkman & Syme 1979, Colon 1991, Reynolds 1994), Every prospective study looking at this issue found higher survival rates for cancer patients with higher levels of social support (Cassileth 1988, Colon 1991, Eli 1992, Goodwin 1987, Maunsell 1995, Reynolds 1990, 1994, Waxler-Morrison 1991). Social support interventions were also found to increase survival in two of three studies where a group of cancer patients receiving a social support intervention was compared to a control group (Fawzy 1993, Gallert 1993, Spiegel 1989). Further weight was added to these results by the fact that the two studies with statistically significant results (Fawzy 1993, Spiegel 1989) were also those that used randomized group selection, giving them much more external validity than the other, nonrandomized study by Gallert et al. (1993). Siegel et al. (1989) found that women with late stage breast cancer randomized to receive social support group interventions lived nearly twice as long, and Fawzy et al (1993) found that only three of 34 melanoma patients randomized to receive group education and support intereventions died after seven years compared to ten of 34 who did not. there was also a trend for decreased recurrence, with seven recurrences in the group receiving group interevention compared to thirteen in the control group.
Social Support, Human Contact, and Childhood Development
One of the great tragedies of the 20th century has been the suffering of children in Romanian orphanges that occurred under the rule of Nicolae Ceausescu. Two different teams of researchers have studied these children and come to heart rending conclusions. The children have suffered extremely high rates of developmental delay, mental retardation, delirium, and death. Because these children received adequate food, clothing, shelter, and medical care when sick, the researchers concluded that these children suffered and died because of lack of physical and emotional contacts during their infancy. The first quotes are from a letter published in JAMA in 1992 (Rosenberg 1992).
Since the downfall of Nicolae Ceausescu's communist regime
in Romania in December 1989, several almost barbaric institutions
for children have been discovered throughout the country. Because
of draconian probirth policies implemented by Ceausescu coupled
with Romania's status as one of the poorest countries in Europe,
children were frequently abandoned by their parents and placed
in state-run orphanages. As a result, approximately 40,000 abused
and neglected children languish in these orphanages...
Prior to 1989, it was estimated that 35% of these children died every year. During September of 1991 we conducted a neuropsychiatric assessment of the entire population of one of these orphanages. One hundred and seventy patients resided in this institution, and all had been declared "irrecuperable".
The orphanage was severely understaffed... This understaffing resulted in such minimal child-staff interaction that 75% of the children did not know their own name or age... It should be noted, however, that the director and many of the attendants had a true desire to help these children but did not have the means, or the training, to do so... 85% of the children had no family contact whatsoever. (page 3489)
The researchers report the results of their neurospychiatric
assessment in table 1 on page 3489. They found that fully 94%
of the children had developmental language and speech disorders,
40% were mentally retarded, 26% had muscular atrophy, 22% were
"completely immobile", 14% suffered from delirium, 12%
had epilepsy, 10% had autism, and 4% had psychosis.
Another description of these children is given by a husband and wife team from Harvard Medical School and School of Public Health, Mary Carlson and Felton Earls (Carlson & Earls 1997). Their analysis is both moving and comprehensive, and extended quotes from their work follow.
The situation of infants and children living in state-operated
residential institutions in Romania provides a setting in which
the consequences of severe social deprivation can be examined.
These children experience a form of social care in which their
medical and nutritional needs are met, but but their social and
psychological needs are not. We believe it is scientifically and
ethically imperative to analyze the developmental deficits of
such children within the context of the social and material resources
available to them... Study of the defecits or capacities of the
decontextualized child can lead to invalid attributions of intrinsic
causation within the child (eg. genes for temperament or IQ)...
Studying children in a situation of extreme deprivation provokes such a strong reaction that pursuing an ethical voice to govern one's work would seem crucial. We intend to... become advocates for these children at the same time that we assess the consequences of their living conditions. ...
The demonstration of direct relation between tactile modality and social deprivation was established in the laboratory of Henry Harlow where it was shown that... tactile (but not visual or auditory) deprivation was a critical determinant of the autistic-like behavioral syndrome that resulted from early social deprivation. These studies were continued by Mason and many others, including one of the authors of this article. (pp. 419-420)
The authors go on to give a detailed account of the mechanisms by which touch induces healthy responses in brain neurotransmitters, receptors, and neuronal development, and go on to describe how increased cortisol (glucocorticoids) can inhibit this process. They then describe the condition of these children, and outline a small program that successfully reversed much the damage that had been done.
The muteness, blank facial expressions, social withdrawal,
and bizarre stereotypic movements of these infants bore a strong
resemblance to the behavior of socially deprived macaques and
chimpanzees. Most of the children... had experienced severe tactile/social
deprivation due to the high child:caretaker ratios and custodial
rearing practices. ... we discovered an early enrichment program...,
organized by an American psychologist, Joseph Sparling. In this
program, two groups of 2-9 month old infants were randomly assigned
to either a social/educational enrichment program with child:caretaker
ratio of 4:1 or left in standard depriving conditions with a child:caretaker
ratio of 20:1. ...
In the 9 month period necessary to obtain funding, this intervention program lost its support. Thus, after 13 months of enrichment, children in the intervention group were once again living in the depriving conditions. The children in the intervention group had shown significantly accelerated physical growth and mental/motor development compared to the control group during the enrichment period, but 6 months after the program ended they were no longer superior to the control children (as measured on the Denver Development Screening Test). Measures of weight and height, head, triceps and chest circumference, and mental and motor performance (using the Bayley Scales of Infant Development) revealed that the intervention group had lost the advantage gained from the enrichment experience. At this same time, we measured cortisol levels using the non-invasive method of saliva sampling to determine its level, diurnal variation (cyclic daily variation), and its reactivity to a stressful event... The control group levels can be seen (Fig 2) to rise significantly at noon, compared to intervention group levels. Significant correlations were found between levels of cortisol and physical growth (Denver Developmental Scale) as well as mental and motor performance (Bayley Scale). (pp. 422-424)
The authors later provide a brief description of other studies showing memory loss and brain damage (neuronal death and shrinkage of the hippocampus) in adults who were victims of prolongued stress, and discuss chronically elevated cortisol as a possible cause.
This study of psychologically deprived and stressed young children
not only carries implications for deficient learning and memory,
but also may convey a life-long vulnerability to certain psychiatric
disorders. The results of this research will be compared to clinical
studies of psychiatric conditions in adults that reveal similar
factors of HPA (hypothalamus-pituitary axis) dysregulation, hippocampal
neuron degeneration, and declarative memory loss. ...
The most profound similarity with the work in rodents is the finding of significant hippocampal shrinkage in patients with post-traumatic stress disorder. The presence of shrinkage is strongly associated with declarative memory deficits... Both changes in hippocampal volume and verbal memory loss have been associated with the degree of cortisol elevation in adults with Cushing's disease. Elevated levels of cortisol associated with memory impairment are seen in depressed adults and adolescents, and elevated levels of exogenous glucocordicoids administered for control of asthma have been shown to produce memory deficits and other cognitive changes in children. (p 426)
Finally, Carlson and Earls provide the following comparison to conditions in the United States, where child neglect is also present.
Although this research undoubtedly has implications for the nature of affiliative relations in Romanian society, we are increasingly concerned about the consequences of the growing numbers of children under age 5 who live in poverty in this country (a rate that has increased from 15% to 26% over the past 20 years). When this reality is coupled with the increasing rates of maternal unemployment, which is the objective of "workfare", and the insufficient supply of satisfactory child care services, the enduring negative effects on child well-being for a large segment of American society should be appreciated. (page 426)
Chapter 4: Voodoo Hexing, Root Work, Bone Pointing, and AIDS
We have seen how stress and social isolation can cause immune deficiency that resembles AIDS, and also how they can cause dementia and increased rates of chronic and often fatal illnesses. The most dramatic syndrome caused by stress, however, is a fatal wasting syndrome that results when a "voodoo hex", is cast in certain traditional societies. Physicians observing this phenomenon postulate that the power of such a hex is derived from the group beliefs of the person, their family and their society. Such syndromes are not limited to humans, however.
Stress-Induced AIDS in Wild-Caught Baboons
A study that looked at the effects of severe stress on the health of monkeys found that some monkeys who had been subjected to severe social harrassment and attack from their peers showed a relentless wasting syndrome that usually proved fatal. The authors comments were quoted at the beginning of this paper, but bear repeating:
Wild-caught vervet monkeys... occasionally showed a syndrome
of cachexia associated with persistent diarrhea, anorexia, and
dehydration that usually proved fatal. Those animals appeared
to be socially subordinate and to have suffered an atypically
high rate of social harrassment and attack from their peers. Two
animals died as early as one month under such conditions, and
others died after six months to 4 years in captivity...
The fatal outcome, caused by severe prolonged social stress, induced classic pathology associated with stress, namely gastric ulcers and adrenal hyperplasia (adrenal hyperplasia is caused by chronic excess cortisol secretion). In these animals we also found unique insidious degeneration and resultant depletion of neurons in the hippocampus... Similar degeneration was also found in cortical neurons. (Uno 1994, page 339)
Of all the adverse health effects that have been described in this paper, this description most resembles the syndrome that is called "AIDS".
The Voodoo Hex
Walter Cannon, the renowned professor of physiology at Harvard School of Medicine who first described the hormonal effects of the "fight or flight" response, was also the first to publish a review of the phenomenon that he called "Voodoo death". He compiled reports from a number of Western-trained physicians who lived in areas of the world where native inhabitants believed in, and practiced, this phenomenon (Cannon 1957). These physicians attempted to rule out other explanations for the deaths, such as poisoning. Here are a number of excerpts from this classic article:
Dr. S.M. Lambert of the Western Pacific Health Service wrote
to me that on several occasions he had seen evidence of death
from fear. In only one case was there a startling recovery...
When Dr. Lambert arrived at the mission (in Mona Mona in North
Queensland, Australia) he learned that Rob (the chief helper at
the mission) was in distress and that the missionary wanted him
examined... He was impressed by the obvious indications that Rob
was seriously ill and extremely weak. From the missionary he learned
that he had had a bone pointed at him by Nebo (a local medicine
man) and was convinced that he must die. Thereupon Dr. Lambert
and the missionary went for Nebo, threatened him sharply that
his supply of food would be shut off if anything should happen
to Rob. At once Nebo agreed to go with them. He leaned over Rob's
bed and told the sick man that it was all a mistake, a mere joke-indeed,
that the bone had not been pointed at him at all... That evening
Rob was back at work, quite happy again, and in full possession
of his physical strength. (page 183)
Dr. Lambert (also) wrote to me concerning the experience of Dr. P.S. Clarke. One day a Kanaka (a local native resident) came to his hospital and told him he would die in a few days because a spell had been put upon him and nothing could be done to counteract it. The man had been known by Dr. Clarke for some time. He was given a very thorough examination, including an examination of the stool and of the urine. All was found normal, but as he lay in bed he gradually grew weaker. Dr. Clarke called upon the foreman to come to the hospital to give the man assurance, but on reaching the foot of the bed, the foreman leaned over, saying, "Yes, doctor, he will soon die". The next day at 11 o'clock in the morning he ceased to live. A postmortem examination revealed nothing that could in any way account for the fatal outcome. (pages 183-184)
Dr. J.B. Cleland, professor of Pathology at the University of Adelaide, has written to me that he has no doubt that from time to time the natives of the Australian bush do die as a result of a bone being pointed at them, and that such death may not be associated with any of the ordinary lethal injuries... In his letter to me he wrote, "Poisoning is, I think, entirely ruled out in such cases." (page 184).
Cannon also provides the following eloquent description of how the reaction of the hexed person's community and family combine to multiply the force of the words of the medicine man. These words emanate from the early part of this century into ours with prophetic power. The description is chilling in its similarity to what often happens in people diagnosed HIV positive.
Now to return to the observations of W.L. Warner regarding
the aborigines of northern Australia.
There are two definite movements of the social group, he declares, in the process by which black magic becomes effective on the victim of sorcery. In the first movement, the community contracts; all people who stand in kinship relation with him withdraw their sustaining support. This means everyone he knows -all his fellows- completely change their attitudes towards him and place him in a new category... The organization of his social group has collapsed, and, no longer a member of a group, he is alone and isolated. During the death illness which ensues, the group acts with all the outreachings and complexities of its organization and with countless stimuli to suggest death positively to the victim, who is in a highly suggestible state. In addition to the social pressure upon him, the victim, himself... through the multiple suggestions which he receives, cooperates in the withdrawal from life. He becomes what the attitude of his fellow tribesmen wills him to be. Thus he assists in committing a kind of suicide.
Before the death takes place, the second movement of the community occurs which is to return to the victim in order to subject him to the fateful ritual of mourning... The effect of the double movement in the society, first away from the victim and then back, with all the compulsive force of one of its most powerful rituals, is obviously drastic. Warner (1941) writes:
An analogous situation in our society is hard to imagine. If all a man's near kin, his father, mother, brothers, sisters, children, business associates, friends, and all other members of the society should suddenly withdraw..., refusing to take any other attitude but one of taboo and looking at the man as already dead, and then after some little time perform over him (death rituals), the enormous suggestive power of this two-fold movement of the community can be somewhat understood by ourselves. (page 185)
Perhaps an analogous situation is not so hard to imagine occurring in our society, after all, given the similarities between what is described above and what is experienced by someone diagnosed "HIV positive". A study of the effects of curses and hexes on family dynamics was published in the American Journal of Psychiatry in November, 1970 (Raybin 1970). The author provided detailed case histories of four families in which a member of the family had been "cursed" or "hexed", focussing on the emotional and psychological affects of these curses on the individuals. These hexes often resulted in severe emotional despair and repeated suicide attempts, as well as disruption of social ties. He states in his conclusion that
The four clinical vignettes have illustrated family mythology in general, and curses and prophecies in particular, whether they be direct or implied. These communications can effectively disrupt or devastate a family, or they can serve to maintain a precariously balanced equilibrium... The dynamic issues involved in myths and curses vary with the individual family. (p. 620)
A more recent article by Meador appeared in the Sothern Medical Journal in 1992. Dr. Meador gave case histories of two people who received death-hexes from medicine men. The two men had very different outcomes, apparently due to the ability of one of their physicians to alter the belief structure of the patient. One of the most astounding elements of his case histories is that one of the men was a Haitian given a death hex by a medicine man, while the other was an American given a death hex unintentionally because of a false positive liver scan which appeared to indicate widespread metastatic cancer, when in actuality there was none. The "medicine man" who placed this second hex was Dr. Meador, himself, the author of the article.
The first patient, a poorly educated man near death after a hex pronounced by a local voodoo priest, rapidly recovered after ingenious words and actions by his family physician. The second, who had a diagnosis of metastatic carcinoma of the esophagus, died believing he was dying of widespread cancer, as did his family and his physicians. At autopsy, only a 2 cm nodule of cancer in his liver was found. (page 244)
The actions of the physician whose patient made a dramatic recovery were truly remarkable, and involved something more akin to theatre, rather than medical treatment:
The patient had been ill for many weeks and had lost a large
amount of weight. He looked wasted and near death. Tuberculosis
or widespread cancer was considered the likely diagnosis. The
patient refused to eat and continued a downward course depsite
a feeding tube.
He soon reached a stage of near stupor, coming in and out of consciosness, and was barely able to talk. Only then did his wife ask to speak with Dr. Daugherty privately... The wife told him that about 4 months before hospitalization, the patient had an argument with a local voodoo priest. The priest summoned him to a local cemetery late one night, and... annonced that he had "voodooed" him, that he would die in the very near future.
Dr. Daugherty spent many hours that evening pondering... what he could do to save this moribund man. The next morning he gathered 10 or more of the patient's kin at the bedside; they were trembling and frightened to even be associated with this doomed man. Dr. Daugherty announced in his most authoritative voice that he now knew exactly what was wrong. He told them of a harrowing encounter at midnight the night before in the local cemetery where he had lured the voodoo priest. Dr. Daugherty reported that he had... choked the priest against a tree nearly to death until the priest described exactly what he had done. Dr. Daugherty announced to the astonished patient and family "That voodoo priest made some lizard eggs climb down into your stomach and they hatched out some small lizards. All but one of them died leaving a large one which is eating up all of your food and the lining of your body. I will now get that lizard out of your sustem and cure you of this horrible curse." With that he summoned the nurse, who had, on prearrangement, filled a large syringe with apomorphine (a powerful emetic for inducing vomiting). With great ceremony, Dr. Daugherty squirted the smallest amount of clear liquid into the air and lunged towards the patient, who by now had gathered enough strength to be sitting up wide-eyed in the bed. Although he pressed himself against the headboard trying to withdraw from the injection, Dr. Daugherty delivered the entire dose of apomorphine. With that he wheeled about, said nothing, and dramatically left the ward.
Within a few moments the patient began to vomit. When Dr. Daugherty arrived at the bedside the patient was retching, one wave of spasms after another. His head was buried in a metal basin. After several minutes of continued vomiting and at a point judged to be near its end, Dr. Daugherty pulled from his black bag, carefully and secretively, a live green lizard. At the height of the next wave of retching, he slid the lizard into the basin. He called out in a loud voice, "Look what has come out of you. You are now cured. the voodoo curse is lifted."...
The patient's eyes widened and his mouth fell open. He looked dazed. he then drifted into a deep sleep within a minute or two, saying nothing. The sleep lasted until the next morning. When he awoke, he was ravenous for food. Within a week the patient was discharged home, and soon regained his weight and strength. he lived another 10, or more, years, and died of an apparent heart attack. No one else in the family was affected...
I reflected on this case for many years. I could make no sense of it until I read Walter Cannon's classic paper, "Voodoo Death". (pages 244-245)
Dr. Meador goes on to describe Cannon's paper, and summarizes the aspects necessary to cause a voodoo hex to succeed, including deep belief in the hex by the victim, the family, and the community, as well as initial social isolation followed by expectant preparations for death. Before describing the American man who died after a false liver scan, he asks the following question:
Even if such a strongly held belief could cause death, most Westerners think of hexing as a bizarre superstitious practice limited to ignorant people. It has no pertinence to modern Western society... does it? (page 245).
This patient died with only a small patch of pneumonia and
a small nodule of cancer in his liver. His wasting syndrome was
unresponsive to antibiotics, and he died "thinking that he
was dying of cancer, a belief shared by his wife, her family,
his surgeons, and me, his internist" (page 246). Meador asks
yet another question of the reader: "If the first patient
was cured of a hex, did the second die of a hex?".
Some of the descriptions of the first patient's illness bear remarkable resemblance to AIDS. The patient "had lost a large amount of weight". He looked "wasted and near death". Tuberculosis or widespread cancer was considered the likely diagnosis, and tuberculosis is one of the most common "AIDS-defining illnesses". Several types of cancer are also considered AIDS-defining. The patient "continued a downward course depsite a feeding tube", showing that malnutrition alone did not explain his demise. He also suffered from severe dementia.
Kaada (1989) presents a review of research into the opposite of the placebo effect, dubbed the "nocebo" effect. This is the negative effect on health associated with harmful beliefs and psychological stressors. He comments on voodoo hexing and the ability to resist its power as follows:
"In its most extreme, nocebo-stimuli may cause death,
as in voodoo-death in
primitive societies, an example of the fear-paralysis reflex. Whether the outcome is
positive or negative is determined, inter alia, by the subject's possibility of coping with the situation."
This could explain why some people live for years after an HIV diagnosis with no ill health, while others succomb in much shorter time.
Also quoted in the introduction of this book wasa brief quote from a special article to the Lancet (Milton 1973). Dr. Milton was am Australian physician who commented as follows:
There is a small group of patients in whom the realisation
of impending death is a blow so terrible that they are quite unable
to adjust to it, and they die rapidly before the malignancy seems
to have developed enough to cause death. This problem of self-willed
death is in some ways analogous to the death produced in primitive
peoples by witchcraft ("pointing the bone")...
Throughout questioning his answers are minimal, and as soon as the questions stop he is silent... He does not have the obvious signs of extreme anxiety or fear. Blood pressure, pulse, and respiration remain normal... Within a month of the onset of this syndrome the patient will almost certainly be dead. If a necroscopy is carried out, ... there will often appear to be no adequate explanation for the cause of death.
A similar syndrome is associated with the custom of "pointing the bone" in primitive societies... Pointing the bone is essentially a magic spell cast by a witch-doctor into the spirit of the victim. The Australian aborigines believe that all disease is the result of disharmony of the spirit. If the spirit can be disturbed by such spells, illness should follow... Any hope of escape becomes unthinkable, and, provided the victim holds the necessary beliefs, death follows the witch-doctor's spell. Obviously, the method is ineffective against those who do not hold the necessary beliefs...
The Melanoma Clinic at Sydney hospital (where Dr. Milton worked) often admits patients with incurable melanoma who are beginning to show all the features of self-willed death. As soon as the patient feels that something can be done to help him, ... his mental attitude improves. This improvement may be so dramatic that there is danger of the medical staff believing that various treatments offered ... have prolonged the patient's life by an organic effect. (pages 1435-1436)
This last description could explain the widely propogated belief that new protease inhibitor "cocktails" are prolonging people's lives, especially since controlled clinical trials do not show reduction in death rates. This topic will be addressed in a later section.
Another paper on hexing appeared in the Journal of the American Medical Association in 1975 (Cappannari 1975). This case was different from other in that it occurred in the United States, and did not involve a professional "witch doctor" but rather a woman considered to have magical powers. The person hexed was the woman's duaghter-in-law, which adds a new dimension to the classic tension between mothers and women who marry their sons. It all began when the woman in question found she was pregnant and her mother in law, who "did not like her" told her that her baby would be born dead.
The patient maintained that she did not worry about this threat,
in spite of her mother-in-law's reputation in the community as
being a "bad lady" who "cast spells".
In September the baby was born dead at full term. that evening the patient experienced abdominal pain, nausea, vomiting and diarrhea. In November (with persistence of her symptoms) she went to a local hospital and a diagnosis of sickle cell trait was made (which ordinarily produces no symptoms). Continued symptoms precipitated the first admission to Vanderbilt University Hospital in January 1972, when regional enteritis was diagnosed on the basis of findings on x-ray and biopsy. In addition to treatment with corticosteroids and sulfonamides, therapy with isoniazid was begun.
In June, the patient and her husband separated. She noted that "he was tired of me being sick all the time"... He said that "he didn't want to leave, but something had power over him and was making him do it". In September (one year after the still-birth) the patient was readmitted because of weight loss. Dosages of corticosteroids were increased, and she was tube-fed. When she left the hospital her weight was 47kg (105 lb) compared to her normal range of 63 to 68kg (140 to 150 lb) before pregnancy. (p. 938)
The patient learned formally that a hex had been placed on her by her mother-in-law, and went to an "herb doctor" who told her to "throw away all she owned of her husband and his mother's possessions in order to free her of the hex" (p. 938) Unfortunately this did not work and she "began to doubt that the hex was gone". Soon she learned of a new hex placed on her.
In July, (nearly two years after the still-birth) her husband
served her with divorce papers and said "I must do this...
I'm under another power, and besides, you will die in January
anyway." He repeated this prophecy to her before remarrying
in December, when he disappeared from her life. (According to
the patient's mother his present wife is said to be losing weight).
This dire prophecy was given additional weight by a physician
who told the patient she would always have her disease and that
it would eventually "kill" her.
Since her weight had fallen to 33 kg (72 lb - about half of her normal weight) and she had begun to look as if she might die, she was readmitted to the hospital. At that time a psychiatric opinion was requested. She was laconic (spoke little), appeared depressed, but was not anxious or psychotic. Concerning the hex, she said "I don't know if I am going to die or not, but I believe my stomach trouble was caused by her spell."... She would not participate in the interview, but let her mother answer questions. It was clear her mother believed in the hex and in the validity of the gypsies as much or more than her daughter... But then she added with emotion, "She will not die until the Lord is ready for her. His power is the greatest of all." ...
The psychiatric consultant suggested that a fundamentalist black Baptist minister (who was also involved in voodoo) talk with the patient. He briefly interviewed the patient and informed her that the hex was "all in her head". Then he read biblical passages concerning the casting out of devils, whereupon she entered a hypnoid-like state from which she later emerged, saying that she felt better. The next day she said that she had "forgotten" about the hex and did not wish to be reminded of it. ... Her mother said she was angry about people bringing up "things which were upsetting her". ...
She gained weight. Her spirits improved greatly after February 1 (she was predicted to die in "January"), although she continued to have abdominal cramping... She observed that her hex was never real, that she only had "regional enteritis," and concluded "anybody can be fooled". (pp. 938-939)
The authors provide some brief comments:
It seems clear that this patient and her omnipresent mother
were torn between two distinct systems of belief: one, the supernatural,
including especially a belief in hexing.., and the other, involving
contemporary allopathic medicine...
It is pertinent that the mother-in-law had a reputation for casting spells and was viewed in the community as a "bad-lady"... This case is complicated by the patient's having regional enteritis. Although there is some controversy about the psychosomatic aspects of this disease, there is evidence that it is related to psychosocial stress and that psychodynamic factors are of etiological importance. Several independent reports emphasize the role of emotional stress in the precipitation of symptoms. (p. 940)
There was evidence of psychosocial stress with the chaotic and disruptive marital situation, as well as severe object loss with the birth of the dead infant... Thus, the clinical picture is also consistent from a psychosomatic viewpoint even out oif context of the hex, which in itself may be looked on as a form of psychic stress.
One evidently adverse suggestion by a physician to the patient to the effect that she would not recover was all too similar to her husband's prophecy that she would die in January. It constituted a blatane example of the inadvertent hexing sometimes performed by physicians. ...
If this case were classic of hexing, with total belief by the patient (and mother) in magical powers of the mother-in-law, the patient should have died as scheduled... A person may, of course, subscribe to more than one belief system at a time, even when such systems are logically or empirically contradictory. Most of the medical literature on voodoo deals with voodoo death. The mechanisms that cause death are still under discussion, but the full acceptance of witchcraft by the victims is characteristic in these reports. In this case, the persons involved subscribed in part to two differing systems of disease causation and cure. Indeed, this vacillation may have prevented this patient's death.
While it is certainly possible that "hexing" had
nothing to do with this patient's illness. The fact that her symptoms
began improving immediately after a spiritual intervention induced
a "hypnoid-like state" and then again after she outlived
her predicted date of death, however, suggests otherwise. The
physicians involved in her care evidently agree, as their comments
In this case the hex was more vague, and death did not result. Instead, a period of severe chronic illness was created, that lasted over two years.
Campinha-Bacote provided an excellent overview of "voodoo illness" in an article in the journal, Perspectives in Psychiatric Care in the winter of 1992 (Campinha-Bacote 1992). He also describes, in much more detail than the other authors cited so far, what the voodoo religion is like and who practices it.
Voodoo illness involves a belief that illness or death may
come to an individual via a supernatural force. Other terms for
this illness include "root work", a "hex",
"conjuring", a "trick", "black magic",
"conjure illness", "hoodoo", "voodoo",
"witchcraft", or a "spell". Voodoo illness
is classified as a culture-bound syndrome, that is, as an illness
that varies from culture to culture. ...
Voodoo is derives from the word vodun, which means "spirit". In the African Haitian belief system, God or "Gran-Mat" is acknowledged as creator of heaven and earth. this Gran Met delegates certain spirits ... to serve as intermediaries between God and man. The voodoo priests or priestesses practice sorcery and conjuring, as well as the voodoo religion, in an attempt to maintain harmony with these spirits. the priests are expected to be knowledgable about black magic in order to counteract malignant forces.
The author then goes on to describe how the voodoo religion affected and interacted with the culture of African slaves in America, and how this has affected current day beliefs in some members of African American communities. After this, she describes common symptoms of "voodoo illness".
Conjure doctors and folk healers report that symptoms typically
fall into two broad categories: gastrointestinal and behavioral.
Gastrointestinal symptoms include diarrhea, nausea, vomiting,
food not tasting right, and "falling off" (unexplainable
weight loss). Behavioral symptoms include bizarre behavior, delusions
and hallucinations. ...
Generally, the victim believes in the power of the person who administered the hex, and realizes he/she has been hexed or at least suspects it.
Left untreated, voodoo illness can progress to voodoo death. While voodoo death is not surprising to the folk healers who understand the belief system that victims hold, to Western health workers such death is a shocking and mystical phenomenon. ... (In the United States) hexing practices are no longer restricted to rural isolated communities ... Nor is a belief in voodoo illness restricted to the poor, uneducated, or lower socioeconomic classes. Indeed, the Western health worker is more likley to encounter (this phenomenon) than ever before.
Generally speaking, Western medicine treats these individuals as having either psychological or physiological problems. the spiritual and cultural dimensions of the client's presenting problem are often overlooked, except by the folk medicine practicioner, who sees no distinction between the mind, body and spirit. ... Western medicine classifies voodoo illness under the heading of psychiatric disorders, listing diagnostic criteria in the Diagnostic and Statistical Manual of Mental Disorders, 3d ed., Revised (DSM-III).
Campinha-Bacote also provides a brief description of several proposed mechanisms.
Western medicine has posed several different etiological explanations for voodoo death. As early as 1942, Cannon (1957) explained magical death in terms of the response of the autonomic nervous system to extreme emotion; in such cases death was thought to be caused by the exhaustion of the sympathetic nervous system. In contrast, Richter (1957) believe death was due to the excessive response in the parasympathetic nervous system, which was a result of extreme feelings of helplessness. Lex (1974) proposed that voodoo death involves stimulation of both the parasympathetic and sympathetic nervous systems. Other explanations of voodoo death have included the power of suggestion and pharmacological poisoning.
The next study to be reviewed documents similar types of severe,
chronic illnesses, which the author feels were caused by a voodoo
hex and the powerful beliefs that were generated.
Golden (1977) provided a description of voodoo hexing that he observed while serving as a peace corps volunteer. His article was published in the American Journal of Psychiatry. Although the author is not a physician, he provides perhaps the best research summary of all, as well as an excellent discussion comparing the "hexing" that occurs in a traditional society with similar phenomena that occur in Western society. He describes both the practice of hexing as he observed it, as well as the effects of such a curse on someone he knew quite well, his landlady.
As a Peace Corps volunteer teacher I spent two years in West Africa. There I lived in an area where the voodoo cult originated, and where cursing and hexing were actively practiced. Vodu in the Ewe dialect of the West african village where I lived means "one to be feared". ...
Disobedience of tribal custom is punished by fines, disgrace, banishment, or, when the infraction is particularly serious, by curse death, which means certain death to the victim. My landlady was fatally affected by such a curse... For a year or so she had been suffering from severe and acute attacks of abdominal pains. She had had exploratory surgery performed by European doctors ... Towards the end of my Peace Corps tour I noticed that she was losing weight and saw her less and less often. When she died, she was buried at the outskirts of the cemetery. When I asked a friend of mine why, I was told that she had been cursed by one of the yehwe, one of the major cults of the village, because she had been an adulteress.
For the curse to be successful, the victim has to be made aware that he or she has been cursed. ... Death comes slowly but surely over a period of months. When the curse becomes known, the victim's family and friends as well as the entire community withdraw their support. The victim becomes an outsider to the few cohesive and organized activities of the village ...
Feeling Hopoeless and helpless, the victim withdraws, thus furthuring his or her isolation ... Although the threat to life is not acute, the emotional strain of feeling hopeless is evident over an extended period of time. The victim fatigues easily in order to conserve the energy needed to protect threatened resources from the emotionally overstressful situation. The victim remains in a state of chronic fatigue and melancholia, and ... he or she simply dies.
Unlike the curse death in this village, curse deaths in other parts of Africa have been reported to occur immediately after rthe curse has been placed. ... When cursed with all the drama of the ceremony, the victim dies suddenly. Many physicians have speculated on the physiological basis of such curse death as well as other types of death caused by emotionally stressful situations. ...
In the village I lived in, belief in the power of such hexes is wholehearted. In areas where the belief is weaker, the victim seems more amenable to treatment. ... when curses and hexes are effective, overdependency and a feeling of powerlessness also occur. ...
Furthur, psycho-physiological forms of giving up are often seen in (Western) hospitals. Patients ... told of their imminent death have been known to react by withdrawing, eating and drinking poorly, and socially isolating themselves; at times these reactions result in premature death. (pp. 1425-1426)
I have used the words of many others throughout this book to shape the argument presented here. It is perhaps fitting, then, that I close with the words of two people intimately involved with HIV and AIDS. One is a "long-term survivor" named Clair Walton, who created and coordinates a network of support for long-term survivors (Walton 1999). The other is a man who worked with hundreds of people diagnosed with AIDS in the early 1980's, and wrote an eloquent spiritual description of what they were going through (Cecchi 1984).
Clair Walton is the Cordinator of the International Long Term Survivors Network, a group of people diagnosed HIV positive who have lived at least seven years with no illness, and who have never taken AIDS medications. She recently wrote an article about her experiences as a person that has decided to challenge the prevailing belief that HIV will kill her:
Such is the power of the hiv/aids spell. On several occasions
I have had people say to me, patronizingly or even gleefully,
that they knew someone just like me, who thought the way I did,
then got sick and died. ...
Part of the process for me has been to challenge the taunts of those who seem to relish warning me of my impending death. I am, though, a little confused as to the message being transmitted to me. If they are trying to warn me, do they think it never occured to me? Do they think I have escaped the most destructive message of hiv/aids for the last fifteen or so years? ... I wonder if those who make such remarks understand the damage they cause when they relentlessly push the inevitability of illness and death? ... I wonder how people, who hardly know me, think they know me, let alone compare me to someone with different histories, philosophies, etc., whom they probably didn't know either? ...
I attended a conference in Cape Town, South Africa, organised by the Global Network of People Living With Hiv/Aids. It was an incredible experience ... What struck me as odd, but I have since come to see as the norm, is the way the session on long term survival was pushed out of the main programme. ... It was in Cape Town that I consciously took my life back and began the retreat from being an hiv clone. ...
In setting up the Long Term Survivor's Network and gathering information on long term survival, I have been challenged on the use of the term, survivor. The argument being that if an hiv test is not an indication of future ill health then we haven't survived, as we had nothing to survive. I would dispute that, for we have survived an assault on the very basic human spirit; ostracism of society, poisoning of the mind by fear, attempts to control our sexual and reproductive needs, as well as pressure to take toxic and experimental drugs. No mean feat! ...
There is a saying that Nelson Mandela used: "Our deepest fear is not that we are inadequate. Our deepest fear is that we are powerful beyond measure." (pp. 16-17)
It is clear what Clair Walton thinks can powerfully undermine
her health, and it does not appear to be "HIV".
A similar view was eloquently expressed by Robert Lee Cecchi in 1984, in an article that was published in the Annals of the New York Academy of Sciences (Cecchi 1984). He wrote about the people, primarily male homosexuals, who were being diagnosed with AIDS in the early years of the epidemic, before any "antiretroviral" drugs were being given. Mr. Cecchi speaks from within the experience of working with hundreds of people diagnosed with "AIDS", and demonstrates that the populations affected by HIV already experience tremendous amounts of spiritual, social, and psychological stress. From this perspective, it is easy to see how a devastating diagnosis like being diagnosed "HIV positive" could well be the final blow.
He wrote the article before "HIV" had been targeted as the cause, and although they had spent several years in a futile search for a common infectious agent, the scientific and gay male communities were still firmly convinced that the syndrome was infectious in nature. The discussion below applies only to a small subset of gay males, those most susceptible to damage that emotional and spiritual stressors can cause. Thus, the generalizations below are skewed by the fact that the author worked primarily with gay males who were diagnosed with "AIDS", and thus his article does not necessarily represent gay males as a whole very well. Although the diagnosis "HIV positive" did not exist, the belief in an infectious plague among gay males could still be able to create a self-fulfilling prophecy, especially among those most susceptible. It is clear from Mr. Cecchi's words that the people he worked with were highly susceptible due to a lifetime of severe stress and societal rejection.
Through the words below one finds that even in the early years of the "epidemic", the thesis of this book was being eloquently expressed. The lines quoted below combine well with some of those quoted earlier by Walter Cannon as examples of people who saw clearly just how devastating the consequences of social dispossession, rejection, isolation, and fear could be, and who also saw that the convenient excuse of an infectious agent or some other organic cause ignored significant social, emotional, psychological, and spiritual dynamics.
Most of the theories about the cause of the acquired immune
deficiency syndrome point to a single agent, typically a virus,
that has attacked the immune system and damaged it, making us
vulnerable to any of a variety of viruses, parasites, fungi, and
Many sciences, ... such as those of psychoneuroimmunology and psychiatry, need to be alerted to the importance of this syndrome in helping to establish the link between our minds and our health, our bodies and our lives. ...
I postulate that the affected communities may already be immune deficient; that all of the syndromes may be opportunistic infections coming out of that deficiency; that the immune breakdown may be a result of stress associated with lack of positive self-image, inability to express feelings and anger, inability to complete relationships, loss of family, lack of community nurturance, lack of supportive role models, and lack of self-acceptance and identity. That this breakdown is an illness of the disenfranchised, the outcasts of society, has already been intimated. Studies have shown that in some areas 85% of the gay male community is immune deficient ...
What is being protested, in this instance, is the persecution of same-sex orientation by a culture where feelings are given little importance and emotional needs vital to a person's well-being are ignored. It is in this area that we have a choice. Choice to continue participating in a life unsupported and unrecognized or choice to facilitate change in a society that has forgotten that all men are created equal.
The greatest obstacle towards completing this process towards universal acceptance is the severity of the grieving process. The gay community and the medical community are both suffering from bereavement overload. With the intensity of our grief we may well lose sight of our goal. ...
The second greatest disadvantage of the process toward universal acceptance is that the "benefits" gained by having an illness - increased love and attention, a lessening of responsibility and demands, permission to focus on the needs of self rather than the opinions of others - often hamper recovery.
My spiritual overview is experiential and comes from my own sense of the way things are, and the following opinions come from my experience, from anecdotal evidence gathered while talking to and working with more than 400 people with AIDS in the last 17 months. Insights were easy to gain as the AIDS patients version of the story reinforced my own idea of what was true.
Psychological stress has been documented to be immune-suppressive. ... Acceptance in society enhances whatever coping methods we have devised to counteract or adapt to that stress. ... AIDS is an illness affecting many people who are in society's disfavor, people cast out and rejected for their differences.
Many homosexual men, when asked to express their feelings, reply with a narrative of the circumstances in their life; they do not know how to describe the feelings associated with these circumstances. Their feelings are repressed and they believe that they must hide who they are.
Early on, gay men realized that the only way for them to get comfortably through the pubescent period was to hide the feelings that made them assume they were different. Repressed anger, confusion, and frustration welled up inside as they looked unsuccessfully for role models ... A lack of relationships led in turn to an underdeveloped self-image and nonacceptance of self...
Sexual freedom brought with it an underdeveloped sense of relationship, sexual freedom left many with a sense of being good enough, but just temporarily, just for one night only, furthur damaging a healthy sense of self-worth. Repeating sexual encounters became an addictive process that gave momentary psychological relief, but was unable to create a satisfying unity or foster bonds.
Drug use, both prescription and recreational either lessened the internalized feelings of worthlessness or produced euphoria, releasing one's true feelings from within. Some men felt good about themselves only when they were high, though inevitably that high time must end, intensifying their original feelings. Hard drug use eventually destroyed those individuals who could not make the adjustment back.
A subculture slowly coming out of hiding had no single issue like this epidemic, which tragically pulled together a sense of family. Community nurturance could have been the substance needed ...
Each act of injustice chipped away at our defense systems, until, weakened, we have accepted ideas not our own; society's ill will has become an opportunistic infection of the mind, and badly managed stress set up a battle which we have lost, resulting in illness, frequently terminal illness.
Many patients have admitted to me that they do not want to die, but that they see no reason to live. Especially damaging are the isolation methods employed in treating people with AIDS, feeding the already established feelings of alienation and causing the patient to furthur withdraw into guilt and depression. ...
Studies have shown that people become ill following stressful life situations. People become terminally ill after chronic stress. Historians have suggested that the spread of the Black Death of Europe in the fourteenth century was partly encouraged by the stress of urban living at the time and that its disappearance coincided with improved social conditions and better living standards for ordinary people. ...
People with AIDS have frequently presented with central nervous system involvement - from fevers, weight loss, seizures, personality changes, lethargy, depression, and weakness to organic brain impairment, perceptual discrepancies and confusion. Care must be taken to evaluate whether these are symptoms of infection or the results of neuropsychiatric changes incurred from prolonged stress. ...
Nurses who struggle with the confusion of conflicting infectious disease recommendations must be reminded that this very isolation has forced them to stop touching the patient. The absence of this tender, loving care, which is the foundation of nursing, hinders the pateint's will to live. ...
To the gay community at large I say that we must work together to adapt to the stressors in our life, to be supportive of ourselves, to create family. Change is continual; it is the only constant in the universe ... Don't buy into the idea that you are less than you know yourself to be. Nurture yourself and each other. This is the coping method needed to create self-worth.
If you believe in the single-agent theory as the cause of AIDS, then regard stress as the variable that made us susceptible. Add repeated insult to the theory and it becomes multifactorial.
Now let us all work together harmoniously, as equal partners, to put an end to this epidemic. (pp. 286-289)
It seems clear that the contradictions and confusions that
riddle the science behind "HIV" as the cause of "AIDS",
which have been documented in this book, point inevitably backwards
to the words spoken here. I believe that an end to the epidemic
is within our reach, and I have seen people make miraculous recoveries,
without the use of "antiretrovirals", simply by coming
to believe that HIV is "harmless". They must maintain
these beliefs in spite of often desperate and angry attempts to
convince them otherwise. A few examples do not prove anything,
however, and do not do justice to the complexity of human existence.
Ultimately, you will have to decide what is right, by listening to your experience, and by listening to the experiences of others.
Are the Toxic Effects of Anti-AIDS Drugs Being Blamed on HIV?
In 1995, the number of people dying from AIDS in the United States began to drop, and when deaths due to AIDS dropped in 1996, this was quickly offered as proof that the new drugs were working. As noted in this paper earlier, however, CDC statistics clearly show that new AIDS cases started dropping in 1993, several years before protease inhibitor cocktails were introduced which would seem the most obvious explanation. In addition, in 1993 the number of AIDS cases doubled overnight when the definition of AIDS was changed for the third time. Previous changes had resulted in more and more illnesses being officially dubbed "AIDS defining conditions", including things like certain yeast infections, cervical cancer and lymphoma which are relatively common in people of the same age group as most HIV positive people. Therefore, just about any serious condition that happens to occur in a person diagnosed "HIV positive" could now be officially blamed on HIV, along with any infectious process. The 1993 definition change included people who had low T-cell counts. The trouble is that a lot of these people were clinically completely health, which means that an artificial inflation of AIDS cases occurred. These new cases were at low-risk, and thus the average life-expectancy of people diagnosed with AIDS would be expected to increase, no matter what medications were used.
So what studies do exist that support the widespread claims that new AIDS medications have revolutionized the treatment of AIDS. These claims are not based on any controlled studies, but rather on clinical observations and media reports. The accepted way to ensure that these anecdotal stories not a result of the placebo effect or observer bias is to perform "placebo controlled", randomized, double blind studies. These studies are sadly lacking in the case of protease inhibitor cocktails, AZT, and other AIDS drugs.
There have been a large number of studies looking at the effectiveness and safety of PI cocktails, but only two have actually looked at clinical health. All of the other ones focused exclusively on "viral load", which earlier sections of this book have revealed to be a questionable marker of HIV activity. A random testing of the population revealed that a large majority of people who have "viral loads" are HIV negative on the antibody tests, which is why the "viral load" test is only given to people who have already tested positive on the antibody tests.
One would expect that lots of studies would be available documenting clear clinical benefits, but that is simply not the case. The fact that only two of the hundreds of controlled studies actually look at clinical health raises serious questions about whether bias and placebo response is involved in the anecdotal media reports of drug-related cures. Many such reports do not even mention clinical health, but refer to the "virus rebounding in their blood streams" as proof that people are getting sick. If one looks more carefully it is often obvious that the people in question are healthier without the drugs, because the drugs are associated with debilitating side effects in a majority of people who take them. One also must rightfully ask how this entire multi-billion dollar industry of anti-AIDS medications was established on statistically insignificant evidence. When billions of dollars and thousands of careers are at stake, the potential for bias is enormous, and one must be very careful about making conclusions from such incomplete reporting.
The two studies that do claim health benefits, and not just "viral load", are of minimal value (Hammer et al 1997, Cameron et al. 1998). They did not find statistically significant reduced death rates. Both were stopped early, which biases the results in favor of the drugs, since the study will be stopped at a statistically advantageous time. The Hammer study suffered from very incomplete reporting, making it difficult to assess toxicity or results. In addition, the Hammer study broke their own study design in order to increase their statistical significance. By combining two separate treatment groups, the statistical "P value" was artificially increased. In addition, the gross underreporting of "AIDS defining" events make this study of little or no value.
The second study by Cameron et al (1998) was of better quality, but its results suggest greater toxicity than benefit. People given the full drug regimen had extremely high toxicities compared to placebo recipients, including 50% with diarrhea, another 52% with nausea, 29% vomiting, 28% circumoral parasthesia (numbness and tingling around the mouth), and 25% weakness. With these extremely high toxicities, it is easy to see how th double-blind could be easily penetrated by both patients and clinicians. Fully 21% of the people taking the three drug combination dropped out of the study before the 4.5 months were up, which again hopelessly biases the results. In spite of all these favourable biases, although there was some reduction in "opportunistic infections", the authors found little or no reduction in mortality, as a graph on page 546 clearly indicates. They mask this failure by lumping death statistics in with opportunistic infection statistics, citing reductions in the probability of "AIDS progression or death", a practice which seems designed to confuse or mislead people who read the study rather than to educate them. the toxicities described here occurred over the short space of 4.5 months, and the risk of giving these drugs for years on end has never been assessed.
Both these studies use a "placebo" which is actually a completely unproven combination of AZT with another DNA chain terminator like ddI or ddC. This alone eliminates these studies from any meaningful scientific discourse, unless the "placebo" combination has been shown to be at least safe, something that can only be done by testing it against a true placebo. This was never, ever done.
The argument thus far is simply that the new protease inhibitor cocktails are completely unproven, open to bias, and may be due to placebo effects. many prominent scientists, however, take the argument quite a bit furthur. They argue that the very drugs used so wantonly with people diagnosed "HIV positive", could very well be causing much of the illness and death that is blamed on "HIV".
Are the effects of AZT and other "antiretrovirals"
being blamed on HIV?
Many people are more comfortable with a physical cause of disease, and thus might reject the idea that emotional, psychological, social, and spiritual influences could cause such devastating illness. People like this may be unconvinced by the portions of this book that deal with such "soft" sciences, but may still be curious what causes the symptoms in people diagnosed with AIDS, given the problems with the HIV hypothesis that I outlined in the first part of this book. To these people, the following section may make more sense. In the same way that some people question whether cases of "voodoo hexing" could actually be caused by poisoning, some people may question whether AIDS could be caused by poisoning. I again do not claim to "prove" the arguments here, but rather to present the evidence so that the reader can decide. I include a number of direct quotes to make this somewhat easier.
AZT, ddI, ddC , protease inhibitors and other drugs termed "antiretrovirals" have been hailed as breakthroughs in AIDS treatment. As described above, what may surprise just about everyone, including people who have been diagnosed "HIV positive" and their physicians, is that there is not even a single controlled study showing a statistically significant reduction in mortality using these agents. The studies used to test their efficacy rely exclusively on measurements of "viral load". The only studies published that claim positive outcome were short-term and did not have statistically significant results (Cameron et al. 1998, Hammer et al 1997). Even if they do have results, however, the possibility of a placebo response is a likely possibility, given the fanfare that has surrounded them since their introduction. Finally, because of the harsh side effects, it is unlikely that any kind of double-blind can be maintained in such a study.
In the opening segment of this book I cited a study from 1950 in which syrup of ipecac, which normally causes nausea and vomiting, cured women who were already suffering from nausea and vomiting (Wolf 1950). The women were told that it was a new drug that eliminated nausea and vomiting, and this belief was apparently powerful enough so that their symptoms went away. Thus it was shown that if people believe in a drug, it can have positive effects, at least for a short while, even if it is normally highly toxic. If administered over a longer period, however, the initial benefit may fade, while the toxicities remain. After reading the following evidence, one may well see how this could explain the anecdotal stories of success with AZT and other "antiretrovirals", as well as how some of the toxic symptoms caused by these drugs, could be later blamed on HIV.
Although the newer "antiretrovirals" like ddC, ddI, and d4T, have analogous mechanisms of action and similar toxicities to AZT, they have not been studied as extensively and therefore are not discussed in as much detail in the studies outlined below. The major exception to this is "HIV
Dementia" as discussed near the end of the essay. (See glossary of brand names below that under which these drugs are sold.)
1) Glaxo Wellcome puts the following warning in large, bold-faced, capital letters at the start of the section in the 1999 Physician's Desk Reference that describes AZT (referred to under the name Retrovir or Zidovudine).
"RETROVIR (ZIDOVUDINE) MAY BE ASSOCIATED WITH SEVERE HEMATOLOGIC TOXICITY INCLUDING GRANULOCYTOPENIA AND SEVERE ANEMIA PARTICULARLY IN PATIENTS WITH ADVANCED HIV DISEASE (SEE WARNINGS). PROLONGED USE OF RETROVIR HAS ALSO BEEN ASSOCIATED WITH WITH SYMPTOMATIC MYOPATHY SIMILAR TO THAT PRODUCED BY HUMAN IMMUNODEFICIENCY VIRUS."
An earlier version of the Physician's Desk Reference, published in 1992 made the connection even clearer:
"It is often difficult to distinguish adverse events possibly associated with Zidovudine administration from underlying signs of HIV disease or intercurrent illness."
Warnings like this should bring about a great deal of concern,
especially given the litany of contradictions and confusion surrounding
the science of "HIV" as the cause.
Allow me to translate some of the above warnings. "Granulocytopenia", also called "neutropenia" means that the primary cells of the immune system, neutrophils, have been depleted, along with some other cells, eosinophils and basophils, which are less numerous but still important to immune function. This condition can be mild, moderate, or severe. The clinical course of severe neutropenia, as described in the basic pathology textbook, Pathologic Basis of Disease by Robbins (5th Ed.), which is used in most medical schools to study pathology, describes what happens to people with severe neutropenia.
CLINICAL COURSE: The symptoms and signs of neutropenias are those of bacterial infections. ... In severe agranulocytosis with virtual absence of neutrophils, these infections may become so overwhelming as to cause death within a few days." (Robbins, p.631).
This sounds disturbingly similar to a description of AIDS. Although CD4 T-cells are the first cells supposedly attacked by "HIV", "later stages of HIV infection" are often associated with loss of neutrophils. Robbins also states, in italics, that "the most severe forms of neutropenias are produced by drugs." AZT was claimed to specifically attack HIV replication by interfering with DNA replication. What is not mentioned in any textbook is that AZT has been found in five studies performed after its rushed FDA approval to be equally toxic to T-cells, the very cells whose absence is blamed on HIV, by inhibiting T-cell DNA replication in exactly the same fashion. (2) AZT may cause an initial increase in T-cells, but in relatively short time the T-cells, neutrophils, and other immune system cells begin to decline. This artificially increased T-cell count was shown to have no bearing on survival in the best and most well-controlled study available on AZT, the Concorde Study, which also found that people who were given AZT earlier died faster. This study will be reviewed below.
Another strongly worded warning appears in the 1996 edition of the USP DI: Drug Information for the Health Care Professional .
"Because of the complexity of this disease state, it is
often difficult to differentiate between the manifestations of
HIV infection [sic] and the
manifestations of zidovudine (AZT). In addition, very little placebo controlled data is available to assess this difference." (pages 3032-3034)
2) An example of a study that documented the toxic effects that AZT has on people's immune systems was published in the Annals of Hematology in 1994. AZT was given to 14 health care workers who were exposed to HIV-contaminated blood through needle sticks and similar accidents. As we saw in previous studies, the likelihood of any of them contracting HIV is extremely remote, about 1 in 333, which is even less than the probablity of finding someone who is HIV positive when randomly picking from the general population. Thus it is no surprise that none of them actually became "HIV positive" as a result of their needle stick. This is not the reason for including this study here, however. This type of study is important because the toxicity observed cannot be blamed on HIV, as is quite likely to happen in people diagnosed "HIV positive", so the toxicities are openly admitted to be caused by AZT and documented as such. Fully half of the 14 workers had to quit the drug because of severe toxic side effects, and the study was stopped early before more damage was done. Only 11 of the 14 people could continue to take the drug for more than four weeks. Neutropenia developed in 36% (4 of 11) of the people who completed 4 weeks of AZT treatment. The three people who could not make it to four weeks dropped out due to "severe subjective symptoms". One worker had to be stopped prematurely because his neutropenia was so severe that he developed an upper respiratory tract infection. What is truly remarkable in this study is that these side effects developed in only 4 weeks, while patients with "HIV positive" status often take AZT and other similar drugs for years. The dosage of AZT included in current protease inhibitor "cocktails" is much lower, which may be one reason why people are "living longer with HIV" today than they were five years ago when high doses of AZT were regularly given to everyone diagnosed "HIV positive" whether or not they showed any sign of illness.
3) An article in the New England Journal of Medicine (4) looked at the muscle wasting caused by AZT and compared it to muscle wasting, called "myopathy", that has been presumed to be caused by HIV. Their comments in the abstract are revealing: "We conclude that long-term therapy with Zidovudine can cause a toxic mitochondrial myopathy, which... is indistinguishable from the myopathy associated with primary HIV infection...". Robbin's text on pathology also contains sections on mitochondrial myopathy, stating that this kind of muscle wasting results in severe weakness. It also states that "this group may also be classified as mitochondrial encephalomyopathies." Encephalomyopathy, in lay language, means widespread damage to the brain and spinal cord.
4) "HIV Dementia": Although most retrospective studies
have not found AZT to be associated with "HIV dementia",
these studies were uncontrolled and thus open to all sorts of
confounding variables and biases. One of the better controlled
studies did find that "HIV dementia"
was twice as likely to happen in people taking AZT. In this study, published in the journal Neurology (5), the authors state:
"among subjects with CD4+ cell counts < 200/mm3, the
developing HIV dementia among those reporting any antiretroviral use (AZT,
ddI, ddC, or d4T) was 97% higher than among those not using this
Because the authors include only people with low CD4 T-cell counts in their comparison, it is less likely that people took AZT because they were already sick. They go on to discuss sensory neuropathy, which is a degeneration of sensory nerves:
"In addition, the findings of our analysis seem to confirm
observation of a neurotoxic effect of antiretroviral agents. Numerous studies
have linked the use of ddI, ddC, and d4T to the development of toxic sensory neuropathies, usually in a dose-response fashion."
These studies are but a sample of the evidence that suggest that AZT and other "antiretrovirals" used as monotherapy or as parts of protease inhibitor cocktail regimens are causing a variety of AIDS-like symptoms which are being blamed on HIV. Unfortunately, the beliefs about HIV are so strong that many of the author's of the studies come out supporting the use of the drugs. A notable exception is the article in Pharmacology and Therapeutics, which provides a thorough and devastating critique (2).
A LIKELY EXPLANATION FOR THE "COURSE" OF AIDS
Based partly on this evidence, a compelling argument can be made that much of what we call AIDS is a self-fulfilling prophecy which might happen as follows:
a) The severe, acute psychological stress of being diagnosed
"HIV Positive" is quickly transformed into a severe,
chronic psychological stress of living with a prediction of a
horrifying decline that could start at any time. This causes a
suppression of the immune system, with selective depletion of
CD4 T-cells as documented in the main section of this book. In
addition, people are more likely to be tested for HIV when there
is already some health problem present, so that the psychological
stress adds to significant stress due to the illness already present.
These illnesses are often severe and chronic in nature. It is
not necessary, however, for prior illness to be present. These
factors have been studied in healthy people where they create
the very same immunosuppression and immune dysregulation that
may later be called "AIDS".
b) After testing positive, people are often put on a variety of powerful medications as a preventative measure and/or for treatment of actual infections. These include long-term regimens of the most potent broad-spectrum antibiotics, as well as "antiretroviral" agents like AZT, ddI, ddC, and protease inhibitors. Although the toxicities of the "antiretrovirals" have been outlined above, antibiotics also often have debilitating side effects which are easily blamed on HIV, including immune suppression. Perhaps more significantly, they lead to a complete disruption of the normal microbial flora present in the gastrointestinal system. The healthy balance of flora in the gastrointestinal tract and elsewhere in the body is one of the most important protectors against infection (8). If this is not enough, these antibiotics also often lead to the development of multidrug-resistant strains of bacteria, fungi, and viruses, which can later ravage a person's system, especially if their immune system is not fundtioning very well.
c) Once the immune system starts to crack under the strain of the emotional stress, previous health problems (if there were any), and disrupted natural defenses, the diagnosis of AIDS is made. If not already on "antiretrovirals", then the person will now definitely be started on them, with all of the toxic effects described above.
d) The new "cocktails" are to be given until the patient dies, with no exceptions, if possible. This is because of the theory that mutant, drug resistant, HIV will flourish if they go off of their treatment. Patients who abandon "antiretroviral" treatment would then, theoretically, be a public health threat because they might infect others with their superpowerful, mutated "HIV". Thus, aside from considering their own health, the patient has a larger social responsibility to stay on the "cocktail", no matter how debilitating the "side effects" are. It is heavily stressed that the patient must not miss a single dose, if at all possible. When the patient's health begins to fail, the failure is blamed on the effects of this "mutated HIV", possibly due to the patients poor compliance. Rarely are the drug toxicities and complications caused by the treatment held responsible.
Some people seem to respond well (at least temporarily) to these "antiretroviral" regimens. The reasons for this are unclear, but may be related to:
1) Direct actions of the drugs on many possible pathogens including, possibly, HIV.
2) Toxic substances have been observed to stimulate the release
of T cells from the bone marrow, before eventually exhausting
the supply and causing immune cell depletion and anemia. The initial
rise in CD4 counts seen in this case would be interpreted as improved
immune function when it is actually the beginning of immune exhaustion.
3) Relief of the severe psychological stress due to the powerful belief that these drugs are "life-saving". This is often reinforced by rising CD4 counts and falling "viral load", which are doubtful and non-specific markers of actual health.
Scientific studies attempting to document positive effects of protease inhibitor (PI) "cocktails" are of questionable value. Every one has been stopped early, like stopping a sporting event when the home team is ahead. This skews any attempt at finding benefit. Even worse, all of the studies of protease inhibitor combination therapy have been stopped before statistically significant reductions in mortality is even reached (1). In addition, the control groups' "placebos" were 2 antiretroviral drugs with no protease inhibitor. If the "antiretrovirals" are part of the problem then these so-called "placebo controlled" trials will not reveal it very well. Stopping the trials early was also the case with AZT monotherapy, until the Concorde study finally went to completion and found greater deaths and "adverse events" in the group that got AZT as a preventative measure. The other group, in which people were only given AZT after being diagnosed with an AIDS-defining condition, had about 25% fewer deaths. Of the 172 Concorde participants who died all but 3 were on AZT at some point. (For more discussion of the Concorde see appendix (1)(9)(10)
The idea that mutated strains of HIV are capable of causing health problems has been completely disproven by the work of David Rasnick, who published his results in the Journal of Biological Chemistry. (11). Thus, the decline seen in most patients is NOT due to "mutated HIV". A much more simple answer is that the combined effects described above finally take over completely, and often irrevocably.
Concorde: MCR/ANRS randomized double-blind controlled trial of immediate and deferred zidovudine [AZT] in symptom-free HIV infection. Although the difference in survival between the participants who started AZT immediately (Imm) and those who were deferred (Def) until the onset of AIDS-Related Complex (ARC) or AIDS was not considered significant by the Concorde report (estimated 3-year probabilities of death were 8% Imm and 6% Def), other "events" were. "Adverse events", such as leukemia, anemia, neutropenia, etc., were at least 300% higher in the Imm group over the three year trial. A fact what is often missed when reading the Concorde report is that of the 172 (96 Imm, 76 Def) participants who died all but 3 were on AZT at some point. This is because 418 participants in the Def group switched to AZT part way through the trial; 74 for "personal reasons", 204 due to low CD4 count and only 109 (26%) due to progression to ARC or AIDS, which was the point of the trial. Ironically, one of Concorde's finding was that CD4 counts are not a useful marker for disease progression. In other words, people who weren't really sick were put on AZT, their T-cells rose, and in spite of this more of them had "adverse events" and more of them died. Was the cause of death HIV or AZT? (9)
Glossary of generic & brand names, (class of drug) for "antiretrovirals" AZT:
ZDV, Retrovir®, Zidovudine (NA) 3TC: Epivir®, lamivudine (NA) ddI: Videx®, didanosine (NA) d4T: Zerit®, stavudine (NA) nelfinavir mesylate: Viracept® (PI) indinavir sulfate: Crixivan® (PI) nevirapine: Viramune® (NNRTI) ritonavir: Norvir® (PI) saquinavir mesylate: Invirase®, Fortavase® (PI) delavirdine mesylate: Rescriptor® (NNRTI) abacavir: Ziagen® (NA) efavirenz: Sustiva® (NNRTI) -others- Combivir®: combines AZT & 3TC (NAs)
1) Lancet; 1998: Volume 352; Supplement 5.
2) These studies of T-cell damage are part of a comprehensive discussion of the extreme toxicity of these drugs. Pharmacology and Therapeutics 1992; Volume 55: 201-277.
3) Annals of Hematology 1994; Volume 69: 135-138.
4) New England Journal of Medicine. 1990; 322(16) : 1098-1105.
5) Neurology. 1994;Volume 44: 1892 -1900.
6) Science. November 21, 1997; 278: 1399-1400.
7) Ader R, Felten DL & Cohen N. Psychoneuroimmunology. Second Edition. San Diego: Academic Press, 1991
8) Kolliadin V., DESTRUCTION OF NORMAL RESIDENT MICROFLORA AS THE MAIN CAUSE OF AIDS, Aug. 1996
9) New England Journal of Medicine 1992; 326: 437-443
10) Lancet 1994; 343: 871-881.
11) Journal of Biological Chemistry 1997; Volume 272 No. 10: 6348-6353.
United States Pharmacopeial Convention (1996). USP DI: Drug Information for the Health Care Professional, 16th Edition. pages 3032-3034.
0% (0 of 4) Ho, NEJM 324(14), 1991, p961
0% (0 of 3) Shaw, NEJM 324(14), 1991, p954
0% (0 of 2) Cooper, Lancet 340, 1992
17% (1 of 6) Shaw, Lancet 341, 1993, p1099
9% (2 of 22) Piatak, Science 259, 1993 )
1) ?title? New England Journal of Medicine, vol?? September 11, 1997.
Alberts SC, Sapolsky RM, Altmann J (1992). Behavioral, endocrine and immunological correlates of immigration by an aggressive male into a natural primate group. Hormones and Behavior 26; 167-178.
Axelson DA, Doraiswamy PM, McDonald WM, Boyko OB, Tupler LA, Patterson
LJ, Nemeroff CB, Ellinwood EH Jr, Krishnan KR (1993 ). Hypercortisolemia and hippocampal changes in depression. Psychiatry Res May;47(2):163-73.
Azar ST, Melby JC (1993). Hypothalamic-pituitary-adrenal function in non-AIDS patients with advanced HIV infection. Am J Med Sci May;305(5):321-5.
Auger I, Thomas P, De Gruttola V, Morse D, Moore D, Williams R, Truman B, Lawrence CE (1988 Dec 8). Incubation periods for paediatric AIDS patients. Nature ;336(6199):575-7
Bacellar A, Munoz A, Miller EN, Cohen EA, Besley D (1994). Temporal trends in the incidence of HIV-1 related neurological diseases: Multicenter AIDS cohort study. Neurology ; 44:1892-1900.
Bacchetti P, Moss AR (1989, Mar 16). Incubation period of AIDS in San Francisco. Nature; 338 (6212): 251-3
Bacchetti P, Jewell NP (1991 Sep). Nonparametric estimation of the incubation period of AIDS based on a prevalent cohort with unknown infection times. Biometrics ;47(3):947-60
Bailey NT (1997). A revised assessment of the HIV/AIDS incubation period, assuming a very short early period of high infectivity and using only San Francisco public health data on prevalence and incidence. Stat Med Nov 15;16(21):2447-58
Balter M (1991). Montagnier pursues the mycoplasm-AIDS link. Science 251; 271.
Balter M (1997, November 21). How does HIV overcome the body's T-cell bodyguards? Science 278: 1399-1400.
Benson H (1997). The nocebo effect: History and physiology. Preventive Medicine 26; 612-615.
Berkman L & Syme S (1979). Social networks, host resistance, and mortality: a nine year follow up study of alameda county residents. Am J Epidemiol; 109(2): 186-203.
Binik YM (1985). Psychosocial predictors of sudden death: a review and critique. Soc Sci Med; 20(7):667-80.
Bird AG (1996). Non-HIV AIDS: nature and strategies for its management. Journal of Antimicrobial Chemotherapy 37 Suppl B, 171-183.
Blatt SP, Lucey CR, Butzin CA et al. (1991). Total lymphocyte count as a predictor of absolute CD4+ percentage in HIV infected persons. JAMA 269; 622-626.
Bonneau RH, Sheridan JF, Feng N, Glaser R (1993). Stress-induced modulation of the primary cellular immune response is mediated by both adrenal-dependent and adrenal independent mechanisms. Journal of Neuroimmunology; 42; 167-176.
Bremner J et al. (1995). American Journal of Psychiatry 152; 973.
Britton S, Thoren M, Sjoberg HE (December 20, 1975). The immunological hazard of Cushing's syndrome. British Medical Journal 4; 678-680.
Brooke SM, de Haas-Johnson AM, Kaplan JR, Manuck SB, Sapolsky RM (1994 Aug). Dexamethasone resistance among nonhuman primates associated with a selective decrease of glucocorticoid receptors in the hippocampus and a history of social instability. Neuroendocrinology ;60(2):134-40.
Bruneau J, Lamothe F, Franco E, et al. (1997). High rates of HIV infection among injection drug users participating in needle exchange programs in Montreal: Results of a cohort study. American Journal of Epidemiology; 146; 994-1002.
Cameron DW et al. (1998). Randomised placebo controlled trial of ritonavir in advanced HIV-1 disease. Lancet; 351; 543-549.
Campinha-Bacote J (1992). Voodoo illness. Perspectives in Psychiatric Care 28(1); 11-17.
Cannon WB (1957). "Voodoo" death. Psychosomatic Medicine; 19:182-190. (reprinted from American Anthropologist; 44: 1942).
Carlson M & Earls F (1997). Psychological and neuroendocrinological sequelae of early social deprivation in institutionalized children in Romania. NY Acad of Sciences; 807; 419-428.
Carney WP, Rubin RH, Hoffman RA, et al. (1981). Analysis of T lymphocyte subsets in CMV mononucleosis. The Journal of Immunology 126(6); 2114-2116.
Cardo DM et al. (1997). A case-control study of HIV seroconversion in health care workers after percutaneous exposure. New Engl J Med 337(21); 1485-1490.
Cassileth BR, Walsh WP, Lusk EJ (1988). Psychosocial correlates of cancer survival: a subsequent report 3 to 8 years after cancer diagnosis. J Clin Oncol; 6(11): 1753-1759.
Castle S, Wilkins S, Heck E, Tanzy K, Fahey J (1995, September). Depression in caregivers of demented patients is associated with altered immunity: impaired proliferative capacity, increased CD8+, and a decline in lymphocytes with surface signal transduction molecules (CD38+) and a
cytotoxicity marker (CD56+ CD8+). Clin Exp Immunol;101(3):487-93
Cecchi RL (1984). Stress: Prodrome to immune deficiency. Annals of the New York Academy of Sciences 437; 286-289.
Challakeree K, Rapaport MH (1993, August). False positive HIV-1 ELISA results in low risk subjects. Western Journal of Medicine; 159(2); 214-215.
Chaney RH et al. (1985). Inability to cope with environmental stress: peptic ulcers in mentally retarded persons. J Psychosomatic Research;29(5);519-524.
Chiodi F, Albert J, Olausson E, et al.(1988) Isolation Frequency of Human Immunodeficiency Virus from Cerebrospinal Fluid and Blood of Patients with Varying Severity of HIV Infection. AIDS Res Hum Retrovirol ;4:351-358.
Christeff N, Michon C, Goertz G et al. (1988). Abnormal free fatty acids and cortisol concentrations in the serum of AIDS patients. Eur J Can Clin Oncol; 24(7): 1179-1183.
Christeff N, Gharakhanian S, Thobie N et al. (1992). Evidence for changes in adrenal and testicular steroids during HIV infection. J Acquired Imm Def Syn; 5: 841-846.
Coe CL (1993). Psychosocial factors and immunity in nonhuman primates: A review. Psychosomatic Medicine 55; 298-308.
Cohen SI (1988). Voodoo death, the stress response, and AIDS. Adv Biochem Psychopharmacol; 44:95-109.
Colon EA, Callies AL, Popkin MK, McGlave PB (1991). Depressed mood and other variables related to bone marrow transplantation survival in acute leukemia. Psychosomatics,; 32(4): 420-425.
Concord Coordinating Committee (1994). Concorde: Randomised double-blind controlled trial of immediate and deferred Zidovudine in symptom-free HIV infection. Lancet ;343:871-881.
Coodley GO, Loveless MO, Nelson HD et al. (1994). Endocrine function in the HIV wasting syndrome. J Acquired Imm Def Syn; 7: 46-51.
Cordes RJ & Ryan ME (1995). Pitfalls in HIV testing. Postgraduate Medicine 98(5); 177-189.
Coutinho RA (1998). The Amsterdam Cohort Studies on HIV infection and AIDS. J Acquir Immune Defic Syndr Hum Retrovirol ;17 Suppl 1:S4-8.
Crary B, Borysenko M, Sutherland DC et al. (1983a). Decrease of mitogen responsiveness in mononuclear cells after epinephrine administration in humans. J Immunol 130; 694-497.
Crary B, Hauser SL, Borysenko M et al. (1983b). Epinephrine-induced changes in the distribution of lymphocyte subsets in peripheral blood of humans. J Immunol 131; 1178-1181.
Dalakas MC, Illa I, Pezeshkpour GH, Laukaitis JP, Cohen B, Griffin JL. (1990, April 19) Mitochondrial Myopathy caused by long-term Zidovudine therapy. New England Journal of Medicine ; 322(16):1098-1105.
de Harven E (1998). Retroviruses: the recollections of an electron microscopist. Reappraising AIDS 6(11); 4-7.
DeLeon MJ, McRae T, Tsai JR et al. (1988). Abnormal cortisol response in Alzheimer's disease linked to hippocampal atrophy. Lancet 2; 391-392.
Duesberg PH (1992). AIDS acquired by drug consumption and other non-contagious risk factors. Pharmacology and Therapeutics ;55:201-277.
Duesberg PH (1993, Aug 11). The HIV gap in national AIDS statistics. Bio/Technology 11; 955.
Duesberg P (1996). Inventing the AIDS Virus. Regnery: Washington, DC.
Eastwell HD (1987). Voodoo death in Australian aborigines. Psychiatr Med; 5(1):71-3.
Eli K, Nishimoto R, Mediansky L, Mantell J, Hamovitch M (1992). Social relations, social support and survival among patients with cancer. J Psychosom Research; 36: 531-541.
Engle GL (1971). Sudden and rapid death during psychological stress: Folklore or folk wisdom? Ann Intern Med 74; 771-782.
Engle GL (1968). A life setting conducive to illness: the giving-up-given-up complex. Bull Menninger Clin 32; 355-365.
Esterling B & Rabin BS (1987). Stress-induced alteration of T-lymphocyte subsets and humoral immunity in mice. Behav Neurosci; 101; 115-119.
Fawzy FI, Fawzy NW, Hyun CS, Elashoff R, Guthrie D, Fahey JL, et al (1993). Malignant melanoma: effects of an early structured psychiatric intervention on recurrence and survival six years later. Arch Gen Psychiatry; 50: 681-9.
Feeney C, Bryzman S, Kong L, Brazil H, Deutsch R, Fritz LC (1995, Oct). T-lymphocyte subsets in acute illness. Crit Care Med; 23(10):1680-5.
Gallert G, Maxwell R, Siegel B (1993). Survival of breast cancer patients receiving adjunctive psychosocial support therapy: a 10 year follow up study. J Clin Oncol; 11(1): 66-69.
Gallo RC, Salahuddin SZ, Popovic M, et al (1984). Frequent Detection and Isolation of Cytopathic Retro-viruses (HTLV-III) from Patients with AIDS and at Risk for AIDS. Science ; 224:500-502.
Gerberding JL (1994). Incidence and prevalence of HIV, hepatitis B virus, and cytomegalovirus among health care personnell at risk for blood exposure: Final report from a longitudinal study. J Infect Dis 170; 1410-1417.
Giberson PK, Weinberg J (1995 Oct). Effects of prenatal ethanol exposure and stress in adulthood on lymphocyte populations in rats. Alcohol Clin Exp Res;19(5):1286-94 (Published erratum appears in Alcohol Clin Exp Res 1996 May;20(3):600)
Gold P (1984). Memory modulation, neurobiological contexts. In Lynch, McGaugh, & Weinberger (Eds.), Neurobiology of learning and memory (pp.374-382). New York: Guilford.
Golden KM (1977, Dec). Voodoo in Africa and the United States. Am J Psychiatry; 134(12):
Goodwin JS, Samet JM, Hunt WC. Determinants of survival in older cancer patients. J Natl Cancer Inst, 1996; 88(15): 1031-1038
Gorochov G, Neumann AU, Kereveur A, Parizot C, Li T, Katlama C, Karmochkine M, Raguin G, Autran B and Debré P (1998). Perturbation of CD4+ and CD8+ T-cell repertoires during progression to AIDS and regulation of the CD4+ repertoire during antiviral therapy. Nature
Medicine 4: 215-221.
Greenberg and Fisher, From Placebo to Panacea, New York, John Wiley and Sons,
Grossman Z and Herberman RB (1997). T-cell homeostasis in HIV infection is neither failing nor blind: modified cell counts reflect an adaptive response of the host. Nature Medicine 3: 486-490.
Gurvits T et al. (1996). Biological Psychiatry
Guyton AC & Hall JE (1996). Textbook
of Medical Physiology. Saunders; New York
Hamilton JD et al (1992). A controlled trial of early versus late treatment with Zidovudine in symptomatic HIV infection. New England Journal of Medicine ;326:437-443.
Henderson DK et al. (1990). Risk for occupational transmission of HIV type 1 associated with clinical exposures: a prosepctive evaluation. Ann Intern Med 113; 740-746.
Hendriks JC, Medley GF, van Griensven GJ, Coutinho RA, Heisterkamp SH, van Druten HA (1993 Feb). The treatment-free incubation period of AIDS in a cohort of homosexual men. AIDS ; 7(2):231-9.
Herbert TB & Cohen S (1993). Stress and immunity in humans: A meta-analytic review. Psychosomatic Medicine; 55;364-379.
Ho DD et al. (1995). Rapid turnover of plasma virions and CD4 lymphocytes in HIV-1 infection. Nature 373; 123-126.
Hockenberry J (1993, March 28). State of the Emergency, on ABC-TV's Day One.
Holmes TH (1956). Multidiscipline studies of tuberculosis.In P Sparer, Ed: Personality, Stress, and Tuberculosis. New York: International Universities Press.
House et al. (1988). Social relationships and health. Science ;241:540-545.
Ikemi Y & Nakagawa S (1962). A psychomatic study of contagious dermatitis. Kyoshu Journal of Medical Science; 13; 335-350.
Jensen TS, Genefke IK, Hyldebrandt N et al. (1982). Cerebral atrophy in young torture victims. New England Journal of Medicine; 307:1341.
Junker AK, Ochs HD, Clark EA et al. (1986, Sep). Transient immune deficiency in patients with acute Epstein-Barr virus (EBV) infection. Clin Immunol Immunopathol 40(3); 436-446.
Kaada B (1989, Mar 10). Nocebo--the opposite of placebo. Tidsskr Nor Laegeforen ;109 (7-8): 814-21.
Katz et al (1997). Projected incidences of AIDS in San Francisco: The peak and decline of the epidemic. Journal of Acquired Immune Deficiency and Human Retrovirology 16:182-189.
Keller SE, Weiss JM, Schleifer SJ et al. (1983). Stress-induced suppression of immunity in adrenalectomized rats. Science; 221; 1301-1304.
Kennedy S, Kiecolt-Glaser JK, Glaser R (1988 Mar). Immunological consequences of acute and chronic stressors: mediating role of interpersonal relationships. Br J Med Psychol; 61(Pt 1):77-85.
Kiecolt-Glaser JK, Ricker D, George J (1984). Urinary cortisol levels, cellular immuno-competency, and loneliness in psychiatric inpatients. Psychosomatic Medicine; 46(1): 15-23.
Kiecolt-Glaser JK, Dura JR, Speicher CE et al. (1991). Spousal caregivers of dementia victims: Longitudinal changes in immunity and health. Psychosomatic Medicine; 53;345-362.
Kiecolt-Glaser JK, Glaser R (1992). Acute, psychological stressors and short-term immunological changes. Psychosomatic Medicine; 54;680-685.
Kreiss JK, Kitchen LW, Prince HE et al. (1985). Antibody to human T-lymphotrophic virus type III in wives of hemopheliacs. Ann Internal Med 102;623-626.
Laudenslager M, Ryan SM, Drugan RC, et al. (1983). Coping and immunosuppression: Inescapable but not escapable shock suppresses lymphocyte proliferation. Science, 221;568-570.
Learmont J, Tindall B, Evans L, et al (1992). Long-term symptomless HIV-1 infection in recipients of blood products from a single donor. Lancet ;340:863-867.
Lemp GF, Porco TC, Hirozawa AM, Lingo M, Woelffer G, Hsu LC, Katz MH (1997 Nov 1).
Projected incidence of AIDS in San Francisco: the peak and decline of the epidemic. J Acquir Immune Defic Syndr Hum Retrovirol ;16(3):182-9.
Leserman J, Jackson ED, Petitto JM, et al. (1999) Progression to AIDS: the effects of stress, depressive symptoms, and social support. Psychosomatic Medicine; 61; 397-406.
Levenstein S et al. (1995, October). Sociodemographic characteristics, life stressors, and peptic ulcer. A prospectice study. J Clin Gastroenterol;21(3):185-192.
Levenstein S & Kaplan GA (1998, January). Socioeconomic status and ulcer. A prospective study of contributory risk factors. J Clin Gastroenterol;26(1):14-17.
Lewi DS, Kater CE, Moreira AC (1995 Mar-Apr). Stimulus of the hypophyseal-adrenocortical axis with corticotropin releasing hormone (CRH) in acquired immunodeficiency syndrome. Evidence for activation of the immune-neuroendocrine system (article in Portuguese). Rev Assoc Med Bras;41(2):109-18.
Lex B (1974). Voodoo death: New thoughts on an old explanation. American Anthropologist. 818-823.
Lopez JF, Chalmers DT, Little KY, Watson SJ (1998 Apr 15). Regulation of serotonin1A, glucocorticoid, and mineralocorticoid receptor in rat and human hippocampus: implications for the neurobiology of depression. Biol Psychiatry ;43(8):547-73.
Lortholary O, Christeff N, Casassus P, Thobie N, Veyssier P, Trogoff B, Torri O, Brauner M, Nunez EA, Guillevin L (1996 Feb). Hypothalamo-pituitary-adrenal function in human immunodeficiency virus-infected men. J Clin Endocrinol Metab ;81(2):791-6
Luecken LJ et al. (1997). Stress in employed women: Impact of marital status and children at home on neurohormone output and home strain. Psychosomatic Medicine; 59;352-359.
Lui KJ, Darrow WW, Rutherford GW 3d (1988 Jun 3). A model-based estimate of the mean incubation period for AIDS in homosexual men.Science ;240(4857):1333-5
MacKenzie WR, Favis JP, Peterson DE et al. (1992). Multiple false positive serologic tests for HIV, HTLV-1, and Hepatitis C following influenza vaccination. JAMA; 268(8); 1015-1017.
Magarinos AM, Verdugo JM, McEwen BS (1997). Chronic stress alters synaptic terminal structure in the hippocampus. Proceedings of the National Academy of Sciences USA; 9;94(25): 14002-14008.
Maunsell E, Brisson J, Deschenes L (1995). Social support and survival among women with breast cancer. Cancer; 76(4): 631-7.
Meador CK (1992 Mar). Hex death: voodoo magic or persuasion? South Med J;85(3):244-7
Membreno L, Irony I, Dere W, Klein R, Biglieri EG, Cobb E (1987 Sep). Adrenocortical function in acquired immunodeficiency syndrome. J Clin Endocrinol Metab;65(3):482-7.
Milton GW (June 23, 1973). Self-willed death or the bone pointing syndrome. Lancet 1; 1435-1436.
Momose JJ, Kjellberg RN, Kliman B (1971). High incidence of cortical atrophy of the cerebral and cerebellar hemispheres in Cushing's disease. Radiology 99; 341-348.
Natelson BH (1980). Effect of multiple stress procedures on monkey gastroduodenal mucosa. Brain Res Bull; 5 Suppl 1;59-61.
Newsome B (1999, March 7). Personal communication.
Norbiato G, Bevilacqua M, Vago T, Clerici M (1996, July). Glucocorticoids and interferon-alpha in the acquired immunodeficiency syndrome. J Clin Endocrinol Metab;81(7):2601-6
Norbiato G, Bevilacqua M, Vago T, Taddei A, Clerici (1997, Oct). Glucocorticoids and the immune function in the human immunodeficiency virus infection: a study in hypercortisolemic and cortisol-resistant patients. J Clin Endocrinol Metab; 82(10): 3260-3.
Ohl F, Fuchs E (1999 Jan). Differential effects of chronic stress on memory processes in the tree shrew. Brain Res Cogn Brain Res;7(3):379-87.
Okie S (September 2, 1997). AIDS: Health officials launch a new campaign to determine how widespread the virus is. The Washington Post, Health Section page 12.
Omkar S (1998, November). Victory Over Fear. Peace; 70(11); 1-4.
Ornish D (1997). Love and Survival: the Scxientific Basis for the Healing Power of Intimacy; Harper Collins; New York.
Padian NS, Shiboski SC, Glass SO et al. (1997). Heterosexual transmission of HIV in Northern California: Results from a ten-year study. American Journal of Epidemiology 146(4); 350-357.
Pakker NG, Notermans DW, de Boer RJ, Roos MTL, de Wolf F, Hill A, Leonard JM, Danner SA, Miedema F and Schellekens PTA (1998) Biphasic kinetics of peripheral blood T cells after
triple combination therapy in HIV-1 infection: a composite of redistribution and proliferation. Nature Medicine 4: 208-214.
Papadopulos-Eliopulos E, Turner VF, Papadimitriou JM (1993). Has Robert Gallo proven the role of HIV in AIDS? Emergency Medicine; 5: 135-147.
Papadopulos-Eliopulos E, Turner VF, Papadimitriou JM (1995). A critical analysis of the HIV-T4-cell-AIDS hypothesis. Genetica 95; 4-24.
Pariante CM, Carpiniello B, Orru MG, Sitzia R, Piras A, Farci AM, Del Giacco GS, Piludu G, Miller AH (1997). Chronic caregiving stress alters peripheral blood immune parameters: the role of age and severity of stress. Psychother Psychosom;66(4):199-207.
Philpott P (1999). Personal communication. The statement and list of signatories can be viewed at www.virusmyth.com/aids/group.htm for the original 500 signatories. Later signatories are listed in installments at www.virusmyth.com/aids/statement/index.htm, www.virusmyth.com/aids/statement/list3.htm, www.virusmyth.com/aids/statement/list2.htm,
Physician's Desk Reference (1992).
Physician's Desk Reference (1999).
Piatak M, Saag MS, Yang LC, et al. (1993). High levels of HIV-1 in plasma during all stages of infection determined by quantitative competitive PCR. Science 259; 1749-1754.
Popovic M, Sarngadharan MG, Read E, et al. Detection, Isolation,and Continuous Production of Cytopathic Retroviruses (HTLV-III) from Patients with AIDS and Pre-AIDS. Science 1984; 224: 497-500.
Proffitt MR & Yen Lieberman B (1993, June). Laboratory diagnosis of HIV infection. Infectious Disease Clinics of North America 7(2).; 203-215.
Rasmussen OV, Lunde I (1980). Evaluation of investigations of 200 torture victims. Dan Med Bull 27; 241-243.
Rasnick D (1997, March 7). Kinetics analysis of consecutive HIV proteolytic cleavages of Gag-Pol polyprotein. Journal of Biological Chemistry:Volume 272 No. 10, pages 6348-6353.
RaybinJB (1970, November). The curse: A study in family communication. American Journal of Psychiatry; 127(5); 617-618.
Reynolds P, Kaplan G (1990). Social connections and risk for cancer: prospective evidence from the Alameda County study. Beh Med; 16: 101-110.
Reynolds P, Boyd P, Blacklow R (1994). The relationship between social ties and survival among black and white breast cancer patients. Cancer Epidemiological Biomarkers Prevention; 3(3): 253-259.
Rich JD, Merriman NA, Mylonakis E et al (1999). Misdiagnosis of HIV infection by HIV-1 plasma viral load testing: A case series. Ann Internal Med 130(1); 37-39.
Richter C (1957). On the phenomenon of sudden death in animals and man. Psychosomatic Medicine; 23(3); 191-198.
Roederer, M. (1998) Getting to the HAART of T cell dynamics. Nature Medicine 4: 145-146.
Rosenberg DR, Pajer K, Rancurello M et al. (1992). Neuropsychiatric assessment of orphans in one Romanian orphanage for "unsalvageables". JAMA 268(24); 3489-3490.
Russek LG & Schwartz GE (1997). Perceptions of parenteral caring predict health status in mid-life: A 35-year follow-up of the Harvard mastery of stress study. Psychosomatic Medicine; 59:144-149.
Sapolsky RM, Uno H, Rebert CS, Finch CE (1990 Sep). Hippocampal damage associated with prolonged glucocorticoid exposure in primates. J Neurosci ; 10(9):2897-902.
Sapolsky RM (1996, August 9). Why stress is bad for your brain. Science 273; 749-750.
Sapolsky RM, Alberts SC, Altmann J (1997, Dec). Hypercortisolism associated with social subordinance or social isolation among wild baboons. Arch Gen Psychiatry 54; 1137-1143.
Sarngadharan MG, Popovic M, Bruch L, et al (1984). Antibodies Reactive to Human T-Lympho-trophic Retroviruses (HTLV-III) in the Serum of Patients with AIDS. Science:224:506-508.
Sasuga Y, Asakura M, Miyamoto S, Bodaiji N (1997 Oct). [Influence of chronic variable stress (CVS) on the association of glucocorticoid receptor with heat-shock protein (HSP) 90 in rat hippocampus].[Article in Japanese] Nihon Shinkei Seishin Yakurigaku Zasshi ;17(5):193-200
Sayre KR, Dodd RY, Tegtemeier G et al. (1996). False positive HIV-1 Western Bloy tests in noninfected blood donors. Transfusion 36; 45-52.
Schmitz SH, Scheding S, Voliotis D, Rasokat H, Diehl V, Schrappe M (1994). Side effects of AZT prophylaxis after occupational exposure to HIV-infected blood. Annals of Hematology; 69:135-138.
Schwartz DH et al. (1997). Extensive evaluation of a seronegative participant in an HIV-1 vaccine trial as a result of a false positive PCR. The Lancet 350; 256-259.
Sivak SL & Wormser GP (1985). How common is HTLV-III infection in the United States? New England Journal of Medicine 313; 1352.
Schupbach J, Popovic M, Gilden RV, et al (1984). Serological analysis of a Subgroup of Human T-Lymphotrophic Retroviruses (HTLV-III) Associated with AIDS. Science;224:503-505.
Seligman M, Warrel DA, Aboulker JP et al. (1994). Concorde: MCR/ANRS randomized double-blind controlled trial of immediate and deferred zidovudine [AZT] in symptom-free HIV infection. Lancet 343: 871-878.
Sheline Y et al. (1996). Proc Natl Acad Sci 93; 3908.
Spiegel D, Kraemer H, Bloom J, Gottheil E (1989). Effect of psychosocial treatment on survival of patients with metastatic breast cancer. Lancet; 2: 888-91.
Starkman MN, Gebarski SS, Berent S et al. (1992). Hippocampal formation volume, memory dysfunction, and cortisol levels in patients with Cushing's syndrome. Biological Psychiatry; 32: 756-765.
Stefanski V, Engler H (1998 Jul). Effects of acute and chronic social stress on blood cellular immunity in rats. Physiol Behav;64(5):733-41
Taylor JM, Kuo JM, Detels R (1991). Is the incubation period of AIDS lengthening? J Acquir Immune Defic Syndr;4(1):69-75.
Thygesen P, Hermann K, Willinger R (1970). Concentration camp survivors in Denmark. Dan Med Bull 17; 65-108.
Tornatore KM, Venuto RC, Logue G, Davis PJ (1998). CD4 and CD8 lymphocyte and cortisol response patterns in elderly and young males after methylprednisone exposure. J Med; 29 (3-4); 159-183.
United States Pharmacopeial Convention (1996). USP DI: Drug Information for the Health Care Professional, 16th Edition. pages 3032-3034.
Uno H et al. (1989, May). Hippocampal damage associated with prolonged and fatal stress in primates. J Neurosci;9(5):1705-1711.
Uno H et al. (1994). Neurotoxicity of glucocorticoids on the primate brain. Horm Behav; 28(4):336-348.
Valleroy LA, Mackellar DA, Karon JM, Janssen RS, Hayman CR (1998). HIV infection in disadvantaged out-of-school youth: Prevalence for US Job Corps entrants, 1990 through 1996.
Journal of Acquired Immune Deficiency and Human Retrovirology 19: 67-73.
Verges B, Chavanet P, Desgres J, Vaillant G, Waldner A, Brun JM, Putelat R (1989 Nov). Adrenal function in HIV infected patients. Acta Endocrinol (Copenh);121(5):633-7.
Verney-Elliott M (1999). "Virtual viral load" tests. Continuum 5(5); 56-58.
Walton C (1999). What makes a survivor? Continuum 5(5); 16-18.
Waxler-Morrison N, Hislop TG, Mears B, Kan L (1991). Effects of social relationships on survival for women with breast cancer. Soc Sci Med; 33(2): 177-183.
Wei et al. (1995). Viral dynamics in HIV-1 infection. Nature 373; 117-122.
Weyer J (1987, Nov-Dec). On the mean incubation time of AIDS infections. Infection ;15(6): 413-416.
Williams RC Jr, Koster FT, Kilpatrick KA (1983). Alterations in lymphocyte cell surface markers during various human infections. Am J Med 75; 807-816.
Wolf S (1950). Effects of suggestion and conditioning on the action of chemical agents in human subjects: the pharmacology of placebos. Journal of Clinical Investigation; 29; 100-109.
Zachar V, Mikulecky M, Mayer V, Mackay I, Frazer I (1988 Oct). A biometrical view on normal values of CD4 and CD8 lymphocyte counts in peripheral blood. Pathology; 20(4):358-60