Appendices & references to this work

"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.

Preface

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 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 Beliefs?
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.
 

"Proof"
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...?
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 HIVpositive.

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 transmitted.
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 blood.
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 day.
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".
 

BOOK 2

The Effects of Severe, Chronic, Psychological Stress:
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, by stress. 
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.
 

Chapter 1: The Effects of Stress and Social Isolation on T-lymphocytes
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. 
(page 1682-3)
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 other animals
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 (Rasmussen 1980).
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 pati