COCAINE & MARIJUANA SUPPRESS IMMUNE CELLS
Narcotics cause immune suppression, concludes a study published in the November, 1997 issue of the American Journal of Respiratory and Critical Care Medicine (156:1606-1613).
Dr. Michael Roth of UCLA and his colleagues evaluated a special type of immune cell - the alveolar macrophage - which is crucial in defending human lungs against just the sort of microbial infections common in AIDS patients. Roth obtained samples of these cells from HIV-negative habitual smokers of crack cocaine, marijuana, and cigarettes, and also from non-smokers. He found that the immune cells from smokers of crack and marijuana were "severely limited in their ability to kill both bacteria and tumor cells" and that the findings "demonstrated that habitual smoking of either impairs the
antibacterial and tumoricidal activities of human alveolar macrophages."
Lung infections are among the most common conditions that are classified as "AIDS" in patients who test HIV-positive. Those conditions include tuberculosis (a transmissible bacterial infection), Pneumocystis carinii pneumonia (an opportunistic fungal infection), and recurrent pneumonia
involving any other sort of microbe. Alveolar macrophages protect against both bacterial and fungal infections, but Roth considered only bacteria
in his study.
According to a December, 1997, Reuters report, Roth explored this topic because "pulmonary [lung] toxicity has been linked to the use of these two drugs" and he wanted to "examine [their] effects on the lung microenvironment." Many sorts of bacteria and fungi reside in healthy humans, and are held to sub-pathologic levels by various immune cells, including macrophages. This balance between microbes and immune cells constitutes the pulmonary microenvironment. The suppression of immune function in the lungs can permit normal microbial residents to replicate out of control and reach population densities that are diagnosable as pneumonia. For patients who happen to test HIV-positive, physicians classify these opportunistic pneumonias as "AIDS," and blame them on HIV.
Roth's data upends this convention, which ignores an immune suppressive capacity for narcotics.
Roth noted that his findings "strongly support epidemiologic reports and case studies linking the use of marijuana and cocaine to opportunistic infection, HIV infection, and the progression of AIDS." How does Roth reckon that HIV fits into this association? Given HIV's innocuous nature and usual scarcity, coupled with the toxicological mechanisms and molecular abundance that typify recreationally consumed narcotics, Roth's data support those who regard drugs as AIDS-causing factors, and HIV as a mere spectator. - Paul Philpott
HEROIN USE BOOSTED BY BELIEF THAT HIV CAUSES AIDS
The availability of heroin that is so pure it can be snorted, coupled with the belief that snorting rather than injecting will protect users from AIDS, has contributed to a resurgence in American heroin usage, Reuters reported December 31, 1997. "The ability to snort heroin like cocaine means that it eliminates needles and the risk of AIDS," said the head of the the Drug Enforcement Agency's New England district, George Festa. "So its use is spreading."
We wonder what the effect on usage would be if Americans knew that the consumption of even HIV-free narcotics - by any means, injection or otherwise - places users at increased risk for AIDS conditions. We also wonder what Fest meant when he said that a "lack of memory on the part of youth" helped enable heroin's increased popularity.
What is it that Fest remembers about the popularity of heroin-injecting in previous generations that he thinks would discourage potential heroin-snorters today? That users wasted away? That they developed dementia? That they developed pneumonias?
How ironic that Fest considers "celebrity heroin chic" to be the other factor fueling consumer interest in smack. After all, few have done more than celebrities to promote the idea that HIV on injection needles - rather than the narcotics that pass through them - is responsible for the
appearance of AIDS conditions in drug users. Sometimes, we note, the same celebrities who participate in the HIV-AIDS publicity crusade are exposed as narcotics users. - Paul Philpott
AZT INCREASES MORTALITY, COCKTAILS UNPROVEN, FIVE UK SCIENTISTS ASSERT
AZT monotherapy for symptom-free HIV-positive people increases mortality, and there's no good reason to think that protease inhibitor cocktail therapy is any better, two groups of British medical scientists stated in separate letters to the editors of prestigious academic journals.
In a letter published in the March 27, 1997 New England Journal of Medicine (336[13]), Andrew N. Phillips, PhD, of London's Royal Free Hospital School of Medicine, and George Davey Smith, MD, of the University of Bristol, responded to an editorial which had stated that, "All persons with HIV infection who have CD4 cell counts below 500 should be encouraged to begin antiretroviral therapy." Phillips and Smith offered this counter view:
No randomized trials in asymptomatic patients have established that those treated early survive any longer than those for whom treatment is deferred. Extended follow-up of patients in one trial, the Concorde study, has shown a significantly increased risk of death among the patients treated early (Darbyshire, "Australian randomized trials of zidovudine in symptomatic HIV infection." Presented at the Fifth European Conference on Clinical Aspects and Treatment of HIV Infection, Copenhagen, Denmark, September
26-29, 1995, abstract). The suggestion is that the situation is different for combination therapy. But where is the evidence...? On average, [recently infected] patients are not at serious risk [of developing AIDS conditions] for more than five years, and there is no evidence that the efficacy of treatment lasts this long.
In 1990, after the results of the AIDS Clinical Trials Group (ACTG) 019 study in patients with CD4 counts of less than 500 cells had been published, a patient with a CD4 count of 450 would have been advised to start monotherapy with zidovudine. We now tell such a patient that, in fact, follow-up data for up to 4.5 years since that time have shown no survival benefit from the early use of zidovudine (Volberding, "The duration of zidovudine benefit in persons with asymptomatic HIV infection," JAMA
272:437-42, 1994) and that if the patient starts using a second nucleoside drug now, the benefit will be smaller than if he or she had waited and started to use zidovudine at the same time as a second nucleoside drug (Corey, NEJM 335:1142, 1996). There is no more hard evidence now of the benefits of early therapy than there was in 1990. We need new randomized trials to determine whether the notion that was probably not true in the era of zidovudine monotherapy -- that early therapy prolongs survival as compared
with deferred therapy -- is now true."
Of course, Phillips and Smith are totally conventional in their other opinions about HIV, AIDS, and anti-HIV therapy. They assume that symptom-free HIV-positive people are bound to develop AIDS conditions, hence their use of the term "early" to describe treatment in the absence of AIDS.
And within this context, when patients who have received treatment only after an AIDS condition has appeared do better than patients who have received treatment in the absence of a history of any AIDS condition, Phillips and Smith assume this is because symptom-free treatment reduces the "benefit" of treatment administered after the presumably
inevitable symptoms arise. They fail to recognize that these drugs may offer no benefits, just toxicity, and that the "reduced benefit" of "early treatment" is better described as increased toxicity from a longer treatment duration. In other words, they don't realize that their criticism suggests the possibility that forsaking antiviral treatment altogether might be the best option of all.
An October, 1997, letter to Nature Medicine (3[10]:1052) makes the same points (with the same omissions) as Phillips and Smith, but the authors -- Abraham Karpas of Cambridge University's Hematology Department, Stephen Ash of London's Ealing Hospital, and Douglas Bainbridge of the Royal London Hospital -- are more aware of the fundamental toxic effects of these drugs. The authors
were responding to what they called a "medico-political commentary" by Richard Wurtman of MIT's Department of Brain and Cognitive Sciences.
"We wish to point out that his optimistic scenario for HIV is not real," they wrote. "Wurtman implies that the drugs are selective for HIV. In fact, they inhibit normal cell division. It is established that AZT causes anemia universally, and in the Concorde trial, on extended follow-up its toxicity caused significantly higher mortality. The protease inhibitors are also cytotoxic [cell-killing]."
They declare the clinical results to date to be "far from anything that could be called a therapeutic success."
In reply Wurtman cited the "extraordinary fall" in American AIDS deaths, which he attributed to government programs that make "cocktail" therapy, which includes AZT and retroviral protease inhibitors, "available to all who need it." Naturally he failed to acknowledge that American AIDS death rates started dropping years before retroviral protease inhibitors became available. - Paul Philpott
FREE NEEDLE PROGRAMS SPREADING HIV?
Junkies who participate in free needle programs, which are designed to "reduce the spread of HIV," actually have a higher HIV incidence than junkies who don't receive free needles, a team of researchers announced in a paper published in the American Journal of Epidemiology
("High rates of HIV infection among injection drug users participating in a needle exchange program in Montreal," 146:994-1002, 1997).
"Although most studies report beneficial effects in terms of behavior modification, a direct assessment of the effectiveness of needle exchange programs in preventing HIV infections has been lacking," the authors stated. In other words, previous studies showed that needle exchange programs really do cause participants to curb behaviors regarded as risks for HIV transmission, such as sharing drug needles. But this study was the first to test the idea that such behavior modification would result in fewer junkies becoming HIV-positive.
The researchers, from a university hospital in Montreal, recruited area dope injectors and randomly enrolled about half in a needle exchange program. Participants in such programs can bring used drug needles to participating centers, and exchange them free of charge for new needles.
Supporters of the infectious AIDS model generally believe that such programs will reduce the amount of unsterile needles circulating among junkies, and that this will lead to fewer new cases of HIV-positivity. Critics oppose tax dollars being used to facilitate self-destructive activities. Some believe that narcotics themselves can cause AIDS conditions even when delivered by clean, HIV-free needles.
The authors monitored their subjects for two years and found that of the initially HIV-negative junkies, those who participated in the needle exchange program were nearly three times more likely to become HIV-positive than those who did not participate.
Neither infectious nor noninfectious AIDS models offer a clear reason why this should be the case. However, the paradox demonstrates yet another instance of HIV proponents stridently promoting a costly public policy without any factual support for it, only to find that careful research -- once conducted -- yields data that contradict their claims.
An earlier study, published in 1997, documented a complete failure for North America's largest needle exchange program - which distributes two million needles per year - in Vancouver, British Colombia (Strathdee, AIDS 11[8], July, 1997). Nearly ten years after the implementation of this program in 1987, 23% of Vancouver's dope shooters test positive, and an equal fraction of positive and negative needle junkies (40%) report having participated in the exchange program. - Paul Philpott
DAVE SONNTAG, TOXICOLOGIST REAPPRAISER IN CINCINNATI
In pursuing my PhD in Toxicology, I have become very interested in Peter Duesberg's book, Inventing the AIDS Virus, and his assertion that AIDS is more a disease of drug abuse than of HIV infection. It raises important questions that deserve serious consideration. Although he has received a "cold fusion" cold shoulder from many institutions, we would enjoy having Duesberg address one of our Environmental Health Department seminars here at the University of Cincinnati. I believe our multi-disciplinary team of molecular toxicologists, biostatisticians, and environmental health experts would receive him fairly.
Duesberg's view in many important ways agrees with my own research and study of the biochemical affects of narcotics and certain pharmaceuticals. The human body responds to the presence of these toxic substances with detoxification processes that cause what is called "oxidative stress." Interestingly, oxidative stress causes immune cells to die and retroviruses - like HIV - to replicate.
Since AIDS conditions are correllated with both HIV and drug consumption, this creates a "chicken or the egg" dilemma of causation versus correlation. Does HIV replication create the oxidative stress that kills off T-cells? If so, then people who have HIV and take drugs (legal or illegal), may
be speeding their demise, since these substances speed the replication of HIV. Or, instead, does oxidative stress from the processing of foreign compounds lead to T-cell death, and - coincidentally - HIV replication? If so, then HIV expression may simply be a biomarker for oxidative stress caused by exposure to toxic substances.
Dave Sonntag can be reached at sonntag@one.net, and is a graduate student in the Toxicology Division of the Department of Environmental Health, University of Cincinnati. He holds a BS in biology and chemistry, and a MS in Public Health from the University of Utah. A longer, referenced version of
Dave's thoughts on toxicology and HIV can be found on the web at: w3.one.net/~sonntag/hiv.html.
DOUG ROISE, PATHOLOGIST REAPPRAISER IN NORTH DAKOTA
I am the Pathologist and Laboratory Director at St. Joseph's Hospital and Health Center in Dickinson, North Dakota. I've been skeptical about HIV/AIDS from the beginning. When the official government announcement came in 1984, I was in residency at the United Hospital in Grand Forks. I had read some early articles published before this announcement, in the 1984 Annals of the New York Academy of Sciences. The authors said that AIDS was neither new nor contagious.
Later I heard of Peter Duesberg and read his papers as they were published. In 1991, the North Dakota Medical Association meeting was held here in Dickinson. Being Dickinson's only pathologist, it was my responsibility to prepare a scientific session for the North Dakota Society of Pathology. I
invited Duesberg, and he accepted.
It was a great time for us, but he must have been greatly disappointed. The audience consisted of only about 25 people in a small room. But it was standing-room-only and a few people were standing. Most were pathologists, but there were some clinical physicians there also.
While in Dickinson, he also lectured at other forums to health care workers, nurses, medical technicians, etc., and I interviewed him on one of the local radio stations and together we visited an AIDS patient and his physician in the hospital.
There was a good response to his lectures, which were video recorded, and the videos went out to several people in several directions. I even had a request to send one to someone who worked at Sandia National Laboratories in Albuquerque. I have a friend who runs an orphanage in New Hope, Uganda, and he was very interested in this. He asked me to come over to Uganda and study AIDS.
But for all the interest and momentary skepticism that some people have after they hear a presentation about it, they seem to drift back into believing again that AIDS is caused by HIV. The propaganda is so pervasive. I get letters or notes from colleagues occasionally and they remark that I must by now at last accept that HIV is the cause of AIDS. But nothing has really changed at all. Just ever more science journal articles that are fatally deficient in many ways.
Overall, though, my dissension has been well received at my hospital. I have been on the infection control committee for years and always speak up about it. They haven't kicked me off the committee, and they even take my advice from time to time about policies regarding AIDS. Most of the medical staff members have some skepticism about HIV causing AIDS, but not enough to speak out about it. Again, I think it's the power of propaganda and politics. How could so many erudite scientists be so wrong? This isn't such a difficult question for me because I've seen it before in science and elsewhere.
Roise graduated from the Univ. of North Dakota School of Medicine, and can be contacted at roise@dickinson.ctctel.com
DENISE KALM, GENETICIST REAPPRAISER IN CALIFORNIA
I have a Bachelors of Arts in Genetics from UC Berkeley, where I participated in research under Sy Fogel on recombination theory. I also have a Masters of Science in biochemical genetics from the University of Michigan, where I researched blood abnormalities in the lab. Today I work as a systems
programmer, but keep current with the medical sciences by reading academic journals.
I had a lot of early skepticism about the prevalent theory of AIDS, primarily because of my training on how viruses work. Initially I was drawn by the idea that HIV could behave differently from other viruses. But as time passed I decided that too many things just didn't fit. I waited in vain for the epidemic, living in some fear, as many others did, but AIDS just sat in certain centers of the population.
The CDC should have recognized this, but until I read Duesberg's book, I didn't realize that they are motivated not to. After studying his book, doing more background reading on some of the points he made, and after careful consideration, I can now state that I no longer believe in the viral AIDS theory.
I'm also very concerned about the official therapies. Reminds me of a time in a research lab where we were testing treatments for multiple sclerosis, only to find that in many cases, the cure made them worse. At least in this lab, we dropped the protocol.
Denise P. Kalm lives in Walnut Creek, California, and can be reached at Dpkalm@aol.com