HIV/AIDS Skepticism

Pointing to evidence that HIV is not the necessary and sufficient cause of AIDS

Archive for November, 2010

Selling sickness and huckstering medications

Posted by Henry Bauer on 2010/11/07

Selling Sickness is the title of a book I mentioned in “You are ill — because we say you are” (2010/10/04). My full review of the book has now been published. I was reminded of it by this recent news item:
“Percentage of U.S. adults with hypertension holds steady at 30% — But CDC report shows more people have their high blood pressure under control”.
“Hypertension” means higher than “normal” or “natural”; but how is the normal or natural level determined?
In the United States, the appropriate levels for blood pressure, serum cholesterol, and a number of other physiological variables are defined by advisory panels at the Food and Drug Administration or the Centers for Disease Control and Prevention or other such agency. Those advisory panels typically comprise a majority of researchers who consult for drug companies and who are thereby inclined to the view that treating such conditions is a good thing. As a result, the levels of blood pressure, serum cholesterol, weight (body-mass-index), etc., defined as appropriate or desirable are periodically revised, always in the direction of favoring expanded treatment.
As I pointed out in the post mentioned above, certain physiological changes with age are perfectly natural, including increased blood pressure; yet a large proportion of seniors are taking medications to treat “hypertension”. This recent news item prompts a rhetorical question:
“How likely is it that 30% of the US population could have blood pressure that is higher than appropriate?”

Not content to leave this as a rhetorical question, I decided to look at what the guidelines precisely are. Once again a surprise. I find myself increasingly astonished at the lack of logic, the absence of plain common sense, in official statements about matters of medical science. Concerning blood pressure, the authoritative documents agree that it rises steadily with age, certainly beginning in the teens. At the same time, “hypertension” is defined by a single number irrespective of age!

Various sources agree on how blood pressure typically changes with age between 15 and 64. I found only one source for ages 65-80:

The sources citing these numbers include official agencies like the website “NIH Senior Health”. There is no controversy about the increase in blood pressure with age.

Now, a commonsense definition of “hypertension” — pressure “too high” — would then be some percentage above the known, observed, natural range at any given age; or perhaps for any individual an increase of pressure with age at a significantly higher rate than average, or perhaps a sudden jump.
Instead, the definition of hypertension propagated by official agencies is a single number irrespective of age and equal to the average at age around 65!

“Your blood pressure changes throughout the day. It is usually lowest when you’re asleep, and it rises when you awaken. It also can rise when you are excited, nervous, or active. So it varies throughout the day. A systolic blood pressure of 140 mmHg or higher, or a diastolic blood pressure of 90 mmHg or higher, is considered high blood pressure, or hypertension. Hypertension is the medical term for high blood pressure. . . . High blood pressure currently affects more than 72 million Americans. That’s 1 in every 3 adults” — NIH Senior Health.
So at what time of day should one regard 140 mm systolic as hypertension? When one is active, excited, or nervous, or when  one is relaxed and inactive? When measured in a doctor’s office, where it’s known to be typically higher than when measured at home?

Advice from the U.S. Department of Health and Human Services via the National Heart, Lung, and Blood Institute states:
“A blood pressure level of 140/90 mmHg or higher is considered high. About two-thirds of people over age 65 have high blood pressure. If your blood pressure is between 120/80 mmHg and 139/89 mmHg, then you have prehypertension. This means that you don’t have high blood pressure now but are likely to develop it in the future. You can take steps to prevent high blood pressure by adopting a healthy lifestyle.
Those who do not have high blood pressure at age 55 face a 90 percent chance of developing it during their lifetimes. So high blood pressure is a condition that most people have at some point in their lives” [emphases added].
Well of course they do, since the normal range at age 55 is about 117-143.

The Centers for Disease Control and Prevention (CDC)  also enlightens us about how the proportion of people with “elevated blood pressure” changes with age:

So CDC, just like Big Pharma, is in the business of selling sickness, of persuading us that perfectly normal characteristics of human life are ailments to be treated. And as so often, African Americans seem to be categorized as inherently more diseased than others — or is it possible that there’s a correlation here with the higher proportion of African Americans who excel at various athletic pursuits?

Unfortunately this is not a willful conspiracy, it is the result of good intentions coupled with ignorance and incompetence within an enormously complicated bureaucratic system. Deliberate wrongdoing might be much easier to correct. The problem is this: They all take correlation as proving causation. Because the incidence of strokes goes up with age, and blood pressure goes up with age, why, therefore of course the higher blood pressure is causing the strokes! Makes obvious sense, doesn’t it?

Only if you don’t think about it. First, correlation NEVER proves causation, no matter how plausible the connection might seem. Second, the fact that blood pressure increases starting in the teens is powerful evidence that this is interconnected with other physiological processes, and it may well be that these increases are desirable, that they play an important function, as the rest of the organism also ages.
The variation of blood pressure with stress and with time of day demonstrates its interaction with other aspects of physiology. Since these changes are observed in healthy people, it’s plausible that they are appropriate changes. Blood pressure in older people also responds to external temperature, decreasing when it’s warmer and increasing when it’s colder (Alperovitch et al., Archives of Internal Medicine, 169 [2009] 75-80). By what stretch of some imagination could it make sense to try to force everyone’s blood pressure to below the same fixed value, no matter their age?
But that’s what we do. So it’s hardly surprising that older people in particular are over-medicated, to the extent that “Nearly 40% of the participants used at least one potentially inappropriate medication” — in quite a large a study of older people (>9000 individuals), not in nursing homes, living in France (Lechevallier-Michel et al.,. European Journal of Clinical Pharmacology, 60 [2005] 813-9). I doubt that the proportion would be less in the United States.
These circumstances also explain why “Disease-specific causes of death, especially vascular diseases, could be overestimated in this age group [senior citizens]” (Alperovitch et al., European Journal of Epidemiology, 24 [2009] 669-75). When someone taking medications for hypertension, high cholesterol, and other “ailments”  dies, the death is likely to be attributed to one or more of those “ailments”, not to side effects of the drugs that have been consumed steadily for many years.
This is a little -discussed but crucial aspect of drug “side” effects: the length of time during which a drug is supposed to be taken. Something that shows up in only 1% of cases in a clinical trial lasting 6 months might well show up in a lot of cases when the drug is then being taken lifelong, as is the case with substances “treating” high cholesterol or high blood pressure or seeking to “thin” blood to prevent clots or strokes.
So, for example, not much more than a year after Gardasil vaccine was approved to guard women against cervical cancer, there had been several deaths attributable to it as well as nearly 400 “serious” adverse events (CDC mongers fear and hawks deadly vaccine, 2008/03/13).
Unabashed, an advisory panel to the Food and Drug Administration urged that Gardasil and its competing knock-off Cervarix be administered to boys to prevent genital warts (Gardasil and Cervarix: Vaccination insanity, 2009/09/21). The push for this continues:
“Merck & Co’s Gardasil vaccine is approved for boys, safe and it would be cost-effective, CDC researchers and vaccine experts told a meeting of the Advisory Committee on Immunization Practices Thursday” (HPV shots for boys debated by experts — Gay men would be among groups protected from various cancers by vaccine, CDC says).  “HPV infection is best known as the primary cause of cervical cancer, but it can also lead to cancers of the anus, penis, head and neck. Vaccinating men and boys could prevent some of these cancers.”
Perhaps this continuing push comes because the earlier considerations judged that the possible prevention of genital warts in boys did not justify the high cost ($360) of the vaccination. That high cost did not prevent its inclusion in a federally funded program, though, “the Vaccines for Children Program, a government-funded system that provides vaccines to children eligible for the state-federal Medicaid health insurance plan and other uninsured children”. The new push cites a concern to safeguard gay men in particular:
”cases of anal cancers are increasing in the United States, especially among women, and men who have sex with men. ‘Estimates from various studies indicate that the incidence of anal cancer in men who have sex with men may be as high as 37 cases per 100,000 men’”.
The campaign seems to be working: “36 percent of pediatricians and 24 percent of family medicine physicians are administering the vaccine to males”.
Once again, I’m not pointing fingers at any conspiracy, any willful wrongdoing. These people think they are doing good — just like Tom Lehrer’s “the old drug peddler, doing well by doing good”. The problem is, they think correlations prove causation, even when the correlation is “as high as” 37 cases in 100,000. This incompetence in statistics is matched by ignorance of the problem of drug “side” effects, even though a decade ago already it was reported that there are in the United States “106,000 deaths/year from non-error, adverse effects of medications” (Starfield, JAMA 284 [2000] 483-5).

Anecdotes don’t count as evidence, of course, but they are mighty impressive subjectively. In my bridge group of senior citizens, several have mentioned loss of feeling in their feet. Each one I’ve asked, “Do you take statins?” All have said “Yes”.
An older friend of mine, now dead, was very slight of build, and always found it difficult to persuade his doctors that he should be taking a lower than average dose of most medications. After a bad fall, he suffered a cerebral hemorrhage from which he never recovered. The doctor who supervised his admission to hospital said he should never have been taking the blood-thinning Plavix that his physician had prescribed for him, let alone at the dose he had been using (and he had been using only half of what had been prescribed).

Posted in clinical trials, experts, vaccines | Tagged: , , | 1 Comment »

Intestinal Dysbiosis theory confirmed

Posted by Henry Bauer on 2010/11/05

The thread on Questioning AIDS mentioned in the previous post is not only about oxidative stress and that HAART adds more such damage, it refers also to a number of articles that lend considerable support to Tony Lance’s hypothesis of intestinal dysbiosis:  damage to the intestinal microflora destroys safeguards — in particular against fungal infections — and allows leakage of certain substances from gut to blood which in turn leads to testing “HIV-positive”.
Mainstream work seems increasingly to be edging toward accepting this view. For example:
“the gastrointestinal tract plays a critical role in the pathogenesis of acute HIV-1 . . . infections”
— Mehandru et al., Journal of Allergy and Clinical Immunology, 116 (2005) 419-22.
“The gastrointestinal pathology associated with HIV infection comprises significant enteropathy with increased levels of inflammation and decreased levels of mucosal repair and regeneration”
— Brenchley & Douek, Mucosal Immunology, 1 (2008) 23-30
“Why and how HIV makes people sick is highly debated. Recent evidence implicates heightened immune activation due to breakdown of the gastrointestinal barrier as a determining factor of lentiviral pathogenesis. . . . Translocation of microbial products from the gut, in turn, correlates with increased immune activation in chronic HIV infection and may further damage the immune system . . . . Maintaining a healthy GALT [gut-associated lymphoid tissue] may be the key to reducing the pathogenic potential of HIV”
— Hofer & Speck, Seminars in Immunopathology, 31 (2009) 257-66.
“Reducing the pathogenic potential of HIV” by maintaining a healthy GALT is quite like Montagnier’s assertion, captured in the House of Numbers film,     that a healthy immune system can stave off damage from “HIV” (some discussion here). In practical terms — no theorizing about causes — these mainstream statements mean and recommend  precisely the same as Lance does:
You have more chance of staying healthy, whether you are “HIV-positive” or “HIV”-negative, if you don’t do anything to harm your beneficial gut microflora. Be sensible in terms of lifestyle. Pay special attention to diet, and by all means use probiotics.

*                    *                    *                    *                    *                    *                    *                    *

The mainstream has been unable to identify specific mechanisms by which “HIV” is supposed to kill off the immune system. The currently favored idea seems to be that “HIV” somehow brings about chronic systemic immune activation:
“the increased CD4+ and CD8+ cell death and proliferation is a consequence of virus-induced immune activation, not virus-mediated killing”
— Douek, PRN Notebook, 10(#3) (2005) 9-12.
“Chronic activation of the immune system is a hallmark of progressive HIV infection and better predicts disease outcome than plasma viral load” [emphasis added]
— Brenchley et al., Nature Medicine, 12 (2006) 1365-71
“HIV infection is characterized by chronic immune system activation” (review article)
— Nixon & Landay, Current Opinion in HIV and AIDS, 5 (2010) 498-503.

But how does “HIV” produce that condition?
“circulating microbial products, probably derived from the gastrointestinal tract, are a cause of HIV-related systemic immune activation. . . . These data establish a mechanism for chronic immune activation in the context of a compromised gastrointestinal mucosal surface”
— Brenchley et al., Nature Medicine, 12 (2006) 1365-71
“Microbial translocation has been linked to systemic immune activation during human immunodeficiency virus (HIV) type 1 infection. Here, we show that an elevated level of microbial translocation . . . correlates with AIDS”
— Nowroozalizadeh et al., Journal of Infectious Diseases, 201 (2010) 1150-4.
So, again, precisely the Lance hypothesis: Damage to the gut’s protective functioning allows leakage into the blood of substances not normally there, producing chronic activation so long as the leakage persists. Eventually serious illness can result.

The salient difference between the Lance theory and the mainstream belief is this:
— If Lance is right, then damage to the gut microflora precedes whatever markers may be used to detect what is thought to be “HIV” or to diagnose what is considered “AIDS”.
— If the mainstream view is correct, then “HIV infection” causes the damage to the gut.

Now, according to Sankaran et al., Journal of Virology, 82 (2008) 538-45:
“HIV-induced pathogenesis in GALT [gut-associated lymphoid tissue] emerges at both the molecular and cellular levels prior to seroconversion in primary HIV infection, potentially setting the stage for disease progression by impairing the ability to control viral replication and repair and regenerate intestinal mucosal tissues. . . . deterioration of the intestinal mucosa may initiate rapidly following infection . . . . HIV-induced enteropathy is well established within the first few weeks of infection, potentially even prior to seroconversion” [emphases added].
The examined biopsy samples had been obtained “at 4 to 8 weeks following HIV infection”; 3 of the 4 patients were then HIV-negative, and the 4th seroconverted 2 days before the biopsy. “Four highly active antiretroviral therapy (HAART)-naive patients in the primary stage of HIV infection (4 to 8 weeks postinfection)” were studied. However, it is not explained how these individuals happened to be enrolled in this study and to be under observation even before seroconversion. The only mentioned reason for assuming “HIV infection” were “flu-like” symptoms, and at that time they tested HIV-negative. Cited earlier studies by the same authors give no more specific information about these individuals; the only clue is that the work seems to be associated with the Center for AIDS Research, Education and Services in Sacramento (CA): so perhaps gay men enroll who are concerned that they might be exposed to “HIV” and might at some time seroconvert?
At any rate, it seems permissible to doubt that the date of “HIV infection” could have been accurately known. But in any case this is immaterial for the present purpose. What is clear is that at some time prior to testing “HIV-positive”, these four individuals had experienced damage to the mucosal lymphoid tissue of the sort seen in “HIV disease” or “AIDS”.
That is precisely what Lance’s intestinal dysbiosis theory predicts.
The mainstream belief is that “HIV infection” immediately — albeit it not always! — produces “flu-like” symptoms, but that antibodies do not appear for several weeks. It seems at least equally plausible that damage to the gut’s immune system brings gut leakage and immune activation that immediately causes “flu-like” symptoms. After all, those symptoms — fever in particular — are the direct result of activation of the immune system as it responds to foreign presences.

*                    *                    *                    *                    *                    *                    *                    *

When Tony had first told me of his theory, it came as the answer to what had been for me the most puzzling aspect of the HIV/AIDS story, from the viewpoint of one who had already seen that “HIV” is not what it’s said to be. The puzzle was, why gay men tested “HIV-positive” at such high rates; even though many of them remained seemingly healthy; and why testing positive seemed maximally probable at ages in the thirties or early forties. The intestinal dysbiosis theory explains those: A certain degree of dysbiosis can produce a positive “HIV” test without causing significant ill health; but continuing damage to the gut microflora over a decade or two could bring ill health as well as testing “HIV” positive.

At the Oakland Conference, Tony described how he came to his theory. The abstract, slides, audio, and video of his talk are available at the Conference website.
(The YouTube version of Part 2 seems  to stop before the end of Tony’s talk.)
Watching that video, one must surely be impressed by the strength of character this man has displayed. He disclaims expertise in science, but Tony Lance has demonstrated the single most important feature of doing science properly: an unwavering determination to look at all the evidence and then to seek explanations for it.

Posted in clinical trials, HIV as stress, HIV does not cause AIDS, HIV risk groups, HIV skepticism, HIV tests | Tagged: , | 32 Comments »

HAART makes things worse: Elsevier journal publishes HIV/AIDS heresies

Posted by Henry Bauer on 2010/11/03

Tony Lance alerted me to a discussion on Questioning AIDS started by trueverax with links to some fascinating recent articles about “HIV” and oxidative stress, for example, Gil et al., “Altered oxidative stress indexes related to disease progression marker in human immunodeficiency virus infected patients with antiretroviral therapy”, Biomedicine & Pharmacotherapy (2010), doi:10.1016/j.biopha.2010.09.009; the journal is published by Elsevier Masson France.
This in-press article in an Elsevier journal seems no less heretical than those Elsevier withdrew a year ago from Medical Hypotheses after protests from HIV/AIDS vigilantes. As Tony had remarked, “The opening line probably caused the Perth Group to chuckle — or sob”. Indeed:

“It is generally accepted that oxidative stress (OS) is implicated
in immunological and metabolic abnormalities during HIV infection”

Beginning in the 1980s, the Perth Group has argued:
“That AIDS and all the phenomena inferred as ‘HIV’ are induced by changes in cellular redox brought about by the oxidative nature of substances and exposures common to all the AIDS risk groups and to the cells used in the ‘culture’ and ‘isolation’ of ‘HIV’”.
For example,
“There is no compelling reason for preferring the viral hypothesis of AIDS to one based on the activity of oxidising agents” — Eleni Papadopulos-Eleopulos, “Reappraisal of AIDS: Is the oxidation induced by the risk factors the primary cause?”, Medical Hypotheses 25 (1988)151-162.

The remarkable statement in the Abstract of Gil et al’s article, that the presence of oxidative stress in “HIV/AIDS” is “generally accepted”, is repeated in the text in this way:
“The redox balance is also severely disturbed in HIV infected individuals without HAART [7–13].” Those references are:
[7] Israel et al., Cellular and Molecular Life Sciences, 53 (1997) 864-70.
[8] Romero-Avila et al., Medical Hypotheses, 51 (1998) 169-73.
[9] Sönnerborg et al., Scandinavian Journal of Infectious Diseases, 20 (1988) 287-90.
[10] Favier et al., Chemico-biological Interactions, 91 (1994) 165-80.
[11] Allard et al., American Journal of Clinical Nutrition, 67 (1998) 143-7.
[12] Gil et al., Pharmacological Research, 47 (2003) 217-24.
[13] Pasupathi et al., Journal of Scientific Research, 1 (2009) 370-80.

I noticed that these seven articles, as well as the one in Biomedicine & Pharmacotherapy, are all in journals that do not specialize in HIV/AIDS. Yet the substance of these articles concerns HIV/AIDS more directly than it does anything else. Here’s a little research project for someone who has some time: Ask the authors of these articles whether they had tried to publish in a journal like JAIDS; and if not, why not?

Here’s another interesting fact about these articles: All the work was done outside the United States. Gil et al. worked in Cuba; Israel et al. in France; Romero-Alvira in Spain; Sönnerborg et al. in Sweden; Favier et al. in France; Allard et al. in Canada; Gil et al., 2003, in Cuba but with a co-worker in Italy; Pasupathi et al. in India.
It may not seem surprising, therefore, that none of these articles acknowledge research support from an American source. That is, it may not seem surprising to people not familiar with the fact that the National Institutes of Health (as well as a number of American foundations) do support considerable amounts of research outside the United States. Perhaps especially about HIV/AIDS; much research on HIV/AIDS in Africa, for example, is supported by American money.
But then again, it’s certainly no surprise that the National Institutes of Health would not support research on the role of oxidative stress in the conditions that are labeled “HIV-positive” or “AIDS”.

The discussion on Questioning AIDS also cites another study, from Africa, that reports correlation of “HIV-positive” status with lowered antioxidant activity: Bilbis et al., Annals of African Medicine, 9(#4) (2010) 235-9; not an AIDS-specialist journal, no research support acknowledged.

Now Gil et al. do not state outright that oxidative stress might be the cause of “HIV-positive” or of “AIDS”, they only point out that oxidative stress is present in those conditions. However, given that “HIV” virions have never been isolated from “HIV-positive” individuals, it is no great step from these findings to the stance taken by the Perth Group for more than two decades.
None of these articles cite the Perth work, of course. Even Romero-Alvira, who published in Medical Hypotheses in 1998, does not cite the 1988 Papadopulos-Eleopulos article in Medical Hypotheses.

*                    *                    *                    *                    *                    *                    *                    *

But the greatest heresy of Gil et al. (2010) lies not in pointing out the role of oxidative stress in HIV/AIDS: It is the finding, in a placebo-controlled trial, that HAART makes things worse.
A variety of measures of oxidative stress were used. Three groups of “HIV-positive” individuals were studied: One not subjected to antiretroviral drugs; one treated with AZT/3TC/ IND (zidovudine or Retrovir, a NRTI; lamivudine, a NRTI; indinavir, a protease inhibitor); one treated with D4T/3TC/ NEV (stavudine, Zerit, a NRTI; lamivudine, a NRTI; nevirapine or Viramune, a NNRTI):
“both combination . . . produced an increase in OS [oxidative stress] indexes paralleled to HIV progression marker change”; in the second (D4T) group to the extent that there was “a poor prognostic” under this treatment.
References are cited for the toxicity of HAART, including typical damage to mitochondrial function. The mitochondria are the energy-producing sites of all animal cells and play a significant role in the redox systems within all cells.
Perhaps most significant, it is pointed out that the surrogate markers typically used to assess the success of HAART, CD4 counts and viral load, did show “improvement” under HAART in these studies at the same time as oxidative stress increased:

increasing OS . . . occurs . . .
during apparently successful  HAART.
This  . . .  underline[s] HAART associated toxicity

[emphasis added].

This work serves to explain quite a few things about “HIV/AIDS” and HAART, for example that neither CD4 counts nor viral load is a good predictor of clinical outcomes (Rodriguez et al., JAMA, 296 (2006) 1498-1506).

Another reference cited in this thread on Questioning AIDS confirms the finding of increased oxidative stress as a result of HAART:

“HAART may affect oxidative stress in HIV-1-infected patients
. . . antiretroviral therapy plays an important role
in the synergy of HIV infection and oxidative stress”

(PMID: 19884983, Mandas et al., Journal of Biomedicine & Biotechnology, 2009;2009:749575. Epub 2009 Oct 26 — again, not an AIDS-specialist journal; work done in Italy).

Posted in antiretroviral drugs, clinical trials, experts, HIV as stress, HIV does not cause AIDS, HIV skepticism | Tagged: | 4 Comments »