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Friday, April 15, 2005

Lying by Omission

One of the most heinous crimes committed by the AIDS dissidents is that of lying by omission. I usually more generously refer to this as "cherry picking". It's not as if putting a spin on a research finding is actually that bad (after all, one must weigh up all the evidence before coming to a conclusion - if that's even possible!) but they do it so often and even in the face of clear contradiction.

For example on misc.health.aids one of the loudest dissidents by the name of Paul King quoted a paragraph from a CDC website refering to condom use. He was trying to show that condoms don't protect against HIV.

"At a Washington, D.C., news conference, the 10,000-member Physicians Consortium claimed that the CDC has known for years that condoms offer little protection against sexually transmitted diseases such as gonorrhea, chlamydia, syphilis and genital herpes.

The NIH panel concluded that there was "insufficient evidence" that condoms protect against STDs."

The REAL wording is somewhat different.

"At a Washington, D.C., news conference, the 10,000-member Physicians Consortium claimed that the CDC has known for years that while condoms are 85 percent effective in helping prevent the spread of HIV, they offer less protection against sexually transmitted diseases such as gonorrhea, chlamydia, syphilis and genital herpes.

While finding that latex condoms can be effective in preventing the spread of HIV and in protecting men from contracting gonorrhea from a female partner, the NIH panel concluded that there was "insufficient evidence" that condoms protect against other STDs."

Fox News Story

More recently, another "big" guy on the dissident scene (Chris Tyler, the moderator who stopped me educating the readers of AIDSmyth.Exposed on MSN) wrote into the BMJ listing several studies which he said supported the role of drugs in causing immune suppression.

A prospective study of male homosexuals using psychoactive and sexual stimulants demonstrated that their T-cells may decline prior to infection with 'HIV'. For example, the T-cells of 37 gay men from San Francisco declined steadily prior to HIV infection for 1.5 years from over 1200 to below 800 per ┬Ál (Lang et al., 1989).

In some case they had fewer than 500 T-cells 1.5 years before seroconversion (Lang et al., 1987).

Other studies of the same cohort of homosexual men from San Francisco described extensive use of recreational drugs including nitrites (Darrow et al., 1987; Moss, 1987; Ascher et al., 1993; Duesberg, 1993d; Ellison, Downey and Duesberg, 1995). Likewise 33 HIV-free male homosexuals from Vancouver, had "acquired" immunodeficiency prior to HIV infection (Marion et al., 1989). While this study did not mention drug use, other articles by the authors reported that all men of this cohort had used nitrites, cocaine and amphetamines (Archibald et al., 1992; Duesberg, 1993f; Schechter et al., 1993c).

In 1994, a study of IV drug users in New York (Des Jarlais et al., 1993) showed that "The relative risk for seroconversion among subjects with one or more CD4 count <500>500 cells/uL was 4.53".

A similar study in Italy (Nicolosi et al., 1990) showed that "low number of T4 cells was the highest risk factor for HIV infection", that is, decrease in T4 cells is a risk factor for seroconversion and not vice versa.


When I got around to reading the sources quoted, I got a nice surprise...

I wonder though why Mr Tyler quotes from Des Jarlais but omits the following:

"We studied CD4 cell counts and percentages from 1984 to 1992 among 1,246 HIV-seronegative injecting drug users in New York City, a population at very high risk for exposure to bloodborne pathogens. Severe CD4 lymphocytopenia was rare, and there was no evidence of an increase over time. Of 229 subjects with longitudinal data, only four met the surveillance definition for "idiopathic CD4 lymphocytopenia" (ICL)."

Hardly glowing evidence of support for the drug-AIDS hypothesis!

Marion et al don't actually demonstrate any immune deficiency at all, aside from lack of responses to DNCB (a chemical that can cause skin reactions). Responses to TB protein, candida and trichopyhton were all normal.

Lang et al actually say:

"The three groups were 37 HIV seroconverters, 304 prevalent HIV seropositives remaining free of the acquired immunodeficiency syndrome (AIDS), and 69 men who developed AIDS during observation. Six months before seroconversion, CD4 levels were similar among HIV seroconverters and 356 seronegative controls. Within 18 months of seroconversion, mean CD4 levels fell to the level of the prevalent seropositives at study entry."

I do not think these are very good arguments for the drug-AIDS hypothesis. Lang et al actually is excellent evidence for HIV infection leading to immune failure.


I recently pulled up the Nicolosi paper as well: they looked at around 460 seronegative IV drug users for an average of 10.4 months. Plenty of time to notice a loss of CD4 T cells...


The incidence rate of HIV infection was 7.4 per 100 person-years, equivalent to a one-year risk of 7.3%. Relative risk was higher in subjects who had been using intravenous drugs for less than 2 years (RR = 2.3). In a case-control analysis, recent frequent syringe sharing was the behavioral variable most strongly associated with HIV infection, with the highest risk in subjects sharing often (OR = 6.1, 90% CI = 2.6-14.7). We found no association with the use of cocaine in addition to heroin nor with sexual habits. Among biologic variables, relative risks were increased in individuals whose T4-lymphocyte count was lower than 1,000 at first visit (RR = 8.5, 90% CI = 2.9-24.3) or who were carrying HBsAg (RR = 1.9, 90% CI = 0.8-4.2).


Note that the normal range of CD4 counts is usually quoted as between 500 and 2000 with the average at around 1000. AIDS is judged to occur at a level of 200, since that is when most opportunistic infections start to become more common than background. It's no surprise that an infection (HIV) is more common in those with lower immune function (as judged by CD4 count at any rate). Only HIV infection seems to be capable of dropping CD4 counts below 200, and lower.

Remember - the opportunistic infections are merely the result of AIDS, not AIDS itself...

5 Comments:

Blogger Bennett said...

This damn "debate" was old even before I got into it. Nothing much has changed. The successes of the Protease Inhibitors in the West, social education in Uganda, and blood product screening are ALL consistent with the orthodox view - and yet the dissidents continue to twist the facts to explain it away according to their own fringe view.

I'm seeing more memes from Scheff starting to spread as well - like "the fetus and mother share blood, so why isn't HIV transmitted during pregnancy". Err, because the fetus and mother don't share blood. Sheesh.

Sadly memes that fit with the dissident view (like malaria being AIDS-defining) are going to survive among the ignorant.

I agree entirely that ignorance is forgiveable - what bugs me is that so many dissidents don't want to CHANGE their ignorance through education. In my experience, those that are willing to learn tend to shift sides.

9:46 PM  
Blogger Bennett said...

I agree that it can be hugely detrimental to accept dogma for dogma's sake. I also can see your point of view with regard to antibiotics and AIDS meds, although by "life saving" they are really talking about prolonging life. Everyone dies, in the end.

But denialists do not simply "offer speculative alternative theories", they twist the truth and science, and basically lie to support their own message. Often that message is nothing more than "don't trust the establishment". You also seem to want to spread that message, but complaining about the lack of effective antibiotics and the capitalist medical industry is somewhat different from lying that retroviruses must be lytic and can only be spread from mother to child, as dissidents of the "caliber" of Duesberg do!

I'm all for dissent where appropriate, but not dissent for the sake of dissent itself. That's simply anarchy.

6:34 PM  
Blogger Bennett said...

I truly find that most if not all of Duesberg's arguments are seriously flawed. He lacks any clinical education, and as such has no perspective on a lot of what he talks about. His research in addition in based on far simpler viruses than HIV, so he's extrapolating from a model T Ford to criticise a Dodge Ram truck!

I have written several short articles addressing the allegedly "low" rate of cell infection by HIV. The rate actually comes closer to 25% (1 in 4) in lymphoid tissue. One copy of the article I furnished to the BMJ debate is on this very blog.

The transmission data is interesting, but horribly confounded. The West had massive public information campaigns that resulted in widespread awareness of HIV and how it was spread. Many areas in Africa not only did not do this, but some actively argued against HIV even existing, and later whether it caused AIDS. Those African countries which did enact positive change have done remarkably well (e.g. Uganda).

The reason why there was a fear of a heterosexual epidemic in the west was simply that, at the time, there was no way to test for HIV, and everyone assumed that it was already in the hetero population. It seems that was not the case. Once awareness was there, the chances of it crossing from the homosexual population to the heterosexual population was far less, although it did still occur of course. In Africa in contrast, it was long in the hetero population so their epidemic would be expected to be very different. If HIV had crossed into the west via a different route, no doubt our epidemic would be different.

I get regular questions from people about getting tested. I give the same advice as the Cleveland clinic you mention. I think everyone does. The tactics most dissidents THINK the establishment uses (everyone get tested, then get on the meds) simply don't happen.

In Africa, even in areas previously dominated by HIV-2, HIV-1 is now the most common strain. It is true that the developed world has a different strain of HIV (B-clade) but I don't think there is any evidence that this is any worse or better at being transmitted. The evidence that any strain is significantly more easily transmitted than any other is limited - they all seem to be similar.

However sexual practises are different. Families in the west are smaller, meaning some kind of contraception or relative abstinence is going on! A couple of studies from Africa quite nicely showed that while male-to-female transmission was twice as likely as female-to-male transmission, men were twice as likely to cheat on their wives and get HIV outside the marriage! This worked out to a 1:1 ratio.

The data you quote from Thailand doesn't say that 90% of infected people are male. These are very specific groups being tested: STD infected men seem as likely as women prostitutes to have HIV. That is obvious - similar high-risk groups. Currently the ratio of male to female AIDS cases is 2:8 to 1 (UNAIDS source) and that is after the epidemic starting out in the homosexual popluation. In many ways, Thailand has gone the way that the US and UK feared it would go for them... 88% of cases are now heterosexual, and homosexual transmission is now less than 1%. However, outside of the sex-worked industry infection rates are far lower, as you might expect. Contrary to what Duesberg says, you would NOT expect an STD to spread equally among the sexes, nor would you expect it to spread equally among risk groups (ESPECIALLY not among risk groups). It simply makes no biological sense to assume this.

10:35 AM  
Blogger Bennett said...

The point, is, the 1 in 1000 rate is semi-mythical. It came from a study where condom use occurred in the West. It is not representative of the African situation for all sorts of reasons. In the same way you can't use results from adults to make decisions in children, and you can use disease rates from Manhattan to predict disease rates in rural Texas.

The African situation is only a paradox if you try to extrapolate from Western society and studies. The same studies done is Africa show a far higher rate than 1 in 1000 exposures.

People are not "only really infectious" in the early and late stages. For sure, viral loads are predictive of relative risk, which accounts for some of the bias, but relatively lower risk is not the same as zero risk.

I can see your point about HIV/AIDS being politicized. I agree that this has happened, and that some people are "on the bandwagon". But the point is that the research will still get done and if the work is shoddy and unfounded, it will get found out. The dissidents say that has already happened, but they can only show this by re-writing the rules of virology and biology to fit their ideas.

You ask why Africa has got so bad and the west hasn't - quite simply in the West we caught the epidemic very early on. We highlighted a risk group and had a serologic test and a likely pathogen within 3 years of the disease being described. It is possible that the virus had only been in the US for a few years (the contact tracing was still done to show the spread from person to person). In contrast the virus had likely been in Africa for decades prior to coming to the US, and no-one was expecting this kind of disease. On average people would live for 10 years and spread it around, so there was a tremendous lag time before it got picked up. Quite likely if the epidemic hadn't occured in gay men in the US, it would have had a longer lag time as well. Heterosexuals would have had less rapid initial spread (less concentrated cases), poorly defined risk group (fewer transmission clues). The cluster of KS and PCP cases in the early 1980's wasn't so striking as the fact that they all occurred in young gay men. That's what really grabbed the attention - it has immunosuppressive STD written all over it.

Also, it's clear that you're still believing some of the dissident stuff. African studies do use blood tests, some of the best research has come out of Africa (usually those countries that are turning the epidemic around!). The 1 in 1000 rate is one of the largest myths, I think because people want to hang on a number, and it's easy to remember. This number came from a study looking at the risk of transmission, and the evidence suggests that in that kind of study (knowing that one partner is positive) the use of condoms goes up and frequency of sex goes down. Risky activities such as anal sex and sex during menses also drops. In one study a third of couples stopped having sex altogether! N Engl J Med. 1994 Aug 11;331(6):341-6. "A longitudinal study of human immunodeficiency virus transmission by heterosexual partners. European Study Group on Heterosexual Transmission of HIV."

Other factors come into play, such as concurrent STDs, which are at a higher rate in Africa than in the West.

I find there is usually only a paradox in the mind of questioner, if they're not aware of all the facts, caveats or limitations of the data. Duesberg massively oversimplifies things, you at least have some logic and numbers to back things up! However, from what I can tell you're still comparing apples and oranges by assuming that Western transmission rates are the same as in Africa or other high-rate areas.

As regards Thailand, here is a scary story: 405 HIV+ male blood donors. 405 female partners of these men. 46% of the women were also HIV+, and did not have any other risk factor other than their husbands. 98% of the men reported sex with a prostitute. 98.5% of men did not use condoms with their regular partner. AIDS. 1997 Nov 15;11(14):1765-72.

In one study where condoms were used for 90% of sex acts by prostitutes, and STDs were treated, seroconversion rates were 6.6% annually. In the European study quoted earlier the rates were around 4.8% in inconsistent condom users (0% in consistent condom users). That's quite a difference and highlights the problem in comparing very different groups of people. One study from Texas put the annual risks at 6.8% for never-users and 0.9% for always-users.

If you want to really see the difference, use the magic of compound interest...
0.9% annual infection for 10 years gives you 8.7% population infection prevalence. 6.6% annual rate gives you 50.5% population prevalence (assuming all infections occur in uninfected people and no-one dies).

Now, that's data from serodiscordant couples, so you're assuming that everyone has an HIV+ partner! Clearly that isn't the case. But you can see how it works... It certainly helps explain why an epidemic caught early has behaved far differently than one caught late (US versus South Africa for example).

Incidentally, this is how credit card companies make their money.

11:19 AM  
Blogger Bennett said...

Que - you've not really said anything that isn't obvious.

Of course the Ugandan numbers will decline due to deaths...how else are they going to drop? The point is they've dropped whereas SA is still "levelling off".

As far as Duesberg goes, so far I ave yet to see a sensible point raised by him. Even if he does, he has lied so blatantly so many times, and his "logic" is built on those lies that it hardly matters any more...sad really.

HIV really doesn't do anything any other virus hasn't done somewhere else! The only people who make it mythical and strange are the dissidents, to try to discredit it!

Dissent can be good (you mention the H Pylori story) but only if its true. Duesberg argues that herpes cannot exist. He says that a virus that kills before the teenage years is passed on mother-to-child. He says that a virus he never studied MUST behave in a certain way, for no other reason than he says so. He says that AZT is toxic because studies were halted for cancer therapy, when in fact they were stopped because it wasn't toxic enough...

I could go on. In fact I have - read the rest of the blog ;-)

8:42 PM  

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