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jacob_cannell comments on Open Thread, September, 2010-- part 2 - Less Wrong
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In my last post on Health Optimization, one commenter inadverntently brought up a topic which I find interesting, although it is highly contraversial - which is HIV/AIDS skepticism and rationality in science.
The particular part of that which I am interested in is proper levels of uncertainty and rationality errors in medical science.
I have some skepticism for the HIV/AIDS theory, perhaps on the level of say 20-30%. More concretely, I would roughly say I am only about 70% confident that HIV is the sole cause of AIDS, or 70% confident that the mainstream theory of HIV/AIDS is solid.
Most of that doubt comes from one particular flaw I in the current mainstream theory which I find particularly damning.
It is claimed that HIV is a sexually transmitted disease. However, the typical estimates of transmission rate are extremely low: 0.05% / 0.1% per insertive/receptive P/V sex act 0.065% / 0.5% per insertive/receptive P/A sex act
This data is from wikipedia - it lists a single paper as a source, but from what I recall this matches the official statistics from the CDC and what not.
For comparison, from the wikipedia entry on Gonorrhea, a conventional STD:
So it would appear that HIV is roughly 100-500 times less sexually transmittable than a conventional STD like gonorrhea.
So in my mind this makes it technically impossible for HIV to be an STD. These transmission rates are so astronomically low that for it to spread from one infected person to an uninfected partner would take years and years of unprotected sex.
If you plug that it to a simulation, it just never can spread - even if everyone was having unprotected sex with a random stranger every single day, it would still require an unrealistic initial foothold in the population by other means before it could ever spread sexually.
And of course, if you plug in actual realistic data about frequency of unprotected sexual intercourse with strangers, it's just completely impossible. Bogus. It doesn't work. It can not be an STD.
As gonorrhea (and I presume other STDs) are hundreds of times more transmissable than HIV, their low rates in the population place bounds on HIV's sexual transmission.
Finally, these rates of transmission are so low that one should question the uncertainty and issues with false positives - how accurate are these numbers really?
A few years ago, I entered an online discussion with some outspoken HIV-AIDS skeptics who supported the theories of Peter Duesberg, and in the course of that debate, I read quite a bit of literature on the subject. My ultimate conclusion was that the HIV-AIDS link has been established beyond reasonable doubt after all; the entire web of evidence just seems too strong. For a good overview, I recommend the articles on the topic published in the Science magazine in December 1994:
http://www.sciencemag.org/feature/data/cohen/cohen.dtl
Regarding your concerns about transmission probabilities, in Western countries, AIDS as an STD has indeed never been more than a marginal phenomenon among the heterosexual population. (Just think of the striking fact that, to my knowledge, in the West there has never been a catastrophic AIDS epidemic among female prostitutes, and philandering rock stars who had sex with thousands of groupies in the eighties also managed to avoid it.) As much as it’s fashionable to speak of AIDS as an “equal opportunity” disease, it’s clear that the principal mechanism of its sexual transmission in the First World has been sex between men, because of both the level of promiscuity and the nature of the sexual acts involved. (And it may well be that HIV among heterosexuals would be even rarer if it weren’t constantly reintroduced into the heterosexual population via women having sex with bisexual men, let alone if the sexual transmissions from intravenous drug users were also absent.)
On the other hand, when it comes to African AIDS, it’s hard to say anything reliably. The public discussions of First World AIDS are full of nonsense, but at least there are enough reliable raw data to make some sense out of the situation; in the case of Africa, however, we don’t know anything beyond what we’re told from people with highly suspect interests in the matter, either careerist or ideological, and even if there are some truthful and reasonable voices in the whole mess, it's impossible to filter them out in the sea of misinformation.
Also, here’s a pertinent comment I left on OB in a thread about the recent Medical Hypotheses affair: http://www.overcomingbias.com/2010/05/rip-medical-hypotheses.html#comment-447400
Quite interesting. I didn't really know much about Medical Hypotheses until I posted a link in another thread (as a minor side point) to an article my dad wrote which happened to be in that very journal, and someone pointed out what it was. Strange connection.
A long while ago I found Duesberg's papers and entered into some online debates taking his position. The end result of all that reading moved me into a position closer to yours, but more uncertain. I just went and re-read Duesberg's most recent 2003 paper and noticed it still has a noticeable pull on me after reading it, but after going back and forth several times between the two camps I usually end up somewhere lost in the middle.
Duesberg, even though probably ill-fated in his main quest, has I believe shown that the orthodox establishment has gone wrong at least in part. The history of the whole affair seems like it should be a lesson that we should learn from, a lesson that somehow results in learning and moving towards a more rational scientific establishment, more cleanly divorced from politics. That may be an interesting discussion to have here, if it hasn't already been discussed much. Deusberg suggests a jury process to replace the current peer-review system, which he is highly critical of. That could be an interesting rationalist angle on this.
I'd point out that nobody is claiming that HIV is exclusively sexually transmitted; there are other methods of transmitting it, such as infected needles. Also, Wikipedia cites a paper suggesting that those rates you mentioned are "4 to 10 times higher in low-income countries" and as high as 1.7% for anal intercourse.
I don't know whether or not these facts are sufficient to address your fundamental complaint, but they would make a pretty big difference.
At an (unrealistically?) independent 0.5% chance per act, a 50% chance of transmission would require 139 sex acts — hardly "years and years".
(ETA: yes, unrealistically, according to this abstract found by Perplexed: "However, in comparison with nonparametric estimates, the model assuming constant infectivity appears to seriously underestimate the risk after very few contacts and to seriously overestimate the risk associated with a large number of contacts. Our results suggest that the association between the number of unprotected sexual contacts and the probability of infection is weak and highly inconsistent with constant per-contact infectivity.")
At best, this can show that pandemic AIDS can't primarily result from sexual transmission of HIV, which is evidence that AIDS has causes other than HIV, but also that pandemic AIDS spreads through other means (as suggested here, e.g.).
If you're thinking of rates in the modern developed world, STDs are unsurprisingly more common when and where treatment is less available:
That is for the highest transmission activity - receptive A, so be careful not to cherry pick. Yes - 139 unprotected sex acts. It would take 1390 unprotected insertive A sex acts to reach a 50% chance of transmission.
So with some assumptions, mainly - gay bathouses and no condom use - yes the virus could spread horizontally, in theory. Although that population would necessarily first acquire every other STD known to man, more or less.
But in the general heterosexual population, not a chance. If you compare to the odds of pregnancy from unprotected sex, the insane requisite amounts of unprotected sex with strangers would result in a massive baby epidemic and far more vertical transmissions long before it could ever spread horizontally in the hetero population.
I don't know why you mention "modern developed-world rates" and then have a link to 1901 NY and Africa . . .
You don't need the "at best" qualifier, but yes I agree that is what this shows. Showing that however opens a crack in the entire facade. Perhaps not a critical failure, but a significant doubt nonetheless.
If the orthodox position had updated on the evidence, and instead changed their claim to "HIV is a borderline infectious disease that spreads primarily through the prenatal and blood-borne routes", then I would give them more creedence. Of course, for political reasons alone they could never admit that.
Many non-AIDS STIs, and pregnancy, are curable.
Funny to think of pregnancy as curable, but yes of course that's true. However, it doesn't really change the numbers much.
Also, from what I have read about the early 80's bathouse scene, it is possible that many of those guys did acquire every STD known to man, so at least in that case the sexual transmission route could work even with such terribly low efficiency.
Regardless, it seems strange to label it as a STD from an evolutionary perspective, it doesn't fit that profile, and it seems incredibly unlikely it could have evolved as such.
It's also funny to call babies an epidemic.
Life is a disease. It is transmitted by sex and ends deadly always.
touche!
What are the political reasons? Staying on-message and retaining funding, or something more specific?
Essentially the government committed to a public awareness campaign that HIV was 'rapidly growing' in the heterosexual community, and this became part of the dogma. It is politically motivated - it's anti-sex message appeases religious conservatives while also shifting attention away from the gay bathouse scene, so it sort of benefits everyone politically, regardless of whether it's actually true.
I meant "rates are higher outside the modern developed world". Rephrased for clarity.
I don't see why epidemiology should care about the 50% threshold. The relevant number is the expected number of transmissions per year. Thus independence is irrelevant.[1] At 200 anal tops per year per infected person, incidence should double yearly. And every top requires a bottom, so that's 400 anal sex acts per year for just doubling. It seemed to spread more quickly than that, but maybe 800 and 4x per year works. It seems just barely plausible with this transmission rate. I'm not sure of the details of bathhouses, but I thought that there was a lot of non-anal sex, too.
[1] independence is relevant if 70s gays were systematically different from the people in the study; and they probably were, eg, they probably had higher rates of STDs
Why "more quickly than that"? From Epidemiology of HIV/AIDS in the United States:
This seems to indicate a doubling time of about 2 years.
ETA: Also according to that page, the patient with the first confirmed HIV infection died of AIDS in 1968, so the growth rate of AIDS before 1989 was at most 1.73x per year.
OK, maybe doubling works.
But it's important to distinguish different populations. You should expect it to spread faster through the bathhouse scene than through the rest of the gay community than through the straight community. So it should slow down once it exhausted the bathhouse regulars (something like weekly visits) or when AIDS shut down that scene. If that happened around 1985 and there's a 10 year incubation period, then the 1995 numbers still include bathhouse effects. Diagnoses were increasing at 3x or 4x in the early 80s: 100 in fall '81 to 250 in mid '82 to 1000 in early '83 to 3000 by the end of the year. From '83 to '89 it was merely doubling and it slowed after that. Of course, there are problems with diagnosis numbers early in an epidemic, but death followed quickly, in weird ways, so these numbers are probably good enough. Yes, there were people with AIDS in 60s, but that 1.73x includes time to get to the bathhouse scene.
One problem with this simplified model is assuming every sexual act is with a new partner, which would only be true in the very early stages.
I think your analysis is on the right track though, and it seems barely plausible with this transmission rate, assuming negligible condom use and an intense bathhouse scene. However, in standard theory HIV progresses to AIDS in about 10 years, so this sets a timer which starts removing vectors from the population.
Thus the exact exponent matters considerably. If incidence can only double every year, then after 10 years you get 2^10 ~ 1000 cases.
If incidence doubles every 6 months (quadruples every year), then you get a million cases after ten years.
If you consider that all other STD's would infect this population before HIV, then one has to wonder how that would effect condom use, and how that changes the model.
So do you find the transmission rate and make the model before you decide that HIV was an STD which spread this way, or after?
It assumes that every sexual act is with an uninfected partner. Perhaps that's what you meant, but then I wouldn't have used "very."
I think this is pretty well documented. STDs were routine and not a big deal (treatable!) in the 70s gay scene. Thus they did not cause condom use.
To say that this makes it not an STD is to misunderstand what an STD is.
An STD is not a disease whose transmission method is specialised to the act of copulation. It is merely a disease which is so difficult to transmit at all that only the most intimate of contact has any substantial chance of doing so. What is important about the sexual contact is not the sex, but the blood contact.
In HIV we have something that is so difficult to transmit that even conventional heterosexual intercourse has difficulty. Closer blood contact is required for a high chance of transmission, such as in anal intercourse (the intestinal lining is fragile and not adapted to contact with foreign bodies) or injection from infected needles. This has been known practically since the start from the epidemiology, before any pathogen was identified.
I'm not in quite agreement with both of your points. Yes of course HIV is transmissable only through blood, but I don't agree with that being a good criteria for use of the term "sexually transmitted", especially when other STD's such as gonorrhea are actually effective - they are measurably hundreds of times more sexually transmissable than HIV. This is probably due to both evolved mechanisms that those STDs have (such as ulceration formation) and overall low virality and transmissability of HIV.
So it is ingenous I think to change the categorization. HIV is clearly at an extremum, and perhaps would be better classified as a weakly transmissable blood borne disease, not an STD.
The evolutionary relevance is important here. How did this evolve?
Have you seen these two recent meta-analysis of HIV transmission rates? Comparing them to your numbers, it seems that Wikipedia/CDC have greatly understated the risk for P/A sex acts (due to using older studies?).
Also, according to this page, the transmission rates for genital herpes are similar to HIV for P/V sex acts, so AIDS is not the only STD to have such low transmission rates.
I think the conventional theory is that HIV established an initial foothold by means such as needle sharing, blood transfusions, and P/A sex acts. That seems quite realistic to me. Why do you think it's unrealistic?
No I haven't seen them until now. I haven't really been looking into or thinking about this until just recently.
I originally quoted the wikipedia data, which several us tracked down and analyzed in another thread (it comes from the CDC and originally from a single medium-ish European study which I think did a fairly good job to control for factors such as condom use and what not given the complexities):
Let's compare to the 1st meta-analysis:
it finds 0.04/0.08% for insertive/receptive P/V sex in the 1st world, very similar but slightly lower to the older CDC study (from europe). They find the rates are around 5 times higher in the 3rd world.
For P/A receptive, they find a pooled per-act rate of 1.7%, about 3.5 times higher than the 1st world CDC study. I suspect this is simply because they pooled 1st and 3rd world data together.
This does not show that Wikipedia/CDC have "greatly understated" the risk for P/A sex acts - this data is in agreement. The variance is between 1st and 3rd world studies. The 1st world data is of paramount concern for the historical origin theory of the disease. The 3rd world data is a side point - not historically important and suspect in general, as in fact mentioned in the abstract.
The abstract:
So this supports the original CDC data for the 1st world.
The second meta-study finds a receptive A per act rate of 1.4%, a little lower than the 1st study, and about 2.8 times the 1st world CDC data. They make no mention of what countries, and I assume it mixes 3rd and 1st world data - it is a large meta-analysis of many studies.
There is also some serious wierdness in the 2nd study:
So something doesn't fit - the per act and per partner numbers don't square up at all. Somewhere else someone posted an abstract with a similar result, how basically your chance of infection levels off quickly in couples and is much lower than you think - you are either going to get it or not irregardless of number of sex acts. This suggests that there are some major unknown immunity factors at work or the entire model is wrong.
I think the needle sharing and blood transfusions is far more credible, but the 0.5% ish per act of receptive A in the 1st world could possibly support a sexual vector in the gay bathouse scene, but it is debatable.
The conventional theory requires that HIV came over as a mutated form of harmless simian SIV and spread here, through a single source vector from what I recall. Blood donation might make more sense, but one would have to look at the epidemiological models for that.
Note that in general low-transmission rates aren't that good an argument against it. First of all, a lot of transmission in the US occurred through other forms, especially early in the epidemic (intravenous needle sharing and transfusion of infected blood being two major ones). As others have noted the transmission issue is also generally higher for homosexual rather than heterosexual intercourse.
Frankly, the thing that I most don't understand about people who are skeptical about the HIV-AIDS link is how one explains the fact that anti-virals tailored to deal with HIV work. Even the first-gen treatments such as AZT were used due to the biochemistry of HIV (often targeting reverse transcriptase). And they worked in delaying the onset of AIDS and worked for giving people with AIDS higher life-expectancy. I don't see how one can easily reconcile that with HIV not being the cause of AIDS and I've never heard anything remotely resembling a coherent explanation about this.
The extremely low official transmission rates indicate that HIV is probably not a sexually transmitted disease, as typically understood. According to the published transmission data, it's only effective natural means of transmission is vertical - from mother to child. From what we know about symbiosis and parasites, this should lead one to suspect it is not that lethal.
However that doesn't destroy the hypothesis that HIV could be a unique disease of civilization - a mutation of a formerly limited retrovirus into a more damaging form that spreads horizontally only through extremely unnatural novelties of the modern world - needle sharing and epic promiscuity in some subgroups. It does of course make the overall hypothesis more complex and overall less likely, but it doesn't destroy it outright.
This is very difficult to prove ethically, and certainly hasn't been shown to satisfaction. Consider how immensely difficult it has been to understand the real health effects of fat in the diet, for example. In the 80's and 90's, we thought it was oh so simple. Today we (the wise) realize how profoundly ignorant we were then, and still are today. I think part of the rational reappraisal for the strength of the HIV hypothesis should come from a similar update.
In other words one can only cling to a high degree of certainty about the HIV hypothesis when one is profoundly ignorant concerning the depth of one's ignorance about the complexity of human health.
That's the theory.
Ahh the world would be so simple if that was true. The AZT clinic trial was ended prematurely and double-blindness could not be maintained due to side effects. The skeptics claim that later studies show that AZT increases long term mortality, not the other way around.
You need to realize how impossible it would be to concretely show what you presume to high certainty. You would basically need a double blind study with two control groups, one receiving plazebo, and compare total mortality. One immediate problem is any noticeable side effects would immediately end the blindness - and the retrovirals certainly have side effects.
And even showing that AZT or drug X reduces mortality in HIV+ patients does not lead to the conclusion that HIV is the cause, or that AZT or drug X has any effect on HIV. Supplementing patients with vitamin D, or changing their diet, or feeding them aspirin, or any number of other changes could also decrease mortality, but have nothing to do with the viral theory.
Health is complex.
So I don't know what evidence you have for these claims. The original AZT study can be found here. It handled placebos just fine.
And AZT is just one example of many anti-retrovirals. 3TC and ABC have also been used. Moreover, there are studies which show that the the standard drug cocktails work better than AZT or 3TC alone. That makes sense for the standard model of HIV as the cause of AIDS.
There seems to be an issue here involving what level of evidence is necessary. From a Bayesian stand point you can't ever "show" anything in the sense that you want. But the overall pattern of evidence can still give you a probability close to 1 that HIV is the primary cause of AIDS.
http://www.ncbi.nlm.nih.gov/pubmed/3299089
Ah you read this while I was editing it.
Yes I have browsed that abstract, although I can't see if there is a full copy of the whole thing. Notice the link to the toxicity right next to it:
The toxicity of azidothymidine (AZT) in the treatment of patients with AIDS and AIDS-related complex. A double-blind, placebo-controlled trial.
Notice that it has serious toxicity side effects, including bone marrow supression, and thus it can massively damage the innate immune system.
This is evident in the abstract itself:
The original AZT study could not possibly be placebo controlled, due to the high toxicity - this is basically chemotherapy. Now chemotherapy can be effective, but it can not be double blind.
Furthermore, due to high toxicity, only a fraction of patients actually completed the intended trial:
Only 27 out of 245 AZT subjects completed the full 24 weeks! One in the AZT group of 245 died in this period, but how many more in the AZT group would have died if they had been able to complete the full 24 week chemotherapy trial?
These were crazy times. These patients were very ill and very worried. It was a full scale terror panic. It was obvious who was on placebo and who wasn't, and from what I have read, placebo patients were swapping and trading pills with AZT patients who couldn't finish. It was many things, but not double-blind.
Here is what would be required to prove with > 99% certainty that HIV is the sole cause of AIDS:
Take a random sample of perfectly healthy test subjects. Now inject half of them with HIV and half with a placebo, and follow their health over the long term. That is about the only test that could get you 99% accuracy, and it is obviously not ethical.
So, instead we have to make due with what we have.
And again, showing that AZT improves long-term mortality - which the AZT trial clearly did not show, only shows that AZT improves mortality in sick AIDS patients. It doesn't tell you much else about HIV as a theory.
It's important that we agree on that subpoint - for it has nothing to do with the level of evidence.
There are many, many things that could improve mortality in sick AIDS patients. Stoss therapy, better diet, more sex, aspirin, etc etc. Do you think that proving a mortality decrease correlation in any of these categories would 'prove' they are the true cause of AIDS?
It also makes sense for the common sense model that reducing AZT doses down from outright lethal to mildly poisonous but tolerable 'works better'.
jacob_cannell:
There have been documented cases of accidental HIV infection of lab workers and dental patients that are not too terribly far from such a controlled experiment. See: S.J. O'Brien and J.J. Goedert, "HIV causes AIDS: Koch's postulates fulfilled," Current Opinion in Immunology, Vol. 8, Issue 5, October 1996, pp. 613-618.
UPDATE: Ungated link to the paper here.
The article (listed as a "guest editorial", I note for completeness) has the following citations in the relevant section:
52. Weiss SH, Goedert JJ, Gartner S, Popovic M, Waters D, Markham P, Veronese FD, Gall MH, Barkley WE, Gibbons J et al.: Risk of human immunodeflciency virus (HIV-1) infection among laboratory workers. Science 1988, 239:68-71.
53. Reitz MS Jr, Hall L, Robert-Guroff M, Lautenberger J, Hahn BH, Shaw GM, Kong LI, Weiss SH, Waters D, Gallo RC, Blattner W: Viral variability and serum antibody response in a laboratory worker infected with HIV-1 (HTLV-IIIB). AIDS Res Hum Retroviruses 1994, 10:1143-1155.
54. Guo HG, Waters D, Hall L, Louie A, Popovic M, Blattner W, Streicher H, Gallo RC, Chermann JC, Reitz MS: Nucleotide sequence analysis of the original isolate of HIV-1. Nature 1991, 349:745-746.
55. Wain-Hobson S, Vartanian JP, Henry M, Chenciner N, Cheynier R, Delassus S, Martins LP, Sala M, Nugeyre MT, Guetard D et al.: LAV revisited: origins of the early HIV-t isolates from Institut Pasteur. Science 1991, 252:961-965.
56. Wolinsky SM, Wike CM, Korber BTM, Hutto C, Parks WP, Rosenblum LL, Kunstman KJ, Furtado MR, Munoz JL: Selective transmission of human immunodeficiency virus type-1 variants from mothers to infants. Science 1992, 255:1134-1137.
57. Morbidity Mortality Weekly Report of the Center for Disease Control: Revised classification system for HIV infection and expanded surveillance case definition for AIDS among adolescents and adults (1993). 1992:1-19.
I'm not a skeptic, but I am a bit surprised that three infected lab workers is considered evidence worth mentioning. I'm accustomed to seeing clinical studies with fewer than 100 patients treated as merely suggestive, and several hundred or even thousands of patients necessary to convince regulatory authorities that there is a real phenomenon. So when I read that "three laboratory workers...became infected", it strikes me as anecdotal. Of course you take what you can get, but still, it seems a small group.
My experience is with pharmaceuticals, which could explain the difference. But still, there's a difference to be explained.
On the upside, if three is worth mentioning, then maybe one is worth mentioning, which would mean that Seth Roberts's self-experimentation may be worthwhile.
Ok, so I have finished reading O'Brien and JJ Goedert. I think the accidental lab worker cases probably have low utility in distinguishing between pathologic HIV and passenger HIV theories, but the animal SIV studies potentially fulfill the ideal experiment design. If animals injected with pure close SIV analogs to HIV develop AIDS-like illness, that is about as good as evidence as one could hope for.
For the lab worker infections, they say that the genomes are close to the clonal strain used in the lab, but they don't have a good probalistic model for this:
threefold more or less variation doesn't sound like much to me, and regardless even assuming they did all get infected via the lab, it doesn't mention treatment, so we don't know if they were treated with AZT or what.
I think the animal models are more interesting - as all the drug cofounding variables are eliminated and everything is controlled.
The authors discuss 3 animal models - baboons, some wierd knockout mice with human t-cell graphs, and finally SIV injected into rhesus monkeys. They spend the most time discussing the latter paper so I looked into it.
"Induction of AIDS in Rhesus Monkeys by Molecularly Cloned Simian Immunodeficiency".
In short, all 5 of the monkeys injected later become seropositive, and 50% of them progress to AIDs-like illnesses and die. Presumably some are naturally resistant.
There is a potential issue to this otherwise smoking gun, which is that it appears they had to inject whole culture of T-cells, as the virus can not be isolated directly into plasmid vectors:
But if all they had then was provirus integrated into PBL ( peripheral blood lymphocytes ), then one must wonder about the risk of graft versus host disease, and transfusion reaction in general. Basically, the foreign T-cell line can actively invade and cause all kinds of havoc. Perhaps they have controlled for that and I'm completely off, but I don't see where they mention it.
OBrien and Goodart conclude:
I haven't seen mention of 'inactivated' sivmaca239 yet in 80, but maybe it is in 83 or 84. However, if they are forced to infect live T-cells because they can't produce viable clonal plasmid, this seems to have a major confounding factor in graft vs host disease. I'd like to find a knowledge skeptic take on this - perhaps Duesberg confronts it, not sure yet.
If he doesn't confront it, then that doesn't look so good for his position.
It appears to me that you are noting different weaknesses, different alternative explanations of the results, in each experimental protocol. I imagine that could appear to happen if there were a strong publication bias for results in favor of the hypothesis (e.g. with medicinal prayer studies), but that has not been demonstrated.
From what I understand, there is strong reason to suspect such bias in the animal models, as many other animal tests were conducted previously attempting to show SIV causing AIDS, and they uniformly failed. From what I have read, the SIV injections failed to do anything in chimps. We don't know how many other rhesus monkeys were injected, but I find it highly unlikely that the five in this study (3 out of 5 of which developed immune defeciency) were the first.
That bias is interesting and it would be useful to have a metastudy covering all the animals that have been injected, but of course most naturally occuring strains of species specific virus should be expected to be harmless. So the 'bias' doesn't really tell you much and is expected either way.
I'll look to see if there is any skeptic review of the SIV injections which did succeed, because in my mind that is fairly strong evidence. If HIV analogs cause AIDS-like illness in primates when they hop species or traditional barriers, this is a good experiemental model for HIV crossing over into humans and causing illness, and is far stronger in my mind than the murky epidimelogical data with all of it's drug cofactor issues.
The lab monkeys are in a controlled environment - we know they weren't using drugs, weren't fed AZT, etc etc.
Yes, but were they treated with chemotherapy agents such as AZT which cause bone marrow and immune supression? (I am asking before I read the article)
For the controlled experiment example, it would have to be double blind the entire time. Nobody would ever know who got placebo and who didnt', and no difference in treatment regimens either way - all on the same diet, same lifestyle, etc etc. I highly doubt the accidental cases fit that profile.
I'm not sure you are allowed to demand that specific piece of evidence.
If you want absolute certainty, you need to fulfill koch's postulates, which is the medical disease variant of experimental physics, and is well grounded.
So yes, in questions of science, we do demand specific evidence for near-certain proof, but naturally when that is not possible for whatever reason, we can still update based on other evidence and reach well grounded conclusions.
First of all, you never have absolute certainty. Proof is for math and alcohol. You may also want to read the Sequences relevant to Bayesian reasoning especially about how 0 and 1 are not probabilities.
Note also that even outside a Bayesian context, Koch's postulates are a rough framework. For example, sometimes there is great difficulty growing an organism in a culture (Koch's second postulate requires this), and sometimes only a fraction of a population may be symptomatic. Even Koch was willing to treat the first postulate as a guideline rather than a hard and fast rule; he worked with multiple examples of microorganisms that showed up in some healthy people but didn't cause disease In fact we know now that this very common. Many causes of minor infections, such as staph, are present on everyone. It then takes some problem, such a wound, or disruption of the immune system to cause the person to become unhealthy. For viral examples, look at asymptomatic herpes or HPV.
Frankly, referring to Koch's postulates like this are one of the things that makes many people with medical knowledge not take the HIV-AIDS skeptics very seriously. As a general heuristic, cranks like to take old ideas and try to use them to argue against some modern result even when that idea isn't used in the current form or isn't as absolute as they make it out to be. This seems for example to occur frequently with creationists who use an oversimplified form of Mendelian genetics that seems to date prior to the work of Hardy, Weinberg, and Fisher. As a way of preventing this signal, referring to such things as Koch's work can be done, but you need to be clear that you understand the limitations it has. Otherwise, it just sets off alarm bells.
S.J. O'Brien and J.J. Goedert (1996) (the paper cited by Vladimir_M) specifically references Koch's postulates. The accidental infection of laboratory workers is only one of five items cited in reference to (I believe) #3, "The cultured microorganism should cause disease when introduced into a healthy organism."
jacob_cannell:
From what I see, O'Brien and Goedert don't report about this. However, Cohen's Science article to which I linked above provides more details about the cases of infected lab workers, claiming that two of them didn't receive any antivirals until the progress of AIDS was well underway:
http://www.sciencemag.org/feature/data/cohen/266-5191-1647a.pdf
I have seen that, but I don't take it as strong evidence of anything either way.
Clearly HIV antibodies are correlated with ill-health, poor immune function and low CD4 counts - that was established in the very beginning by Gallo et all and is the entire basis of their original claim.
But the competing hypothesis is not the null hypothesis, the competing hypothesis is that the HIV presence is a marker of some severe immune function failure, and that HIV itself is a largely harmless vertically transmitted retrovirus - like all the others. If it does become active, it is because something is already seriously wrong.
So of course if you have a lab, and you are testing lab-workers deathly afraid of contracting HIV, in either theory some may come up HIV+, and in either theory those that test positive will be ill.
This is very different than the intentional infection test you need to establish strong causation along a koch's postulate principle. I think one of the stronger flaws in current HIV theory is the chimpanzee models - they have many HIV similar retroviruses (SIV's), they are common in wild chimps, are all vertically transmitted, and don't appear to be problematic for chimps. If HIV killed chimps outright, the mainstream theory would have some more ammo.
Instead the theory is that HIV came from a chimp SIV and somehow became lethal and horizontally transmissable at the same time in humans. But from the studies of sexual transmission - it is only weakly blood transmissable. So overall, it's alot to swallow. I think it is plausible that this happened and HIV causes novel problems in humans, but it certainly has not been well demonstrated, mainly because HIV doesn't cause specific symptoms and it is extremely difficult to properly dissociate other causitive factors. As Duesberg notes, the cocaine/meth craze boomed in the 80's right as the AIDS epidemic started - they overlap perfectly.
Deusberg's theory is that drugs specifically are a major cause of the immunosupression, which I think has some absolute validity, but we should also notice that there are other causes, and some people just have poor immune health, and this has been the case for long before HIV came on the scene.
I think that, in general, viruses that jump species barriers are more lethal in their new hosts than their old ones. Selection pressure tends to make viruses that are transmitted from individual to individual less dangerous over time, not more, because a dead host can't spread the virus. So the fact that chimps tolerate SIV better than humans tolerate HIV isn't a strike against the "HIV is mutated SIV" theory.
Also, there exists a more direct counterexample: FIV, feline immunodeficiency virus, is an HIV-like virus that is commonly found in lions. It doesn't harm lions very much, but it's lethal to domestic cats, which haven't co-evolved with the virus the way lions have. (Specifically, lions compensate for the loss of T-cells to the virus by producing them in much larger numbers than other animals do.)
jacob_cannell:
According to O'Brien and Goedert, however, the strains of HIV found in these accidentally infected individuals were effectively identical to those from the source of their accidental infection, showing much less difference than is usual for strains taken from two random patients. This looks like powerful evidence against the competing hypothesis. On the other hand, it seems like there have been disputes about the validity of these identification procedures, and Duesberg and other skeptics raised some specific objections to them back then. However, this gets into technical issues that I'm definitely not competent to judge on.
(I should add that I haven't delved into the references provided by O'Brien and Goedert, which Robin has conveniently listed in his above comment, to see if their summary of the facts is accurate and complete.)
Ever since I've read in Guinea Pig Zero about test subjects who feel that they'll never be able to afford medical care and cheat on the requirements of an experiment (for example, not following dietary changes they've signed on for), I've been that little bit more dubious about drug studies.
It takes courage to voice a low but not negligible degree of doubt in a emotionally salient mainstream position. I would expect it to result in almost as much social punishment as in the case of outright denial. (Emotional backlash isn't good at math.)
More concretely, I would roughly say I am only about 70% confident that HIV is the sole cause of AIDS, or 70% confident that the mainstream theory of HIV/AIDS is solid.
I am surprised that those two confidences happen to be the same. Is it not a distinct possibility that HIV is, in fact, the sole cause of AIDS even when the mainstream theory is itself rubbish? (For example, if the theory got important details such as mechanism completely wrong.)
I like this sentence.
I tend to think of "HIV being the sole cause of AIDS" as the central tenet of the mainstream theory, but sure that could be true even if much of the details are wrong. Actually, I think many within the mainstream would admit most of the details are wrong - last I checked all the important details, such as how the retrovirus could come active after many years and damage T-cells and what not are all still hot research items.
And most of the specific results have been failures - no vaccine yet, just some drugs with a bunch of side effects which may or may not even improve mortality, etc etc.
I find hypotheses in the middle more likely overall - examples: that HIV is a mostly harmless retrovirus but in some people with (X, Y, Z cofactors) it can cause immune damage.
And I yes, I am at least mildly concerned about taking an HIV skeptic position in a public internet forum - and just thinking about the reasons for that causes me to slightly update to be more skeptical.
I find denialism in all forms simply fascinating. I wonder if you could indulge my curiosity.
You find your arguments completely convincing. Yet they are based on publicly available statistics and rather obvious and common-sense kinds of reasonings. So, I have to wonder, what do you think is wrong with the cognitive apparatus of all those medical and research professionals who believe that HIV == AIDS and is an STD?
Why don't they reach the same conclusions as you? Are they stupid? Just haven't thought of the train of thinking you use? What are your guess as to where they are all going wrong? Why none of them has realized the simple truth and shared it with colleagues?
Incidentally, I have a hypothesis as to what is wrong with your reasoning, which I will share on request, but I really want to understand how you reconcile your own certainty with the opposing certainty of people who (on paper) seem far better qualified on this subject.
I will indulge your curiosity in a moment, but I'm curious why you use the politically loaded term "denialism".
As far as I can tell, it's sole purpose is to derail rational dicussion by associating one's opponent with a morally perverse stance - specially invoking the association of Holocaust Denialism. Politics is the mind-killer. In regards to that, I have just been spectating your thread with Vladimir M, and I concur wholeheartedly with his well-written related post.
There is no rational use of that appelation, so please desist from that entire mode of thought.
Firstly, I don't think nearly as many quality researchers believe HIV == AIDS as you claim, at least not internally. The theory has gone well past the level of political mindkill and into the territory of an instituitionalied religion, where skeptics and detractors are publically shamed as evil people. I hope we can avoid that here. Actually, I think most intelligent researchers, if they could afford to be honest, would admit that HIV is the major indirect causitive factor, but this is not the same as saying HIV == AIDS. Likewise, I think most would admit that HIV is not quite an STD, not really at all.
Finally, even though I just said what I think is "wrong [with] the cognitive apparatus of all those medical and research professionals", namely that it is more an issue of politically charged public positions; I should also point out that even by the standard of your implied criteria - which seems to consist of counting up scientists for or against, it is even less clear that HIV == AIDS can be supported on that criteria. (which I do not favor as a rational criteria regardless). There are a large number of skeptics on public record for that hypothesis even considering the huge social stigma associated with adopting such a position in public. The HIV==AIDS hypothesis has far more skeptics on record than String Theory, for comparison.
But regardless, counting scientists is not a good rational criteria.
If you want to get into a discussion about rationality and reasoning in highly politicized issues such as this, that is an interesting side topic. But otherwise don't stoop to the moral high ground of politicized orthodoxy - just provide your hypothesis.
This is Less Wrong, not Mere Mainstream.
Actually, though you may not believe me, Holocaust denialism hadn't even occurred to me. In the portion of the blogosphere that I follow, it applies most frequently to AGW denialism, with the AIDS denialists second, evolution denialists third, and the anti-vaccination crowd getting an honorable mention.
The wikipedia article on HIV that you reference has a section entitled "AIDS Denialism".
But now that you mention it, why do you consider Holocaust denialism morally perverse? I thought that questioning PC conventional wisdom was considered a Good Thing here.
No, I don't believe I do. I wouldn't want to further offend you.
My hypothesis is pretty simple. You are using the wrong numbers.
When I Googled, the first few hits I found suggested 0.3% per coital act as a lower bound on heterosexual transmissibility with the risks increasing by 1-2 orders of magnitude in case of genital ulcers and/or high viral loads. I don't think that it is particularly difficult to understand the epidemic spreading in Africa as an STD when these higher numbers are used.
I did look at this study providing smaller numbers and this paper critiquing it, as well as this abstract mentioned in the wikipedia article. It was pretty clear to me that the kinds of low numbers you were using to argue against HIV being an STD are actually based on monogamous couples who are regularly examined by physicians and have been instructed in the use of condoms to prevent transmission. Those numbers don't apply to the most common cases of transmission, in which ulcers and other factors make transmission much more likely.
That is the hypothesis I was going to offer. When you suggested that you only had a 20-30% level of doubt of the orthodox position, I simply had no idea that it was such a strong and assured 30%.
Please see my response below concerning the perjorative "Denialist", and why such perjoratives have no place here.
You haven't offended me.
The google hits you mention are just websites, not research papers - not relevant. There is no reason apriori to view the ~0.3% per coital act transmission rate as a lower bound, it could just as easily be an upper bound. You need to show considerably more evidence for that point.
The data on wikipedia comes from the official data from the CDC1, which in turn comes from a compilation of numerous studies. I take that to be the 'best' data from the majoritive position, and overrides any other lesser studies for a variety of reasons.
This may be 'clear to you', but the Wikipedia data comes from a large CDC sponsored review considering aggregates of other studies to get overall measures of transmission. This is the orthodox data! I highly doubt it has the simple methodological errors you claim. And even if you did prove that it does have those errors, then you are only helping the skeptic case - by showing methodological errors in the orthodox position, and the next set of data should then come from the heterodox camp.
If I can take the liberty of butting in...
Here's the table of data I believe you're referring to:
It cites references 76, 77 & 79, all of which turn out to be publicly available online. That's good, because now I can check the validity of Perplexed's claim that the studies backing your CDC data used samples of relatively healthy, well-off people who lack some risk factors.
I took ref. 76 first. It reports data from the "European Study Group on Heterosexual Transmission of HIV", which recruited 563 HIV+ people, and their opposite-sex partners, from clinics and other health centres in 9 European countries. (Potential sampling bias no. 1: HIV+ people in European countries are more likely to have access to adequate healthcare than many Africans and Americans.) It also says:
That fits Perplexed's claim that the study's couples were "regularly examined by physicians" and "instructed in the use of condoms to prevent transmission". It's not clear whether they were "monogamous", but the study did exclude "[c]ontacts reporting other risks of HIV infection and those with other heterosexual partners with major risks for HIV infection". I also see another sampling bias: if the man & the woman in a couple disagreed on their questionnaires, that couple was blocked from the study. I would think that such couples have a higher risk of transmitting HIV (as I'd guess they're more likely to be couples where someone's lying about their sexual history); if so, the study's more likely to lowball HIV transmission risks.
What about refs. 77 & 79? Where did their data came from? It's pretty clear that they used the same European Study Group data. From 77:
And 79:
To be explicit: the three studies you're citing (via the CDC) are based on one data set, and Perplexed's characterization of that data is essentially accurate. That adds credence to his claim that the transmission rates you're citing don't represent HIV transmission rates in other situations.
Incidentally, tables 2 & 3 of ref. 76 suggest that HIV transmission risk is not only associated with type of sex act, but also with the HIV+ partner's infection stage, especially (I did not expect this!) for male partners of HIV+ women. Maybe more evidence that there's more to HIV transmission risk than who's putting which organ in which orifice?
By all means. While you were writing this I was reading 76 and writing my own reply.
Ah I hope he wasn't claiming this, because they certainly were anything but healthy, with around 20% being hardcore IV drug users, 23% transfusion recipients, 10% hemophiliacs, and overall high rates of STD's.
I noticed the discrepancy about sexual history part but I didn't see how to factor it. They are relying on self-reporting to make any of these links.
Err, no, because his characterization is based on the idea that these couples were using condoms frequently, but the study specifically shows that is not the case - see my reply to Perplexed.
If you want to characterize this study, fine, but don't pretend that these are "regular couples regularly using condoms" - that is not what the study claims.
And finally this is the orthodox data. I mean if you want to reject ... ok .. and then we move to searching for other data which supports our relative positions . . . to the extent we have positions.
Perhaps it would be best to agree what the ideal study would be and precommit to that ideal in a sense? And then we could look for other studies that may be closer. Of course in the real world they will rarely be clear cut.
I quite agree that they weren't healthy in absolute terms; I just meant that they were relatively healthy for people with HIV. Compared to HIV+ people in much of the rest of the world, especially sub-Saharan Africa, I'd expect this European study's subjects to have (on average) better nourishment, better healthcare, stronger immune systems, less exposure to infectious disease, much less exposure to parasites, and a far lower rate of promiscuity & prostitution. I should've been more explicit that that was the sort of comparison I had in mind.
Looking at your reply, I think we disagree about whether or not Perplexed was hinting that the couples were consistently using condoms. I didn't think Perplexed was implying anything more than that most cases of HIV transmission involve people who weren't regularly reminded to use condoms. So I took his statement at face value, in which case it's surely true (unless European doctors have come up with a way of counselling couples "about the risk of HIV infection and safer sex practices" that doesn't involve advising condom use!).
I don't believe Perplexed or I are pretending that these are normal couples who continually use condoms. I think it goes without saying that these weren't "regular couples" — after all, "regular couples" don't visit hospitals and clinics to get HIV infections checked out. Whom are you quoting?
I reject your interpretation of the data, rather than the data. The study probably gives a fair idea of transmission risks among faithful Western couples living in the 1980s/90s who regularly see doctors...but for that reason (among others) it's likely to underestimate transmission risks in other demographics.
I think you're probably right on that point. I suspect that looking at per-sex act transmission risks isn't going to be very enlightening about whether or not HIV causes AIDS. It would be better to have data from
(each bullet point getting more restrictive). I don't know if there are such data, but it would get us closer to the original question than big-picture arguments about transmission risks.
I generally agree with most of this except perhaps the last part - I doubt that promiscuity and prostitution varies that much from 3rd and 1st world.
I think he was implying that the reminders led to condom use, but this was in fact not the case according to the study itself (possibly because they excluded many of the condom users, some aspects of the study's design are not all that clear to me).
Not quoting, just paraphrasing. He was implying that the heterosexual couples receiving counseling were not indicative of a typical HIV hetero population, but the study designers of course realized that and were at least attempting to gather representative data.
Ok, whether HIV causes AIDS is a larger topic. My original point was just about the orthodox claim that HIV is sexually transmitted, which I believe is rather obviously bogus according to the orthodox's own data. I hope you can see how the orthodox could go wrong there and some of the political factors at work.
As to the larger HIV == AIDS issue, I largely agree with your ideal data criteria, but one potential issue is whether we are comparing HIV to the null hypothesis or to some other hypothesis. I don't think any reasonable skeptic claims that HIV is not at least correlated with AIDS - Richard Gallo may be many things, but he is probably not stupid nor a charlatan.
So it would be better to compare the orthodox HIV hypothesis vs the Drug/Lifestyle Hypothesis (which predated HIV). Some immediate concerns are that one must take care to then define AIDS reasonably without circular reference to HIV (which precludes some data)
The next concern would be that either way, previously healthy people don't get HIV or AIDS, in reality or according to either theory. The risk groups are all unhealthy in various ways.
All that being said, Duesberg does indeed provide data very close to what you are proposing. There are some groups of HIV+ who, for whatever reason, have refused mainstream treatment. There aren't many such people, but he cites a study about a group in Germany - they are called long term non-progressors (which is kind of funny when you think about it - AIDS is progress?).
Anyway, this study is small, only 30-40 people IIRMC, but it is long lasting and only a handful have died. He calculates their death rate as measurably lower than the death rate of HIV+ treated patients, and uses this as a major piece of evidence.
here .. that part is on page 402 (it's a large journal excerpt or something - not really that long)
An interesting read overall, would like to read a good rebuttal.
Quite possibly, but note that I was comparing the subjects in the European study with the rest of the world, rather than all of the 1st world. The study's screening procedures probably cut out quite a few people who have a lot of sex.
I think I do. (I hope I do!) Still, I do see the orthodox belief that HIV can be transmitted sexually as being compatible with the CDC numbers. The CDC transmission rates are surely below the average real-world HIV transmission rate (due to the nature of the European study sample), and there are features of the data that are easier to explain if we acknowledge that HIV's sexually transmitted: the condom-using couples had lower HIV transmission rates than the non-condom users, men who (claimed to have) had period sex with HIV+ women were at higher risk of transmission than men who (claimed to have) avoided period sex, and so forth. So I continue to disagree that the HIV-is-an-STI view is "obviously bogus according to the orthodox's own data".
It might even preclude the Duesberg/Koehnlein data you link. Page 402 says the study's of "AIDS patients", and it's not clear from the immediate context what definition of "AIDS" was used for the study. All 36 of the patients (you were right about the study's size!) are listed as being HIV+, which suggests to me that the AIDS diagnoses were made (at least partly) based on HIV+ status, as is standard practice.
I would have thought that healthy people are capable of getting HIV? Getting pricked with an HIV-infected needle works, as does sexual transmission. A lot of people in high-risk groups are unhealthy, of course, but there are surely unlucky people who get HIV without prior major illness.
I looked up long-term nonprogressors on Wikipedia (not the most reliable source, but anyway), and it looks like many long-term non-progressors have genetic traits that make them better able to resist HIV, or have a weaker form of HIV.
I also saw that the group in Germany Duesberg's talking about all come from Kiel, a relatively small city (population about 240,000). I'm wondering whether the people living there could be more likely to have HIV-resistant genes. Or maybe the form of HIV circulating there is less virulent? (Or both?)
I should say upfront that there's no way I'm rebutting all 30 pages of the article (I really doubt the game's worth the candle), but I can comment a bit more on the little German study.
The first thing that jumps out at me is the lack of detail. I'm curious about how Koehnlein discovered the subjects for the study (personal contact?) and whether they included all of the eligible patients they found. I also wonder how Koehnlein followed up patients, and how regularly. How rigorously do they track the patients to make sure they're staying off HIV drugs & illicit drugs? How often do they check on them to see whether they're still alive? When was the last follow-up? The article's dated mid-2003, but it looks like Koehnlein's added no new subjects to the study since 2000, and the latest update is from 2001 (when the 3 dead patients died). It would be very interesting to know how many of the remaining 33 patients are still alive 7-9 years on. I looked for later publications by Koehnlein on his study and didn't find any (which is a bit of a red flag in itself).
I'm also not sure that some of these "AIDS patients" had AIDS in the first place. This looks like the CDC's definition of AIDS: typically, you have to HIV, and either a CD4 count below 200 ("or a CD4+ T-cell percentage of total lymphocytes of less than 15%") or one of a list of AIDS-defining illnesses. (You might dispute using HIV+ status as part of the definition of AIDS, but it makes no difference with Koehnlein's subjects because they all had HIV.) The table doesn't offer enough information about CD4 T-cell percentages to check whether they're less than 15%, but it does give CD4 counts and list what appear to be the patients' "initial AIDS-indicator symptoms".
So I look at case 1. His CD4 count is 256. His initial symptom was "Herpes zoster". The Wikipedia/CDC list of AIDS-defining diseases does not include herpes zoster, only chronic ulcers due to herpes simplex. It's not clear that the patient actually had AIDS when Koehnlein included him in the study. Moving on to case 2, she's marked as asymptomatic and no CD4 count is given. What was the basis for her AIDS diagnosis?
I sorted the 36 cases into 3 groups: a "questionable diagnosis" group (patient was asymptomatic/had symptoms clearly not on the AIDS-defining illness list, and their CD4 count was explicitly given as >200), a "definite AIDS" group (patient had an illness clearly on the AIDS-defining list, and/or a CD4 count explicitly <200), and an "unsure" group (cases that didn't fit the other two groups). I put cases 1, 8, 9, 17, 19, 20, 23, 24, 25, 27 & 35 in the "questionable" group; cases 3, 4, 6, 12, 13, 21, 30, 31, 32 & 36 in the "definite AIDS" group; and cases 2, 5, 7, 10, 11, 14 (they had pneumonia, but only recurrent pneumonia and/or PJP is AIDS-defining), 15, 16 (they had toxoplasmosis, but it's not said whether it was in the brain), 18, 22, 26, 28, 29, 33 & 34 in the "unsure" group.
So the Koehnlein's study's effective sample size & death rate seems to be sensitive to how rigorously one defines AIDS. As I see it, only 10 of the 36 cases unambiguously have AIDS, and counting deaths in that subgroup leads to a death rate of 20% as opposed to "only 8%". I think Koehnlein's data are interesting, but there are a multitude of reasons not to take Duesberg's 8% vs. 63% comparison at face value.
Well the best cure for doubt is to actually read the papers referenced. For example, following the links from your reference to the abstract of the actual paper which generated the numbers brought me to this abstract. I think you should read it.
The issue isn't methodological errors in the studies - the studies clearly describe the methodologies used and their limits. The issue is trying to use the numbers in ways that they are not designed to be used. It is not the orthodox folks that are doing that. It is you that is doing that.
Ah, so do the numbers come with little instruction manuals that say "CAN ONLY BE USED TO SUPPORT ORTHODOX POSITION"? Haha sorry, couldn't resist.
OK, I'm game, I will now look into the CDC studies, but let's be clear on the trace ..
it starts with the wikipedia chart which has the ref note 80 linked here, which points to this, which in turn lists refs 76, 77, and 79 for P/V sex, which are (in order):
76: Comparison of female to male and male to female transmission of HIV in 563 stable couples
77: Reducing the risk of sexual HIV transmission: quantifying the per-act risk for HIV on the basis of choice of partner, sex act, and condom use
79: European Study Group on Heterosexual Transmission of HIV. Heterosexual transmission of HIV: variability of infectivity throughout the course of infection
I'll comment more after I have read these.
You will find that #77, the Varghese et al paper, can be found online by Googling the title, and that it gets its 0.1% number for heterosexual transmission from the paper whose abstract I recommended.
I'm pretty sure you will find that all of these papers involve monogamous couples. If you give it some thought, you will realize that there is just about no other way to come up with a solid empirically-based number. And I again urge you to read that abstract - particularly the bottom third.
Haha ok this is kinda funny, but the abstract you linked to which is the source of the data in Varghese(77), is just 76! - the couple comparison from the European Study Group which I linked to and have been trying to parse. 79 appears to be another chapter from that same book, but I haven't looked at it yet.
So before we get into 76 - the source of the stat you don't like in 77, I need to backup and remember your original claim about the data:
Your implied point appears to be that couples in this study use condoms frequently. Surprisingly, this is not the case - only a surprisingly small number of couples reported consistent condom use (out of 500+),
Contraceptive behaviour:
No regular contraceptive 12 (10/86) 20 (43/212) Oral contraceptive 18 (7/40) 23 (26/114) Intrauterine device 10 (1/10) 28 (7/25) Condom* 0(0/11) 18 (6/33)
These people were using other methods of birth control more than condoms.
and they further removed consistent condom users from the data:
No, it is not. The reference leading to the abstract is the absolute risk described in the first paragraph of page 40 of Varghese. It is reference 28 of Varghese.
You are apparently following the references (21) appearing in Table 1 of Varghese. But these are relative risks (relative to felatio). Not at all what I meant.
My point about condom use came from an earlier reference that I had supplied which discusses a study that took place in Uganda in 2005. And I didn't say that they used condoms frequently, I said that they were monogamous couples who got regular medical inspections and had been counseled regarding condoms. And in this study, as I recall, there was no exclusion of condom users.
It didn't occur to me either, and seemed strange. That word does have strong negative connotations in my mind, but only because I associate it with stupid people denying true things and refusing to update on evidence. I thought the comment that referred to was incorrect, but it seemed more like honest confusion of the sort that clarification would dispel than denialism.
Some history then of exactly why the word conjures strong negative correlations is in order.
Look at the wikipedia entry for "denialism". It originates with holocaust denialism, was then applied to skeptics of HIV==AIDS, and then later to other areas.
Peter Duesberg, the leading HIV==AIDS skeptic, is a German of non-Jewish descent raised in Nazi-era Germany, so it's use against him and his followers adds extra moral angst. It is just about the deepest insulting connotation one can use. It is a signal of stooping to the ultimate low, that, in running out of any remaining rational argument, one must invoke deep moral revulsion to stigmatize one's opponent.
In my view, the term is a serious Crime of Irrationality, it is an empty ad-hominem and should be seen as a sign of great failure when one stoops to using it as a name-calling tactic against one's opponents.
That being said, I don't think Perplexed has this view, and that wasn't his intention. I am just giving background on why the word should not be used here.
Those who don't subscribe to HIV==AIDS, should just be called skeptics.
Do we call proponents of quantum loop gravity String Theory Denialists? It's ridiculous.
Should we call those who subscribe to HIV==AIDS to be Inquisitors, Mcaurthy-ists, or Witch-hunters?
I do.
Oh please. Stop trying to pretend you have the rationalist high ground here. You don't.
This is a truly impressive bit of sophistry. You have succeeded in phrasing your objection in a manner such that a casual observer, unfamiliar with the topic under discussion, would think that you were being completely sincerely intellectually curious, while at the same time employing a coded epithet unmistakable to those already inclined to agree with you. This is a very common tactic, but I have rarely seen it done so skillfully. Bravo sir!
Now leave and go do it someplace else. This is lesswrong, not realclimate
Mr Hanson on "asexual" AIDS transmission: "Africa HIV: Perverts or Bad Med?".
As I say in my comment there, it looks as though there are probably good reasons why this is not a very common perspective.
Perhaps vulnerability to transmission is partially dependent on prior immune health. That would predict faster spread where health-in-general is worst, ie Africa, as observed, and also explain the discrepancy between prevalence and observed traqnsmission rates. I also recall reading an article about a widely afflicted demographic in the US (a particular subset of gays in a particular city - I don't recall which one), which suggested that they had already weakened their immune systems with drugs and sleep deprivation.
The other possibilities are that the transmission rate you quoted is wrong for some reason, or that the sexual transmission aspect has been overstated, and most transmission is through reused needles and other blood-borne vectors.
Note that spreading the idea that the transmission rate of AIDS is low has negative utility, regardless of whether it's true or not, since it would encourage dangerous behavior.
This is untrue. Consider a similar claim: "spreading the idea that very few passengers on planes are killed by terrorists has negative utility, regardless of whether it is true or not, since it would encourage dangerous behavior."
Informing people of the true risks of any activity will not in general have negative utility. If you believe a particular case is an exception you need to explain in detail why you believe this to be so.
In the case of infectious diseases, there are large unpriced negative externalities involved. Everyone doing what is individually rational, given true beliefs about transmission rates, is likely not socially optimal, because the expected individual cost of a risky action is less than the expected social cost. Giving people false beliefs about transmission rates can improve social welfare by shifting the expected individual cost closer to the expected social cost.
Are you talking about free rider problems with health care costs under a partly or fully socialized health care system or something else? STDs seem to be less of a problem than more easily transmitted diseases like flu for most negative externalities I can think of.
And also, if you take some risky action that increases your chances of get infected, that also increases the chances of everyone else getting infected (causally, via yourself getting infected and then infecting others).
I'm not sure I get your point here. Whether it's more or less of a problem doesn't seem relevant to the original claim that spawned this subthread.
It's relevant to using your negative externality argument to support the original claim. To be consistent you would have to argue that we should make even more effort to avoid spreading the idea that airborne diseases like flu have low transmission rates (if true) than the idea that STDs have low transmission rates. Are you advocating a general policy of deliberately misleading people about the risks of various activities in an effort to correct for negative externalities? I'm pretty sure more efficient and robust approaches could be found.
It would be consistent with Wei Dai's claim just to argue that we should make an effort to not reveal how low the transmission rate of influenza is among people who don't wash their hands; we know that hand-washing is a large factor in transmission, but actual transmission rate numbers are still low enough to fail to convince people to wash their hands.
From a brief study of those particular numbers (I worked on a team modeling the spread of H1N1), I feel like we already mislead the public about the numbers themselves by being truthful as to the societal benefits and somewhat optimistic about the individual benefits of hand washing. If you believe more robust methods are more efficient, by all means, advocate for them, but I'm reasonably happy with the current situation.
From another perspective, blood-borne pathogens are particularly worth focusing on because they are easier to control. If we could encourage the entire population of the world to behave safely (not reuse needles, use condoms for sex, etc.), it would be a fairly minor change for individuals, but could eradicate or nearly eliminate HIV over time. With the flu, safe behavior will limit the damage of seasonal infections, but it's not realistic to actually eliminate the virus. Thus, over the long term, I think the negative externalities of HIV might outweigh those of influenza.
I think government policy makers and public health authorities already use a variety of approaches to reduce negative externalities related to infectious diseases, including subtle misinformation, such as making efforts to correct people's beliefs about transmission rates when they are too low, but not when they are too high (anything really obvious wouldn't work in a free society like ours). But it seems clear that large negative externalities still exist. What other approaches do you have in mind, and why haven't they thought of it already?
I think we're starting from quite different assumptions about how society works. I don't believe that government policy makers or public health authorities are very rational. Even to the extent that they are rational, I don't believe that their incentives are such as to reliably lead them to decisions that maximize utility by the kind of utilitarian calculus you seem to be assuming. So to the extent that we agree negative externalities exist (and I suspect we differ a fair bit on what they are and to what extent they exist) I have very little expectation that government policy makers or public health authorities will tend to take actions that minimize them.
What did you mean when you said "I'm pretty sure more efficient and robust approaches could be found"? You're not offering any concrete ideas yourself, and apparently you weren't thinking of government health authorities when you wrote that, so who is supposed to find and apply these approaches?
I think you're on to something, but wouldn't that cause officials to overstate transmission rates rather than understate them?
What is especially strange to me is that the government pushed a fear campaign for HIV and promoted as a dangerous STD for the mainstream hetero community, but neglected to double-check their official statistics, which rather clearly destroy the STD theory. Perhaps it's just an honest mistake, but I don't think so. From what I have read, they have spent time trying to get honest statistics. So they overpromoted the STD message, regardless of the actual statistics.
Regardless of what HIV actually does or is, public campaigns to reduce needle sharing and reduce unprotected sex are probably net public goods.
However, on the other hand, if AIDS is really caused by drug toxicity, then at least some people are actively being harmed by spending energy in the wrong protections.
But I agree with your central point, and it applies to vaccines especially - they don't really have much of an individual benefit, but if enough people can be convinced to vaccinate, the entire epidemic can be curtailed or completely avoided.
That needs some clarification. Most people cannot distguish between a risk being somewhat low, and it being extremely low, so we need to be careful about the transition from numbers to qualitative divisions. The risks of being killed in a plane crash are so low that unless you're a pilot, you should ignore them; and overestimating the risks of flying would cause too much driving, which is more dangerous. In the case of AIDS, the probability of transmission may be "low", but none of the numbers given are so low that they would justify skipping any of the common safety precautions, so we shouldn't describe the probabilities involved as low in the presence of people who can't do the utility computations themselves.
Topical.
So as an addendum to this, I found this blog which I am now reading as it has an updated view from the HIV skeptic position. Here is a post analyzing a recent study showing that cocaine can cause AIDS
CONCLUSION: Use of crack cocaine independently predicts AIDS-related mortality, immunologic and virologic markers of HIV-1 disease progression, and development of AIDS-defining illnesses among women
The 1st commenter had an inside view which I thought was especially interesting:
This certainly supports my eyewitness accounts of back in 1987 when several friends and acquaintances consciously or subconsciously decided that an HIV positive diagnosis surely meant death in 2 to 5 years, which led them onto severe crack and cocaine binges up until they were finally put on AZT monotherapy. Sad to say what the results were. Now they’re all part of the statistics. Can I say self-fulfilling prophecy?
Cocaine is a drug that a) can damage the immune system and b) reduce appetite. It isn't at all unreasonable that HIV positive individuals who were heavy cocaine users would therefore progress to full AIDS faster than others. Note also that a 2-5 timespan isn't that far off from the timespan one would expect from HIV infection to emergence of AIDS given no treatment. Note that the study authors don't seem to think that this is at all unusual and nowhere do they claim that the use of crack cocaine was somehow causing AIDS.
Sure, but it makes it more difficult to dissociate what the cocaine and virus are doing independent of each other, ie it makes it difficult to tease out the cause and effect from the correlation.
Right, but that makes it just weak evidence. So it isn't very useful for the claim that cocaine somehow causes AIDS.
Well not quite, because cocaine was causing AIDs-like symptoms before HIV was presumed to be around, even if the great rise of cocaine use in the 80's in the west happens to correspond exactly with the rise of AIDS.
What's your source for this? Looking at the cocaine statistics and AIDS statistics myself, I'm not seeing this correspondence. What I do see is that cocaine use dropped to a fraction of its peak level by 1990, while AIDS kept rising.
Just go down to the graph in your first link and look at the emergency room drug mentions and see the cocaine serge - it does indeed correspond to the AIDS epidemic. Deusberg's 2003 paper has more on this, but it's in the data you linked. From the emergency room data it looks like cocaine use was still growing up to 2001, but my point was with the rise. AIDS peaked in the mid 90's from your data link.
This much at least is something that should be relatively easy to confirm to a reasonable level of satisfaction. It would seem to require only a microscope, as syringe and a sufficient sample of people with AIDS. Has anybody ever founds someone with AIDS who did not have HIV? If not is that because nobody has bothered to take a close look? If so then I would certainly support your questioning of the standard of research supporting the mainstream position.
According to skeptics, yes, in all but name. The standard skeptical argument is that AIDS, as it is currently defined, includes HIV+ as a necessary diagnostic criterion, and that this is a circular definition: if someone presents with all the symptoms of AIDS, but tests HIV-, then they are defined to not have AIDS. This means that 100% of diagnosed AIDS patients will be HIV+, just by definition, not due to a meaningful correlation.
The skeptical position here is that you can't actually see a virus with an optical microscope (which I believe is true), and "HIV tests" are actually just testing for HIV antibodies (or substances alleged to be HIV antibodies), not HIV itself.
I'm not endorsing these positions, just passing them along, btw.
Thankyou. I'm not familiar with the subject and wanted the information.
Yes, unless one defines AIDS as a collection of symptoms plus HIV. I forget the name, but any definition of AIDS which does not include HIV has some HIV-.
Now on the other hand, AIDS is a syndrome of immune supression, not a disease, so there of course could be other things that cause a similar syndrome.
If you are interested in venturing down that rabbit hole, read a little Duesberg:
(warning: reading his papers may result in general increased skepticism about the medical establishment)
http://www.duesberg.com/papers/chemical-bases.html
Now that is a familiar mistake - and a negligence that does real damage. I'm more familiar with the mental side of the medical establishment so have seen, for example, ADD symptoms lumped together and medicated presuming there is only one distinct etiology. Looking at a brain scan could tell them the difference easily enough.
That would be surprising - purely because my existing skepticism is already significant. All the more so after I spent some time involved in medical research myself. Scary stuff. "Hang on, wait. you want me to do what with the data?"