Discussions on the Challenge
Dean
Our publication of the CDC numbers and the inferences we have drawn from them has sparked an enormous amount of commentary, most of it good and healthy. You can read responses from other bloggers here, here, here, here, here, here, here, here, here, here, here, here, here, here, here, and here. Our own discussion (thread here) has also generated, I think, some particularly worthwhile reading no matter where you come down on this question.
But of all the discussions on all the blogs so far, I believe that commenter Dan Fendel has given the most complete and concise response:
Those of you who are accusing Dr. Bialy of trying to use misleading information have only yourselves to blame. It's pretty obvious from the shape of his first graph that this must represent new cases. The total couldn't drop like that unless AIDS patients were dropping like flies, which wasn't the case in the 1990's. Nowhere did he say that this graph represented total cases. That wouldn't make sense.
You misunderstood him, and missed the point. If the number of people with the virus stays constant, then although the number of people getting sick might go down due to drugs, there's no explanation for why it went up in the first place. It's not just that they gave the name AIDS to a previously un-named disease. The AIDS-identified diseases - such as Kaposi's sarcoma and pneumocystis - were known but extremely rare. Suddenly they became more common, simultaneous with a major drug-use life-style change. Try reading Peter Duesberg's June 2003 paper. "The Chemical bases of the various AIDS epidemics: recreational drugs, anti-viral chemotherapy, and malnutrition," from which the graphs are taken. It's all laid out clearly.
As I have said, I will publish, unedited, any response from any public health official, epidemiologist, or professional researcher who wishes to refute the data presented in Dr. Bialy's article, or the implications we have drawn from same.
All Related Posts (on one page) | Some Related Posts:









As for the drugs and lifestyle argument, that theory would/could be complementary to the rise of AIDS. And there could be a compromise point: what if HIV DOES cause AIDS (though other things can as well), or is a co-factor, and the rise in illegal drug use, etc., spurs the process?
Again, I don't have a judgment on this, but the latency of the virus seems to speak to the initial spike, from my limited interpretation. Just throwing up challenges.
Also, there have been a number of challenges to there being 1,000,000 HIV infected persons in 1985 that have gone unanswered. As has been mentioned by others,that number is a GUESS, and is NOT based on data. How could it be, when HIV was discovered in 1984?
Good thing I really like your blog, because this is exactly the sort of thing i usually ignore. i'm pragmatic; i let the scientists figure out how, I'm ok that AIDS is being successfully combatted. now, to the discussion at hand.
To me, the strongest piece of evidence and one that is virtually impossible to overcome despite this data is that aids is being successfully treated through the treatment of hiv.
if these graphs are true, and let's assume they are, then perhaps something else is going on. i don't know what that is. but hiv and aids are linked; that much is a fact.
part of the problem is the shortness of the sample in the second graph. it's only 15 years. aids has a long latency period. the assumption, if i understand you correctly, is that there's always been a million people with hiv and suddenly aids spiked up and down and something else must have caused it.
problem is, we don't know that from the data. the sample period is too short. and even if we did have the data, that wouldn't clear hiv, especially in light of the fact of successful treatment. no, hiv is guilty of being a murdering little shit, we have the proof. now, can hiv kill without an accomplice? that we don't know.
the straightness of that line in the second chart is odd, particular considering that the U.S. population has increased during that time. one million folks are infected by hiv in the US? how many are being treated right now? are mostly the same folks?
we may be looking at a second factor, let's call it factor x. i say we lean on his pal hiv and see if he'll talk.
I can see why very few people are bothering to continue a serious discussion with you and Mr. Bialy. If my opponents in a debate brought to the table an attitude of "well, yeah, I may be lying and misrepresenting the data I claim supports my arguments, but you're just a goddamned idiot if you believed what I was saying, lol!" I certainly wouldn't stick around very long to hear what else they had to say.
"It's pretty obvious from the shape of his first graph that this must represent new cases."
Well excuse me for not being an epidemiologist and knowing these things that are just plain obvious. Yes, now that I know what I know it's pretty "obvious". It's obvious in the sense that if you know what to look for, it's clear. But it's not "obvious" in the sense that any idiot should be able to see it.
Forgive me for being a little miffed, but I don't think that an appropriate response to this discussion was to insult your readers.
There is NO WAY to have a meaningful discussion about a portion of a graph that is based on an estimate and doesn't include all the data.
Furthermore, it's irresponsible to discount the change in AIDS diagnosis criteria that is responsible for at least a portion of the cases that make up the steep portion of the spike.
And Dan, I did read the Duesberg paper. I read it before you did. His data are 1) patently false as presented(mislabeled graphs, as discussed here) and 2) intentionally misleading (see the table of data wrt drug use and HIV, and peruse the actual papers he references).
There's a reason this work isn't being published in Nature or JAMA. It couldn't pass the editorial and peer review standards. And that's no conspiracy.
I find this to be awfully compelling, myself. You've got studies that control for all the relevant factors, with the only primary variable being the presence of HIV. The babies with HIV get AIDS, the babies without don't.
I'm on your side, but I suspect the answer to your question would be, "Because the HIV+ babies were receiving drug treatment for their presumed viral illness, while the HIV- babies were not." One thing that those who disagree with the "HIV is a primary cause of AIDS" hypothesis contend is that the very drugs used to "treat" AIDS are in fact causing it in many cases. The drugs can make a person very sick, especially the older ones (I don't think anyone disputes this). If you're treating one child and not the other, there is a difference between them other than their HIV status.
Is this addressed anywhere? Are there studies of how these drugs act in those who are HIV- that would disprove the notion that they cause AIDS?
There is certainly a correlation between HIV and AIDS. While there are some cases of AIDS (or something very similar) without HIV they are exceptionally rare. Considering how difficult it is for HIV to be transmitted it is puzzling that nearly all people who have AIDS also have HIV if HIV is not at least a partial cause for AIDS.
I have found it to be very difficult to make any reasonable determinations about the effectiveness of drug treatments of HIV/AIDS. AZT seems to be a terrible drug as it is highly toxic and effectively destroys a great deal of the body and the bodys immune system. Its widespread use greatly muddles the data on AIDS, as I see it. AZT as part of the "AIDS cocktail" may be effective, but I have not been able to find any studies that clearly demonstrate that. There are many studies that give that indication, but there have also been flaws and issues with most of them that bring question to their reliablility (patients receiving different treatments such as transfusion apart from AZT, comparisons with differing definitions of AIDS, etc).
All in all, I think that neither case is clear. There is much reason to question the HIV/AIDS Hypothesis, but there is also reason to question the Chemical/AIDS hypothesis. My concern is that one is being treated is true and the other false.
For an example of how sketchy their "drugs cause AIDS" claim is, check out my latest post at MUSC Tiger, which is in the trackbacks.
If you'll note the dates on the studies, some of them were published before the drugs were widely available.
Aaron -
The toxicity of AIDS drugs is highly overstated. As MUSC Tiger points out at http://themusctiger.com/blog/index.php?p=420, since the ready availability of AIDS treatments, people have been living LONGER with AIDS, and the number of new AIDS cases has DECLINED. If AIDS drugs CAUSED AIDS, then these numbers should be the OPPOSITE. That is, if AIDS drugs caused AIDS, we should see MORE cases of AIDS and a SHORTER lifespan among those taking the drugs. But that's not what the data shows.
Indeed, this is the problem with the whole "AIDS drugs cause AIDS" argument. AIDS came first, and the drugs came later. In the world I live in, causes precede effects, not the other way around.
Here are my thoughts on the twins studies.
First of all the assertion that "Newborn infants have no behavioral risk factors for AIDS." is not exactly true. Yes, they have no behaviors of thier own that put them at risk, but the behaviors of their mother during pregnancy can very much put them at risk.
As for the rest of it, it certaily proves correlation between HIV and AIDS, but not clearly that it is the cause. Was the infected twin infected because of a problem in his/her immune system or did HIV cause a problem in the immune system?
A big question, that I have not been able to find the answer to, is were the mothers or the HIV infected twins treated for their HIV during the study? We know that AZT damages an immune system and it's introduction would undermine the studies.
Some of those studies took place before AZT was avaiable and used for AIDS treatment.
The MUSC Tiger graph is interesting, but not compelling to me, simply because there are so many factors aside from the AIDS drugs that are involved.
It certailnly could be due to the effectiveness of AIDS drugs that the lives of AIDS patients has been lengthend.
It also could be due to more widespread desting and early diagnosis is allow us to record more of the lives of AIDS patients by traking their progress earlier, and their lives are not greatly lengthened.
It could also be related to better treatment for the diseases that kill AIDS patients, rather than due to the treatments for AIDS.
It could also be because of any number of lifestyle and/or environmental changes that are not curretly believed to be a factor in the development in AIDS.
I'm not saying any or all of the above are true or false, just that they all are plausible explinations for the data the MUSC Tiger presented.
No, it couldn't... we are talking about AIDS as a definable condition, <200 White count/ viral lode >50000. Early HIV testing would bear little impact on it.
It could also be related to better treatment for the diseases that kill AIDS patients, rather than due to the treatments for AIDS.
See, this is what happens when you only provide one graph... true it COULD be due to anything, but it's most likely due to HIV drugs.
It's most likely due to HIV drugs b/c we know clincally with HAART administration that patients see a decrease in viral lode (to almost a dormant level, though still present) and a resultant increase in white cell count.
Honestly, the case is closed.
Also I'm not avoiding the question of AZT's toxicity, I have read it in many sources and didn't realize it was disputed. I'm looking for valid sources and will present them when I find them.
"No, it couldn't... we are talking about AIDS as a definable condition, < 200 White count/ viral lode > 50000. Early HIV testing would bear little impact on it."
Testing would bear a great impact on it. If I have no symptoms and am not tested, how do you know what my T-Cell count or Viral load is? It used to be that only people who showed symptoms were being tested and therefore diagnosed as having AIDS. Now far more people are being diagnoses before they show outward symptoms. Does it not make sense that more people are being diagnosed in earlier stages then?
"It's most likely due to HIV drugs b/c we know clincally with HAART administration that patients see a decrease in viral lode (to almost a dormant level, though still present) and a resultant increase in white cell count."
Can you provide me with a source for this? I would be very interested to see proof that this is occuring.
Sorry for the poor quoting above, everytime I tried to blockquote or italicise the sections I would get an unclosed tag error, but the tages were all properly closed.
http://www.niaid.nih.gov/publications/hivaids/23.htm
Umm, simply observing AIDS patients isn't going to keep their disease down. What these graphs demonstrate is that the PROGRESSION of the disease is slower since the introduction of these drugs.
Also Aaron P:
That doesn't account for the decrease in NEW cases, though. If we're treating these diseases better, patients live longer, true, but contracting and subsequently surviving any of these diseases DOESN'T HAVE ANYTHING TO DO with meeting the criteria for an AIDS diagnosis. The decrease in NEW cases is directly attributable to drug intervention against HIV.
Jenks is right. Case closed.
http://www.niaid.nih.gov/publications/hivaids/13.htm
Simple, you present with symptoms well before it has any impact on your long-term survival. (This is what frequently happens) You most likely initially present with oral Candidiasis. Luckily for you, you can now be given HAART and flagyl (to treat the fungus) so you don't risk developing something that can really hurt you like PCP.
I am referring to the graph that was presented on MUSC Tiger's side, not the graphs here. What I am referring to is the fast that AIDS patients live longer today than they did in 1994 (with a gradual increase every year between). This has nothing to do with new cases as you pointed out. New cases have nothing to do with what I was descibing above.
The DATA cannot be refuted only the inferences drawn by the doctor which are insane and don't pass the muster of basic logic.
Again, if you read the post, you will see that I make the point that you have to look at ALL the data to get a clear picture of things. Nothing can be fully explained in one graph, which give critics the opportunity to poke holes in them.
Either I am not understanding you or you are not understanding me.
The graph on MUSC Tiger's page measures time from diagnosis to death in AIDS patients. One reason for this is that, in 1994 patients were not diagnosed with AIDS as early.
Prior to the diagnosis we do not know how long they had AIDS, so we cannot say definitively how long their survival with AIDS was.
What I do know is that today far more people are tested and likely to be diagnosed early for AIDS than were in 1994. Does that mean they are not surviving longer? No, they could be. I'm simply saying that cannot colclude that from such an uncontrolled study.
I'm not sure what you intend with your last comment. I have been reading a great deal of information and trying to look at all of the data presented. I simply am not seeing anything on either side of this debate that closes the case, and am pointing out the problems I see when I see that claim.
I would be happy for either side to prove their case to me, I simple haven't, as yet, seen it.
http://www.fda.gov/bbs/topics/NEWS/NEW00070.html
I'm sorry but this is just not true. You are applying the strides in HIV testing to full-blown AIDS. HIV has an undeterminable latency before white counts are depleted enough to cause AIDS symptoms. People present to doctors with clinical symptoms because they notice things that bother them. It was just as easy to diagnose someone with AIDS (it begins with a clinical observation of symptoms followed by testing viral load and white count) now as it was in 1994.
Just look up information on the clinical effectiveness of HAART (and stop being so hung up on AZT) if you require convincing. For AIDS, HAART regimines have been the closest thing to a miracle drug.
So you are saying that people are not being diagnosed with AIDS prior to having symptoms? How then do we have so many identifications of people who have AIDS (HIV+ plus low T-cell count) yet don't have symptoms?
Sure AIDS was just as easy to diagnose in 1994 as it is now, but people are only diagnosed when they go to the doctor. Are you saying that people who test positive for HIV are not more likely to be tested for AIDS?
I have read some information on HAART and am continuing to do so.
My "hang up" with AZT is simply that it's introduction has tainted a lot of the evidence that HIV causes AIDS, from what I see.
Yes, that is what I am saying. It is impossible to be diagnosed with AIDS without any AIDS defining conditions. These asymptomatic people are HIV+ and most likely have a white count of over 200 and low viral load.
If you have a white count below 200 and have no infections, you either live in a hermeticly sealed chamber or are the luckiest person on earth. Gotta go to work now, fun talk though.
You first link shows a lot of studies that set out to disprove the hypothesis that AZT causes AIDS, and I believe they show that to be the case. I don't believe that AZT causes aids, merely that it greatly impears the health of those who take it and damages the immune system.
AZT may temorarily prevent the onset of AIDS, studies do seem to indiate that. That may or may not be related to it's effect on HIV, however.
The animal studies link is very interesting and I plan to look more into that. I am reluctant to rely only on the summaries of studies for information.
You have a point, and perhaps I have overestimated that factor a bit. It is unlikely that someone with such a low T-cell count would have no opportunistic infection. I wonder, however, how many would go to the doctor in 1994 compared to now. Especially people that are high risk for AIDS, and what factor that plays in the time between diagnosis and death.
I'm french and chemist
I apologize for my poor english
I have found some links about the toxicity of AZT
Here a link from Thailand :
Ruengpung
and
http://www.nhrbc.org/paper1.1.html
http://www.nhrbc.org/paper1.2.html
http://www.nhrbc.org/paper1.3.html
http://www.nhrbc.org/paper1.4.html
http://www.nhrbc.org/paper1.5.html
http://www.nhrbc.org/paper1.6.html
You can retain the conclusion of the abstract :
The french-British Concorde study shows :
and
abstract :
abstract
full text :
full
Reardon &al have demonstrated that AZT reacts readely and totally
with thiols at 25°C :
abstract
and the full text :
full
It is realy an oxidoreduction. I have found in the site of the
university of Jussieu (Paris), that cysteine (a thiol) can be oxidized
in sulfate (with cysteine dioxygenase).
jussieu
NB : sodium sulfate is known to give diarroea !
Reardon give all the reduced forms of AZT, mainly aminothymidine,
which is the main metabolit of AZT (outside glycuronate, which is not
truly a metabolit).
When you read the paper from Marmor &al.
marmor
they quotes :
"Low serum thiol levels predict shorter times-to-death among
HIV-infected injecting drug users."
and the paper from De Rosa &al.
stanford
they quotes(p 923) :
"NAC administration is associated with increased survival"
It become clear that the administration of AZT, which can only deplete
the thiols levels, can only decrease survival !
I'm french and chemist
I apologize for my poor english
I have found some links about the toxicity of AZT
Here a link from Thailand :
Ruengpung
and
http://www.nhrbc.org/paper1.1.html
http://www.nhrbc.org/paper1.2.html
http://www.nhrbc.org/paper1.3.html
http://www.nhrbc.org/paper1.4.html
http://www.nhrbc.org/paper1.5.html
http://www.nhrbc.org/paper1.6.html
You can retain the conclusion of the abstract :
The french-British Concorde study shows :
and
abstract :
abstract
full text :
full
Reardon &al have demonstrated that AZT reacts readely and totally
with thiols at 25°C :
abstract
and the full text :
full
It is realy an oxidoreduction. I have found in the site of the
university of Jussieu (Paris), that cysteine (a thiol) can be oxidized
in sulfate (with cysteine dioxygenase).
jussieu
NB : sodium sulfate is known to give diarroea !
Reardon give all the reduced forms of AZT, mainly aminothymidine,
which is the main metabolit of AZT (outside glycuronate, which is not
truly a metabolit).
When you read the paper from Marmor &al.
marmor
they quotes :
"Low serum thiol levels predict shorter times-to-death among
HIV-infected injecting drug users."
and the paper from De Rosa &al.
stanford
they quotes(p 923) :
"NAC administration is associated with increased survival"
It become clear that the administration of AZT, which can only deplete
the thiols levels, can only decrease survival !
I'm french and chemist
I apologize for my poor english
I have found some links about the toxicity of AZT
Here a link from Thailand :
Ruengpung
and
http://www.nhrbc.org/paper1.1.html
http://www.nhrbc.org/paper1.2.html
http://www.nhrbc.org/paper1.3.html
http://www.nhrbc.org/paper1.4.html
http://www.nhrbc.org/paper1.5.html
http://www.nhrbc.org/paper1.6.html
You can retain the conclusion of the abstract :
The french-British Concorde study shows :
and
abstract :
abstract
full text :
full
Reardon &al have demonstrated that AZT reacts readely and totally
with thiols at 25°C :
abstract
and the full text :
full
It is realy an oxidoreduction. I have found in the site of the
university of Jussieu (Paris), that cysteine (a thiol) can be oxidized
in sulfate (with cysteine dioxygenase).
jussieu
NB : sodium sulfate is known to give diarroea !
Reardon give all the reduced forms of AZT, mainly aminothymidine,
which is the main metabolit of AZT (outside glycuronate, which is not
truly a metabolit).
When you read the paper from Marmor &al.
marmor
they quotes :
"Low serum thiol levels predict shorter times-to-death among
HIV-infected injecting drug users."
and the paper from De Rosa &al.
stanford
they quotes(p 923) :
"NAC administration is associated with increased survival"
It become clear that the administration of AZT, which can only deplete
the thiols levels, can only decrease survival !
Can you delete my two redundant posts. Thank's
Normally, in the scientific community, one scientist postulates a theory backed by research and experimentation, describing how he achieved his results and conclusions. Normally, the science world has an opportunity to examine these conclusions fully before any are confirmed and postulated to the public.
This was not the case with HIV-AIDS. No, that was a bandwagon quickly hopped on by every pharmaceutical company, every lobbyist, and all the media... and hence by the public, who never knew there was no such testing of Gallo's theories. (read Jon Rappoport's AIDS, INC. for a very enlightened view)
I recall reading an article some time ago that prior to the current cocktail of drug treatments being used, most AIDS patients expired of respiratory causes, but that since AZT (a failed chemotherapy drug shelved in 1961) has become the treatment norm, they now expire from liver/kidney failure. Does it take rocket science to spot a problem?
Liam Scheff reports that the criteria for AIDS diagnosis vary around the world, and that in Africa, a case of dysentery can be cause for that diagnosis. Again... what is wrong with this picture?
Quite frankly, given the foregoing, I am forced to conclude that something stinks to high heaven in the whole mess. I don't need any more statistics; I will look instead to the ones who opted for immune-boosting and healthy living instead of a death diagnosis, and are still thriving today.
Until the public stops handing responsibility for their health over to institutions filled with white-coated "experts" whose very jobs depend not on wellness, but on illness, and starts to use their God-given free will as it was intended, people around the world will continue to be fodder for that machine. We've
"let George do it" and "George" has done us but good... and didn't even kiss us first.
http://www.altheal.org/statistics/fiala.htm
Samba Diallo
BTW, some of you might want to look at the figure in the Duesberg paper that the graphs I presented are adapted from. They have a missing part that is as bewildering, almost, as the point I made by extracting only two of the data sets there.
Look at the data from Africa. What? How can that be?
Either the CDC is full of it or the WHO is. You decide. Pres. Mbeki has. But then again he is only an economist and the president of a country.
It's a nice idea, but it's not mathematically accurate.
Total HIV cases are not necessarily proportional to new AIDS cases. People who have HIV for a few years are more likely to develop AIDS then people who just got HIV.
A change in the latency period (which was announced long ago) would also change the shape of the AIDS curve.
A very simple explanation for the rise in AIDS is that new HIV cases rose rapidly in the 70's and early 80's (doesn't contradict any data presented here, also conventional wisdom - I'm not making stuff up to fit the data).
These people would have died later, causing an increase in AIDS during the late 80's and early 90's.
A flat HIV rate in the 80's would represent LOW amounts of new HIV cases. After all, according to your data, not many people were dying of AIDS, and a flat HIV total means AIDS deaths = new HIV cases. Because less people in the 80's were getting HIV, AIDS dropped in the 90's.
If you don't believe me, do a computer simulation.
Dan Fendel's assertion stands, especially to those that did not forget the terms "infectious" and "incurable" which the NIH uses.
"If the number of people with the virus stays constant, then although the number of people getting sick might go down due to drugs, there's no explanation for why it went up in the first place."
It is not the first time (and i suspect not the last) that i've seen similar reactions, although it IS the first time I witness them in the blogosphere.
Another little skirmish come and gone, but it will be remembered, if not by History, by some of the participants. Cheer up Dean, and welcome to the AIDS wars. This is how the [smaller and least ugly] battles usually end, in my experience. But one can never know beforehand the nonlinearly cumulative result. So keep it up.
Somebody once said that the task of science was not to answer questions but to question answers (Theodore Schick, i think). It follows that since in our day most answers ARE given by science, science has to question "scientific" answers. Kinda tricky.
Samba
Samba
I'm not saying that these data prove the HIV hypothesis. In fact, I think almost any hypothesis can fit these data, which means that nothing can be proven.
I AM saying that the claim that the data are inconsistent with the HIV hypothesis is just plain wrong.
The HIV hypothesis is based on other data, but I'd rather not analyze t5hose data in this particular thread, as it is a bit off topic.
If we assume the data on HIV seropositivity is correct (around 1e6 and constant since the introduction of the test, these numbers are obtained by extrapolation from the testing of millions of blood donations made by people of all ages and gender, army service recruits-mostly young men/women-, requests by doctors for their patients, regular testing of health workers, etc.), an incubation period between 5-15 years (median 10 years), and incurability, then by 1995 the number of AIDS cases and likely deaths) should have been around 1e6 too. Now, our french chemist friend has provided references to the most extensive AZT trial done (the Concorde study) that was the basis on which AZT monotherapy is no longer used, so we agree that AZT after 1987 cannot have made the difference.
Now after 20 (!) years the number of AIDS cases (assuming all deaths were prevented by the "good" HAART, widely available only since 1995) has not reached the million yet.
And this does not even deal with the problem of why there aren't any new infections for an STD (when other STDs have gone up in the same period). Where are they?
The problem as i see it is that if AIDS was not declared as INVARIABLY developing after HIV infection and INVARIABLY fatal by the NIH the diffculties would melt away, but since it is declared as inevitably following HIV seropositivity and fatal, after 20 years the million should have been reached and exceeded.
Do you agree?
Samba
It is simply a mistake to compare total HIV cases with new AIDS cases, because people live with HIV for several years and thus have a chance to accumulate in numbers.
Thus, if HIV+ people live for 10 years, total HIV will be roughly 10 times the AIDS rate.
For the same reason, there have not been 20 million HIV cases. You're counting everyone for every year that they live, giving you much more than the real amount.
-----------------------------------
Assessment of the epidemiological situation 2004
The estimated number of diagnosed AIDS cases for 2002 in the United States is 886,575. Adult and adolescent AIDS cases total 877,275, including 718,002 cases in males and
159,271 cases in females, with women accounting for an increasing proportion of people living with HIV and AIDS (PLWHAs). In the same period, 9,300 AIDS cases were estimated in children under age 13.
The estimated number of deaths of persons with AIDS is 501,669, including 496,354 adults and adolescents, and 5,315 children under age 15.
------------------------------------
I am working with TOTALS now...
Now, if we have a million HIV positives estimated today, we obviously have to subtract those people who died of AIDS (about half a million). That would mean that if HIV = AIDS half a million new people have turned seropositive since 1985 since HIV seropositivity is constant and they will inevitably develop AIDS and die although the "life prolonging" drugs will postpone their death.
Half a million new HIV infections in 20 years makes about 25,000 new infections per year in the last 20 years (25,000 x 20 = 500,000).
This is exactly the discordance evidenced in the two original graphs, corrected or no. 25,000 people each year go HIV+, roughly compensating the deaths to keep the HIV+ total constant, but AIDS cases go down after 1994 or so. I say AIDS cases, NOT AIDS deaths. As I understand it, for the stats we are working with the CASES change the total number of HIV+ only if they die, in which case they are subtracted from the total number of HIV+ and added to the AIDS deaths. How can the CASES go down if 25,000 people a year are, theoretically, newly infected? Even if they survive indefinitely they are CASES anyway.
However, this would be easily explained if you assume that HIV testing measures something pretty constant in the population not related to the AIDS deaths. Then deaths and infection could go in separate ways.
Samba
Samba
I'll post more on this, probably tomorrow or the day after. I'm pressed for time--Rosemary will be delivering our son any minute now--and am waiting on clarification for a couple of questions so I can make sure we all have a completely unobfuscated understanding of what we're looking at.
To resume:
The GRAND total for HIV+ would be the million alive today plus the half million dead, that would be that TOTAL HIV+ increased from 1e6 in '85 to 1.5 million in 2004 (but half a million died).
In the absence of anything that will prevent AIDS development (that is what i call AIDS cases) how come AIDS case development has slowed down?
Samba
Perhaps I am still misinterpreting you, but the figure of 25,000 new HIV+ cases per year seems to be an average. If the figure goes up and down (while averaging 25,000), AIDS cases will go up and down (a few years later).
Now, you might say that if the figure of new cases goes up and down, total HIV+ will go up and down, not remain constant. I have 2 replies:
1) AIDS cases are volatile mainly before 1996, (and fairly stable afterwards). These are cases deriving from HIV infection in the 80's, when the claim that total HIV+ remained constant is the most iffy.
2) If new infections outpaced AIDS deaths by, for example, 25,000 during a given year, this would raise total HIV+ cases by only 2.5%. New infections could outpace deaths for a few years, then deaths could outpace new infections, and the total HIV+ cases would wobble only by a few percent (and AIDS cases would rise and then fall). This would not be detectable at the accuracy of the estimates in the total HIV+ data.
This is the problem with trying to prove ANYTHING from the total HIV+ data. Small deviations in total HIV+ can mean large deviations in new HIV+ cases, completely changing the interpretation of the data. And the data are so unreliable (considering the way they were derived) that small errors are virtually certain, and large errors are fairly likely. It would be much better to study groups of known individual HIV+ cases.
(Also, notice that the graph shows that the 1995 estimate WAS thought to be off by a few percent, relative to the improved estimate for 1996. The 1985 data are probably even worse. Even the latest data include an estimate of 200,000 undetected HIV+ cases (if I understood the CDC site correctly), which suggests a significant potential error.)
Re:
"In the absence of anything that will prevent AIDS development (that is what i call AIDS cases) how come AIDS case development has slowed down?"
Delaying AIDS development (as the treatments are believed to do) will lead to less AIDS cases during the years following introduction of the treatment, even if it doesn't affect AIDS cases in the long run. And we don't quite have data for the long run.
However, i think that anyone taking the medication (and supposedly then not dying, and even excelling in sports as some publicity suggests) would be counted as (treated) AIDS cases and should add up to the total. As I understand it, total HIV+ are estimates, but AIDS cases (in the US) are just about all reported, so the estimates are not likely to affect those numbers significantly.
Maybe you are right, but I see a trend to go down, even if my 25,000/year new HIV+ is only an average. Maybe as jfr suggests (and i agree with him if this is the case) the original rise was more due to the massive amounts of AZT given than anything else...?
Anyway, if we assume the HIV+ estimates (for the 80s at least) are iffy then the whole discussion is useless, as you say. But if so then it is hard to imagine why the CDC planned its strategy (whatever that was beside clean needles and condoms) according to it. Kind of irresponsible, maybe? And it still does not explain the descriptor "epidemic by infectious agent" given so early unless they were biased from the start to an infectious cause.
Anyway, the data for Africa, considering that over here antirretrovirals are not available, should be similar to the US data before the "good antirretroviral therapies" came about. And, according to UNAIDS, there was/is a good correlation (in Africa, not in the US) between infection estimates (HIV+, which should be even "iffier" than in the US given the lack of HIV tests) and AIDS cases/deaths. I just wonder, specially since in Africa the virus has been around for a longer time but has not yet stabilized as it did so quickly in the US ....
Anyway, thanks for your time, but i do think something is really really wrong, and too much of African AIDS is so much extrapolation and racist crap that i think you would be surprised if you start looking at it (the site i posted in the first comment is only the beginning of it).
Have a good life,
Samba
I look always to the chemical function of these ARV. Only AZT is oxidant. If you scrutinize the recent publications, you will see that the thioxolane-ARV are practically the only potent drugs against the decrease of CD4. All the regimens content 3TC or FTC.
Glaxo has patented AZT the 16 march 1985
People who have been declared P24 positive in the middle 80th, without any symptom of full blown aids, have certainly received AZT from this moment.
What make me suspiscious against AZT is the thai trial from Ruengpung, who says that :
and this study from Yamaguchi
They demonstrate that AZT is at least as oxidant as hydrogen peroxide. In the book of the french professor of chemistry Maurice Bernard, we can find the redox potential from HN3/NH4(+), which is 1,96 V, making AZT more oxidant as permanganate (The replacing of H in HN3 by a secondary carbon may decrease the redox potential to 1,6 - 1,7 V).