Friday, September 01, 2006

Is Dean Esmay Dishonest? or Just Ignorant?

Here he is repeating a lie told by Hank Barnes:

Lancet Study

The Lancet just published a massive study of over 20,000 AIDS patients and determined that anti-retroviral drugs do not increase the lifespan of AIDS patients. They increase leukocyte counts and reduce "viral load," but do not save lives. HAART is a failure, in other words.

Well now. Isn't that mysterious?

The original lie, told by Hank, is about a study in the Lancet :


HIV treatment response and prognosis in Europe and North America in the first decade of highly active antiretroviral therapy: a collaborative analysis

Which shows that even though improvements to HAART have continued to decrease HIV viral load and increase CD4+ T-cell counts over the past ten years. There has not been a corresponding reduction in deaths or progression to AIDS during the first 1 year of treatment.

It doesn't say anything about lifespan, indeed it would be very difficult to learn anything about lifespan in a study that followed patients for --wait for it-- ONLY a single year!

Despite Dean's ignorant assertion: "HAART is a failure, in other words.", the graph below shows an example of the effect Haart has had in decreasing death from AIDS.





























http://content.nejm.org/cgi/content/abstract/338/13/853
(UPDATE: The graph actually comes from this paper, the above URL is for an earlier paper with a similar figure by the same first author.)

Hank Barnes' take on the paper is far more dishonest and is precisely the sort of quote mining and slanted coverage, ignoring the main facts in order to prop up a failing agenda, that can be expected of Intelligent Design Creationists and other "deniers" of reality.

"In short, T-4 cells increased, viral load decreased -- but patients did not live any longer as a result of these wonderous drugs."
No Hank, the drugs do increase lifespan versus placebo, even in the first year of treatment. Even AZT monotherapy does that, and HAART is a vast improvement over AZT alone.


(Click to enlarge.)
(Update: Graph is from figure 2 of:
Ann Intern Med. 1990 May 15;112(10):727-37.




The safety and efficacy of zidovudine (AZT) in the treatment of subjects with mildly symptomatic human immunodeficiency virus type 1 (HIV) infection. A double-blind, placebo-controlled trial. The AIDS Clinical Trials Group.
What the Lancet study showed was that deaths in the first year were not further reduced during the past ten years as refinements to HAART continued to decrease viral load and increase CD4+ T cell counts.

Interestingly, neither Hank nor Dean mention these facts from the study:

"The proportion of heterosexually infected patients increased from 20% in 1995–96 to 47% in 2002–03, and the proportion of women from 16% to 32%."
Perhaps because they're both rather fond of the erroneous contentions that:

1. HIV cannot be transmitted by heterosexual sex, and
2. That HIV cannot be a sexually transmissable disease because there are more men than women infected.

Number one is of course an abject lie or base stupidity depending on who is saying it.

Number two is simply an erroneous conclusion based on an improper understanding of what a founder effect is, and how that could lead to an increased number of males infected when HIV was first introduced to the male homosexual population in North America and Europe.

I fully expect Dean to accuse me of ad hominem attacks. Please note, I am not saying you should disregard what Dean says because he is ignorant, I am saying you should disregard what Dean says about HIV/AIDS because what he says is wrong! He's wrong because he's ignorant of what the Lancet study actually says.

I believe Dean's ignorance in this case is because of his reliance on Hank, so I've sent him a copy of the paper. No response, no retraction of his earlier statements, will mean a check mark in the dishonest category for Dean in my book.

UPDATE: I'm sorry Dean, was that a yes to both questions?

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Comments on "Is Dean Esmay Dishonest? or Just Ignorant?"

 

Anonymous Anonymous said ... (9/01/2006 7:13 PM) : 

I vote lazy. As in can't be bothered to take the time to actually read what a scientific paper says.

Dale

 

Blogger Dr. Roy Hinkley said ... (9/01/2006 10:07 PM) : 

I don't know Dale. Here he is commenting on Padian again in the comments to the Lancet post:
http://www.deanesmay.com/posts/1157097975.shtml#81547

"if you look carefully you'll discover that out of thousands of these couples over a period of years, not one single HIV- person turned HIV+."

Thousands of couples?

Surely he's troubled himself to read Padian by now?

Looks like he's dishonest to me.

 

Blogger Pharma Bawd said ... (9/02/2006 11:02 AM) : 

Either way Dale, if he can't be bothered to learn the truth about HIV and AIDS or if he just won't tell the truth, he should follow his own advice and stop talking about it.

Especially if the best he can do is to be a pompous jerk when he says things as ignorant as this:

"HAART is a failure, in other words.

Well now. Isn't that mysterious?"

 

Blogger Dean Esmay said ... (9/06/2006 9:04 AM) : 

Sorry, not thousands. Oh gosh. It's leaping on simple mis-statements like that that have from the beginning made me believe that HIV's defenders are basically nasty, dishonest people--that because they can't defend the science on the merits, they have to rely on dumbshit little things like that to get anywhere.

I have only just now received the paper. I'll look at it, thank you. I noted immediately that the authors' own interpretation is given as "Virological response after starting HAART improved over calendar years, but such improvement has not
translated into a decrease in mortality." Which, perhaps, would be careless wording on their part. I'll look at the study.

Oh by the way, that chart you give showing AIDS deaths down as HAART goes up? I've tried getting the actual source data on that to verify, but like so much else that CDC and NIH put out, that turns out to be more difficult than it should be.

 

Blogger Dean Esmay said ... (9/06/2006 9:07 AM) : 

Oh by the way, can you source for me the studies which compare HAART to placebo?

You certainly can't expect me to take that AZT chart seriously considering that we know now that the original AZT studies (which I've read) were contaminated.

 

Blogger Pharma Bawd said ... (9/06/2006 3:36 PM) : 

Dean said:

“Sorry, not thousands. Oh gosh. It's leaping on simple mis-statements like that that have from the beginning made me believe that HIV's defenders are basically nasty, dishonest people...”

Fair enough Dean, I accede that I can be a real bitch over an order of magnitude.

Thanks for taking a look at the Lancet paper. There are legitimate criticisms to be made based on it. But, upon reading it, I think you’ll find that this:

“"Virological response after starting HAART improved over calendar years, but such improvement has not translated into a decrease in mortality."”

Refers only to the first year of HAART treatment. It is not comparing non-HAART to HAART and saying there is no decline in mortality. It is comparing 1995-96 HAART to 2002-03 HAART and saying that there is no difference in mortality during the first year on HAART. ie: deaths average a little less than 2% during the first year of HAART.

In no way does it say what you said:

“anti-retroviral drugs do not increase the lifespan of AIDS patients.”

They do, as shown in this 1998 NEJM paper by Palella et al. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&dopt=AbstractPlus&list_uids=9516219&query_hl=1&itool=pubmed_docsum

“I've tried getting the actual source data on that to verify, but like so much else that CDC and NIH put out, that turns out to be more difficult than it should be.”

What is it exactly you want to verify? Is there a thread about these difficulties at your place? If you can give me a link I’ll read about it there instead of asking you to repeat everything.

The graph of AZT monotherapy comes from this paper:

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&dopt=AbstractPlus&list_uids=1970466&query_hl=1&itool=pubmed_docsum

AZT vs combination of ARVs is here
http://content.nejm.org/cgi/content/abstract/335/15/1081

These are randomized, double-blind, placebo controlled trials. I don’t have HAART vs combination therapy at my fingertips but I’m sure I can dig something up.


However regarding a placebo controlled study of HAART, I’m sure you know it hasn’t been done. I’m sure you know that medical ethics prevent it.

In light of what we do have, AZT proven to be more effective than placebo, combination therapy has been proven to be more effective than AZT monotherapy, and HAART has been proven to be more effective than combination therapy:

A vs B, B wins. In B vs C, C wins. In C vs D, D wins.

It’s pretty difficult to believe that D (HAART) is not quite a bit better than A (placebo) given the data.

In addition to these trials, the Palella NEJM 1998 paper is a good study showing the effectiveness of HAART vs combination therapy vs monotherapy vs no therapy.

“In a failure-rate model, increases in the intensity of antiretroviral therapy (classified as none, monotherapy, combination therapy without a protease inhibitor, and combination therapy with a protease inhibitor) were associated with stepwise reductions in morbidity and mortality. Combination antiretroviral therapy was associated with the most benefit; the inclusion of protease inhibitors in such regimens conferred additional benefit.”

http://content.nejm.org/cgi/content/abstract/338/13/853

I think I have all these references as electronic files. If you need any send me an email at my profile here and I'll forward them. I can't attach documents to your contact email at your site.

 

Anonymous Chris Noble said ... (9/09/2006 8:44 PM) : 

The next question is who told Hank about this study.

I don't think Hank is a regular Lancet reader.

The average "rethinker" has not read a significant number of "orthodox" papers. All they ever do is cite a select few that they think provide support for their preconceived idea that HIV does not cause AIDS.

 

Blogger Pharma Bawd said ... (9/10/2006 1:52 PM) : 

You have a point Chris, Hank may not have read the paper. Hank cites p. 453 for the below quote:

"Virological Response after starting HAART improved over calendar years, but such improvement has not translated into a decrease in mortality."

Since 453 is in the body of the paper I had assumed Hank at least looked at it. Turns out the quote is in the abstract on page 451. So Hank may not have actually looked at the paper and is just quote-mining the abstract.

Googling the abovequote, there is a discussion of the paper at http://groups.msn.com/aidsmythexposed/general.msnw?action=get_message&mview=0&ID_Message=24660
posted by David Crowe 8/16/2006. Mr. Crowe did not make this erroneous interpretation in his post but several commenters did.

The abstract is also posted at http://hiv.researchtoday.net/archive/3/8/2475.htm with no discussion. And of course its been up on PubMed. I happened to read the paper as soon as it came out online and figured there would be great mischief made from it. I never expected this particular interpretation though.

I expect after reading it, Dean will find several arguments to make that are at least based on the findings of the paper. An actual discussion of the paper’s implications could be interesting, if it tends toward Hazard Ratios etc. it might be nice to have a statistician around. So please check back in Chris.

 

Anonymous Chris Noble said ... (9/10/2006 6:51 PM) : 

Hank may have been given a copy of the paper but I strongly doubt he was just browsing the Lancet.

Perhaps a bigger hypocrisy is that whenever "rethinkers" are presented with a study that shows a cohort with HIV+ members developing AIDS and HIV- members not progressing to AIDS the first retort is that the two groups were not properly matched.

In this current studies the demographics and type of co-infections changed markedly over time.

For some strange reason "rethinkers" are not complaining about the groups not being matched.

PS. I am not a statistician.

 

Anonymous Richard Jefferys said ... (9/11/2006 2:53 PM) : 

The Lancet paper contains two analyses of mortality, one just looking at one year after starting ART and a second analysis (available in a supplemental table on the Lancet website) looking at two years after starting ART.

Here are the data for the different time periods.

One year after starting ART:

1995/96: total n=1232 #deaths=27 (2.2%)
1997: 4785 98 (2.1%)
1998: 4583 85 (1.9%)
1999: 3699 67 (1.8%)
2000: 3203 63 (2.0%)
2001: 2783 49 (1.8%)
2002/03: 1932 25 (1.3%)

Two years after starting ART:

1995/96: 1232 53 (4.3%)
1997: 4785 151 (3.2%)
1998: 4583 144 (3.1%)
1999: 3699 109 (3.0%)
2000: 3203 99 (3.1%)
2001: 2783 69 (2.5%)

So, in fact, mortality has declined in the later periods whether you look at the one or two year mark (although, predictably, the difference is more evident after two years) The reason that the authors state that it's unchanged is based on the hazard ratios where the differences weren't large enough to be statistically significant (the hazard ratios were also based on the data from 98 which was picked as the reference year). Given that people in the later period were starting with around 200 CD4s, you can compare the two-year mortality data with that from natural history studies of untreated HIV infection. You will find that the number of untreated people surviving at two years after the CD4 drops below 200 is >10 fold less than the number surviving in this cohort study of people on ART (~97.5% of people still alive at two years).

So the people that have claimed that the Lancet article shows that ART does not reduce mortality are just plain lying. This includes D. David Steele, Dean Esmay, Anthony Liversidge, Neville Hodgkinson and Celia Farber.

 

Anonymous Anonymous said ... (9/11/2006 5:55 PM) : 

You are right, Richard, and I think that the american aids rethinkers compromise themselves by not accepting that the HAART is beneficial.

But we can completely explain the success of the HAART by considering the intrinsic chemical properties of every substance, and not their "antiviral" properties.

It is now certain that the death of the CD4 is due to the oxidizing stress provoked by an immune activation. The fact of using at present reducing substances on the place of the AZT, which is an oxidizer by its azide moiety, allows to reduce this oxidizing stress and thus to decrease this syndrome of immunodéficience.

In particular, Epivir and Emtriva are probably easily hydrolyzed in reducing aldehydes in the presence of an strongly electrophilic environment rich in cation nitrosyle.

 

Anonymous Richard Jefferys said ... (9/11/2006 10:15 PM) : 

Activation of CD4 T cells causes activation-induced cell death. Are you suggesting you can prevent activation-induced cell death with antioxidants?

And why do you think untreated HIV positive people have higher levels of immune activation (including CD4 T cell activation) than their HIV negative counterparts? Why do the levels of immune activation reproducibly and significantly correlate with viral load (whether it's measured by branched DNA or RNA PCR)?

 

Anonymous Anonymous said ... (9/11/2006 11:51 PM) : 

The HIV-positive persons not treated by the HAART have obviously higher levels of immune activation in this hypothesis, because, if it is indeed about an excess of oxidation by the oxidized nitrogenous compounds which is responsible of this immune activation, the use of the HAART is going to oppose to it, and to decrease it, allowing to avoid the cellular apoptose.

In this hypothesis, the viral load represents a DNA (or ARN) mutated in a specific way by the type of used oxidizer, but containing constants connected to the chemical phenomenon of oxidation. (For example, alterations can appear when the guanidine is oxidized in 8-hydroxyguanidine). It is thus logical to notice an increase of this viral load.

As the HAART contains antioxidizers, yes, immune activation is doubtless prevented by these antioxidizers.

 

Blogger Pharma Bawd said ... (9/12/2006 8:25 AM) : 

"(For example, alterations can appear when the guanidine is oxidized in 8-hydroxyguanidine). It is thus logical to notice an increase of this viral load."

No it isn't. Oxidation of guanidine to 8-hydroxyguanidine is not possible as guanidine does not have an 8 atom. Not to mention the fact that guanidine is not a component of either DNA or RNA.

So perhaps you mean guanine?

That still doesn't make any sense as oxidation of guanine could have no effect on increasing viral load.

Not only would such a single base change not have a large impact on viral load measurements, but the C-8 of guanine is not involved in DNA base pairing. So such an oxidation of guanine would not be expected to effect viral load at all. Particularly, it would not be able to produce the large increases in viral load seen in AIDS patients.

 

Anonymous Anonymous said ... (9/12/2006 10:01 AM) : 

You are right, Pharma Bawd, I written too quickly.
It is naturally about the 8-oxo-deoxy-guanosine. Guanidine is iminourea.
But 8-oxo-deoxy-guanosine is a major oxidative lesion in DNA and is responsible for mutation and cancer.
For instance, this paper show exactly what I have said : 8-oxo-deoxy-guanosine catalyse misincorporation of adenine in preference to accurate incorporation of cytosine.

Error-prone replication of oxidatively damaged DNA by a high-fidelity DNA polymerase.
Hsu GW, Ober M, Carell T, Beese LS.
Nature. 2004 Sep 9;431(7005):217-21. Epub 2004 Aug 22

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&dopt=AbstractPlus&list_uids=15322558&query_hl=3&itool=pubmed_docsum

What is ;ore serious, it is that it was shown that AZT provoked this oxidation of the dG in 8-oxo6dG :

AZT treatment induces molecular and ultrastructural oxidative damage to muscle mitochondria. Prevention by antioxidant vitamins.

J G de la Asunción, M L del Olmo, J Sastre, A Millán, A Pellín, F V Pallardó, and J Viña
J Clin Invest. 1998 July 1; 102(1): 4–9.

http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=509058

 

Blogger Pharma Bawd said ... (9/12/2006 1:56 PM) : 

Be all that as it may, I don’t see how any such modification of DNA or RNA could increase HIV viral load measurements.

AZT and HAART both decrease viral load. Under your hypothesis wouldn't you expect AZT to increase viral load?

 

Anonymous Anonymous said ... (9/12/2006 3:18 PM) : 

All the studies show that the AZT in monotherapy has a very weak incidence on the viral load, while the addition of 3TC made fall considerably.
Certainly, the AZT makes it fall for a moment, but did not it replace in these studies of the other substances which deteriorated considerably the biologic parameters?
The bactrim, for example is a powerful oxidizer by its group isoxazole, and, at the beginning of the AIDS, has strongly aggravated the disease.

Rapid disease progression in human immunodeficiency virus type 1-infected individuals with adverse reactions to trimethoprim-sulfamethoxazole prophylaxis.
Veenstra J, Veugelers PJ, Keet IP, van der Ven AJ, Miedema F, Lange JM, Coutinho RA.
Clin Infect Dis. 1997 May;24(5):936-41.

According to the laws of the organic chemistry, compounds with connection NO are more oxidizing than those containing a connection NN.

It would seem logical to think that the passage of bactrim to AZT gets a decrease of the viral load

On the other hand, at naive patients, as the new-born, the results are very contrasted, as well as this study shows it

Effect of perinatal short-course zidovudine on the clinical and virological manifestations of HIV-1 subtype E infection in infants.

Sutthent R, Chokephaibulkit K, Piyasujabul D, Vanprapa N, Roogpisuthipong A, Chaisilwatana P.

J Clin Virol. 2002 Jul;25(1):47-56.

On the other hand, the fact of using reducers (epivir, emtriva, to lopinavir) make fall at once the viral load, and improves the health of the patients.

The viral load is obtained by PCR using primers, which are fragments of DNA which we do not apparently find in the human genome. But the mutations in the junk DNA could not create these "viral" DNA?

 

Anonymous Chris Noble said ... (9/12/2006 5:14 PM) : 

There is a "theory" of sorts in "rethinker" circles that oxidising substances can somehow cause the human body to assemble RNA or DNA sequences that match the PCR primers used in viral load tests.

The PCR primers used are somewhere around 17-23 bps so someone can calculate the probability of this happening by chance.

You have to wonder why HIV sequences that are obviously retroviral are generated. The PCR primers are chosen for their specificity.

Why doesn't the same process produce millions of other random sequences.

The whole thing is just an ad hoc attempt to avoid facing the reality.

 

Blogger Pharma Bawd said ... (9/12/2006 8:54 PM) : 

"But the mutations in the junk DNA could not create these "viral" DNA?"

No.

Try multiplying 1/4 times 1/4 twenty times, then multiply that product times itself. The odds of what you're suggesting would be a little bit worse than that.

Also, the patients taking AZT in your study only had twice as much 8-oxo-dG as untreated controls. There's no way this would be enough to produce such widescale mutation.

Even if it did, it's mathematically impossible to randomly create two exact primer complementary sequences on a single peice of c-DNA.

Then this would have to happen in every single HIV+ person with a detectable viral load.

There is no way oxidative damage of DNA could possibly be responsible for increased viral load.

 

Anonymous Anonymous said ... (9/12/2006 9:36 PM) : 

Why to suppose that these processes can be totally unpredictable? And not dependent of the nature of the oxidizer? Is it the premisse which seems logical, either an experimental observation?

 

Anonymous Chris Noble said ... (9/12/2006 9:48 PM) : 

Why to suppose that these processes can be totally unpredictable? And not dependent of the nature of the oxidizer? Is it the premisse which seems logical, either an experimental observation?

Why suppose it is non-random when you cannot provide a mechanism?

Why do the sequences generated just happen to match highly conserved regions of the HIV genome?

Why do a huge range of substances that you put under the label of oxidising agents all produce the same sequences?

Without a plausible mechanism you might as well claim that microscopic pink unicorns assemble the DNA.

I am also interested in why testing positive to antibodies to HIV-2 correlates with viral load tests with HIV-2 specific primers and likewise for HIV-1 antibody tests and primers. Wild coincidence?

 

Anonymous Anonymous said ... (9/13/2006 3:06 AM) : 

"Why do a huge range of substances that you put under the label of oxidising agents all produce the same sequences?
"

The oxidizing properties of the AZT are due to the electrophilic nitrène which forms spontaneously by loss of nitrogen. This nitrène is going to react with the water to give an alkylhydroxylamine, a strongly mutagène compound.

The metabolic reduction by the aldehyde oxydase of nitrocompoundss and of isoxazoles leads to hydroxylamines. The metabolic oxidation of the secondary (methamphetamine) and the tertiary amines (cocaine) leads to hydroxylamines after transposition in the case of the tertiary.

We can thus put forward from a resemblance of the mutagenic agent, and thus from a resemblance in the alterations.
Besides, the suites of bases present different functional groups (carbonyles, methyl), and it is normal in chemistry that the interaction between the reagent ( hydroxylamines ) and the substratum sees its speed varying according to the environment.

In Africa, where many of chloramphenicol is used, would it provoke a light variation of the alterations?

 

Blogger Pharma Bawd said ... (9/13/2006 5:24 AM) : 

Anonymous,

It's not the alterations that are the problem, its how do you happen to get, around, 20 nucleotides to mutate into precisely the same sequence as the primer binding sites from the HIV genome?

Please do the calculations I suggested above. Do them by hand on a piece of paper and then see how likely it is to occur by chance.

Then consider that people who have not been treated with AZT develop high viral load measurements. Then consider that HAART even, if it is a reducing substance, would not correct previous mutations in the genome if they occurred because of, for instance, oxidative stress. Then consider that when such amplification products are sequenced they all give some version of the HIV genome...

There is a list of reasons why your hypothesis is completely incapable of explaining the data.

At this point we're rather far afield of the topic of this post so I'll ask you not to continue discussing this here.

Thank you.

 

Anonymous Anonymous said ... (9/13/2006 8:36 AM) : 

See you, Dean, how Pharma Bawd runs away when we dig a little the chemistry of the disease!!!

I shall not thus write any more on this subject.

Bye.

 

Blogger Pharma Bawd said ... (9/13/2006 8:51 AM) : 

Sure thing, you don't understand the basics of genetics so I'm running away.

 

Anonymous Anonymous said ... (9/13/2006 9:09 AM) : 

It is the chemistry which governs the genetics and not the opposite. The models used in genetics are much less reliable than those used in chemistry.

 

Blogger Pharma Bawd said ... (9/13/2006 9:39 AM) : 

Unfortunately for you it's the laws of probability that you're up against.

Look, obviously you're interested in this theory of oxidation, go do some more reading about genetics, PCR, mutation, and probability and you'll be able to understand why your theory is wrong.

Then you can revise it or look at other alternatives.

 

Anonymous Chris Noble said ... (9/14/2006 2:42 AM) : 

As far as I can make out according to the Perth Group a diverse range of substances including sperm, poppers and AZT all cause AIDS because of their alleged potent oxidising capabilities.

For some unknown and inexplicable reason these substances also cause the production of HIV antigens, HIV antibodies and HIV RNA and DNA sequences.

At the same time they also for some unknown and inexplicable reason cause the progressive depletion of one perticular subset of cells.

If you can provide a plausible mechanism for this then go ahead.

 

Anonymous Anonymous said ... (9/14/2006 6:33 AM) : 

The DNA has a step of 10 bases by turn of helix. Roughly, the primer (for direct PCR, not for RTPCR) corresponds to two turns of helix. In the "proviral" DNA, bases do not follow each other in a regular way, furthermore, they are close to the tenth base which follows, because of packing of bases.

Do you really think that all the environments are alike and that the action of an oxidizer as the hydroxylamine will be unpredictable?

Do not you know the existence of regioselectivity, which makes that the attack of an electrophile ( oxidizer) will not be made wherever? Of more the nature of the hydrophobic forces which govern the stability of the DNA is still unknown (de Voet, de Voet, 1998).

Thus the knowledge of the nature of the DNA obtained after mutation cannot amount with care of a calculation of probability. If it is it that we learn in biology, well, it is to be revised.

Chris, the description of the metabolism of the different nitrogenous oxidizers begins only to fill out, we cannot again know everything. For my part, I think that the pivots of this lethality are nitrogen monoxyde and hydroxylamine, which form a rédox couple. The first one being at the origin of the cellular apoptose by forming of peroxynitrites, the second being a powerfull mutagneic agent.

 

Anonymous Anonymous said ... (9/18/2006 10:25 PM) : 

Over at his blog today Dean wrote OK, I've read the study. Twice now. I admit that some of the language is dense and, as a non-biologist, I can't understand all of it. I understand most of it, but some of it still confuses me. But, to be fair to the study's authors, they were not writing for laymen like me. Nevertheless, they wrote this conclusion:
Interpretation: Virological response after starting HAART improved over calendar years, but such improvement has not translated into a decrease in mortality.
In short, the virus (measured by PCR amplification) went down, and the leukocytes went up, but the patients didn't actually live longer. During the first year anyway.


Sorry Dean, but no, you didn't understand what you read. You may have thought you did but you didn't. The virus didn't go down - the proportion of patients with virus below a set level (500 copies per ml) after six months of treatment went up. The CD4+ leukocytes pretty much stayed the same after 1998 (which was the year to which the authors compared other results) and it wasn't that patients didn't live longer during the first year - it was the proportion of patients who survived the first year (which was already at ~98% in 1998 by the way) didn't increase when corrected for CD4+ counts and viral loads.

Dale

 

Blogger Pharma Bawd said ... (9/19/2006 9:51 AM) : 

There you go again Dale, always arguing from authority.

How can I be expected to understand what this paper says unless you send me your CV?

 

Anonymous Anonymous said ... (9/19/2006 10:23 AM) : 

I don't know, Pharma Bawd, but somehow I think you'll manage. However, just in case ...

Dale, B.Sc., M.Sc., Ph.D

(Hope that helps!)

 

Blogger Pharma Bawd said ... (9/19/2006 11:36 AM) : 

Hah! See there, you're not even a member of the National Academy of Sciences. Duesberg's right again.

 

Anonymous Anonymous said ... (9/19/2006 2:09 PM) : 

Hah yourself, Pharma Bawd. This wasn't about how Duesberg interpreted the Lancet paper but about how Dean did. And HE isn't an NAS member either!

Dale

 

Blogger Pharma Bawd said ... (9/19/2006 3:49 PM) : 

Yeah, I think that's fairly obvious!

His attack on you in his response to me seemed wholly uncalled for. If there was anyone arguing based on credentials rather than evidence in those old threads, it was Harvey not you.

Dean's whole argument that people should read papers and question scientists and their funding kind of falls apart when they aren't able to get the basic premise of the research right. At least one of his commenters tried to explain to Dean how he was wrong about the Lancet paper.

The whole thing makes me understand how someone can be pushed to write something like this.

 

Anonymous Anonymous said ... (9/19/2006 6:04 PM) : 

I find it funny - anyone can question the orthodoxy but Dean requires you to have 'credentials' to defend it.
(I couldn't open your link.)

Dale

 

Anonymous Chris Noble said ... (9/19/2006 9:45 PM) : 

Dean still insists: Now in 2006, a Lancet study has concluded that the AIDS cocktails do not increase lifespan.

The likely answer to your original question is a) ignorant and b) incapable of understanding a scientific paper.

He has had, what, a week to read the paper and he still cannot understand what it does and does not conclude. The paper is not that complicated.

Dean should give up any pretence that he is picking sides based on scientific merit.

 

Blogger Pharma Bawd said ... (9/20/2006 11:00 AM) : 

Dale, try this URL:

http://www.uwgb.edu/dutchs/PSEUDOSC/SelfApptdExp.htm

 

Anonymous Chris Noble said ... (9/20/2006 8:54 PM) : 

http://www.apa.org/journals/features/psp7761121.pdf#search=%22unskilled%20and%20unaware%22

 

Blogger Pharma Bawd said ... (9/21/2006 8:04 AM) : 

Yeah, I love that Chris! I about busted a gut when you posted that for Wilhelm Godschalk at Aetiology.

That's a classic.

 

Anonymous Chris Noble said ... (9/23/2006 8:50 PM) : 

Dean has set himself up as the arbiter of what is and what isn't science and he cannot even comprehend what possible conclusions can be made from this study after reading it twice.

Perhaps there should be a simple comprehension test given to such individuals. It's all very good for Dean to insist on credentials for everybody else but where are his. And I don't mean a PhD just a demonstrated ability to read and understand scientific papers.

Despite his backpedalling to "just asking questions" Dean has been quite adamant previously in saying that HIV cannot cause AIDS. Celia Farber attempts the same trick by claiming that she is just reporting on the "controversy". In reality she is consistently arguing for one side of the imaginary controversy. If you are going to pretend to be impartial at least do a good job.

Even if Dean was in reality "just asking questions" what is the point if he can't understand the answers?

 

Blogger Pharma Bawd said ... (9/23/2006 9:27 PM) : 

Have you read this Chris?
http://www.bookslut.com/features/2006_09_009885.php

Celia says she lets the data speak for itself, then says the exact same thing about this paper that Hank and Dean said.

"But what I just told you about is a ten-year perspective(sic) study. And when they looked over those ten years the utopian dream did not pan out. Their HIV levels are going down, whoop-dee-doo, but they are not living longer. It’s a very strange position to be in. Those of us on the skeptical side have never been more right but we have never been more hated."

You can't even argue with such ignorance.

I do agree with her on one point though, they have never been more right!

 

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