DEATH, ANTIRETROVIRAL DRUGS, and COGNITIVE DISSONANCE
Posted by Henry Bauer on 2008/05/09
No sooner had I remarked on cognitive dissonance (HIV/AIDS ILLUSTRATES COGNITIVE DISSONANCE, 29 April 2008 ) than a truly hair-raising instance of it turns up: the increasing rate of deaths caused by antiretroviral drugs is said to require clinical trials in which these drugs would be tried out on even healthier people.
Most “AIDS” deaths now are from liver failure, cardiovascular problems, and the like, which are clearly “side” effects of the antiretroviral drugs. By refusing to acknowledge this, however, a recent article interprets the data as calling for administering these drugs to even more people, people whose immune systems are even healthier by the official criterion of CD4 counts in the blood. Under the current guidelines, treatment is recommended for asymptomatic HIV-positive people who have never had an AIDS illness at CD4 counts <200, and it is said to be optional between 200 and 350. Now, it is suggested, treatment should perhaps be recommended at counts even higher than 350:
“Reductions in AIDS-related morbidity and mortality following the advent of combination antiretroviral therapy have coincided with relative increases in chronic non-AIDS end-organ diseases among HIV+ patients….
Higher CD4+ counts on antiretroviral therapy are associated with lower rates of non-AIDS diseases and AIDS. These findings … motivate randomized studies to evaluate the effects of antiretroviral therapy on a broad set of clinical outcomes at CD4+ counts greater than 350 cells/µl.” (emphasis added; Baker et al., CD4+ count and risk of non-AIDS diseases following initial treatment for HIV infection, AIDS 22: 841)
That recommendation is based on the belief that antiretroviral drugs increase CD4 counts, and that higher CD4 counts are not only somehow associated with better health but actually cause better health and prognosis. That belief is not justified by much and long-accumulated data, however. It’s been known at least since the Concorde results published in 1994 that CD4 counts (in the blood) do not correlate with better clinical outcomes, and the large Antiretroviral Collaboration published in 2006 reported that HAART increased rather than decreased the incidence of adverse events (sources cited at p. 169 in The Origin, Persistence and Failings of HIV/AIDS Theory). In between there have been a range of articles pointing the same way, for example the finding that viral load and CD4 counts are not correlated:
“Presenting HIV RNA level predicts the rate of CD4 cell decline only minimally in untreated persons. Other factors, as yet undefined, likely drive CD4 cell losses in HIV infection” (Rodriguez et al., JAMA, 296  1498-1506).
Note that the decline of CD4 counts in HIV-positive people remains to be explained and is not owing to the amount of purported virus measured supposedly by viral load.
Yet Baker et al. in their 2008 publication cite a 1997 paper for the beneficial effect of HAART in restoring CD4 counts, while neglecting to mention “immune restoration syndrome”, described already in 1999: the phenomenon in which supposedly restored immune-system function leads to death rather than health; and Baker et al. cite a 1998 paper reporting declining mortality, very few years after HAART was introduced, while ignoring the Antiretroviral Collaboration published in 2006 that found increased mortality.
Correctly cited are no fewer than 10 independent studies, published between 2002 and 2007, that found increased incidence of and death from liver, cardiovascular, and renal diseases, and from some cancers, among HIV-positive people on antiretroviral treatment. In their own study, remarkably, Baker et al. want to ascribe this to “prolonged survival” achieved by antiretroviral treatment. Yet the median ages of their patients who suffered or died from these non-AIDS illnesses was between 40 and 44, ages at which one does not normally expect a noticeable rate of death from cancer, or from liver or heart “end-organ” failure. Those conditions are typical effects of drugs.
Not only does the selective citation of data and the manner of interpretation adopted by Baker et al. allow much room for questions to be raised, so does the very manner in which they report the data. Here is their summary (their Table 1; “FIRST” is an acronym for the Flexible Initial Retrovirus Suppressive Therapies trial):
Please look at the numbers carefully. 188 total deaths are reported, of which 89 are from AIDS and 27 from non-AIDS “events”. “AIDS” and “non-AIDS”, one might imagine, are mutually exclusive categories that together cover all possibilities; yet 188 minus 89 minus 27 leaves 72 deaths unaccounted for.
Only several paragraphs below the table are these referred to: “16 were a result of sepsis/shock, 17 from respiratory failure or pneumonia, 17 from other cardiovascular causes (arrhythmia, heart failure, pulmonary embolus, or aneurysm), and 20 were due to unknown causes”.
How are these 17 cardiovascular-caused deaths different from the 5 reported in the Table as “non-AIDS cardiovascular”, since apparently they are not “AIDS”?
Why were not all those 72 deaths acknowledged as “non-AIDS”?
What possible reason is there not to regard these deaths as plausibly occasioned by the antiretroviral drugs?
Furthermore, what is one to say about a study in which 20 deaths — 20 out of 188, a little over 15% — are attributed to unknown causes? Who was in charge here? How were the patients being monitored? Who signed the death certificates? Why were no autopsies performed in cases of doubt about the cause of death? In a study specifically aimed at elucidating ways of decreasing mortality, what possible excuse is there for such lapses? (And, not by the way, what does this say about the quality of the editorial review and refereeing practices of this journal?)
Enough of rhetorical questions: There were actually 99 non-AIDS deaths and 89 AIDS deaths. All the causes of the non-AIDS deaths are conditions typically associated with “side” effects of drugs. Since the median age of the patients was about 40, it is more than plausible that they were caused by the antiretroviral drugs. Indeed, the latest version of the official Treatment Guidelines states (at p. 13):
“In the era of combination antiretroviral therapy, several large observational studies have indicated that the risk of several non-AIDS-defining conditions, including cardiovascular diseases, liver-related events, renal disease, and certain non-AIDS malignancies … is greater than the risk for AIDS in persons with CD4 T-cell counts >200 cells/mm3; the risk for these events increases progressively as the CD4 T-cell count decreases from 350 to 200 cells/mm3.”
When there are more deaths from scenario A than from scenario B, one might prefer the latter. In other words, better NOT to use antiretroviral treatment, especially with people who initially present with no symptoms of illness and who are treated only because of laboratory tests (“HIV” and CD4) of doubtful validity and significance.
But even accepting the article’s basic premises, note that there is mention of only a correlation between CD4 counts and risk. Anyone should feel free to interpret all this differently, namely: People with higher CD4 counts (in the blood) are better prepared to stave off physiological insults than those with lower counts, and they are therefore better able to resist the toxic effects of antiretroviral drugs. Apparently, the higher one’s CD4 count, the longer one is likely to survive HAART. Recall Julianne Sacher’s explanation of why CD4 counts in the blood vary dramatically from time to time: these cells move to those parts of the body that are under attack (AIDS AS INTESTINAL DYSBIOSIS, 23 February 2008; ALTERNATIVE TREATMENTS FOR AIDS, 25 February 2008).
Baker et al., however, choose to sum up their findings thus:
“Serious non-AIDS diseases, such as liver, cardiovascular, renal, and non-AIDS cancers, have contributed significantly to morbidity and mortality among HIV-infected patients because of the introduction of potent combination ART. It is unclear to what extent this is due to chronic immunosuppression, complications of ART, coinfection, or other established risk factors . . . .
we have established an association between latest CD4+ levels and risk for end-organ diseases not attributable to AIDS following initiation of ART. Further research is needed to establish whether HIV-related immune depletion truly leads to more frequent non-AIDS diseases, and to examine the underlying mechanisms.”
In my view, it is implausible to the point of perversity to suggest “chronic immunosuppression, coinfection, or other established risk factors” as possible reasons for the increased mortality in the same breath as “complications of ART”, given that all the death events are from occurrences well known to typify iatrogenic events; they are typical “side” effects of drugs.
It also seems to me highly irresponsible to suggest “further research” that involves exposing yet more and healthier people to drugs whose toxicity is beyond doubt.
This entry was posted on 2008/05/09 at 8:46 am and is filed under antiretroviral drugs, clinical trials, experts, HIV does not cause AIDS, HIV/AIDS numbers. Tagged: cognitive dissonance about HIV/AIDS, death from antiretroviral drugs, iatrogenic deaths, toxicity of antiretroviral drugs. You can follow any responses to this entry through the RSS 2.0 feed. You can leave a response, or trackback from your own site.