HIV/AIDS Skepticism

Pointing to evidence that HIV is not the necessary and sufficient cause of AIDS

Posts Tagged ‘lying with statistics’

HAART, heart disease, & lying with statistics

Posted by Henry Bauer on 2010/01/19

Brian Carter had asked: “More proof of drugs causing disease?”
in connection with the piece,
“Increased presence, severity of coronary artery plaques in HIV-infected men”
(ScienceDaily, 8 January 2010):
“The HIV-positive participants had longstanding infection, were generally healthy, and the great majority were receiving antiretroviral therapy” [emphasis added].

Seemed likely that the answer would be “Yes” to Brian’s question, so I got the original article, “Increased prevalence of subclinical coronary atherosclerosis detected by coronary computed tomography angiography in HIV-infected men” (Lo et al.). I was surprised to read that duration of HIV infection was significantly associated with coronary plaque build-up “after adjustment for age, traditional risk factors, or duration of antiretroviral therapy” [emphasis added]. If HAART was causing the coronary disease, then longer HAART should correlate with more disease, surely!

Well, consider that statement carefully: It doesn’t deny that duration of antiretroviral therapy is associated with plaque build-up; it just says that HIV infection is independently associated with plaque buildup. But reading the whole article reveals that there’s actually no good evidence that plaque build-up is associated with “HIV” in absence of HAART.

Many studies have indicted HAART for increasing coronary risks, notably the protease inhibitors which disturb fat metabolism. That was reported already within a year or two of the first use of protease inhibitors, which had also been reported to produce hyperglycemia and hemolytic anemia (Massip et al.). “Use of HIV PIs is associated with atherogenic lipoprotein changes and endothelial dysfunction. Because these metabolic and vascular changes predispose to atherosclerosis, monitoring and treatment of dyslipidemia in patients taking these medications is warranted (Stein et al.).

HAART doubles the risk of coronary heart disease in young adults (Currier et al.) and “the proportion of deaths attributable to non-AIDS diseases increased and prominently included hepatic, cardiovascular, and pulmonary diseases, as well as non-AIDS malignancies. Longer time spent receiving HAART and higher CD4 cell counts at HAART initiation were associated with death from non-AIDS causes. CD4 cell count at time of death increased over time” (Palella et al.). HAART also is associated with an increased thickness of carotid-artery deposits (IMT): “Antiretroviral-treated patients had a higher median IMT than the untreated patients (0.94 vs. 0.85 mm, P = 0.006; Fig. 3). Furthermore, among all HIV-infected participants, increasing duration of HAART (rho 0.20, P < 0.001), protease inhibitor use (rho 0.19, P < 0.001), and nucleoside analogue use (rho 0.23, P < 0.001) were each associated with thicker IMT. These relationships remained significant after adjustment for traditional cardiac risk factors and the duration of HIV diagnosis (P < 0.024 for all)” (Hsue et al.).
((However, this unequivocal statement is followed by equivocations in the article’s Discussion section — “Compared to uninfected controls, carotid IMT was higher among all groups of HIV patients, irrespective of antiretroviral treatment or the level of viremia”; yet also “antiretroviral therapy and advanced immunodeficiency likely contribute independently to atherosclerosis in HIV patients”. The equivocation may be inevitable since the HIV-negative “controls” had lower coronary risk factors, so the study could not possibly identify “HIV” as the cause of more coronary disease:
“The  HIV-seropositive patients were older than the controls (48 years compared to 43 years) and more likely to have smoked in the past. The HIV-seropositive patients were also more likely to have had a prior history of coronary artery disease and a prior history of hypertension, whereas the controls had a higher LDL cholesterol [112 vs 103] and HDL cholesterol [47 vs 42.7]”. My cardiologists asserted that the risk factor is actually HDL/LDL ratio, desirably >0.3 and ideally >0.4. Here we have controls with 47/112 = 0.420, in other words no risk factor, and “HIV-positives” with 42.7/103 = 0.414, indistinguishable from controls. In other words, “HIV-positives” in this study had unquestionably higher risk factors, making any implication of “HIV” highly questionable. You can’t claim significant results if the controls aren’t proper controls, no matter how you dice and slice the numbers.))

The Treatment Guidelines issued by the National Institutes of Health surely represent an official mainstream consensus, and they are clear that HAART is associated with increased organ failure including adverse coronary events:
“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 [14-19] 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” (emphases added; p. 21, 3 November 2008).

How then could Lo et al. claim that HIV infection was significantly associated with coronary plaque build-up “after adjustment for . . . duration of antiretroviral therapy”?

In point of fact, some of the reported data do show an effect of HAART on plaque build-up — albeit there’s a certain amount of statistical legerdemain to wade through, and the need to THINK about whether the statistical calculations make sense.

The authors’ affiliations are with programs in Nutritional Metabolism, Cardiovascular Imaging, and Internal Medicine, entirely appropriate for examination of arteries and the like, but not necessarily for statistical analysis. It may be, of course, that one or more of the authors is expert in statistics, but it isn’t confidence-building to read that
“Two-tailed probability values are reported and statistical significance was assumed when P value was less than 0.05. All statistical analyses were performed using JMP (SAS Institute Inc., Cary, North Carolina, USA) and SPSS (SPSS Inc., Chicago, Illinois, USA).”
Expert statisticians tend to groan and roll their eyes heavenward when non-statisticians use such readymade statistics software packages and feed data into them without thinking knowledgeably about whether a particular mode of analysis makes sense.

Lo et al. used imaging to measure degree of atherosclerosis “in HIV-infected men”, with a sample of 78 and 32 controls of HIV-negative men matched for cardiovascular risk factors, and they found significantly more plaque in the “HIV-infected”. Then, among the HIV-infected only, they compared those with plaque (32) and those without (46) and found statistical significance at the p<0.05 level for several parameters (Age, Race, Framingham risk score, Duration since HIV diagnosis, CD4+/CD8+ T-lymphocyte ratio, Total cholesterol, Triglycerides, Cytomegalovirus titer), but not for antiretroviral treatment:

Note that ALL of the measures of HAART duration are higher in the plaque group. That these differences do not reach significance at the p<0.05 level is no evidence, however, against the previously well-established fact that antiretroviral treatment causes coronary disease. At a minimum, one would say that while the numbers do not add statistically significant evidence, they are consistent with the expectation that HAART causes coronary disease:
— For one thing, the sample sizes are not large enough to produce statistical significance in a multivariate analysis with so many variables.
— Second, comparing mean years of treatment is not the best way to look for possible causation of coronary disease. One would like to see a graph or data set showing the raw data for each individual, because one wants to test for the presence of a threshold effect or some other non-linear dose-effect or duration-effect relationship: it is perfectly feasible, perhaps even to be expected, that a certain period of years on antiretroviral treatment would produce no discernible plaque but that accumulation might progress relatively rapidly once plaque has begun to form.
— Third: One would like the data for individuals also because of certain apparent incongruities, for instance the much shorter periods on protease inhibitors than on antiretroviral treatment as a whole, since HAART is generally thought to have protease inhibitor as one of the typical components.
— Above all, though, the manner in which these numbers are presented makes it easy to overlook that the best indicator of whether HAART causes coronary disease is to compare “HIV-positive” people who have never been on HAART at all with those who have been. Here, there is no significant difference found, with p=0.16 too large. But hidden in plain view is the fact that the number of individuals NOT on HAART was only 3 in the no-plaque group and 1 in the plaque group!
NOT on HAART were 3/32  (9.4%) in the no-plaque group and 1/46 (2.2%) in the plaque group. That looks quite significant, and very different from 90.6 vs. 97.8.

“How to Lie with Statistics” by Darrell Huff (1954/1993) and “Damned lies and statistics: untangling numbers from the media, politicians, and activists” and “More damned lies and statistics: how numbers confuse public issues” by Joel Best (2001,2004) point to many other devices for presenting numbers and statistical data to produce a desired impression not necessarily warranted by the data themselves. In the present case, one can legitimately state a priori that it is unlikely to be a good test of the influence of HAART on coronary disease when the proper control group — “HIV-positive” individuals who have never experienced HAART — constitutes only 4 of the sample of 78. Further, any possible effect is hidden rather than exposed when the data are presented only as averages, which leave salient questions unanswerable. For example, the average time since HIV diagnosis is 13.5 years, yet the average duration of antiretroviral treatment is 6.2 and 7.9 years for the two groups but only 4 individuals out of 78 have never had antiretroviral treatment: How many had very short courses? Why? What were the differences in individual treatments? And so on.

Given the small sample size, one might reasonably conclude that statistical analysis could not command the power to deliver statistically significant results, and one would make do with the numbers themselves. And those numbers are perfectly consistent with all the previous reports that antiretroviral treatment increases the risk of coronary disease (and also kidney and liver disease as well as certain cancers). After all, among people never on HAART, 75% (3/4) had no sign of coronary disease and only 25% did, whereas of those who have experienced HAART, 61% showed plaque (45/74).

Above all, the data presented by Lo et al. shows a pronounced increase in cardiovascular disease with longer duration of “HIV infection” AND 74  OF  THE  78  PEOPLE  IN  THE  SAMPLE  HAD  BEEN  ON  ANTIRETROVIRAL  TREATMENT, only 4 had not, and 3 of those 4 showed no sign of cardiovascular disease. Those data are at least equally compatible with the inference that duration of HAART correlates with cardiovascular disease, and comparisons of those with and without plaques confirms that: Those with plaque had experienced antiretroviral treatment 27% longer (7.9 vs 6.2 years), particularly protease inhibitors (52% longer, 4.4 vs 2.2).

Lo et al.: Janet Lo, Suhny Abbara, Leon Shturman, Anand Soni, Jeffrey Wei, Jose A. Rocha-Filho, Khurram Nasir, and Steven K. Grinspoon, “Increased prevalence of subclinical coronary atherosclerosis detected by coronary computed tomography angiography in HIV-infected men” AIDS 24 [2010] 243-53

Massip et al.: P. Massip, B. Marchou, E. Bonnet, L. Cuzin, & J. L. Montastruc, “Lypodystrophia with protease inhibitors in HIV patients”, Thérapie 52 [1997] 615

Stein et al.: James H. Stein, Melissa A. Klein, Jennifer L. Bellehumeur, Patrick E. McBride, Donald A. Wiebe, James D. Otvos, & James M. Sosman, “Use of Human Immunodeficiency Virus-1 Protease Inhibitors is associated with atherogenic lipoprotein changes and endothelial dysfunction”, Circulation 104 [2001] 257-62.

Currier et al.: Judith S. Currier, Anne Taylor, Felicity Boyd, Christopher M. Dezii, Hugh Kawabata, Beth Burtcel, Jen-Fue Maa, & Sally Hodder, “Coronary heart disease in HIV-infected individuals”, JAIDS 33 [2003] 506-12

Palella et al.: Frank J. Palella, Jr., Rose K. Baker, Anne C. Moorman, Joan S. Chmiel, Kathleen C. Wood, John T. Brooks, Scott D. Holmberg, & HIV Outpatient Study Investigators, “Mortality in the Highly Active Antiretroviral Therapy era — Changing causes of death and disease in the HIV Outpatient Study” JAIDS 43 [2006] 27-34

Hsue et al.: Priscilla Y. Hsue, Peter W. Hunt, Amanda Schnell, S. Craig Kalapus, Rebecca Hoh, Peter Ganz, Jeffrey N. Martin & Steven G. Deeks, “Role of viral replication, antiretroviral therapy, and immunodeficiency in HIV-associated atherosclerosis”, AIDS 23 [2009] 1059-67

Posted in antiretroviral drugs, clinical trials, experts, HIV risk groups, HIV/AIDS numbers | Tagged: , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , | 7 Comments »


Posted by Henry Bauer on 2008/08/22

“HIV” is the worst evil in the world, according to HIV/AIDS believers:
— They want to give drug addicts fresh needles, because cocaine and heroin are so much better, so much more healthy than “HIV”; see COCAINE AND HEROIN AREN’T GOOD FOR YOU! [a Golden Fleece Award, 13 June 2008];
— They will treat Africans for worm infestation only if that makes antiretroviral treatment more efficient; see PARASITIC WORMS are *NOT* GOOD for you!, 24 July 2008; ARE INTESTINAL WORMS GOOD FOR US? ARE THEY GOOD FOR AFRICANS? FOR AFRICAN CHILDREN?, 30 December 2007;
— They will provide food to malnourished Africans only if that helps with antiretroviral treatment ; see DRUGS OR FOOD?, 25 December 2007; FOOD IS GOOD FOR CHILDREN, 8 January 2008;
— “HIV” does ALL SORTS of dreadful things, like instigating bone fractures; see TALKING OF HIV’S MAGICAL POWERS…, 29 DECEMBER 2007.

And so on. No doubt about it, “HIV” — or, of course, “HIV/AIDS” — is the worst evil in the world.

Therefore it makes sense to study — and to acquire research grants to study — whether abused women are at greater risk of “HIV” than non-abused women are. If one finds that they are at greater risk, that would provide a compelling reason to regard the abusing and battering of women as a bad thing and perhaps even to look for ways of helping abused women and of trying to prevent such abuse.

A corollary that seems to me obvious, though apparently not to HIV/AIDS believers, is that if abused women are NOT at greater risk of “HIV”, then there’s no need to give further thought to the plight of abused women?

My e-mail friend Andy D. found this as absurd as I did, and drew my attention to the several news items in which the HIV status of abused women is treated as a matter of the highest newsworthiness:

AIDS infection risk higher in abused Indian women, study says” (John Lauerman, Aug. 12, Bloomberg)
“Indian women who are physically and sexually abused by their husbands are four times more likely to have HIV than other wives . . . . AIDS prevention should focus more on mistreatment of women . . . .
India’s AIDS epidemic is the third largest of any country in the world, and infections among women are rising . . . . Health officials should target wives who are forced to have unsafe sex, along with their husbands, for preventive measures, said study author Jay Silverman, an associate professor of society, human development and health at the Harvard School of Public Health in Boston.
’Sexual abuse of adolescent girls and women is driving the HIV epidemic in India and around the world . . . . We need to make it a major priority for prevention.’
The findings echo a 2004 study of women in South Africa, . . . [where] abused women were 50 percent more likely to be HIV-infected than non-abused women, regardless of their own behavior.
’In many settings, women’s risk of HIV is largely driven by the behavior of their male partners,’ said Kristin Dunkle, an assistant professor of behavioral sciences and health education at the Emory Center for AIDS Research in Atlanta . . . .
About 0.73 percent of women who had been physically and sexually abused were infected, compared with 0.19 percent among non-abused women . . . . Almost all the women, 95 percent, reported that they had no extramarital sexual relations themselves . . . . That points to known patterns in the behavior of abusive husbands that puts their wives and children at higher risk of HIV infection . . . . Sexually abusive husbands may force their wives to have intercourse without condoms, or unprotected anal sex, both of which can significantly increase HIV infection risk . . . . The men may also be having risky sex with women outside the marriage, increasing their own chance of infection . . . . ‘We have to get to the men,’ Silverman said. ‘And we have to provide women with reasonable alternatives if they’re being abused, so they can maintain their children and not become destitute.’
. . . . ‘To be truly successful in addressing the spread of HIV in India, we must think of ways to address the all-too-widespread mistreatment of wives,’ said Donta Balaiah of the Indian Council of Medical Research, who helped write the study. The study was supported by the U.S. National Institute of Child Health and Human Development in Bethesda, Maryland, and the Indian Council of Medical Research in New Delhi, which funds and promotes research in the country.”

Another version was in CBC News: “Prevent abuse of women to stem rise of HIV: researchers” (August 12) :
“ . . . . despite a lower prevalence of infection among India’s general population, women account for a rising percentage of HIV cases. . . . ‘married Indian women who experienced both physical and sexual intimate partner violence demonstrated an HIV infection prevalence approximately four times greater than that of non-abused women,’ . . . . The risky sexual behaviour of husbands was the major source of women’s infection . . . . They suggested that doctors and public health officials focus on preventing intimate partner violence to help reduce the spread of HIV/AIDS.”

The scientific publication on which these stories are based is Silverman et al, JAMA 300 [2008] 703-710.


As I said at the outset: The prime reason for trying to do something about abuse of women is apparently to prevent the spread of HIV.

That’s a heartless HIV/AIDS cart-before-horse stupidities. To my mind, any abuse of human beings is a thoroughly despicable and detestable thing, and we should do everything we can think of to prevent it. Naturally enough, the more it can be prevented, the more beneficial COROLLARIES there will be — for the women’s emotional and mental as well as physical health, and that of their family members; and much more. How on earth does “HIV/AIDS” come to take priority over everything else? Perhaps because any mention of it brings the money flooding in?

Note also the HIV/AIDS-typical abuse of statistics and data in this:

“India’s AIDS epidemic is the third largest of any country in the world”
only because India has so large a population. The HIV-positive rate in India is among the lowest in the world. Moreover, the HIV/AIDS guru at the World Health Organization admitted that there had not been and would not be a heterosexually spread epidemic there, see WHO SAYS that WE’VE BEEN VERY WRONG about HIV and AIDS? (Clue: WHO = World Health Organization), 10 June 2008. A year ago, it was conceded that there were about 2.5 million “HIV/AIDS” people in India rather than the 5.7 million estimated earlier (for example, REDIFF: India Abroad — “India’s HIV/AIDS affected reduced to half in revised figures” July 06, 2007; acknowledged in the Silverman et al. article). The earlier number had corresponded to a rate of 0.9%, so the newly estimated rate is 0.4% — as I said, among the very lowest in the world.

“and infections among women are rising”

This illustrates a common way in which statistics are abused for the purpose of misleading. If something starts at zero and then “increases” to barely noticeable, that’s an enormous increase if you express it in percentages!

This device is used pervasively in marketing medicines. “Take XXXXX”, we are assured, and “cut in half” our risk of YYYYY; where YYYYY might be heart attack, stroke, just about anything undesirable. If you are inclined to take this sort of thing at face value, then you should read Malignant Medical Myths by Joel Kauffman (read this for an excellent summary). If the risk of YYYYY is, say, 1%, does it make sense to try to reduce this to 0.5% when the “side” effects of prolonged dosing with XXXXX brings its own tangible risks? The only clinical trials worth attending to are those for which the important data are rarely published: namely, changes (if any) in ALL-CAUSE MORTALITY. If XXXX is good for you, then it should lower ALL-CAUSE mortality, not just the risk of YYYYY.

Silverman et al. further illustrate misleading via numbers with “Despite recent reductions in HIV prevalence among both the general population and many high-risk groups, the percentage of all infections occurring among Indian women (currently estimated at 39%) has continued to rise relative to that among men” [emphasis added].
How impressive that “39%” appears! An enormous “increase”!
But in India the overall rate for women is 0.22% and for men 0.36%, both extraordinarily low by any standards. Yet these trivially low rates allegedly cause India to be “recognized as the source of increasing HIV prevalence among its South Asian neighbors”!
I suppose a prevalence of even 0.4% poses a threat to neighbors like China, Laos, and Pakistan where the prevalence is estimated at 0.1%; let alone to those where it’s estimated at LESS than 0.1% (Afghanistan, Bhutan, Bangladesh, Sri Lanka); but surely the threat is the other way around from Myanmar (1.3%) or even Nepal (0.5%). This is worse than ludicrous.

Silverman et al. reported that “7.68%” (2161) of 28,139 women had been both physically and sexually abused; and “0.73%” (205) tested HIV-positive. A statistical test marked the difference between that 0.73% and the 0.19% among non-abused women as “statistically significant”. Maybe, although we lay people wonder why fewer than 1 in 10 of those “at risk” abused women were actually HIV-positive; but bear in mind that “statistically significant” is not the same as PROVEN. More important, what’s statistically significant is NOT that physical and sexual abuse are CAUSATIVE of testing HIV-positive, only that the two things are CORRELATED; and


Note, too, the usual abundance of assertions about matters that are not known:
“women’s risk of HIV is largely driven by the behavior of their male partners”
— Were all the male partners investigated to arrive at that “largely”?
— And who established “known patterns in the behavior of abusive husbands”?

Where I would thoroughly agree — at least for the purpose of the published study — is that “’We have to get to the men,’ Silverman said”.

I wish the authors had done that, and had tested all the husbands of those abused women of whom 95% had not had extramarital relations, because an essential — but missing — part of the study is to discover, how many of those husbands are themselves HIV-positive. If they aren’t, then they didn’t infect their wives, after all.

My prediction is that very few of those husbands are HIV-positive, certainly many fewer than 95% of them.

Think about it. 0.73% of Indian women are physically and sexually abused and HIV-positive. Each has a husband, so those husbands represent about 0.73% of Indian men (only “about” because the ratio of males to females is not 1 and varies with age). In the overall population of India, however, only 0.36% of men are HIV-positive. Therefore physically and sexually abusive husbands must be twice as likely as other men to be HIV-positive AND ALL OF THOSE MUST HAVE INFECTED THEIR WIVES — a truly remarkable set of circumstances, especially given that the claimed average rate of sexual transmission of “HIV-positive” without use of condoms is about 1 per 1000. It gets only more remarkable when one takes into account that about ¾ of all “HIV transmission” in India is NOT owing to marital sex, if India is at all comparable to Asia as a whole, see HIV/AIDS ILLUSTRATES COGNITIVE DISSONANCE, 29 April 2008. Then the husbands of those poor HIV-positive abused women must themselves be not twice as likely but 8 times as likely as other Indian heterosexual men to be HIV-positive?

The fact of the matter is that testing HIV-positive does not mark infection by a sexually transmitted agent, it is a sign of physiological stress. That physically and sexually abused women are 4 times as likely as untroubled women to be seriously stressed should be no surprise to anyone, not even to researchers who conjure up imaginative grant proposals.

Posted in clinical trials, experts, Funds for HIV/AIDS, HIV absurdities, HIV as stress, HIV risk groups, HIV skepticism, HIV tests, HIV transmission, sexual transmission, uncritical media | Tagged: , , , , , , , , , , , | 1 Comment »

%d bloggers like this: