Pre-exposure prophylaxis: A flawed clinical trial that no one should take seriously

“Daily AIDS drug lowers risk of HIV, study finds” (David Brown, Washington Post, 24 November, 2010),      is how the media ballyhooed a study that is not worth the paper it was printed on (or will be printed on, since it had only been released on-line).
“When gay men at high risk of becoming infected with HIV through sex take a daily dose of antiretroviral drugs, their chance of catching the virus drops by at least 40 percent, according to a new study. The protective benefit could be as high as 95 percent if a person is extremely attentive about not missing a dose, the research on nearly 2,500 men on four continents found.”
But the protective effect could also be as little as zero, even if no dose is ever missed, because the details of this study inspire no confidence at all. The on-line publication was available as of 28 November 2010 at http://www.nejm.org, together with a Supplementary Appendix that contains further details.
As usual, there are general reasons for skepticism: No single publication or study should ever be accepted at face value (“Real science isn’t news”); and the statistical criteria used, p<0.05, may greatly overstate the significance of the results (Matthews, “Significance Levels for the Assessment of Anomalous Phenomena”). But there are also some very specific reasons for not taking this work seriously: the subjects of the study were rather sick people leading highly unhealthy life-styles.
The median age of these men (including some transgendered former men) was about 25 (data in Figure 3). A little over half of them had more than 5 drinks in any given day on which they drank. 1 in every 7 or 8 reacted positive on a syphilis test, and more than a third did so for herpes. Unprotected anal intercourse in the last 3 months was acknowledged by 60% of them, and in the last 6 months by 80%. And 40% reported “transactional sex” during the last 6 months. It is unconscionable to suggest, as the report does, that this group might be representative of “men who have sex with men”. It is representative only of people who work at least occasionally as male prostitutes and who behave in ways conducive to poor health and high risk of all sorts of infection.
Furthermore, a few exceptionally promiscuous subjects might well have had a disproportionate influence on the overall results: Table 1 reports the number of partners in the last 12 weeks as 18±35 and 18±43 for treated and placebo groups respectively, indicating that a few individuals are clear outliers. The same is suggested by Figure S2, where for most of the study period the mean number of partners with whom subjects had receptive anal intercourse was between 4 and 6 while the median was only 1; in anything approaching a normal distribution, mean and median are close to one another (in a truly normal distribution they are identical).
The poor state of health is illustrated by the fact that in both placebo and treated arms more than 1 in 20 of these young men, median age 25, suffered a “serious adverse event” during the median follow-up time of 1.2 years: “Serious adverse events (SAEs) were defined in accordance with the ICH, as any untoward medical occurrence that, at any dose, results in death, is life-threatening, requires inpatient hospitalization or prolongation of existing hospitalization, or results in persistent or significant disability/incapacity”. This is anything but representative of 25-year-old gay men.
Nor were these “Serious” adverse events the only signs of a sick population. Table 2 has about 1 in 8, again in both placebo and treated arms, suffering a grade 3 or 4 event, defined by the Division of AIDS as:
Grade 3 — Severe — Symptoms causing inability to perform usual social & functional activities
Grade 4 — potentially life-threatening — Symptoms causing inability to perform basic self-care functions OR Medical or operative intervention indicated to prevent permanent impairment, persistent disability, or death.
My attempts to determine whether “serious” adverse events in Table 2 included the Grade 4 events was unsuccessful because the detailed information in the Supplement delivered numbers that do not match those in Table 2, presumably because the former omitted events experienced by no more than 25 subjects. Since they are reported separately here, it seems that 17-18% of these young men fell seriously ill in not much more than a year. This is not typical of 25-year-old gay men.

Testing for “HIV-positive” involved two positive rapid tests plus a “confirming” Western Blot or “HIV” RNA. Please recall that Weiss & Cowan have stated, and explained why, neither Western Blot nor PCR nor any other “HIV” test “confirms” infection (“HIV” tests are self-fulfilling prophecies, 10 May 2009).

Even on its own terms, this article contradicts HIV/AIDS theory: Figure S4 shows “HIV RNA level” declining slightly during the first month after seroconversion and then remaining unchanged for as much as 60 months in both placebo and the group treated with ARVs; and the CD4 counts were also essentially the same for those 60 months in both treated and untreated groups. Moreover, “Plasma RNA level was not lower in those reporting higher pill use or in the 3 seroconverters with detectable drug levels” (Supplement, p. 18) — no antiretroviral effect of the antiretroviral drugs, in other words.

So there are ample specific grounds for distrusting the conclusions offered by the authors of this study. Beyond that, there are ample general grounds for never recommending any existing antiretroviral drugs for “pre-exposure prophylaxis”, because that involves administering highly toxic agents to perfectly healthy people. Even this study notes that “Side effects may have contributed to low pill use among some subjects” and “TDF [tenofovir disoproxil fumarate] treatment is known to cause decreases in renal function” — yes indeed, see “Kidney-disease denialism (a special case of HAART denialism)”, 2010/11/20.

The mainstream promulgates such shibboleths as condoms and circumcision being effective in prevention, and HAART being life-saving, even as the actual data in published studies offer as much evidence against these beliefs as for them. One finds acknowledgment that the shibboleths are baseless only when it suits the mainstream to tout some new approach or to repeat the need for more research. Thus here it is admitted, in the context of hyping the present study, that prevention approaches have been singularly unsuccessful:
“Few concepts for the prevention of sexual HIV transmission have been rigorously proven: of 37 late-phase trials, only 6 have demonstrated a significant protective benefit. [1,2] Tenofovir 1% vaginal gel had 39% efficacy in heterosexual women. [2] All other successful prevention interventions were clinic-based and directly observed, including enhanced services for sexually transmitted infections (STIs), [3] male circumcision, [4-6] and a vaccine candidate. [7] None of the successful interventions are known to be effective in men and transgender women who have sex with men (MSM), who carry a major burden of the global epidemic. [8,9]” (Supplement, p. 6).

Survey of Gay Asian Men

Some time ago, Joe mentioned a survey that had been carried out by fridae (“empowering gay asia”).

Here are some of the noteworthy points:
About one-third were celibate or monogamous during the last 6 months; another third had a few sexual partners; and the other third were highly promiscuous. In this connection it is vital to recall the survey’s caveat: “The respondents are not a representative sample of the gay community” — one might add, if indeed one can even speak of a gay community.

The survey’s principal selection bias — self-selection — includes interest in participating in such a survey; some of the responses also suggest an unrepresentatively high frequency of travel and high level of promiscuity. The latter, though, makes the responses concerning sexually transmitted infections (STI) and HIV particularly significant: 24% had experienced an STI in the last 6 months, but only 5% were (known to be) “HIV-positive”.
Between 15% and 30% apparently behaved in what has been called a “fast-lane” style, with 6 or more sexual partners within half a year, and 13% used drugs before or during sex. However, only 75% have had at least one HIV test, so the discrepancy between 5% “HIV-positive” and 24% STI may be smaller than it first seems; probably not all that much smaller, though, because half of those who have never been tested were not tested because they knew that they have no reason to be “HIV-positive”. It seems reasonable to infer that STI is more common than “HIV-positive” by a factor of between 2 and 5.

There seems to be a mixture of concern and lack of concern, or perhaps fatalism, as to HIV. There is general willingness (72-81%) to befriend or work with someone “HIV-positive”, but less willingness (60%) to share food with an “HIV-positive” person. Yet 31% will have sex with someone known to be “HIV-positive” — and that 31% must include a significant number who are HIV-negative themselves, since not much more than 5% of the sample is “HIV-positive”. Moreover, 14% have actually had sex with someone “HIV-positive”, and that 14% likely includes some HIV-negative individuals, since (again) not much more than 5% of the sample is “HIV-positive”.
On another hand, 30% of those who have never had an HIV test give as a reason “fear and denial”.

The survey would seem to demonstrate at least two significant points:
1. Becoming “HIV-positive” is much less common than contracting an STI, even in a group that is notably promiscuous and fast-living.
2. The believed existence of HIV contributes to a certain level of confusion and emotional stress.

The low percentage of known “HIV-positive” individuals in this group is also interesting from the viewpoint of racial demographics. A large proportion of this sample appears to be comprised of Asian men, and copious data, especially from the United States, show that people of Asian ancestry are 30-50% less likely to test “HIV-positive” than are white Americans, including among gay men (pp. 36 (Table 6), 37 (Table 7), 54, 56 (Figure 17), 63, 66 (Table 14), 75-6 in The Origin, Persistence and Failings of HIV/AIDS Theory).

Kidney-disease denialism (a special case of HAART denialism)

Mainstreamers have perfected the ART of explaining away the toxicities of HAART even as they publish illustrations of its statistically significant toxicities. They find  that HAART causes oxidative stress even “during apparently successful HAART”, which “underline[s] HAART associated toxicity”; yet they practice HAART denialism by calling it “life-saving”.
They know that protease inhibitors cause lipodystrophy, but practice denialism by calling it “HIV-associated” lipodystrophy.
They know that HAART causes kidney disease, but practice denialism by calling it “HIV-associated nephropathy”, underscoring how well established this is supposed to be by giving it an acronym, HIVAN (Mocroft et al., “Estimated glomerular filtration rate, chronic kidney disease and antiretroviral drug use in HIV-positive patients”, AIDS, 24 [2010] 1667-78):
“increasing exposure to tenofovir was associated with a higher incidence of CKD [chronic kidney disease] . . . .
Nephrolithiasis was seen in up to 27% of patients treated with indinavir [23,24] and there are numerous studies [25–29] demonstrating that tenofovir is associated with impaired kidney function . . . .”
After 24 months, 1.5% of patients on HAART had developed kidney disease, and 3% had after 36 months. Two other methods of assessing the results gave similar numbers, 0.95 and 0.88 respectively as incidence of kidney disease per year ( = 1.8-1.9% after 24 months, 2.7-3% after 35 months).
Now how could one practice denialism in the face of these statistically significant findings?
Here’s how:
“This study has demonstrated a relatively low proportion of patients developing CKD and that in addition to the traditional risk factors for renal disease, increasing exposure to tenofovir, indinavir, atazanavir and lopinavir was associated with an increased incidence of CKD” [emphasis added] —
A few percent is indeed a low percentage, though one doubts whether properly informed patients would willingly accept that high a probability of losing their kidney function.
The insertion of “in addition to the traditional risk factors” has only one purpose, to defuse the following admission that HAART kills kidneys. Those “traditional” factors include age, hypertension, and diabetes; but they are entirely irrelevant, since HAART independently kills kidneys.
The abstract practices this denialist obfuscation in its first sentence: “Chronic kidney disease (CKD) in HIV-positive persons might be caused by both HIV and traditional or non-HIV-related factors”. What the article fails to say, though, is that the work proves that HAART causes kidney disease but offers absolutely no evidence that “HIV” does.
Admittedly, some patients “at baseline” already had early signs of kidney disease; but given that “HIV” tests react poz to a wide range of disease conditions, it may well be that those individuals tested “HIV-positive” only because they already suffered from some sort of kidney problems — which “treatment” then promptly made worse.
The article’s “Introduction” lays HIV/AIDS belief on the line at once:
“HIV infection is associated with renal dysfunction, including HIV-associated nephropathy (HIVAN), immune complex kidney disease and acute renal failure [1,2], which may be associated with progression to AIDS and death [3,4]. There is increasing evidence that HIV infection of the kidneys is involved with HIVAN [5], whereas other disorders include nephropathy resulting from coinfection with hepatitis B, hepatitis C or syphilis [6,7]; diabetes or hypertension [8] and immune complex glomerulonephritis [9]”.
This is followed by remarkable claims:
“The incidence and occurrence of renal disease has decreased since the widespread introduction of combination antiretroviral therapy (cART) [10,11], with studies suggesting that cART reduces the incidence of HIVAN [12], possibly by slowing the decline in renal function [13,14]”.
I’m awaiting delivery of copies of those references 10-14, but it is curious indeed that Mocroft et al. should cite them in this manner but then, in their abstract and conclusions, point only to kidney damage done by HAART. Evidently their work has superseded and contradicted those earlier claims, yet they cite them here and do not anywhere discuss the conflict with their own findings. To have done so would, of course, have made kidney-disease denialism and HAART denialism more difficult.
The article’s final paragraph seeks to give the impression that kidney damage comes only from tenofovir:
“increasing exposure to tenofovir was associated with a higher incidence of CKD independently of other antiretroviral drugs and traditional CKD risk factors. The increase in risk of CKD was also true for indinavir and atazanavir, whereas the results for lopinavir/ r were less clear. There may be some reversibility in CKD after discontinuation of the antiretroviral drugs, but this requires confirmation in larger studies with longer follow-up”.
While the large effect of tenofovir could not be denied, the attempt to make it seem that there is some doubt about damage from the others is disingenuous, for the incidence-over-time trend is reported as positive in all of these cases, at very high statistical significance, p<0.0001 (Figure 2).
Furthermore, the suggested hope that HAART-caused kidney damage might be reversible is not supported by the earlier observation of “high risk of CKD in the group of people within 12 months of stopping tenofovir”.
The call for more research is routine, of course, and demonstrates the willingness of HIV/AIDS researchers to continue to observe, for the good of science and medicine and humanity, what happens to people who are being slowly poisoned by their “treatment”.
As of January 2009, there were well over 100 clinical trials of tenofovir (Tenofovir and the ethics of clinical trials), including as prophylaxis (Prophylaxis via organ failure and bankruptcy) against contracting “HIV”, some of them using tenofovir in a microbicide (More clinical trials in Africa; Reading HIV/AIDS numbers) despite the horrendous “side” effects that had long been known (To avoid HIV later, damage your kidneys and liver now, 19 January 2008).

Tuskegee and Guatemala were not the last examples
of Mengele-type human experimentation
by doubtless-well-intentioned medical researchers.

Facts versus Faith (cognitive dissonance again)

In my last post I ascribed to cognitive dissonance the inability of mainstream researchers to grasp fully the plain fact that HAART has been demonstrably responsible for a range of quite-often-fatal “side” effects including organ failure (of heart, kidney, and lung in particular) as well as life-long mitochondrial dysfunction, lipodystrophy, bone loss, and bone-marrow damage. (And that is doubtless an incomplete list.)

Another major example of cognitive dissonance is the inability to grasp what the demographics of “HIV” tests demonstrate: namely, that what is measured is not an infectious agent. For instance, people of relatively recent African ancestry invariably test “HIV-positive” more often than others, by not much less than an order of magnitude and often more, when matched for any other demographic variable. (“Relatively recent”, because all modern-sapiens human beings are of African ancestry if one goes back far enough, say more than 100,000 years or so.)

Writing about this, I was led to think back on how difficult it had been for me to see what these demographics meant, even though I had already come to disbelieve that HIV could be the cause of AIDS. If it was difficult for someone who didn’t fully believe HIV/AIDS theory to grasp the heretical significance of the demographics, how extraordinarily difficult must it be for true believers? Thinking along those lines may enable one to appreciate, I think, the power that cognitive dissonance wields.

My first encounter with HIV/AIDS dissidence had been the 1994 Ellison-Duesberg book. Over the years I then read a few other dissident works, finding the viewpoints plausible though not conclusively compelling; for example, I was impressed by Root-Bernstein’s multifactorial hypothesis that included “HIV” as a co-factor.
I began to read intensively about the question only after I had found in Harvey Bialy’s book an assertion about HIV tests that simply could not be correct under the mainstream view. Up to that time, I had not questioned the existence of HIV, its infectiousness, or its detection by HIV tests. I had had no occasion to question those: my introduction to the matter had been through the work of Duesberg, universally accepted as expert retrovirologist, who differed from the mainstream over whether or not HIV caused AIDS, not over its existence or its being a retrovirus. Almost all the dissident material I later encountered also concentrated on that issue of causation, not on what “HIV” tests detected or on the nature of “HIV”.
Bialy quoted a mainstream source to the effect that when the Army began to test potential recruits in the mid-1980s, it found in teenagers all over the country much the same prevalence among females as among males. But that could not be the case, if — as the mainstream view would have it — HIV had entered the USA during the mid-1970s in gay communities in two or three large cities: it could not have spread to teenage females all over the country within 10 years.
Chapter 1 of my book describes how I checked Bialy’s source and then collected as much additional data as I could on the results of HIV tests. That chapter does not describe, however, the state of my mind and emotions during that time. I couldn’t believe what the demographics showed, but equally couldn’t see what was wrong with the data. I tried to get help from other people, not very successfully. This long piece which I wrote as part of that attempt may convey my months-long state of emotional and intellectual turmoil; it shows how difficult it was for me to accept what the data pointed to, how hard I tried to reach some non-heretical interpretation. So pity the true believer faced with the ample conclusive evidence that disproves HIV/AIDS theory.

*                    *                    *                    *                    *                    *                    *                    *

The foregoing was set off by an article by Adimora et al., “Ending the epidemic of heterosexual HIV transmission among African Americans” (American Journal of Preventive Medicine, 37 [2009] 468-71). It makes rather desperate attempts to come to terms with — really, to evade the significance of — the evident fact that recent African ancestry in itself is a reason for testing “HIV-positive”.
Adimora et al. recognize that African Americans test “HIV-positive” at rates similar to those found among people of African ancestry elsewhere (in the Caribbean as well as in southern Africa itself), and that the differences are independent of behavioral and social variables:
“estimates of HIV prevalence among African Americans are strikingly similar to, and in some cases exceed, population-based estimates of HIV seroprevalence . . . reported by several countries in sub-Saharan Africa, Asia, and the Caribbean. . . . Although individual-level sexual behaviors contribute to the disparity in HIV prevalence, observed differences in individual behaviors do not fully explain the marked racial differences in HIV infection prevalence. . . . HIV prevalence among African Americans exceeds that of whites, typically substantially, even in comparisons stratified by education, poverty index, marital status, age at first sexual intercourse, lifetime number of sex partners, history of male homosexual activity, illicit drug use, injection drug use, and herpes simplex virus type 2 (HSV-2) antibody positivity” [emphases added]. In other words,

no economic, social, or behavioral variables explain
the racial disparities in “HIV” status.
Race itself remains as the only correlate.

It may not be immediately obvious why this conclusion should be unthinkable. After all, the Food and Drug Administration has been comfortable with approving heart medication specifically for African Americans. Crestor acknowledges that Asians should be prescribed lower doses than others.
Perhaps the difference lies in the fundamental faith that “HIV” is infectious? Yet it has long been accepted that people of African and Mediterranean ancestry are prone to harbor genes for sickle-cell anemia because those are protective against the effects of malaria, an infectious disease.
All those, however, are physical, physiological, correlates of race. And utterly ingrained in HIV/AIDS believers is the axiom that “HIV” is spread primarily by sexual practices, in other words because of particular types of behavior.
Now, this belief condemns HIV/AIDS theory and practice to restate common racist stereotypes about black sexuality: inherently black behavior leads to being “HIV-positive”. Political correctness then requires this racist viewpoint to be camouflaged by placing the blame for this postulated different racial behavior not on those who behave this way but on their victimization by others; or, as Adimora et al. phrase it, “structural violence”:
“a social system characterized by inequalities in power and life chances of sufficient magnitude to restrict a group of people from realizing their full potential 23 and put them ‘in harm’s way.’ 24 The system is structural because it is ‘embedded in the political and economic organization of our social world’ and ‘violent because it causes injury to people (typically, not those responsible for perpetuating such inequalities)’ 24”.
The effects of structural violence include the higher prevalence of sexually transmitted disease among African Americans and “poverty, the low male-to-female sex ratio, de facto racial segregation, and disproportionate incarceration”.
The central flaw in all this is that the racial disparities in rates of “HIV-positive” remain when those postulated effects of structural violence have been taken into account, as Adimora et al. themselves acknowledged: the disparities are NOT owing to differences in “education, poverty index, marital status, age at first sexual intercourse, lifetime number of sex partners, history of male homosexual activity, illicit drug use, injection drug use, and herpes simplex virus type 2 (HSV-2) antibody positivity”, all the variables that would reveal effects of structural violence.
Another way of parsing the rationalizing by Adimora et al. is this: African Americans always test “HIV-positive” more often than whites. This cannot be owing to the fact of their race, it must be owing to the discrimination they have always suffered. Therefore their sexual behavior and its consequences are not under their individual control.
Of course this too cannot be stated plainly because it’s demeaning, so it is expressed in sociologese jargon that plays around with such abstractions and generalities as “structural violence”. Nevertheless, the meaning remains: The long record of discrimination and unjust treatment has caused contemporary African Americans to be helplessly sexually irresponsible and helplessly promiscuous — irrespective of education, poverty, etc.

What Adimora et al. cannot do by any contortions of semantic obfuscation is to make their argument logically sound, nor can they rescue HIV/AIDS theory from its inherently racist character.

HIV/AIDS grift

[grift:
1.    Money made dishonestly, as in a swindle.
2.    A swindle or confidence game.
— American Heritage Dictionary, 3rd ed.]

“Grift” popped into my head because of this recent news item with an apt choice of name for a new drug:
“FDA approves Egrifta to treat Lipodystrophy in HIV patients”
Despite occasional waffling and evasiveness, even mainstreamers do know that “HIV-associated lipodystrophy” is actually ARV-caused lipodystrophy, perhaps specifically protease-inhibitor-caused lipodystrophy. So here’s an iatrogenic [caused by treatment] ailment that is then to be treated with yet another medication — which, of course, will then have its own “side” effects.
It’s not unique to HIV/AIDS medical practice, unfortunately, that treatment may turn out instead to be iatrogenic illness, which is then sought to be treated by drugs with yet further “side” effects. Ask around, perhaps especially among us senior citizens, how many of us are taking statins and diuretics and blood thinners as well as other medications to counteract the muscle weakness, mental confusion, etc., etc., that are “side” effects of those statins, diuretics, blood thinners that we are supposed to take for as long as we survive.
In this instance, Egrifta not only sometimes lessens the lipodystrophy, as desired, it also produces “joint pain (arthralgia), skin redness and rash at the injection site (erythema and pruritis), stomach pain, swelling, and muscle pain (myalgia) [and] Worsening blood sugar control”.
Note too that these “side” effects showed up already in a 26-week trial. ARVs are to be taken forever, so these effects are likely to get increasingly unpleasant, and additional ones might also show up. Plenty of opportunity to be prescribed medications to control muscle pain, joint pain, blood sugar level, etc.

Not that all HIV/AIDS activists, doctors, researchers and others are consciously propagating a vast confidence racket; they are doing it unconsciously, and they are themselves victims of this racket. As I’ve tried to make plain always, the HIV/AIDS mess is not the result of any conscious conspiracy, it is a reflection of the state of science and medicine in contemporary society.
Researchers and doctors are victims in that they suffer cognitive dissonance. They are unable to conceive that a mainstream consensus could be plain wrong, in this instance HIV/AIDS theory, and therefore they either ignore evidence to that effect or find ways to explain it away, to their own satisfaction at least.
An increasingly common device is to ascribe to “HIV” what are actually the effects of ARVs, as with lipodystrophy. This is increasingly accomplished by ascribing to “HIV” a chronic stimulation or activation of the immune system which produces chronic inflammation that can be blamed for any and every ailment or organ failure.
Osteoporosis, and its precursor, the loss of bone mineral density (BMD), is another “side” effect of antiretroviral drugs that mainstreamers attempt to ascribe to “HIV” itself. Thus the recent news item, “Bone loss more common in HIV”:
“In a group of people with HIV, researchers found eight in 10 had either osteoporosis, the brittle-bone disease that raises the risk of fractures, or osteopenia, abnormally low bone mass that could progress to osteoporosis.  It’s unclear exactly why people with HIV are more likely to experience bone loss, study author Dr. Anna Bonjoch of the Lluita contra la SIDA Foundation in Barcelona, Spain. . . . HIV patients also appear at higher risk of heart disease, cancer, kidney problems, diabetes, and cognitive decline. ‘All these big chronic diseases that increase with age do occur earlier in HIV’”.
The study referred to is “High prevalence of and progression to low bone mineral density in HIV-infected patients: a longitudinal cohort study” by Bonjoch et al., AIDS, 24 [2010] 2827-33. Note that the news report accurately reflected that the article emphasizes “HIV infection” and not antiretroviral treatment. The article’s abstract is truthful in reporting the association, though:
“Factors associated with bone loss and progression were age . . . , low body mass index . . . , time on protease inhibitor . . . , time on tenofovir . . . , and current use of protease inhibitors . . . . Our findings support the importance of applying adequate strategies to prevent bone demineralization and of close monitoring of BMD in HIV-infected patients, specifically in at-risk patients who are taking antiretrovirals that affect bone mineralization” [emphasis added].
Yet note how the authors blend the drug “side” effects with other matters. That age and low body mass index may be associated with bone loss should have been irrelevant, since those associations are also found in HIV-negative individuals; the point is that protease inhibitors and tenofovir are independently associated with bone loss.
A meta-analysis, published 4 years before this study, had demonstrated quite clearly the association between bone loss and antiretroviral treatment (Brown & Qaqish, Antiretroviral therapy and the prevalence of osteopenia and osteoporosis: a meta-analytic review, AIDS, 20 [2006] 2165-74):
“ART-exposed and  PI- exposed  individuals  had  a  higher  prevalence  of  reduced  BMD [bone mass density] and  osteoporosis compared with their respective controls”.
But here too the authors try to find some way to blame “HIV”, for example, “other factors, such as the effects on chronic immune activation [5], appear to be important in the pathogenesis of reduced BMD in HIV, and other studies have failed to show an association with ART in general or PI, specifically”.
The point of a meta-analysis is to determine what the cumulation of studies shows to be the case, namely here that antiretroviral drugs cause bone loss. That a few studies did not report this is irrelevant, since those studies were included in the meta-analysis. Figure 1 shows details of 7 studies, 5 of which individually reported osteoporosis associated with ART, with an overall odds ratio of 2.38 (95% confidence interval 1.20, 4.75); the incidence of bone loss, as one would expect, was greater than of actual osteoporosis, with an odds ratio of 2.5. Protease inhibitors were specifically associated with osteoporosis at an overall odds ratio of 1.57; since this is markedly lower than the overall 2.38 for ART, evidently it is not only the protease inhibitors of HAART that cause bone loss.
And still the authors try somehow to exculpate antiretroviral treatment by emphasizing possibly confounding factors, such as that some longitudinal studies did not find increasing bone loss among HAART-treated individuals. But it is the initiation of HAART that needs to be examined, because bone loss is not rapid, and “the two published studies of treatment-naive HIV-infected patients show decreases in BMD with ART initiation”.
But let’s not accept the evidence too willingly:
“It is  not  clear,  however,  whether  the  decline  in  BMD observed with the initiation of ART can entirely account for  the  increased  prevalence  of  osteoporosis in  ART- treated  patients” [emphasis added].
Since bone loss tends to occur naturally as we age, and also in certain other conditions, for example after menopause in women, of course ART will not account “entirely” for all bone loss; it shouldn’t be expected to.
From the mainstream HIV/AIDS view, though, what is really needed, naturally, is more research:
“Further  longitudinal  studies  of  HIV  patients beginning therapy will be needed to clarify the effect of ART initiation and also provide information on the effect of individual antiretroviral agents on bone density”.
But how much does it matter if HAART does not “entirely” account for osteoporosis? Might it not be wise to abstain from HAART in the case of individuals whose only “symptoms” are being “HIV-positive” and having a CD4 count lower than that currently in vogue criterion (<200? <350? <500?) for beginning treatment?