HIV/AIDS Skepticism

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

Posts Tagged ‘Steven K. Grinspoon’

Human cancers (≥20% of them) are caused by viruses!

Posted by Henry Bauer on 2010/01/23

— at least so says Robert Gallo, co-non-discoverer of the non-AIDS-causing “HIV”.

In “HAART, heart disease, & lying with statistics” (2010/01/19)  I pointed out that Lo et al. (2010) claim statistical significance for an association between coronary disease and “HIV” without benefit of the proper control group, “HIV-positive” people who had never been fed antiretroviral drugs.

One of the earliest instances of the “bait and switch” tactic of ascribing to “HIV” what is actually caused by “treatment” against “HIV” was with lipodystrophy, which became prominent only upon introduction of protease inhibitors (PIs), a fact that doesn’t prevent mainstreamers from talking about “HIV-associated” lipodystrophy instead of PI-associated lipodystrophy. This attempted legerdemain of ascribing to “HIV” what is caused by antiretroviral drugs is widespread and will continue to be so, since an increasing proportion of “HIV-positive” people will suffer “treatment” as it is being extended to people with higher and higher CD4 counts, and is even proposed as prophylaxis in healthy, “HIV”-negative  people whose only “risk factor” is being an African woman. By the time every “HIV-positive” person is on antiretroviral drugs, every “side” effect of the drugs can be asserted to be “HIV-associated”.

Robert Gallo is engaged in an analogous attempted legerdemain by ascribing to viruses, without benefit of evidence, certain human cancers. According to Gallo, history teaches that the importance of infectious agents has been discounted for a century or so, despite periodic reminders: Spanish flu, polio, HIV: “ ‘I arrived in the National Cancer Institute in 1965 and there was a serious search for viruses involved in human cancer and a serious respect for infectious disease as potentially new epidemic disorders . . . . By 1975 the virus cancer programme had been killed and people had come to the conclusion that no virus was involved in human cancer and almost certainly would never be.’” Yet a few years later, those biases had been smashed. “Viruses are now known to be involved in about 20 per cent of all human cancers, maybe more, and we now have one of the great epidemics of all time in our face: HIV” (emphases added; “Keeping focused on eradicating a life-long and killer disease”).

Actually the virus-cancer program was not killed, it self-destructed because no human-cancer-causing viruses had been discovered, despite a mistaken claim by Gallo followed by his continuing insistence that HTLV is a retrovirus that causes leukemia — even as he writes that HTLV “tended to be transmitted within families and to stay within families for generations” (p. 114, Gallo 1991). To most people, even medical scientists and perhaps even virologists, something that stays within families for generations is a heritable genetic factor and not an infectious disease. But Gallo is quite ready to re-write medicine and science just as he feels entitled to re-write history: he ascribes medical advances from the beginning of the 20th century to “an increased understanding of and reliance upon the scientific method” (p. 2); and “over the last fifty years, I see few examples in which the scientific-medical establishment arrived at an important conclusion about a disease and was later shown to be wrong” (p. 297; maybe only “few”, but they’ve been fairly significant, like prions mistakenly thought to be lentiviruses, or bacterially caused ulcers ascribed to psychological stress, or shock treatments and lobotomies); and he describes interferon and cytokines as “non-chemical” (p. 301), as though Wöhler had not destroyed the basis for such distinctions in 1828.

Just a few weeks ago, before I had seen this latest Gallo emission, I’d commented that “ ‘HIV’ has infected virology with cancer-causing viruses” (2010/01/08)  in connection with XMRV, the allegedly “xenotropic” (species-jumping) mouse virus allegedly involved in prostate cancer because SOME prostate cancers can yield bits of “non-chemical” substances that might be interpretable as originating in a virus related to XMRV: HIV/AIDS has provided the precedent for regarding something as a cause just because bits of what might be from it can be found in some proportion of cases. Of course, if there’s a “statistically significant” correlation at the p<0.05 level, calculated by use of a ready-made statistics software package, that proves it scientifically, because in HIV-virology correlation proves causation. After all, the fact that a couple of strains of human papillomavirus (HPV) are correlated with genital warts is clear proof that HPV cause the cancers that are sometimes correlated with such warts.

Gallo is anything but shy, though his memory may be conveniently short. Twenty-five years ago he assured the Secretary for Health and Human Services that an anti-“HIV” vaccine would likely to be ready in a couple of years. Now, more than two decades of nothing but failed vaccine trials later, he interprets the latest failure of such a vaccine quite positively: “ ‘It worked, but all the positive data are in the first six months and after that there’s no protection. So whatever worked stopped working, and we have a good idea of what that might be . . . . I think it’s down to a special category of antibodies that were induced, and it fits with some ideas that we are working on.’ Gallo is understandably reserved about predicting the outcome of research in train, but he believes it could produce interesting results.”  He would obviously make a champion seller of Brooklyn Bridges, not to speak of snake oil; perhaps I should say, he has already shown himself to be such a champion.

The State of California has just added AZT to its list of recognized carcinogens. AZT was administered for more than two decades to “HIV-positive” individuals, and during this time an association was noticed between certain cancers — for example, cervical cancer — and “HIV-positive”. Should not Gallo point out to Governor Schwarzenegger that it isn’t the AZT that causes cancer, it’s the HIV against which the AZT is administered?

But Gallo’s (unsupported and unsupportable) claim that ≥20% of human cancers are virus-caused is far too modest. He unaccountably failed to realize that “HIV” can be indicted for an even more widespread condition that negatively affects human beings, namely, aging. The logic is simply the increasingly common syllogism by which HAART-associated equals “HIV”-associated:

Aging is caused in some part, perhaps very large part, by accumulation of mitochondrial mutations and increasingly poor mitochondrial function (Linnane et al. 1989).
Antiretroviral drugs cause mitochondrial damage.
“HIV-positive” people consume antiretroviral drugs.
QED: “HIV-positive” is associated with mitochondrial damage which leads to aging.

This is not a purely theoretical deduction, moreover: it has been noticed that “HIV-positive” individuals often seem to age very prematurely: “A striking number of HIV patients are living longer but getting older faster — showing early signs of dementia and bone weakness usually seen in the elderly” (David France, “Another kind of AIDS crisis”, New York Magazine, 1 November 2009):
“patients who contracted the virus just a few years back are showing signs of what’s being called premature or accelerated aging. Early senility turns out to be an increasingly common problem . . . . One large-scale multi-city study released its latest findings this summer that over half of the HIV-positive population is suffering some form of cognitive impairment. Doctors are also reporting a constellation of ailments in middle-aged patients that are more typically seen at geriatric practices, in patients 80 and older. They range from bone loss to organ failure to arthritis. Making matters worse, HIV patients are registering higher rates of insulin resistance and cholesterol imbalances, and they suffer elevated rates of melanoma and kidney cancers and seven times the rate of other non-HIV-related cancers. Whether this is a result of the drugs or the disease itself, or some combination, is still an open question . . . .”

It’s an open question only for people who don’t remember the past. Whether “non-HIV-related cancers” are a result of “HIV” is not an open question, it’s an attempt to obfuscate. Under HIV/AIDS theory, the average time from “HIV-positive” to any symptoms of illness is 10 years. Now, “patients who contracted the virus just a few years back are showing signs of what’s being called premature or accelerated aging” [emphasis added].

The determined defenders of the orthodox faith speak in hand-waving fashion which ignores that chronology (among other things). The official line is that the life-saving drugs are enabling HIV/AIDS patients to live longer than ever before, and so to become prone to ailments of old age. What that attempted explaining-away does not explain is that the ailments “of old age” are affecting people in middle age; HAART-treated individuals are not living into old age and getting those ailments. Moreover, in the past, in the early days of actual AIDS, people died from opportunistic infections, not from cancers or other typically old-age conditions.

Gallo 1991: “Virus Hunting: AIDS, Cancer, and the Human Retrovirus: A Story of Scientific Discovery”, BasicBooks

Linnane 1989: Linnane AW, Marzuki S, Ozawa T, Tanaka M. “Mitochondrial DNA mutations as an important contributor to ageing and degenerative diseases”, Lancet 25 (8639) 642-5

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

Posted in antiretroviral drugs, experts, HIV absurdities, HIV risk groups, HIV skepticism, uncritical media | Tagged: , , , , , , , , , , , , , , , , | 35 Comments »

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

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HIV: It can do anything, everything . . . or nothing?

Posted by Henry Bauer on 2008/09/02

Newspost Online (August 30th, 2008 Health, World News)  broke this news: “HIV-infected patients at ‘higher risk of bone fractures’”.
“HIV-infected patients are at a significantly higher risk of bone fractures, according to new study to be published in the Journal of Clinical Endocrinology & Metabolism (JCEM). ‘Prior studies have indicated reduced bone density in HIV-infected patients, but little was known whether fracture risk increased in this population,’ said Dr. Steven Grinspoon . . . . ‘These data are the first to suggest that there is a clinically significant increase in bone fractures among HIV-infected patients’. . . . overall fracture prevalence increased more than 60 percent in HIV-infected patients versus non HIV-infected patients. . . . ‘HIV patients with risk for low bone density should be assessed and potentially treated to prevent fractures . . . . Further research is needed into the mechanisms of bone loss in this population,’ added Dr. Grinspoon” [emphases added; original source is Virginia A. Triant, Todd T. Brown, Hang Lee, and Steven K. Grinspoon, “Fracture prevalence among HIV-infected versus non HIV-infected patients in a large U.S. healthcare system”, J Clin Endocrin Metab, published ahead of print 1 July 2008 —doi:10.1210/jc.2008-0828].

This study may be “new”, but it isn’t the “first” (as also noted in TALKING OF HIV’S MAGICAL POWERS…, 29 DECEMBER 2007 ):
“December 28, 2007 — HIV-positive women have higher risk of bone fractures . . . say the authors of a study published in Osteoporosis International.  Jerilynn Prior . . . and her colleagues compared the medical records of 138 HIV-positive women with the records of 402 HIV-negative women. Both groups were similar in terms of age, bone mineral density, family history of osteoporosis, calcium intake and other factors known to affect bone health. . . . 26 percent of the HIV-positive women had a history of a fragility fracture — a broken bone that occurs as a result of a fall from standing height or less — compared with just 17 percent of the HIV-negative women. . . . Dr. Prior’s team theorized that the difference in fracture rates, despite equal bone mineral density, may be due to the effect of HIV infection within the bone in a manner that does not show up on standard measures of bone health”[emphases added; original source is J. Prior, D. Burdge, E. Maan, R. Milner, C. Hankins, M. Klein, & S. Walmsley, “Fragility fractures and bone mineral density in HIV positive women: a case-control population-based study”, Osteoporos Int (2007) 18:1345–1353, DOI 10.1007/s00198-007-0428-7].

That “60%” in Grinspoon et al. reminded me once again of techniques for misleading by means of numbers. SIXTY is big, impressive; no one wants to take a risk like that. But this is the same sort of sleight of evidence as when people neglect all-cause mortality when considering risks of death (ABUSED WOMEN and “HIV”, 22 August 2008 ). The HIV-negative controls of similar ages already have quite a high risk of bone fracture, more than 1 in 6. To reduce that to perhaps 1 in 4, does it make sense to contemplate treatment with highly toxic antiretroviral drugs, as Grinspoon suggests? Especially since those drugs themselves damage bone marrow and cause osteonecrosis (= bone death) — see Treatment Guidelines, 29 January 2008, pp. 23, 30, 67, 69, 80, 84, 101, 102; mentioned re osteonecrosis are “all protease inhibitors” and, for bone-marrow suppression, ganciclovir, lamivudine, and zidovudine (AZT) as well as (in animal models) stavudine and tenofovir. Drugs listed as causing “overlapping toxicity” through bone-marrow suppression are “amphotericin B, cidofovir, cotrimoxazole, cytotoxic chemotherapy, dapsone, flucytosine, ganciclovir, hydroxyurea, interferon-a, linezolid, peginterferon-a, primaquine, pyrimethamine, ribavirin, rifabutin, sulfadiazine, trimetrexate, valganciclovir, zidovudine”; some of those are used for prophylaxis against PCP, for example.

But in addition to risking damage to the very system — bone — that HIV supposedly puts at some risk, HAART is also known to be a risk factor for “cardiovascular diseases, liver-related events, renal disease, and certain non-AIDS malignancies” (Treatment Guidelines, 29 January 2008, p. 13).

A risk-benefit analysis might well conclude that a 60% increased risk of bone fracture is the risk least to be feared. Or rather, one might conclude that even if “HIV” were definitely known to be the cause of a higher rate of bone fractures. But many HIV-positive people are being treated with antiretroviral drugs already. Did these studies look for differences in tendency to fractures as between HIV-positives on HAART and HIV-positives who were not getting antiretroviral drugs?

NO. They didn’t!


There’s a significant difference between the Grinspoon article and the Prior one: the latter eliminated osteoporosis as a cause of the increased rate of fractures by using a proper control group of HIV-negative people “similar in terms of age, bone mineral density, family history of osteoporosis, calcium intake and other factors known to affect bone health”.

Now, Grinspoon et al. acknowledge that “Comparison with a control population is critical”; however, “Due to database constraints, we could not investigate antiretroviral medication use, smoking, alcohol use, body mass index, socioeconomic status, or medications affecting bone metabolism such as estrogens or steroids”. They used data from a large health-care system and could only accept what was available, they didn’t — as Prior did — use a PROPER control population, namely, one matched in as many potentially confounding variables as possible.

No wonder, then, that Grinspoon et al. see a need for further research. In any case, that’s ALWAYS so with people who derive their living from doing research. And HIV/AIDS is ideal for the purpose, because so many contradictory results keep turning up. For example, does HIV actually have anything to do with bone density and osteoporosis?

Grinspoon says “Yes”, prior studies have shown it; and no fewer than 14 such studies are cited as well as a meta-analysis. Those studies also provide ample reason for further research, because while some of them do find bone density lower in HIV-positive people, a number of studies ascribe this not to HIV but to HAART. Moreover, the Treatment Guidelines, version 29 January 2008, see above, cite many of the components of HAART as known causes of bone-marrow suppression or osteonecrosis. An infinite series of studies will no doubt be required to resolve those (manufactured?) contradictions.

The Prior study is exemplary in spelling out possibly confounding factors and attempting to control for them. For example, it speculates about a possible resolution of the conundrum of higher fracture-rate despite equal bone density: different racial compositions of the study and control groups, because black women have higher bone-density than others do. Also noted is that “HIV+ women in this study had more classical risk factors for osteoporosis, including more systemic steroid therapy, heavier smoking histories, more oligomenorrhea [irregular menstrual periods at intervals >35 days] and more weight cycling, than the control women. They also had much higher rates of injection or illicit drug use. . . . Half of the HIV+ women reporting intravenous drug use had a history of 10-kg weight cycling. The use of narcotics, cocaine or amphetamine and their related weight losses probably account for the higher proportion of HIV+ women who reported oligomenorrhea. . . . HIV+ women had more variable cycle lengths and a tendency toward abnormally short cycles . . . associated with higher viral loads and lower CD4 T-cell counts . . . ovulation is disturbed in HIV+ women . . . . Early menopause before age 40 . . . may also occur more frequently in HIV+ women . . . .”.

But what about the known bone-death and bone-marrow damage that are “side” effects of many components of HAART? The Prior study enrolled “One hundred and thirty-eight HIV+ women”; some were on HAART and some were not: “100 ART+, 38 ART-“. That, it would seem, would be the very first variable to be controlled for. Yet the study does not even mention the relative rates of bone fracture in those two different groups!

It’s not that Prior et al. were unaware of this issue, it’s just that yet another study will be needed to look into it: “It remains to be determined whether part of the reason for increased fractures in this population of HIV+ women relates to the majority of the population who were treated with modern highly active antiretroviral therapy [2]. Literature results are mixed about whether ART use is associated with bone loss because of adverse drug effects or with bone gain as HIV+ women become less ill, more mobile, gain weight, and have less inflammation. Investigation of fracture and BMD [bone mineral density] in these cases by ART use or not, is currently ongoing (Burdge, personal communication).” [Burdge is one of Prior’s six co-authors]

One may wonder how many studies will be needed before it is admitted that, in some patients at least, HAART leads to severely debilitating “side” effects such as lipodystrophy and loss of bone. After all, reactions to many drugs differ from individual to individual; but if some people suffer severe “side”-effects, others are likely to suffer similar effects in milder fashion. With such treatments as HAART, which are continued indefinitely, even mild “side”-effects may become serious after a while. The fact that some studies have not found bone loss to be associated with HAART does not prove invalid other studies that do find such a relationship; it only indicates that there were some unknown differences in the studies, possibly characteristics of the particular people being studied, some being more sensitive than others to those particular effects. So results should surely not be ignored like those of Tebas et al. (AIDS, 14 [#4, 2000] F63-7), that protease inhibitors not only produce lipodystrophy but also more than double the risk of osteopenia and osteoporosis; or those reported by McDermott et al., Am J Clin Nutr., 74 (#5, 2001) 679-86.


As seems so common in HIV/AIDS research, Prior et al. are prepared to credit HIV with almost magical properties: “bone geometry and microarchitecture are of key importance as risks for osteoporotic fracture. Further research is required to explore the geometric properties of bone in HIV+ women . . . .”. If HIV doesn’t de-mineralize the bone, perhaps it alters its structural properties?!

Note that HIV is held responsible not only for possible bone damage, even if only in some occult manner, but also with “more variable cycle lengths and a tendency toward abnormally short cycles . . . associated with higher viral loads and lower CD4 T-cell counts . . . ovulation is disturbed in HIV+ women . . . . Early menopause before age 40 . . . may also occur more frequently in HIV+ women” [emphasis added]:  clearly, it’s taken for granted that viral load and CD4 counts are reliable measures of activity by HIV, and this distracts the authors from the more obvious connection between HAART and bone damage.

All these conflicting reports resolve themselves once it’s realized that testing HIV-positive is simply a marker, analogous to fever, of some disturbance of the system. HIV-positive doesn’t signify the presence of an all-powerful virus, it is a consequence or corollary of any one of a large variety of pre-existing conditions of disturbed health, minor as well as major. If you’re on drugs, or something has disturbed ovulation and menstruation, or you’re under just about any form of physical or emotional stress, you’re more likely than otherwise to test HIV-positive, to have lower CD4 counts, to be generating the bits of RNA that constitute “viral load”.

“HIV” doesn’t cause bone loss any more than it causes liver damage or heart disease; antiretroviral drugs do those things.

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