HIV/AIDS Skepticism

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

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.

5 Responses to “HIV: It can do anything, everything . . . or nothing?”

  1. JH said

    Arthritis Res Ther. 2008;10(2):107. Epub 2008 Apr 18.

    Role of interleukin-7 in degenerative and inflammatory joint diseases.

    van Roon JA, Lafeber FP.

    IL-7 is known foremost for its immunostimulatory capacities, including potent T cell-dependent catabolic effects on bone. In joint diseases like rheumatoid arthritis and osteoarthritis, IL-7, via immune activation, can induce joint destruction. Now it has been demonstrated that increased IL-7 levels are produced by human articular chondrocytes of older individuals and osteoarthritis patients. IL-7 stimulates production of proteases by IL-7 receptor-expressing chondrocytes and enhances cartilage matrix degradation. This indicates that IL-7, indirectly via immune activation, but also by a direct action on cartilage, contributes to joint destruction in rheumatic diseases.

    J Acquir Immune Defic Syndr. 2005 Dec 15;40(5):581-4.
    Increased circulating interleukin-7 levels in HIV-1-infected women.

    Napolitano LA, Burt TD, Bacchetti P, Barrón Y, French AL, Kovacs A, Anastos K, Young M, McCune JM, Greenblatt RM.
    Gladstone Institute of Virology and Immunology, University of California at San Francisco, 94158, USA.

    Sex-based differences in CD4 T-cell (CD4) counts are well recognized, but the basis for these differences has not been identified. Conceivably, homeostatic factors may play a role in this process by regulating T-cell maintenance and repletion. Interleukin (IL)-7 is essential for normal T-cell production and homeostasis. We hypothesized that differences in IL-7 might contribute to sex-based differences in CD4 counts. Circulating IL-7 levels were analyzed in 299 HIV-1-infected women and men. Regression analysis estimated that IL-7 levels were 40% higher in women than in men (P = 0.0032) after controlling for CD4 count, age, and race. Given the important role of IL-7 in T-cell development and homeostasis, these findings suggest that higher IL-7 levels may contribute to higher CD4 counts in women.

    AIDS. 2005 Dec 2;19(18):2077-86.

    Loss of IL-7Ralpha is associated with CD4 T-cell depletion, high interleukin-7 levels and CD28 down-regulation in HIV infected patients.

    Rethi B, Fluur C, Atlas A, Krzyzowska M, Mowafi F, Grützmeier S, De Milito A, Bellocco R, Falk KI, Rajnavölgyi E, Chiodi F.
    Microbiology and Tumor Biology Center, Karolinska Institutet, Stockholm, Sweden.
    OBJECTIVE: Elevated levels of interleukin (IL)-7 are present in the blood of HIV-positive patients and it is known that IL-7 receptor (IL-7R)alpha expression decreases on T cells during HIV infection. The subset(s) of T cells with low IL-7Ralpha and the consequence of low IL-7Ralpha expression for T-cell survival are poorly characterized. DESIGN: The frequency of IL-7Ralpha-negative T cells in HIV-positive patients was studied in relation to CD4 T-cell counts, IL-7 concentration and survival in culture. We analysed IL-7Ralpha expression in different T-cell populations and in relation to Bcl-2 expression. METHODS: Specimens from 38 HIV-1 patients and 17 controls were examined. IL-7Ralpha and Bcl-2 expression in different T-cell populations was studied by flow cytometry. The influence of IL-7Ralpha expression on T-cell survival was studied by culturing T cells in the presence of IL-7. RESULTS: Down-regulation of IL-7Ralpha on T cells correlated with depletion of CD4 T cells (P < 0.001) and also with increased concentration of serum IL-7 (P < 0.05). The decreased IL-7Ralpha expression was associated with low Bcl-2 expression and with the reduced survival capacity of T cells in the presence of IL-7 in vitro. Particularly, T cells with memory phenotype showed a decreased IL-7Ralpha expression in association with CD28 down-regulation. CONCLUSIONS: The positive effects of IL-7 on survival and homeostatic proliferation of T cells might be severely impaired in HIV-infected individuals due to IL-7Ralpha down-regulation. Differentiation towards a CD28-negative memory phenotype in response to chronic activation may lead to an overall decrease of IL-7 mediated survival within the peripheral T-cell pool.

    Nat Med. 2001 Jan;7(1):73-9.

    Increased production of IL-7 accompanies HIV-1-mediated T-cell depletion: implications for T-cell homeostasis.

    Napolitano LA, Grant RM, Deeks SG, Schmidt D, De Rosa SC, Herzenberg LA, Herndier BG, Andersson J, McCune JM.
    Gladstone Institute of Virology and Immunology, San Francisco General Hospital, and Department of Medicine, University of California at San Francisco, San Francisco, California 94110-9100, USA.

    We hypothesized that HIV-1-mediated T-cell loss might induce the production of factors that are capable of stimulating lymphocyte development and expansion. Here we perform cross-sectional (n = 168) and longitudinal (n = 11) analyses showing that increased circulating levels of interleukin (IL)-7 are strongly associated with CD4+ T lymphopenia in HIV-1 disease. Using immunohistochemistry with quantitative image analysis, we demonstrate that IL-7 is produced by dendritic-like cells within peripheral lymphoid tissues and that IL-7 production by these cells is greatly increased in lymphocyte-deplete

  2. Martin said

    While this tidbit isn’t exactly related to this particular posting, it’s still AIDS. In the NY Times editorial today, “The Real Numbers on H.I.V.”, a report from the CDC said that the number of people infected with HIV is 40 percent higher than previously estimated. “The report, based on new technology that allows more precise estimates, found that 56,300 people around the country became newly infected in 2006, well above the 40,000 cited in recent years.”

    Now reading this “carefully”, I would interpret this to mean that they are taking the same data and employing a different statistic (“new technology”) in order to create (generate from whole cloth) a new estimate. This covers up the fact that there are no real data garnered from an accurate survey based on what we know is an unvalidated test.

    Is my interpretation reasonable based on what you know?

  3. Henry Bauer said


    Your interpretation is basically right. What’s “new” is using a technique to differentiate “long-standing” from “recent” infections, a technique that has never been validated and which gave wrong results when applied in a couple of overseas places. That’s fed into a model together with a staggering array of assumptions, to deliver a history of HIV infections back to the late 1970s that’s totally at odds with CDC and peer-reviewed estimates for the first decade or more. It’s not whether to laugh or cry, but fit for SCREAMING . I’m working on a lengthy post about it; it’s the usual problem, doesn’t take long to make and write up mistakes and takes ten times a s long to deconstruct the rubbish.

  4. Martin said

    Hi Dr. Bauer, That’s what I thought. That’s like a chef working at a crappy restaurant with only leftovers with which to create tonight’s special and voila!, the food critic (the journalists) write a great review and tell the readers to go to that restaurant. A new HIV disease: Journalitis Gullibilitosis.

  5. Dear Dr Bauer –

    I have started a blog, inspired by your spirited work here.

    Please pay a visit & honour me with a comment.

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