HIV/AIDS Skepticism

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

Posts Tagged ‘side effects of antiretroviral drugs’

HIV/AIDS theory hurts people

Posted by Henry Bauer on 2009/01/08

My preoccupation with HIV/AIDS began as a purely intellectual pursuit, trying to make sense of contradictory accounts, and becoming hooked as I gathered HIV-test data that seemed to point inescapably toward the conclusion that “HIV” didn’t cause an epidemic and was not the cause of AIDS. But after my book was published, and increasingly since I began this blog, I’ve glimpsed the many human tragedies for which this monstrous mistake has been responsible. Careers of people who testified to the mistake have been wrecked; an unknown number of parents have been forced to feed their babies poisonous substances that hurt and harmed them; an unknown number of relationships have been broken needlessly; on and on. Recently my Google Alert brought in a single day several stories that illustrate the range of damage that the wrong theory of HIV/AIDS has wrought.

Circumcision:
It’s become a shibboleth among HIV/AIDS “activists” and journalists that circumcision reduces the risk of contracting “HIV” by something like 60%. That’s in the face of many studies to the contrary, including from the Centers for Disease Control and Prevention [Rwanda: circumcise all men—even if it means more HIV infection, 3 February 2008]: “Unhygienic Circumcision ‘Increases Risk of Hiv’” (SciDev.Net, London, 28 February 2007); “PRESIDENT Yoweri Museveni has trashed claims that circumcised men are less prone to HIV/Aids infection. . . . “Why are Muslims and Bagisu dying? Who beats the Bagisu when it comes to circumcising men?” . . . Among the Bagisu, a tribe in eastern Uganda, every male, between adolescence and manhood, must be circumcised”; “Circumcised male and female virgins were substantially more likely to be HIV infected than uncircumcised virgins”; “Circumcision does not affect HIV in US men”.

And still the shibboleth is promulgated: “Adopt male circumcision as anti-HIV strategy” (by Sam Anguria, 6 January 2009, on The New Vision — Uganda’s Leading Website; “The writer an
HIV/AIDS specialist”) : “male circumcision should be fully rolled out in Uganda . . . . Leaders should themselves embrace male circumcision and circumcise their male children.”

It’s not as though circumcision of adults were a trivial matter; let alone in much of Africa, which is where the HIV/AIDS dogmatists advocate it

Stigma:
A rather astonishingly stark self-contradiction in HIV/AIDS matters is the plaintive appeal not to stigmatize HIV-positive people — at the same time as it’s insisted that “HIV” is contracted by careless, unsafe sexual behavior, the risk of “infection” being small unless there is a high level of promiscuity, adultery, and anal intercourse — all of them practices that most societies have stigmatized long before AIDS.
KENYA: Unease over new HIV transmission law . . .
NAIROBI, 12 December 2008 (PlusNews) — In June 2006, a young woman in western Kenya died of HIV-related complications and left a list of about 100 people that she said she had infected with HIV. A new law, approved by the Kenyan president but yet to be implemented, is hoping to prevent willful transmission. The HIV and AIDS Prevention and Control Act 2006 has drawn mixed and very sharp reactions. Inviolata Mbwavi, an AIDS activist who went public about her status in 1994, warned that the legislation in its current form appeared to label HIV-infected people as dangerous human beings with whom people should not associate. ‘When you criminalise HIV then we are going back to square [one] of trying to stigmatise the virus even more, yet we have not effectively dealt with the stigma associated with HIV. Why do we want to further burden those who are already burdened by coming up with HIV-specific legislation?’ . . . . ‘We know that the majority of those who know their status are women. What we are doing by passing such a law is therefore to condemn people we are claiming to protect to jail.’ The new legislation has also brought into question the responsibility of HIV-negative people. ‘What we are proposing in the law only touches those already [HIV]-positive. We should also look at the responsibility of those who do not have the virus’ . . . .”
And so on and so forth. When a wrong theory gains acceptance, conundrums and contradictions and mutually impossible things also have to be swallowed whole.

Well-intentioned do-gooder harm:
Kaiser Daily HIV/AIDS Report [6 January 2009]
Global Challenges
“IRIN/PlusNews on Friday profiled a commune operated by HIV advocate Paul Ari designed for HIV-positive people who have experienced stigma and discrimination near Mount Hagen, the capital of Papua . . . . people are able to stay at the commune for as long as they need, and relatives are encouraged to visit to help fight stigma related to the virus”.
Clearly, the way to combat stigma directed at HIV-positive people is to have separate places for them, just as long ago we fought the stigma against lepers by providing them with separate accommodations.

Homosexuality:
Gay men — together with hemophiliacs and people of African ancestry and pregnant women and babies — are among those most harmed by the invention and application of the fallacious “HIV” test. For whatever reason, gay men tend to test “HIV-positive” with a rather high probability even when they are perfectly healthy and remain so (as of the present date, for upwards of two decades). So gay men are among those most threatened by the urging that “HIV-positive” people accept antiretroviral treatment, and “HIV” has delivered yet another arrow for the quiver of the confirmed homophobes and homophobic groups:
“HIV being spread mainly through homosexual relations in Spain” (Catholic News Agency, Madrid, 6 January 2009)
“The Anti-AIDS Independent Committee in Spain has called for behavioral changes among homosexuals in order to reduce the spread of HIV/AIDS, as 2007 data confirms that the disease is more prevalent in the homosexual population. . . . The organization criticized government campaigns that promote condom use, ‘with a message aimed indiscriminately at the population in general and young people in particular, as if everyone were equally at risk, regardless of their habits.’ . . .  the ‘disproportionately high rate of infections can only be explained by much higher promiscuity and a higher risk of homosexual contact.’”

African ancestry:
When panic erupted in a St. Louis school over possible “HIV” infections, I wrote, “What we know from the demographics of ‘HIV-positive’ in the United States is that an individual may test positive after being vaccinated against flu, or taking an anti-tetanus shot, or having TB, or for a large number of other reasons having nothing to do with a life-threatening sexually transmitted virus . . . . We also know that the probability of testing positive for any of those reasons is far greater for people of African ancestry than others; black females in particular are typically 20 times as likely to test positive under one of those numerous conditions. We also know that in the lower teenage years, females are more likely to test positive than males . . . . Those facts cause me to dread the further ‘news’ and rumors that will be leaking out from those ignorant, panicked, ‘everything is normal’, school administrators and health officials in St. Louis.” And, sure enough, it turned out that 99% of the students in that school are black.

Men of African ancestry have been charged with or convicted of having sex while “HIV-positive” in Australia, in Canada, in the United States. In the United States, the average “prevalence of ‘HIV’” is about 0.6%. African Americans are between 7 and 21 times as likely to test “HIV-positive” compared to others, so the average prevalence among African Americans is about 8%. Another demographic fact is that the likelihood of testing positive is greatest at ages in the late thirties to mid-forties. So African Americans in middle age have a chance ≥ 10% of testing “HIV-positive” under such circumstances as having recently been vaccinated or being exposed to some minor health challenge. It struck me as particularly sad that “HIV” should be mentioned in the case of an African American pastor charged with sexual abuse:
“Police: Pastor Charged With Sexual Abuse Has HIV — James Bell Faces Sexual Abuse, Sodomy Charges” (by Stephanie Segretto, WLKY Louisville, 5 January 2009)
“SHELBYVILLE, Ky. — More information about the arrest of a Shelbyville pastor charged with sexual abuse has become public, including his HIV status. . . .
For those who knew Bell, they said it’s hard to imagine he would be facing charges for anything, especially this. . . . neighbors said they will have several people on their minds — Bell’s wife and his three children [emphasis added]”
That “HIV status” will make it seem to most people ever so much worse than the far-from-uncommon sexual lapses of ministers and priests, or the actions of the many men who have sex with young teenagers.
Of course, Bell really behaved irresponsibly in having sex with a 15-year-old. On the other hand, he himself was the one who first reported the fact. And he would be far from the only African American clergyman to be confounded by the news that he is “HIV-positive”, knowing that he was never at risk of contracting a sexually transmitted disease:
“An increasing number of Africans who find themselves HIV-positive are taken aback, knowing that they have never behaved in a pertinently risky fashion, like the Rev. Gibson Mwadime, 53, an Anglican vicar in southern Kenya (Sanders 2006a): ‘I thought AIDS was for prostitutes and truck drivers,’ [he] said … learning about his diagnosis in 2001 was like a slap from God, spurring feelings of betrayal and anger. ‘I lived a faithful life and my wife lived a faithful life,’ he recalled praying. ‘And then you bring this sinful disease upon us?’ Like most of the clergymen, Mwadime said he doesn’t know how or when he contracted the virus. He believes his wife was infected through a blood transfusion during childbirth in 1985. A year later, doctors told the couple their baby girl had tested positive for HIV. But when they were told it was a sexually transmitted disease, they dismissed his advice to get tested themselves” (p. 172 in The Origin, Persistence and Failings of HIV/AIDS Theory).

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That one day’s set of stories is a mere glimpse of the many human tragedies that the HIV/AIDS business has brought. But is everyone at risk, as the mainstream propaganda would have it?

YES;  EVERYONE  IS AT  RISK
If the Centers for Disease Control and Prevention have their way, “HIV” testing will become routine if not universal. Then an increasing number of babies, pregnant women, recently vaccinated individuals, and people exposed to a whole range of health challenges will test positive. After all, the CDC keeps asserting that something like a quarter of all “HIV-positive” Americans don’t know their “status”. That’s about a quarter of a million people.

Some proportion of the newly “diagnosed” will be advised, urged, or forced to consume antiretroviral drugs. Thereupon the numbers of “AIDS” patients dying from non-AIDS events caused by those drugs will increase noticeably. It’s already a majority of them, after all — “In the era of combination antiretroviral therapy, . . .  the risk of several non-AIDS-defining conditions, including cardiovascular diseases, liver-related events, renal disease, and certain non-AIDS malignancies [97-102] 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” (NIH Treatment Guidelines, 29 January 2008, p. 13).
Eventually, the increasing number of diagnosed people who know they could not have been “infected”, and the obviously increasing number of iatrogenic deaths, will bring wealth to a whole population of trial lawyers, and the HIV/AIDS house of cards will soon thereafter implode.

But it would be so very nice if that implosion could happen without so many unsuspecting people having to die first at the hands of misinformed doctors.

Posted in HIV and race, HIV risk groups, HIV tests, HIV transmission, Legal aspects, prejudice, sexual transmission, uncritical media | Tagged: , , , , | 2 Comments »

WHAT HIV DRUGS DO

Posted by Henry Bauer on 2007/12/15

The previous post (OFFICIAL GUIDELINES FOR HIV TREATMENT, 14 December 2007) offered some extracts from the text of the official Guidelines for treating “HIV-1 infected” people, even when they don’t feel ill and are not visibly ill. The Guidelines also have detailed Tables listing the frequent and serious “side” effects of antiretroviral drugs.

The scare quotes are around “side” to emphasize how evasive a euphemism this is. Molecules, chemicals, drugs can’t choose to do only what we want them to do. Any foreign substance disturbs our physiology, which is an intricate system of balances and feedbacks where any one change is likely to induce others as well. The more powerful a molecule, the more likely it is to disrupt our metabolism in multiple ways. Antiretroviral drugs are extremely powerful molecules that can kill cells and block receptors and incapacitate enzymes. As in cancer chemotherapy, antiretroviral treatment kills or disables innocent as well as guilty cells.

All examples in the following are taken from the 1 December 2007 version of the Treatment Guidelines.

* * * * * *

The overriding aim of antiretroviral treatment is to lower viral load or increase CD4-T-cell counts. At several points this seems to take explicit priority over the patient’s condition. For example, as “acceptable [emphasis added] but inferior to preferred or alternative” is included the combination “Stavudine + lamivudine” despite “Significant toxicities including lipoatrophy, peripheral neuropathy, hyperlactatemia including symptomatic and life-threatening lactic acidosis, hepatic steatosis, and pancreatitis” (Table 6b, p. 60).

Drugs “not recommended” for initial therapy include “Indinavir (ritonavir-boosted)” because of “High incidence of nephrolithiasis”, or ritonavir by itself because of “Gastrointestinal intolerance” (Table 7, p. 61). Nevertheless, both indinavir and ritonavir are countenanced for therapy other than “initial”. For example, “Abacavir (ABC) + zidovudine (ZDV) + lamivudine (3TC) only” has “Inferior virologic responses when compared with . . . indinavir-based regimens” (p. 64). Indinavir (trade name CRIXIVAN) is available in “200, 333, 400 mg capsules”, suggesting rather common use, even though the listed “Adverse events” include “nephrolithiasis, GI intolerance, nausea, indirect hyperbilirubinemia, hyperlipidemia, headache, asthenia, blurred vision, dizziness, rash, metallic taste, thrombocytopenia, alopecia, and hemolytic anemia, hyperglycemia, fat maldistribution, possible increased bleeding episodes in pts [patients] with hemophilia” (p. 76). When liver damage (“hepatic impairment”) ensues, it is merely recommended that the dose of 800 mg be reduced to 600 mg (Table 15, p. 82). There is a minimum effective concentration desired when indinavir is used (p. 104), and there is a rationale for using it in pregnant women: “Alternate PI to consider if unable to use nelfinavir or saquinavir-HGC/ritonavir, but would need to give indinavir as ritonavir-boosted regimen. Optimal dosing for the combination of indinavir/ritonavir in pregnancy is unknown” (p. 109).

Ritonavir seems to be widely used to “boost” other drugs even though “Potentially more adverse effect on lipids than unboosted atazanavir”. By itself, ritonavir (NORVIR) is known to produce these “adverse events”: “GI intolerance, nausea, vomiting, diarrhea, paresthesias – circumoral and extremities, hyperlipidemia, esp. hypertriglyceridemia, hepatitis, asthenia, taste perversion, hyperglycemia, fat maldistribution, possible increased bleeding episodes in patients with hemophilia” (p. 77). Once liver damage has ensued, “No dosage adjustment in mild hepatic impairment; no data for moderate to severe impairment, use with caution” (p. 81). What, one might wonder, could possibly constitute “cautious” use?

As noted in the previous post, antiretroviral drugs should not be taken with a multitude of quite commonly used medications; thus “Coadministration of ritonavir with certain non-sedating antihistamines, sedative hypnotics, antiarrhythmics, or ergot alkaloids may result in potentially serious or life-threatening adverse events because of possible effects of ritonavir on hepatic metabolism of certain drugs” (p. 92).
HIV patients must be exceptionally well briefed by their physicians, and exceptionally alert readers of fine print, to understand that these antiretroviral drugs should not be taken with commonly used, sometimes over-the-counter antihistamines, sleeping pills (sedative hypnotics), or anti-migraine compounds (ergot alkaloids). But that list seems not to be exhaustive, because later (Table 21a) caution is advised when using ritonavir together with antifungals (…conazoles), anti-mycobacterials (clarithromycin, rifabutin, rifampin), hormonal contraceptives, a couple of extra statins beyond those earlier mentioned, anti-convulsants, erectile dysfunction agents, and some miscellaneous substances.

Given all these immediate and short-term dangers, it may well be irrelevant that longer-term use of ritonavir has been shown to induce “liver adenomas and carcinomas in male mice” (Table 25).
Similarly worrisome details about many other of these drugs confront the reader. It is discomforting that different members of a given group of drugs are likely to have similar “side” effects, in kind if not in intensity, and that the large number of individual names represents only 3 classes of drugs, two of which are present in the standard “combination” “cocktail” treatment. The third class is represented by only two substances, efavirenz (SUSTIVA) and nevirapine (VIRAMUNE). The former has the disadvantage of neuropsychiatric “side” effects and that it produces birth defects in non-human primates. The latter has been the subject of much controversy because of flawed trials in Africa and the death of a pregnant woman in the USA (Celia Farber, “Out of control”, Harper’s, March 2006). The Guidelines describe its “disadvantages” as “Higher incidence of rash than with other NNRTIs, including rare but serious hypersensitivity reactions (Stevens-Johnson Syndrome or toxic epidermal necrolysis); Higher incidence of hepatotoxicity than with other NNRTIs, including serious and even fatal cases of hepatic necrosis; Treatment-naïve, female patients and treatment-naïve patients with high pre-NVP CD4 counts (>250 cells/mm3 females, >400 cells/mm3 males) are at higher risk of symptomatic hepatic events. NVP not recommended in these patients unless benefit clearly outweighs risk.”
One wonders what conceivable benefits could outweigh those risks. The only ones mentioned are “Less fat maldistribution and dyslipidemia than PI-based regimens”.

Nevertheless, those PIs (protease inhibitors) just judged relatively disadvantageous form part of the standard drug combinations, their advantage being “Save NNRTI for future use”. In other words, it is expected that the standard treatment will be effective only for a limited time. In addition to the fat maldistribution, various of these PIs produce such “side” effects as diarrhea, gastric troubles, hyperlipidemia, and skin rash (pp. 63-4).

Still used is AZT (also called Zidovudine, ZDV), the chemical too toxic to be used in cancer chemotherapy. It is an NRTI (Nucleoside Reverse Transcriptase Inhibitor). The general disadvantage of this class of compounds is “Rare but serious cases of lactic acidosis with hepatic steatosis reported (d4T>ddI=ZDV>TDF=ABC=3TC=FTC)”.
That equation states that d4T is even more dangerous than ddi, which is just as dangerous as AZT/ZDV. Nevertheless, these apparently more dangerous members of this class are in common use. They feature such additional “side” effects as peripheral neuropathy and pancreatitis (ddI + 3TC); peripheral neuropathy, lipoatrophy, hyperlactatemia and lactic acidosis, reports of progressive ascending motor weakness, potential for hyperlipidemia with stavudine use (d4T + 3TC); higher incidence of mitochondrial toxicity with d4T than with other NRTIs ; bone marrow suppression owing to ZDV (Table 9, p. 63).

Table 10 reports some clinical trials of 48-week duration, with 2-7% dropping out because of side effects. Four-drug combinations brought dropout rates as high as 23%. Similarly high dropout rates were experienced with two-drug combinations using ZDV or 3TC. Quite a large number of such trials are listed here, though these are described as no more than “selected” examples.

Table 11 lists details of individual NRTIs, including “adverse events”. Among the inscrutable annotations are “Minimal toxicity” [!!] followed immediately by “lactic acidosis with hepatic steatosis (rare but potentially life-threatening toxicity with use of NRTIs)”, with EMTRIVA (FTC) and 3TC as well as commercial combinations of 3TC with another NRTI as COMBIVIR, EPZICOM, TRIZIVIR.

Table 12 similarly lists NNRTIs (Non-Nucleoside Reverse Transcriptase Inhibitors), and Table 13 lists PIs. Table 14a describes the new class of “entry inhibitors”. Enfuvirtide (FUZEON) produces “local site injection reactions” in almost 100% of patients, increased rate of bacterial pneumonia, and allergic reactions. One wonders how severe the rate of bacterial pneumonia must be to have been noted already at this early stage. Maraviroc (SELZENTRY) offers “Abdominal pain, cough, dizziness, musculoskeletal symptoms, pyrexia, rash, upper respiratory tract infections, hepatotoxicity, orthostatic hypotension”. Table 14b introduces the latest class of drug, “integrase inhibitor”, raltegravir (ISENTRESS), dosage 400 mg twice daily, producing “nausea, headache, diarrhea, pyrexia, and CPK elevation”.

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The treatments are so unpleasant that there is a Table 16, “Strategies to improve adherence to antiretroviral therapy”. Table 17, stretching over 6 pages (84-9), then lists potentially life-threatening and serious adverse events and recommendations for managing them. Table 18 lists “overlapping toxicities” of “HIV-related” drugs. Table 19 cites “black box warnings” for these drugs. Tables 20 and 21 list numerous commonly used medications that should not be taken with antiretroviral drugs.

***********

There’s lots more. Read as much as you can stomach. Bear in mind that these drugs and regimens are intended to kill a retrovirus that has never been isolated in the form of active, infectious particles from HIV-positive people; and that “HIV-infection” is expected to show no symptoms of illness for an average of 10 years after infection, in absence of antiretroviral drugs.

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OFFICIAL GUIDELINES FOR HIV TREATMENT

Posted by Henry Bauer on 2007/12/14

In earlier posts I commented on how ever-changing are the official Guidelines for the use of antiretroviral drugs in “HIV-1 infected” people and how doubtfully based on reliable scientific evidence (“BEST TREATMENT…, 10 December), as well as euphemistic about toxic “side” effects (ANTIRETROVIRAL DRUGS, 12 December). Here are a few bits (from the October 2006 version) to illustrate why my view of these Guidelines is such a jaundiced one. If you suspect that these extracts may be misleadingly out of context, reassure yourself that they are quite representative by reading the latest version, freely available via the Internet.

Page 2: “short term and, even more concerning [sic!], longer term toxicity may limit the duration of treatment needed in what can be seen as a chronic disease. Finally, drug interactions among the antiretroviral drugs and with other necessary drugs are challenging and require special attention in prescribing and monitoring”.
Apart from the clear and worrying statement that prescribing and monitoring are challenging because of numerous interactions with many medications, it’s rather baffling, why longer term toxicity should be of more concern than short-term toxicity? Is this another instance of what has been remarked in some earlier posts, that the experts do not necessarily think about what they are saying or calculating?
If duration of treatment is limited by “short term … toxicity”, that means the patient died or was severely harmed already by a brief course of treatment. How could this be of less concern than “longer term toxicity”? Only if the preoccupation is with treating long enough to kill the virus, forget about the patient.

Page 8:
“—Antiretroviral therapy is also recommended for asymptomatic patients with <200 CD4+ T cells/mm3 (AI).
—Asymptomatic patients with CD4+ T cell counts of 201–350 cells/mm3 should be offered
treatment (BII).
— For asymptomatic patients with CD4+ T cell of >350 cells/mm3 and plasma HIV RNA >100,000 copies/mL most experienced clinicians defer therapy but some clinicians may consider initiating treatment (CII).”
The strongest recommendation, AI (for definitions, see post of 10 December, BEST TREATMENT…), is for antiretroviral treatment for people with no symptoms of illness, purely on the basis of a low CD4-cell count, which in Canada is not even regarded as a reason for treatment (www.phac-aspc.gc.ca/publicat/haest-tesvs/a_e.html, accessed 28 April 2006). That underscores, of course, why “The decision to begin therapy for the asymptomatic patient is complex and must be made in the setting of careful patient counseling and education”.
Indeed! “Asymptomatic” people–people with no sign of ill health–are in these Guidelines recommended strongly (A), moderately (B), or optionally (C) to start “treatment” which in healthy people produces such results as “depression, chronic fatigue, loss of weight and appetite and inflammation of the intestine”.
That description is from a report about a woman wrongly diagnosed as HIV-positive who was recently awarded $2.5 million in damages for malpractice (“Woman misdiagnosed with HIV gets $2.5 M”, Rodrique Ngowi (AP) 13 December 2007). Perhaps some enterprising lawyer will organize a class-action suit against the people who draw up these Guidelines, since they call for asymptomatic people to be fed substances known to be toxic, recommendations made (“offered” to the “patient”!) solely on the basis of lab tests (CD4 counts) that are not universally recognized as validly diagnostic or (“HIV” tests) that are known to be subject to many false positives (http://virusmyth.net/aids/data/cjtestfp.htm) and which have never been proven to detect active virus (SKEPTICISM…, 12 November).

Furthermore,
Page 9: “The optimal time to initiate antiretroviral therapy among asymptomatic patients with CD4+ T cell counts >200 cells/mm3 is unknown. For these patients, the strength of the recommendation for therapy must balance other considerations, such as patient readiness for treatment and potential drug toxicities”.
The phrase beginning “patient readiness” signals clearly enough that nasty side effects are to be expected.

Page 12: “With improved choices of more effective and more convenient regimens, some of the agents or combinations previously recommended by the Panel as alternative regimens have been removed from the list or placed as other possible options”.
Consider how the physician and the patient feel when the treatment they had agreed on and used is removed from the list of recommendations. Give thought to why those previously recommended regimens were withdrawn.

Page 13: “two deaths were attributed to nevirapine use . . . . Symptomatic, serious, and even fatal hepatic events have been observed when nevirapine was initiated in treatment-naïve patients. . . . In some cases, hepatic injuries continued to progress despite discontinuation of nevirapine”.
[Translation: People treated with nevirapine have suffered liver damage that gets worse even after the treatment stops.]

Pages 20-21: “Adverse effects have been reported with virtually all antiretroviral drugs and are among the most common reasons for switching or discontinuation of therapy and for medication non-adherence [emphasis added] . . . in a Swiss HIV cohort . . . 47% and 27% of the patients were reported to have clinical and laboratory adverse events, respectively . . . . Whereas some common [emphasis added] adverse effects were identified during pre-marketing clinical trials, some less frequent toxicities (such as lactic acidosis with hepatic steatosis and progressive ascending neuromuscular weakness syndrome) and some long term complications (such as dyslipidemia and fat maldistribution) were not recognized until after the drugs had been used in a larger population for a longer duration. In rare cases, some events may result in significant morbidity and even mortality.”
Bear in mind that new drugs continue to be introduced, on the basis of similarly brief trials, even though they belong to the same classes of substance as those already known to bring “long term complications”.
“Complications”, of course, is yet another euphemism for really serious sickness or death.

Page 21: “Most drug interactions with antiretrovirals are mediated through inhibition or induction of hepatic drug metabolism . . . . The list of drugs that may have significant interactions . . . is extensive and continuously expanding [emphasis added]. . . . lipid-lowering agents (the “statins”), benzodiazepines [tranquilizers–librium, valium, xanax, etc.], calcium channel blockers [for cardiovascular conditions], immunosuppressants (such as cyclosporine, and tacrolimus), anticonvulsants, rifamycins [antibiotics, typically used in tuberculosis], erectile dysfunction agents (such as sildenafil), ergot derivatives, azole antifungals, macrolides [antibiotics], oral contraceptive, and methadone. Unapproved therapies, such as St. John’s Wort, can also cause negative interactions.”
Consider how frequently people are prescribed one or other (or more) of these, which interact dangerously with antiretroviral drugs.

Page 23: “Treatment failure is often associated with virologic failure, immunologic failure, and/or clinical progression…
virologic failure, immunologic failure, and clinical progression have distinct time courses and may occur independently or simultaneously. . . . These events may be separated by months to years.”.
In other words, “failure” may refer to viral load (“virologic”), CD4 counts (“immunologic”), or condition of the patient (“clinical progression”). But surely it is only the last of these that should matter. That periods of months or years may separate those three phenomena underscores what dissidents emphasize and HIV/AIDS believers try to deny, that there is indefinite or poor correlation at best between the surrogate markers themselves and between them and the health of the patient.

Page 25: “Clinical progression may not warrant a change in therapy in the setting of suppressed viremia”.
Almost incredible, isn’t it? When viremia (viral load) is being decreased, treatment should continue even if the patient is sinking. Another real-life example of what some might think a jocular fantasy, “the operation must continue, even if the patient then dies”.

Page 27: “Information on relationships between concentrations and drug-associated toxicities are [sic] sparse.”
Or, we just don’t know what a safe dosage is.

Page 28: “Lack of established therapeutic range of concentrations associated with achieving the desired therapeutic response and/or reducing the frequency of drug-associated adverse reactions”.
Or, we don’t know what the effective dosage is or what a safe dosage might be.

Pages 30-32 concern “Acute HIV infection”, an intriguing phenomenon that deserves separate consideration. Further sections of the Guidelines deal with treatment of special groups: pregnant women, adolescents, people with other concurrent medical conditions. Those are followed by many Tables, some of which deserve further discussion, as does the membership of the Panel that draws up these recommendations.

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