From April 2023: The drugs don’t work

They just make you worse

This post was published a year ago. I’m reposting it today for new readers.

The only argument that the AIDS mainstream has left is that the drugs “appear” to work, and they waste no time trotting this “fact” out as “proof” that HIV is the necessary and sufficient cause of AIDS. But is this statement provable?

What does “work” even mean, and can a drug’s apparent effectiveness be used as “proof” of the underlying ailment’s causation—especially when a careful analysis indicates that often, the drugs don’t work, and even cause great harm? And how many people are on these drugs, anyway? For the official story that the AIDS drugs have truly eradicated AIDS to be true, wouldn’t it have to be the case that almost everyone eligible ought to be on these drugs for eradication to be possible? If AIDS has truly become a “chronic, manageable condition” thanks to the drugs, wouldn’t it make sense that these drugs ought to have close to 100% uptake, or else there should be many full blown AIDS cases showing up among the unmedicated?

We must also note that there are scientific and logical assumptions that must be met prior to any conclusion being reached regarding the efficacy of these medications. The pathogen said to be susceptible to said medications must have been proven to exist and to be pathogenic. The mechanisms by which the drug is intended to work should be explainable and understood by most. Neither of these assumptions has been met in the case of HIV and AIDS. Also, crucially, the medications need to have been shown, via controlled trials, to actually positively affect clinical health, and not merely have a positive effect on “surrogate markers” such as “viral load” and T cell counts. This has rarely occurred in any clinical trial for antiretrovirals.

The general structure of a “scientific proof,” or the basis of the scientific method, consists of the following simple—not necessarily easy—steps: 1. Make an observation; 2. Ask a question; 3. Form a hypothesis; 4. Make a prediction based on the hypothesis; and 5. Test the prediction. In the case of HIV AIDS, the crucial failure occurred at step 5. Almost every prediction made about HIV AIDS has failed, rendering the hypothesis null and void. The mechanism by which HIV is alleged to kill T cells remains unclear; indeed, there is no evidence that HIV kills T cells at all. It is against this failure to satisfy the scientific method that we must analyze the efficacy of antiretroviral drugs.

(Interestingly, this book I came across makes the statement that “Among the very basic principles that guide scientists, as well as many other scholars, are those expressed as respect for the integrity of knowledge, collegiality, honesty, objectivity, and openness.” There has never, in the case of HIV, been any sort of “collegiality” or “openness” toward views of scientists critical of the HIV AIDS hypothesis. The opposite is true, and it would not go too far to say that the attitude of HIV researchers toward their scientific critics fosters a hostile working environment in AIDS research, thus making true progress near impossible.)

Anyone who has taken an introductory class in formal logic will recall the fact that a false premise logically implies any conclusion. “If pigs can fly, then the sky is blue” is a logically consistent statement, with a conclusion that happens to be true, but it does not prove that pigs can fly, just because the sky happens to be blue, and further, it provides no new information. “If HIV causes AIDS, then the drugs will work” is also a logically consistent statement but one must exercise caution because one cannot assume that HIV causes AIDS in order to prove that it does. “If HIV causes AIDS, then the drugs don’t work” is also logically valid. The AIDS establishment has been taking outrageous advantage of this logical loophole for decades.

When one considers the apparent “overwhelming effectiveness” of anti-HIV drugs in changing the course of the AIDS epidemic, one must carefully consider the numbers. First, combination therapy was only available, at the earliest, in 1995-96 to a limited number of patients, yet AIDS deaths peaked in 1994 before dropping sharply. Putting that aside for the moment, the concept that these medications changed the course of the AIDS epidemic deserves some scrutiny. For AIDS to have morphed from an inevitably fatal disease to a “chronic, manageable condition,” surely it must be the case that almost every HIV-antibody-positive patient in the United States is “retained in care” on these medications. Even a significant untreated minority ought to be showing up as a signal that AIDS, in untreated patients, has not changed.

The monograph by Vivent Health and the Ryan White Foundation, Ending the HIV Epidemic in the United States , indicates in the Introduction that, among those HIV-antibody-positive individuals in the United States that are aware of their status (estimated to be about 88%), only a little more than half are being treated for HIV at all:

According to the CDC, only 63% of people living with HIV engage with HIV medical care at any level [emphasis mine], and fewer are virally suppressed (51%).

If 88% of HIV antibody positive patients are aware of their status, and slightly over half of those are “retained in care,” and only half of those are “virally suppressed,” how is it possible that we are not seeing a massive influx of full blown AIDS patients every year? That’s less than half of HIV positive patients that are even on medication, leaving half a million or so HIV-antibody-positive patients who should be highly susceptible to AIDS. If the drugs are truly so beneficial, we should still be seeing a massive AIDS epidemic among the unmedicated—yet we are seeing no such thing.

Before I dive more deeply into the failures of these medications to prove anything about the alleged pathogenicity of HIV, as well as plausible explanations for any positive effects they might encourage, I would like to examine two examples from recent medical history in which the apparent efficacy of a treatment turned out not to conclusively indicate anything regarding the mechanism of disease. The first is the chemical imbalance theory of depression, and the second is the use of statins to reduce cholesterol in an attempt to lower incidence of heart attacks.

The chemical imbalance theory of depression posits that an imbalance of chemicals such as serotonin, norepinephrine, and dopamine are the organic cause of depression, and that medications such as SSRIs (selective serotonin reuptake inhibitors; they allegedly work by preventing brain enzymes from breaking down serotonin, low levels of which to some predict the onset of major depressive disorder) and others, including mono amine oxidase inhibitors (MAOIs) therefore effectively treat depression. In reality, these drugs not only have extremely variable outcomes among patients, they can also cause great harm to some, and their apparent efficacy is now commonly believed not to support the chemical imbalance theory of depression.

As brief reminder, antidepressants and the chemical imbalance theory of depression were discovered by accident, when, in the early 1950s, TB patients were prescribed the MAOI iproniazid, which had the unusual “side” effect at the time of decreasing the subjects’ depression. Although the medication only worked for some, drug developers embraced the chemical imbalance theory of depression and worked to develop drugs that worked similarly to MAOIs, but with fewer side effects. (MAOIs have a number of inconvenient contraindications.) Prozac was developed in the 1970s and brought to market in 1988, followed by a number of other antidepressants including Zoloft, lexapro, Paxil, and many more.

Their effectiveness has been mixed, with some patients claiming SSRIs and similar medications have saved their lives. However, there are some for whom the medication has no effect, and, even worse, in some segments of the population, particularly young people and adolescents, there appears to be a troubling link between the use of SSRIs and suicidal ideation.

The 2010 book by Irving Kirsch, The Emperor’s New Drugs, provides a comprehensive review of the chemical imbalance theory of depression, ultimately rejecting it:

After a half century of research, the chemical-imbalance hypothesis as promulgated by the drug companies that manufacture SSRIs and other antidepressants is not only without clear and consistent support, but has been disproved by experimental evidence. — Kirsch, The Emperor’s New Drugs

As this 2022 article indicates, the chemical imbalance theory of depression remains highly controversial, despite the apparent yet limited utility of drugs used to treat it.

Almost seven years after finishing his Ph.D., Horowitz said he still hasn't found any compelling evidence. His latest analysis, released in the journal Molecular Psychiatry in July, is yet another review of serotonin research through the years and concludes that there is no solid link between low serotonin levels and depression. 

Many mental health experts not only agree, but say Horowitz's conclusions are nothing new.

Echoing Kirsch’s conclusions, Mimi Winsberg, chief medical officer at Brightside Health, says:

"Depression itself is a very complex and nuanced diagnosis," Winsberg said. "SSRIs don't cure people by raising their serotonin levels." In fact, studies have shown that even artificially lowering a person's serotonin levels does not reliably lead them into a depressed state. SSRIs are more successful for anxiety, rumination, and OCD than for "low-energy" depression cases, Winsberg said.

Turning for a moment to another example, consider the use of cholesterol lowering drugs, statins. This is highly relevant to the use of antiretrovirals for “HIV” infection, because the benefits of these drugs are primarily measured via the change in the surrogate marker of serum cholesterol levels, rather than clinical improvement. However, as an overview of 21 clinical trials indicated, the drop in serum LDL (low density lipoprotein, or “bad” cholesterol) was not correlated with any significant decrease in the risk of heart attacks. This example is relevant to HIV medications, because the efficacy of these drugs as determined by the results of clinical trials is only measured via the use of surrogate markers such as CD4+ T cells and “viral load,” rather than using clinical health as endpoints. We see the same use of the surrogate marker of cholesterol level when it comes to statin drugs, and we also see that said surrogate marker is not a reliably accurate reflection of clinical improvement.

Indeed, the recent history of medicine is replete with examples of medications that have been shown to be either ineffective at what they were advertised to do, or in some cases are dangerous, such as the famous examples of Vioxx—a drug used to treat arthritis that was voluntarily withdrawn from the market due to increased risk of heart attack and stroke—and Celebrex, which is still on the market.

Regarding anti-HIV medication, we have established that “retention in care” and “compliance” to treatment regimes are significantly lower than mainstream AIDS science would recommend, and one significant reason for this is that the adverse effects are so severe and life-disrupting that remaining compliant is not an option for many.

Treatment Guidelines are replete with references to non-adherence, e.g. “Adverse effects have been reported with use of all antiretroviral (ARV) drugs; they are among the most common reasons for switching or discontinuing therapy and for medication nonadherence.”—The case against HIV, Guidelines for the use of antiretroviral agents in adults and adolescents

One does not have to look too far into the past regarding AIDS treatment to be able to see the warning signs that many so called anti HIV drugs may meet a similar fate. From the AZT scandal to the Truvada disaster, the history of AIDS medications appears to be nothing more than a shell game in which a toxic drug is replaced with a slightly less toxic drug. Remarkably, though one aspect of the Truvada lawsuits included the fact that Gilead Pharmaceuticals knowingly withheld a “safer” form of tenofovir, TAF, from patients in favor of prescribing the more toxic TDF before its patent expired, it turns out that “good” Truvada (sold under the brand names Descovy and Genvoya) is also under fire for the same adverse effects of bone loss, kidney damage, and lactic acidosis, according to Shouse Law.

To complicate matters further, Truvada and similar medications are the only game in town when it comes to PrEP, or pre-exposure prophylaxis, but even the mainstream has only confusing information to offer regarding this protocol. Specifically, all PrEP drugs are nucleoside analogues, or nucleoside analogue reverse transcriptase inhibitors (NRTIs), which means that they are DNA chain terminators, and they damage cellular mitochondria and arrest cell growth. These are given to HIV-antibody-negative individuals as so-called preventatives. Had a vaccine been available when it was promised, in the eighties, this use of HIV treatments as de facto vaccines would not be deemed necessary. Regarding PrEP, once—and if—a patient has seroconverted, other classes of medications such as protease inhibitors are added to complete the “combination therapy regimen.” However, according to none other than the NIH, “single NRTI therapy does not demonstrate potent and sustained antiviral activity and should not be used.”

Note that NRTI therapy is THE standard of care for PrEP. If NRTIs alone do not “suppress viral activity,” then what is driving the apparent effectiveness of these medications in preventing seroconversion?

The criterion for effectiveness of ARVs is action in reducing “HIV-positive” or “viral load” or increasing CD4 counts, judged initially by in vitro experiments. But this does not necessarily correlate with clinical improvement of the patient. This is a real-life illustration of the old saw that an operation may be judged by the experts to have been successful even if the patient died. Suppression of "viral load" does not always restore the immune system; level of "viral load" does not correlate with level of CD4 cells and neither correlates with clinical condition of the "patient.” —The case against HIV

Further to the potential harm that these medications are likely to cause—especially when taken for a lifetime—and the fact that anti-HIV drugs are not specific to HIV, patients who are “retained in care” may also have to deal with the phenomenon of immune reconstitution syndrome, or IRIS, in which patients taking antiretrovirals experience “paradoxical” opportunistic infections—a fancy way of saying the drugs themselves are causing acquired immune deficiency in some patients. Per Wikipedia:

There are two common IRIS scenarios. The first is the “unmasking” of an occult opportunistic infection. The second is the “paradoxical” symptomatic relapse of a prior infection despite microbiologic treatment success. Often in paradoxical IRIS, microbiologic cultures are sterile. In either scenario, there is hypothesized reconstitution of antigen-specific T cell-mediated immunity with activation of the immune system against persisting antigen, whether present as intact organisms, dead organisms, or debris. —Wikipedia

Returning to the concept of the anti-HIV drugs completely changing the face of AIDS, some examination of the numbers does not support this assertion. In the blog post Have ARVs saved 3 million life years?, Dr. Henry Bauer, Dean Emeritus of Arts and Sciences at Virginia Tech, shows that, at a cost to the taxpayers of $20 billion per year, HAART can at best be credited for having “saved” only one in eight AIDS victims. So what happened in the nineties that changed the course of the AIDS epidemic, if it wasn’t the antiretroviral drugs?

One factor is the fact that AZT, which was the only game in the early days of AIDS, is so toxic that “When AZT was replaced by “cocktails” (HAART) the death rate of “AIDS” patients almost instantly declined solely because the new treatment was less toxic.” (The case against HIV, section 5)

Regarding the so-called “Lazarus effect:”

Anecdotal reports describe "AIDS" patients on the point of death who recover immediately upon receiving antiretroviral drugs. But any antiretroviral action could only produce a very slow, lengthy effect. The Lazarus Effect demonstrates that antiretroviral drugs are very efficient killers of all cells, bacterial and mammalian, including the lymphocytes that produce inflammation. (The case against HIV, section 5.5)

We must also consider the difference between“Proto AIDS” and “long haul AIDS”— This distinction is imperative to recognize because the fact that AIDS changed around 1990-95 is usually used as “proof” that the ARVs eliminated AIDS, when in fact this is not the case. AIDS deaths peaked in 1994, two years before combination therapy became widespread, and the opportunistic infections that AIDS patients were susceptible to were already moving away from Kaposi’s sarcoma (now considered to be caused by a herpes virus) and pneumocystis pneumonia and toward inflammatory conditions such as cardiovascular disease and neoplasms, as the massive expansion of “AIDS defining conditions” in 1993 implies.

The question remains: If HIV doesn’t cause AIDS, why do ARVs successfully treat AIDS? The answer is: they don’t, and often prematurely end the life of the patient, but situations in which ARVs appear to work—or even provide some benefit for those suffering from serious opportunistic infections—can be easily explained.

ARVs are very powerful killers of biological invaders, by their very nature, and their antibiotic or antifungal or anti-parasitic powers might overcome occult infections; but prolonged use of ARVs is likely to be fatal.

The seeming positive effects of ARVs are actually very easy to explain, especially when it comes to their effectiveness among the clinically very ill. They are potent microbicides, and very effectively wipe out most bacterial infections; they are also strong anti-inflammatories, and inflammation is very common in both HIV AIDS and non HIV AIDS. Furthermore, the potential of the placebo effect should be ignored at everyone’s peril.

Again, according to official estimates, at least half of the HIV-antibody-positive population of the United States is NOT taking antiretroviral therapy, yet the AIDS of the eighties has been over for decades. This should not be the case if it was the drugs that changed the face of the epidemic. Given the disappearance of “proto AIDS” despite nowhere near universal uptake of the “lifesaving drugs,” this phenomenon deserves an explanation. I wonder what that will be.

In conclusion: Anti-HIV drugs cannot possibly be the reason that AIDS became a “chronic, manageable condition” in the nineties because, first, the decline in AIDS began before the widespread rollout of antiretroviral combination therapy; second, because nowhere near the proportion of the HIV-antibody-positive population has been retained in care at the level that would explain the disappearance of “proto AIDS.” They also cause manifest harm to many patients, as evidenced by the fact that liver damage, neoplasms, and cardiovascular events—direct adverse effects of ARVs—are the most common “AIDS defining conditions” or “complications of HIV disease” nowadays, as well as by the numerous lawsuits being filed against AIDS drugs manufacturers. Any transient positive effect of these drugs can be easily explained by their broad spectrum anti microbial and anti inflammatory properties. Furthermore, they are not even specific to HIV, and have been used to treat hepatitis, chronic fatigue syndrome , and even Covid with varying degrees of success. The fact remains, however, that these medications are meant to be taken not for days or weeks, but for years or decades, creating customers of the pharmaceutical industry for life, however shortened and reduced in quality that life may be. What these drugs do NOT do, and CANNOT do, under any circumstances, is prove ANYTHING about the cause of AIDS. Yes, the drugs work very well if your goal is to have both hips replaced and undergo kidney failure, with the consolation prize of (perhaps) “getting to undetectable,” but to call them very specific “miracle drugs” is highly inaccurate.

I don’t ordinarily mix media, but, because the vibe of the song is so appropriate, here is a bonus video for my fellow nineties babies, plus a link to buy my book: