Testosterone blockers to treat “HIV”—is this real?

Yes. It is.

This will be a very short post, but I think it’s important.

I recently had the opportunity to watch the below YouTube video, which features “HIV” positive activist Raif Derrazi interviewing poster presenters at an HIV AIDS conference. Something that caught my attention is that two of the presenters he interviewed discussed the use of spironolactone as a “transcription inhibitor.” That is fascinating to me because for one thing, I thought that NRTIs like AZT and Truvada were “transcription inhibitors?” Why do we need yet another? Plus, I’d heard about spironolactone being used as a testosterone blocker (??), so I was quite curious where this would go.

But even more weird is the fact that spironolactone is approved for use not only as a blood pressure medication—it has diuretic effects—but as a testosterone blocker for trans-identifying males. Why on earth is it being repurposed as an antiretroviral?

Check this out, from Mayo Clinic:

Feminizing hormone therapy typically begins by taking the medicine spironolactone (Aldactone). It blocks male sex hormone receptors — also called androgen receptors. This slows or stops changes in the body that usually happen due to testosterone.

About 4 to 8 weeks after you start taking spironolactone, you begin taking estrogen. This lowers the amount of testosterone the body makes. And it triggers physical changes in the body that are caused by female hormones during puberty.

A very short look into this drug reveals that it is primarily prescribed as a blood pressure medication. However, with the rise in “gender affirming” surgeries and treatments, it has gained new enthusiasm as a “testosterone blocker.” Two of the poster presenters featured in this video enthusiastically discussed spironolactone as a “transcription inhibitor.” Wait, what?

This whole enterprise of “anti-HIV drugs” is completely bizarre. From the advent of AZT in the 1980s—which if you can remember living through it, AZT really was treated as a miracle drug back in the day—to the case of the disappearing protease inhibitors (remember Crixivan?) to PrEP to Truvada to the long-acting injectables to, now, prescribing testosterone blockers as “anti-HIV” medication, it just seems like the entire history of “HIV” research and treatment is one bungled misstep after another. Clearly, the idea that these drugs are specific to “HIV” is completely insane.

Here is a brief explanation of how this is meant to work (emphasis mine throughout):

Here, we show that spironolactone (SP), an aldosterone antagonist approved for clinical use, inhibits HIV-1 and HIV-2 infection of permissive T cells by blocking viral Tat-dependent transcription from the long terminal repeat (LTR). We found that treatment of Jurkat and primary CD4⁺ T cells with SP induces degradation of the XPB cellular helicase, a component of the TFIIH complex, without affecting cellular mRNA levels, T cell viability, or T cell proliferation. We further demonstrate that the effect of SP on HIV infection is independent of its aldosterone antagonist function, since the structural analogue, eplerenone, does not induce XPB degradation and does not inhibit HIV infection. Rescue experiments showed that the SP-induced block of HIV infection relies, at least partially, on XPB degradation. In addition, we demonstrate that SP specifically inhibits Tat-dependent transcription, since basal transcription from the LTR is not affected. Our results demonstrate that SP is a specific inhibitor of HIV Tat-dependent transcription in T cells, which additionally suggests that XPB is a cofactor required for HIV infection. Targeting a cellular cofactor of HIV transcription constitutes an alternative strategy to inhibit HIV infection, together with the existing antiretroviral therapy.

This is really incredible, when you consider that the entire “proof of concept” of the HIV AIDS theory rests entirely on the idea that the reason AIDS isn’t this big scary thing like we saw in the 1980s is because we have found these highly specific drugs, that are laser-focused on “HIV.” Except that, clearly, they are not. From prescribing antiretroviral drugs to long COVID and hepatitis patients, demonstrating their lack of specificity to “HIV”, to using random testosterone blockers as “anti-HIV” medications, we have been fed, since the late 1980s, a complete lie as to the efficacy and safety of “anti-HIV” medication. I hope that, if nothing else, I have managed to convince you that “anti-HIV” drugs are not specific to “HIV.”

Let me know what you think in the comments. I hope you are all keeping warm and safe—here in East Texas it’s been a cold rain, which is an improvement from my time growing up in Canada.