“Paxlovid is effective, but underused”
It also contains an “HIV” protease inhibitor—why?
The propaganda from JAMA is deafening.
Paxlovid Is Effective but Underused—Here’s What the Latest Research Says About Rebound and More
Anyone who watches television has probably seen the Pfizer commercial with the tagline, “If it’s COVID, Paxlovid.”
That might be a catchy slogan, but, apparently, a lot of people aren’t getting the message.
I don’t actually have a television, but I can use my imagination. “A lot of people aren’t getting the message?” Oh brother.
What is Paxlovid anyway? Well, according to the article, “A dose of Paxlovid consists of 2 pills of the protease inhibitor nirmatrelvir and 1 pill of ritonavir, which boosts nirmatrelvir’s concentration in plasma to the target therapeutic range by slowing its metabolism in the liver.” What are Nirmatrelvir and ritonavir? According to Wikipedia, Nirmatrelvir is “an antiviral medication developed by Pfizer which acts as an orally active 3C-like protease inhibitor.” Where things get interesting is with regard to the second ingredient, ritonavir. Let’s see what Wikipedia has to say about this “antiviral” medication.
Ritonavir, sold under the brand name Norvir, is an antiretroviral medication used along with other medications to treat HIV/AIDS.[4][5][6] This combination treatment is known as highly active antiretroviral therapy (HAART).
Wait a minute. Aren’t “anti-HIV” drugs supposed to be highly specific to HIV? (Oh, wait—they’re not. Click the link, it’s worth it.) Why are we prescribing antiretrovirals for Covid? Apparently it is a “strong CYP3A inhibitor.” CYP3A is an enzyme that is involved in healthy liver function. You may recall that one of the major side effects of the HIV protease inhibitors, when they came out in the 1990s, was liver failure, which must be at least part of why—and you may not be aware of this—most of the commonly prescribed multi drug therapies for “HIV” no longer involve a protease inhibitor at all any longer. Just check out the formulations of the popular drugs Genvoya, Triumeq, and Biktarvy, for starters. I thought those were the medications that ended the AIDS epidemic.
The article goes on to state that “However, the treatment is contraindicated for some patients because ritonavir slows the metabolism of a variety of medications, leading to excessively high concentrations.” Isn’t that code for “it’s toxic?” (The Wikipedia page even says ritonavir is used at least in part to “boost the concentration in the liver” of Nirmatrelvir—that doesn’t sound dangerous at all.) But never fear, there is an alternative for those who can’t handle the toxicity of taking an “anti-HIV” drug for a short lived respiratory illness—remdesivir (manufactured by our favorite pharmaceutical company, Gilead.) I’ll just leave that there.
Now we move on to the panic about hospital overrun and hand wringing about how just not enough patients are taking Paxlovid, darn it! (I have a family friend that was prescribed Paxlovid and described the experience as terrible, so that might be part of it.)
“The number of hospitalizations for COVID right now are much higher than for flu,” Pragna Patel, MD, MPH, chief medical officer in the Coronavirus and Other Respiratory Viruses Division of the CDC’s National Center for Immunization and Respiratory Diseases, pointed out in an interview with JAMA.
One likely reason: relatively few eligible patients are getting nirmatrelvir-ritonavir, the preferred treatment for keeping mild to moderate COVID-19 from progressing to severe disease.
A retrospective study published in January of this year found that only 12.2% of 309 755 eligible adult outpatients received nirmatrelvir-ritonavir. The patients, seen from January 2022 through December 2022, received care from the National Veterans Affairs Healthcare System. The proportion of eligible patients prescribed the treatment did increase over the course of the study, the authors noted, but by December still had only reached 23.2%.
Here is another reason that patients might not be falling for the Paxlovid garbage quite as quickly as they fell for the mRNA garbage (emphasis mine):
Perhaps the main reason nirmatrelvir-ritonavir has been underused is the rebound phenomenon, usually described as the return of symptoms and test positivity a few days after completing treatment and appearing to have recovered.
[…]
An observational study published in November 2023 compared rebound rates of 130 treated and 241 untreated patients who were eligible for treatment. The treated and untreated groups had similar baseline characteristics. Researchers collected daily reports for 10 days from each patient about symptoms and medication use as well as respiratory specimens for polymerase chain reaction (PCR) testing from March 2022 to May 2023.
Patients who completed treatment reported experiencing fewer symptoms and had a lower viral load than those who weren’t treated, the authors found. However, those who were treated had a greater occurrence of symptom rebound compared with untreated participants (32% vs 20%) and viral load rebound (27% vs 7%).
Ah, the famous “rebound”—in other words, the medication doesn’t do what it’s supposed to do. This reminds me of immune reconstitution syndrome, also known as immune reconstitution inflammatory syndrome or IRIS, a phenomenon in which HIV positive people sometimes develop paradoxical opportunistic infections after initiating antiretroviral therapy. But don’t worry, people! A study was conducted to try and sweep the fact that the medication is useless and potentially harmful under the carpet:
In contrast to the studies published in November, 2 papers that appeared a month later in Morbidity and Mortality Weekly Report (MMWR), one by Patel and CDC colleagues and the other by FDA scientists, both concluded that among patients with COVID-19, virological rebound rates were similar between patients treated with nirmatrelvir-ritonavir and those who were not.
[…]
“We were worried that rebound got linked to Paxlovid, and folks might be hesitant to take it because of rebound,” Patel said in explaining why she and her colleagues conducted their study.
Once again, they’re saying the quiet part out loud, if only we will listen. Why was the study conducted? To address “Paxlovid hesitancy,” apparently. (Is that a term, like vaccine hesitancy?)
I’m getting tired of the propaganda, so let’s wrap this up. The article itself is far longer than it needs to be. The last section asks: when is the best time to begin treatment? Immediately, of course. Hit hard, hit early, remember? And let’s don’t forget the importance of TESTS.
Treatment is supposed to begin as soon as possible after a COVID-19 diagnosis and within 5 days of symptom onset, according to the nirmatrelvir-ritonavir label.
[…]
That said, starting treatment within a day of symptom onset might be tricky for some people because rapid antigen tests can yield false-negatives. These results should be confirmed right away with a PCR test if possible or another antigen test in 48 hours, according to the CDC.
The whole thing is such a neat little package, isn’t it? Let’s normalize PCR for diagnosis and toxic medicines for therapy, all while making the drug company executives very wealthy on the backs of this endless testing/treatment cycle. We’ve seen it before; there is nothing new under the sun.
I’ll just end on this final note, from the “when to initiate treatment” section:
Their study also found that early treatment may be associated with a significantly higher risk of viral burden rebound, although the number of late-treated patients who experienced rebound was too low to be certain.
So the study that was supposed to make Paxlovid look better actually indicated quite clearly that it is ineffective? Don’t fret, though, the article concludes by noting that “many promising Anti-Viral treatments for Covid” are just around the corner! It ending on that note seems to be a pretty clear indication that the study authors are well aware that Paxlovid is at best useless and at worst, dangerous. Who are they trying to fool?
Do you know anyone who’s taken Paxlovid and what their experience was like? I’d love to know in the comments!
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This is so fascinating. The part that struck me was the part where Paxlovid (the Ritonivir portion), was DESIGNED to slow the liver down. The liver is a detox organ. In Chinese medicine they refer to the liver as The General, because it's in charge of everything. Yes, we need the other organs, but the liver has a central role in the body's entire homeostasis. I follow a doctor who treats all kinds of maladies in people purely by helping them repair liver damage. Western medicine thinks of a healthy liver as something that doesn't have elevated liver enzymes, but he says that sub-clinical liver injury is at the heart of many peoples' health struggles. What he points out was the only thing that made sense to me in my case.
He's developed a fascinating theory called Toxic Bile Theory. Bile is mostly known as a fat emulsifier, that's its widely known function, but in fact the liver dumps toxins of all sorts into the bile and tries to transport them out of the body through the poop. But the liver gets messed up, even mildly, and the bile starts doing things it shouldn't be doing. The bile ducts actually become damaged (leaky) and the bile and all the toxins the body is trying to get rid of instead back up into the bloodstream. This is actually a thing, there are functional tests for this called Serum Bile Acid tests. The more bile acids you have the blood, the sicker you are. Type 2 diabetics have twice as much bile floating around their blood as non-diabetics for instance.
Well, this doctor discovered that all kinds of disease states are associated with this bile in the blood condition, and one of the things that can make something appear short term to seem better is by slowing the liver down, which means less bile is being excreted and thus less backing up where it doesn't belong in the blood and thus making a person sick.
So there we go, Paxlovid slow the liver down giving a person a temporary reprieve from symptoms, and when it's withdrawn, the bile starts flowing again, and in the injured liver state back up into the blood making the person symptomatic again.
His presentations are interesting, they're based on the work of a researcher who back in the 80s I believe discovered this process and has written a bunch of papers on it (Anthony Mawson).
Paxlovid is a temporary fix that ends up making the problem worse in the long run because pharmaceuticals in general cause liver injury and thus this processes called subclinical cholestasis.
Some have said that Long Covid is the new name for Aids.
Aloe, I encourage you to familiarize yourself with Rebecca’s work. It’s not possible for her to encapsulate the entirity of it in every post. There is such thing as Covid as a reference to human unwellness since humans do and have always had varying degrees of wellness.
Sooner or later Rebecca’s work will focus on the phenomenon which some call Covid since Long Covid or something with a name to that effect will replace the function of deception that was previously known by the name of Aids.
In simple terms however I do agree that there is no such thing as Covid (or of Aids).