Jumping the Snake
Notes on the Bryan Ardis / Stew Peters collab., "Watch the Water."
A review of the Bryan Ardis interview by Stew Peters, in which snake venom is the explanation for, well, everything.
I like Stew Peters. I don’t know if he’s an op.
Peters’ persona combines tinfoil-hat histrionics and Teetotaling Joe Sixpack straight-talk; neither seems authentic, and yet both sincere. Like de Bergerac stepping in after the anti-media’s scripted avatars have forgotten their lines, Peters is a breath of fresh air; there’s always a certain panache to his work, and yet one struggles to imagine that nearby ladies are swooning at the sight or sound of him.
And whether Peters is an op or not, his mission seems to be to transcend the official anti-media narrative, and find the fringe. He is always looking for the next shark to jump; his pursuit is one of creativity. In this way, you can appreciate his efforts on an artistic level.
So I want to acknowledge that “Watch the Water,” like all his output, stands as a work of art, and make it clear that I will not be reviewing it in the terms that are truly appropriate to it. My goal here is instead to offer a simple overview and comments on the theory advanced by Ardis, in case the reader prefers not to have to watch the interview for themselves.
In other words, the following is covered by “spoiler alert.” However, I will not be ruining the big reveal of what was on the back of the fortune cookie at Pei Wei.
More Complete than it Needs to Be
Ardis’ theory manages to cover just about all the bases. I propose to organize the theory as follows:
Snake venom peptides are being added to water supplies by private contractors under the auspices of the CDC.
The CDC’s Wastewater Surveillance system is essentially a They-brag of this activity.1 (Ardis doesn’t apply a name to the They in his theory, nor does he say “They” with a capital T very much. Instead, he alludes to an evil force currently waging war against Heaven on Earth. However, his theory makes frequent reference to the same overt displays of conspiracy (brags) as do theories about Masonic and Satanist conspiracies.) However, the surveillance was kept secret until September, 2020.
This is supported by the CDC’s own ability to report increases in positive samples in advance of recognized increases in “cases” (otherwise, it wouldn’t be a very useful surveillance system).
Snake venom peptides are in Remdesivir.
26:30: Gilead, who developed Remdesivir, purchased an Oceanside, CA facility from Genentech in 2011, the same year a set of Genentech employees began a project to map the Indian Cobra (Naja naja) genome and venome-ome (Genentech itself had already been purchased by Roche in 2009).2 While Ardis asserts that Gilead brought “55 Genentech executives” on board, it merely appears that they offered current employees continued employment at the same facility (shocking).3 However, it is pretty funny that the Genentech cobra genome study was literally published in January, 2020.
“Remdesivir as snake venom” accounts for:
The high toxicity of Remdesivir as revealed before its Emergency-Authorization for severe (inpatient) Covid-19. Here Ardis is primarily referring to the Ebola trial, as he has done before. However, Remdesivir merely failed to show improvement against baseline mortality in the Ebola trial.4 The real-world data for its use for severe Covid-19 is likewise ambivalent.5 (I say this as someone who thinks Ardis is probably correct that the NIH treatment protocol in general is driving 10,000s of unnecessary deaths in the US.6)
The white-to-yellow color of Remdesivir, and the storage and dilution requirements.
The contra-indication of Remdesivir with HCQ. Ardis asserts (28:00) that HCQ has been known since 2005 to block nicotine receptors in the brain-stem which are affected by cobra venom. I am not sure if there is a citation for this. He thus proposes that HCQ is contra-indicated because it mitigates harms from snake venom neurotoxins in Remdesivir.
Remdesivir instructions, which include checking prothrombin time before and after administration. Indeed, a small but still higher-than-placebo percentage of recipients experienced an increase in prothrombin time (a clot formation speed test) in the NIAID ACTT-1 trial, potentially indicating anticoagulant effect.7 Cobra venom includes potent anticoagulant peptides. (But… Covid-19 is associated with substantial clotting…)
“Covid-19 as snake venom poisoning” is further supported by:
Observations of toxin-like peptides by Brogna, et al.8
Post-ICU findings by Snider, et al. at the University of Arizona.9 Blood samples from Stony Brook, New York Covid-19 patients (whom Ardis presumes were treated with Remdesivir) revealed that severe Covid-19 features excessive secretion of sPLA2-II, a pro-inflammatory molecule common in mammalian tissue. In high amounts, sPLA2-II causes cell lysis and vascular damage, and possibly partial paralysis (hence why it is also found in bee, wasp and rattlesnake venom). Severe Covid-19 patients who went on to die had sPLA2-II levels over 10 times of normal. This study prompted an on-the-nose headline from the University press.10 However, it so happens that for the patients at Stony Brook in early 2020, treatment with HCQ was more common in both the severe (but recovered) and death (non-recovered) cohorts.11 Also, sPLA2-II is a pro-coagulant.
Pulmonary cytokine storms. Naja naja venom was found to prompt severe inflammatory tissue damage in the lungs after abdominal injection in mice.12
Elevated D-dimer after Covid vaccination (as reported by Charles Hoffe13). Elevated D-dimer can be a useful marker when clinically evaluating snake venom poisoning, per a Medscape Q&A document dramatically read to the camera by Peters.14
Loss of sense of taste and smell. Ardis asserts (43:00) that healers who suck snake venom out of bites lose their taste and smell for long periods. I do not know if there is a citation for this.
Disparate impact on individuals with demographically-associated pre-existing conditions. Ardis asserts (43:30) that the snake venom peptides were essentially curated to target organs that are affected by metabolic diseases (most snake venom contains a large tool-bag of toxins, so this is plausible in general, but hardly seems like an accurate way to target victims).
Thus, snake venom poisoning via tap water and Remdesivir account for the illness and deaths attributed to SARS-CoV-2. Ardis believes that “Covid-19 is not a respiratory virus of any kind” (33:20). It is not clear if Ardis is ruling out that there still is a virus (as in, a virus that still contains elements of the snake venom “bioweapon” but does not actually drive the real-life illness that we term Covid-19).
Hence why monoclonal antibodies are effective against (tap water- and Remdesivir-vectored) Covid-19 (what we term “antivenom” is simply antibodies against venom15), and also why monoclonal antibodies have been aggressively suppressed by Federal authorities or ignored by the media.
Hence why HCQ is effective (blocking nicotinic receptors), and counter-indicated, as suggested by the unclear 2005 citation as noted above. Ardis further cites a 2019 study proposing nicotinic receptor therapy as a treatment for snake venom neurotoxicity.16
Hence the early observations that smokers were under-represented in severe cases,17 and why the Federal authorities made such a pointed effort to encourage quitting smoking. (Note that all three of these bullets are still potentially valid leads in any non snake-venom theory in which the media/government is also intentionally sabotaging treatment, and I’ve always meant to revisit the mystery of whether smoking has a protective effect at some point.)
Thus, SARS-CoV-2 either does not exist or is not driving illness and deaths attributed to it.
However, the studies from early 2020 that report homology between the SARS-CoV-2 spike protein and snake venom peptides are still part of the supporting evidence for Ardis’ theory.18
Likewise, the aggressive fact-checking prompted by snake-origin conspiracy theories based on these studies is corroborating evidence for the link between Covid-19 and/or SARS-CoV-2 and snake venom.
Likewise, the murder of Bing Liu, the University of Pittsburg researcher who was expected to announce “very significant findings” on the cellular mechanisms of SARS-CoV-2 pathogenicity,19 presumably corroborates the “Covid-19 as snake venom” theory (again suggesting that the SARS-CoV-2 spike protein is evidence of the nature of the disease even if the virus isn’t causing the disease).
Thus, since the Covid vaccines code for whatever is in Covid 19 and/or SARS-CoV-2, the Covid vaccines are also causing venom-poisoning in recipients.
And so presumably, we should consider these findings regarding the spike protein to apply to the product coded by the mRNA vaccines. However, Ardis isn’t very prescriptive here. All he seems to support is the notion that the mRNA codes for snake (venom) genes of some type (another element of They-brag, in that snakes are a Biblical representation for sin and Satan).
Ardis is on the right track when he proposes that the most coherent rationale for choosing snake venom (“the original bioweapon”) for Covid-19 and/or SARS-CoV-2 and for the mRNA transfections would be essentially symbolic. So, if you are inclined to think that the virus or its spike protein was designed in a lab, Ardis’ argument remains interesting, even if you don’t buy the parts about the tap water or Remdesivir.
However, Ardis doesn’t actually offer a lot of compelling evidence for the “venom”-ness of the spike protein. Beyond that, it’s not a very useful theory beyond speculating about the state of mind of those who may have designed the virus. Maybe the spike protein has bits of snake venom. But snake venom is a grab-bag of peptides that interact with host molecules; which is already the definition of a viral protein as well.
Rattlesnake venom contains a relative of sPLA2-II, which is expressed in all human tissues. SARS-CoV-2 infections were found by Snider, et al. to prompt extreme secretions of sPLA2-II by these same tissues, mimicking venom-poisoning. Out-of-control bacterial infections leading to sepsis also promote extreme secretions of sPLA2-II, mimicking venom-poisoning.
Charles McCall, lead researcher from the Wake Forest School of Medicine on the study, refers to the enzyme as a "shredder" for its known prevalence in severe inflammation events, such as bacterial sepsis, as well as hemorrhagic and cardiac shock.
Previous research has shown how the enzyme destroys microbial cell membranes in bacterial infections, as well as its similar genetic ancestry with a key enzyme found in snake venom.
The protein "shares a high sequence homology to the active enzyme in rattlesnake venom and, like venom coursing through the body, it has the capacity to bind to receptors at neuromuscular junctions and potentially disable the function of these muscles," Chilton said.20
So the “venom-ness” of SARS-CoV-2, which is only weakly supported by Ardis’ evidence to begin with, wouldn’t imply that the virus is or isn’t derived from snake venom peptides. In evolutionary terms, snake venom peptides are “designed” by the biology of the creatures who are bitten by them - just as viral proteins are “designed” by the hosts that are infected. So in either case the host - ourselves - writes the “script” for what a bioweapon-designer will come up with. All that really matters is that SARS-CoV-2 appears to have some direct toxic properties (as do many other molecules belonging to common microbes, including those responsible for routine childhood infections).
So in general, Ardis’ theory is more complete than it needs to be. It is thus not without merit, but likewise not without some rather astonishing flaws:
Even if Remdesivir is toxic (which would be hard to know, given that it is only administered to high-risk patients), Ardis misconstrues almost all of the evidence. In particular, he trips up with the Snider, et al. study (HCQ, not Remdesivir, was given to most patients).
If Remdesivir contains anticoagulant cobra venom peptides, it cannot account for the hypercoagulation pathologies observed during Covid-19. The virus and specifically the S1 unit of the spike protein, not cobra anticoagulant peptides, are the obvious candidate for these effects.21
(Again, I want to stress that I am not opposed to the more general idea that the official treatment regimen is increasing deaths from infection.)
The detection of virus in wastewater does not imply that tap water contains what is being measured in the wastewater. (Obviously Ardis is being sloppy here. If the CDC has contracted wastewater surveillance, that neither implies nor rules out that it has also logistically insinuated itself into the water supply; it merely proves that the CDC is aware that water exists.) Wastewater surveillance has been used in lower-test-rate contexts (such as with polio in developing nations), and may or may not offer an advantage for tracking SARS-CoV-2 in the US. It depends on how widespread testing is in a given region at a given time, the buffer between high and low false-positives in the beginning of a wave, the delay between initial viral shedding and the onset of symptoms, etc. Likewise, wastewater surveillance has always had creepy deep-state / NGO collaboration overtones.22 It’s the chemtrails of poop.
If the Covid vaccines code for snake venom, in Ardis’ theory, then they also “vaccinate” against themselves, as well as the tap water and Remdesivir. Naturally, the first thing is true if the spike protein is simply considered to be toxic in general (so that doses beyond the first may in fact be less toxic, thanks to previously-primed antibodies, but this depends on the speed with which antibodies are ramped up - obviously the spike has to be expressed in the first place for ramp-up to occur). The other two things, however, suggest that the “They” are intentionally trying to disarm their own bioweapon. Ardis at least could have buttressed his theory with some sort of reference to variants as “alternate peptides” or something. Perhaps we will have to wait for the sequel.23
Edit: For a less generous review of “Watch the Water,” see Stephanie Brail’s take at Wholistic.
If you derived value from this post, please drop a few coins in your fact-barista’s tip jar.24
Suryamohan, K. et al. (2020.) “The Indian cobra reference genome and transcriptome enables comprehensive identification of venom toxins.” Nature Genetics. 52, pages 106–117 (2020)
Mulangu S. et al. (2019.) “A randomized, controlled trial of Ebola virus disease therapeutics.” N Engl J Med. 2019;381(24):2293–2303.
If it is either helping or harming, the signal is hard to make out given the low rate of severe disease in infection overall (Gottlieb, R. et al. “Early Remdesivir to Prevent Progression to Severe Covid-19 in Outpatients”) and the high rate of death once patients have already progressed to severe disease (Ader, F. et al. “Remdesivir for the treatment of hospitalised patients with COVID-19: final results from the DisCoVeRy randomised, controlled, open-label trial”).
This paradox ironically puts Remdesivir in the same boat as HCQ, Ivermectin, etc. But unlike those other therapeutics, Remdesivir doesn’t seem to have any doctors that believe it can prevent progression to severe illness to an extent that justifies outpatient use. Additionally, Remdesivir is a nucleoside analog, like Molnupiravir - and all nucleoside analogs are likely toxic and represent a net-negative approach to treating viral infections (see “Doppelgänger”).
Here Ardis appears to cite Table 8 in https://www.gilead.com/-/media/files/pdfs/remdesivir/eua-fda-authorization-letter.pdf
Brogna, C. et al. “Toxin-like peptides in plasma, urine and faecal samples from COVID-19 patients.” F1000Res. 2021; 10: 550.
Snider, J. et al. “Group IIA secreted phospholipase A2 is associated with the pathobiology leading to COVID-19 mortality.” J Clin Invest. 2021;131(19):e149236.
Brandt, Rosemary. “Like Venom Coursing Through the Body: Researchers Identify Mechanism Driving COVID-19 Mortality.” (2021, August 14.)
The higher rate of HCQ treatment in the Severe (but not Deceased) cohort may be a signal for efficacy against death, or it could be a reflection of differences in how individuals (samples) were selected in each group, etc.
Al-Mamun, M. et al. (2015.) “Histopathological Alterations Induced by Naja naja Crude Venom on Renal, Pulmonary and Intestinal Tissues of Mice Model.” Biotechnology Journal International, Page 119-125. 2015.
The authors do not use the phrase cytokine storm but report “extensive [pulmonary] tissue damages and showing inflammatory cellular infiltration and alveolar haemorrhage.”
See Hirschhorn, Joel. “From shots to clots: considerable medical evidence of COVID vaccine-induced blood clots.” (2021, August 11.) LifeSiteNews.
Szigeti, R. “How are elevated D-dimer levels interpreted?” (2019.) Medscape.
A login-circumventing snapshot of the article is available on Wayback http://web.archive.org/web/20200615051647/https://www.medscape.com/answers/2085111-196749/how-are-elevated-d-dimer-levels-interpreted
And yet somehow Veritasium hasn’t yet been deplatformed for his unhinged “anti-snake-venom-vaxx” rant last month. This heartless, pro-snake-venom luddite is a menace to public health!
Albulescu, L. et al. (2019.) “A Decoy-Receptor Approach Using Nicotinic Acetylcholine Receptor Mimics Reveals Their Potential as Novel Therapeutics Against Neurotoxic Snakebite.” Front Pharmacol. 2019; 10: 848.
The balance of evidence seems to support the initial reports, but this may simply be a matter of which bias was represented more often in studies.
Studies finding that smokers were more at risk may have been biased by counting non-SARS-CoV-2 infections based on similar symptoms, before testing was widespread (Hopkinson, N. et al. “Current smoking and COVID-19 risk: results from a population symptom app in over 2.4 million people”); studies finding the opposite may have been biased by high rates of smoking in the test-negative pseudo-control-group (Meini, S. et al. “The Paradox of the Low Prevalence of Current Smokers Among COVID-19 Patients Hospitalized in Nonintensive Care Wards: Results From an Italian Multicenter Case-Control Study”).
These issues aside, a 2021 review concludes that most research finds smokers to be under-represented in SARS-CoV-2 infections (Simons, D. et al. “The association of smoking status with SARS-CoV-2 infection, hospitalisation and mortality from COVID-19: A living rapid evidence review with Bayesian meta-analyses (version 11)”).
Ardis is a bit vague in which studies he is citing. However, reader “Sandokhan” previously supplied an extensive list of citations for the link between SARS-CoV-2 and snake genomes in a comment to a post in February:
Certainly Sars-Cov-2 did not originate in bats.
Cobra genome and Sars-Cov-2 genome MN908947:
The researchers used an analysis of the protein codes favored by the new cor.onavirus and compared it to the protein codes from cor.onaviruses found in different animal hosts, like birds, snakes, marmots, hedgehogs, manis, bats and humans. Surprisingly, they found that the protein codes in the 2019-nCoV are most similar to those used in snakes. […]
See “Department Mourns the Passing of Dr. Bing Liu” and Armus, Teo. Beachum, Lateshia. “Coronavirus researcher killed in Pennsylvania murder-suicide, police say.” (2020, May 6.) The Washington Post Democracy Dies in Darkness.
See Grobbelaar, L. et al. “SARS-CoV-2 spike protein S1 induces fibrin(ogen) resistant to fibrinolysis: implications for microclot formation in COVID-19.” Biosci Rep. 2021 Aug 27; 41(8): BSR20210611.
2 Watch 2 Watery.
(Housekeeping notice for longer-term subscribers: Going forward, I am replacing the monthly “drive” model with per-post donation solicitation. However, I will continue to try to create value for long-term readers via monthly “magazine-worthy” articles!)