The Snake Venom Hypothesis - An Analysis
Let's look at the points raised by Dr. Bryan Ardis (PhD) DC
Is there snake venom in SARS-COV-2? My video below. Short answer: no.
Is there anything useful that came out of this viral snake venom hypothesis? Yes, my video on this topic below.
During the last few days more and more KoolBeens asked if I had reviewed the snake venom hypothesis. I also saw an increasing number of commenters just writing SNAKE VENOM under some videos. Considering that I am busy studying and then presenting/reporting contemporary health matters, it is difficult for me to pay attention to theories that are dime a dozen now a days. Still, it became clear to me that KoolBeens are interested in hearing my review of this topic. Here goes.
My colleagues and friends have addressed many of the points from the presenter of this hypothesis. Read these articles here, here, and here.
Considering the exhaustive analysis by my colleagues above, I will focus on the following points from Dr. Bryan Ardis (PhD Doctorate in Chiropractic) and some questions that I am seeing repeatedly from the KoolBeens.
Context
My colleague Bryan has based some of the venom theory on this rather weak study. In this study the authors present that the COVID patients have toxins in their urine and stool samples. This study is weak as it uses urine samples from two patients and stool samples from three. Additionally their control group is not correct. For example, we will want a COVID patient’s inflammatory biomarkers to be verified by comparing to the biomarkers of other patients that may have infections from non SARS-COV-2 pathogens. This will help verify if these markers the researchers saw are produced by SARS-COV-2 or not. Instead the researchers compared COVID patient samples to healthy individuals’ samples. Healthy individuals do not have inflammation going on, neither are they taking any medicines, etc.
(Imagine my surprise that this toxins study got reviewed, accepted, and printed. That says something about the journal as well.) A doctor’s comment on this study sums up the issues (go to the comments section.)
Ernesto de Bernardis, ASP SR, Italy
I don't understand why the Authors' hypotheses about the origin of these peptides don't include the host response during severe inflammation or ARDS, or during a pharmacological therapy similar to those given to COVID patients.
The paper compares peptides from COVID patients with those from healthy controls, but doesn't include controls with other diseases, e.g. inflammatory diseases, other viral diseases, or people treated with the same medications that were administered to their sample of COVID patients.
So, I guess it can't be excluded that the findings aren't specific to COVID and that might be common to other conditions.
It is interesting to note that authors backtrack their observations in response to the comment by Dr. Ernesto de Bernardis.
In the above cited toxins study the authors say that the patients had high levels of Phospholipases, Metalloproteinases, and Conotoxins. Despite this study being weak we will discuss these toxins in the discussion below as Bryan uses it to base his hypothesis of snake venom.
Let’s continue our discussion.
Bryan also misinterprets the university of AZ study and article to imply in this video (at minute 3) that SARS-COV-2 contains/is snake venom because phospholipase A2 - IIA (sPLA2-IIA) is found in the cobra venom and also in the dying COVID patients. He also mentions that a colleague of his said that they see sPLA2-IIA sequence in vaccine patents as well.
He mentioned here (minute 4:39) that a person send him a note that this venom theory helps them make sense of why children get less severe COVID. The note said that it is higher levels of melatonin in children protecting them from the snake venom (sPLA2-IIA) because melatonin can help against the cobra venom.
Pre-Discussion
Before we start, some answers to worried KoolBeens’ questions below:
Question: will I be passing this venom to my partner during sex?
Answer: phospholipase (PLA) is not known to become part of semen from the other destinations. However, it is found in the sperm so that it can help with the ova activation.
Question: will I shed this snake venom?
Answer: no, phospholipase does not shed through our breath.
Question: what part of the virus (SARS-COV-2) contains this venom?
Answer: none, SARS-COV-2 does not have a phospholipase sequence in it.
Discussion
Phospholipase A2-IIA (sPLA2-IIA)
Phospholipase is an important enzyme found in most animals including us.
The function of phospholipases is to digest/breakdown or remodel the cell membranes. Cell membranes are made of phospholipids. (Note: enzymes that break down various structures are usually named after the structure with an “ase” postfix. Phospholipase [PLA] breaks down phospholipids.)
In nature many types of PLA are found. Their categories are based on what part of the phospholipid molecule they attack and the outcome of the attack. Here is an excerpt from the article linked above:
As protein sequencing methodologies advanced in the 1970’s, it became apparent that these enzymes had an unusually large number of cysteines (over 10% of the amino acids) and as secreted enzymes, that they were all in the form of disulfide bonds. It was further recognized that in the case of PLA2, cobras and rattlesnakes had six disulfides in common, but one disulfide bond is located in distinctly different locations. This led to the designation of Type 1 and Type 2 for cobras (old world snakes) and rattlesnakes (new world snakes), respectively.2 During that same period, studies on the porcine pancreatic digestive enzyme that hydrolyzes phospholipids led to the determination that this mammalian enzyme (and also the human pancreatic enzyme) had the same disulfide bonding pattern as cobras and hence the designation as IB with the cobra enzyme as IA.
PLAs are secreted from pancreas to help digest meat in food.
PLAs are also able to help reshape and remodel our cell membranes. This is an important homeostatic function. And, we need it.
sPLA2-IIA (same enzyme that is present in Cobra, Rattle Snake, Scorpio, and Bees’ venom) is released from our cells in response to infections. The reason is that our body when infected knows that we need to kill these pathogens. A good way to break these pathogens is to break their cell walls/envelops. And, sPLA2-IIA does this function. This is why PLA release is an important event during infections. Excerpt from the article below:
sPLA2s exhibit a large variety of cellular functions, though the specific function varies by group or subgroup. The major functions will be summarized below and include the ability to kill Gram-positive and Gram-negative bacteria thereby affecting host defense against bacterial infections.44 sPLA2s also show antiviral activity.
Fortunately SARS-COV-2 is an enveloped virus (has a membrane/envelop made of phospholipids). This makes SARS-COV-2 prone to an attack from sPLA2-IIA.
It is understandable that the dying patients will have a higher level of sPLA2-IIA because they are under intense infective state and their bodies are making a lot of sPLA2-IIA to kill the pathogens.
It is not the virus that is the venom, it is our bodies producing venom against the virus. However, this high level of sPLA2-IIA is counterproductive and ends up causing damage to our cells. This cell damage in turn contributes to the organ damage leading to organ failure and our death in some cases. These events are part of the immune response in our body. In severe cases this response is called cytokine storm.
It is worth repeating, it is our body’s response to infection that creates the cytokine storm. And, the cytokine storm has many inflammatory and destructive molecules produced including high levels of sPLA2-IIA. This response is what causes the damage and death, and not only the tissue damage by SARS-COV-2. In fact in some HIV patients SARS-COV-2 has been present for more than a year without much issues. (I have discussed this case study from South Africa in one of my videos.)
Sadly, the University of AZ article had a title that provided ammunition to Bryan. Their title is (and I kid you not): Like Venom Coursing Through the Body: Researchers Identify Mechanism Driving COVID-19 Mortality.
Bryan used this title to strengthen his hypothesis. Maybe believing that people will not read the article. I read it. In this article the researchers specifically say:
"In other words, this enzyme is trying to kill the virus, but at a certain point it is released in such high amounts that things head in a really bad direction, destroying the patient's cell membranes and thereby contributing to multiple organ failure and death."
Now, what does release mean in the above excerpt? Researchers clarify it in their article:
The sPLA2-IIA enzyme, which has similarities to an active enzyme in rattlesnake venom, is found in low concentrations in healthy individuals and has long been known to play a critical role in defense against bacterial infections, destroying microbial cell membranes.
When the activated enzyme circulates at high levels, it has the capacity to "shred" the membranes of vital organs, said Floyd (Ski) Chilton, senior author on the paper and director of the UArizona Precision Nutrition and Wellness Initiative in the university's College of Agriculture and Life Sciences.
So far we have seen that the virus is not a snake venom, instead it is our body and immune system trying to kill the virus using hundreds of mechanisms including releasing PLA2.
Metalloproteinases
This is another toxin that the study mentions. Metalloproteinases are actually also enzymes that are produced by our body in high amount during infections. Interestingly Zinc is needed by these enzymes. Hence, patients with severe infections can become Zinc deficient.
Metalloproteinases are also found in the venom. But, again like PLA this enzyme is our body’s production and not the SARS-COV-2.
Conotoxins
Conotoxins are toxins present in sea snails of genus Conus. These snails are predatory and release conotoxins to paralyze their prey. Researchers are trying to convert these into pain killing meds.
Now, this toxin is not produced by our body. The paper in which these are mentioned have such small cohort size (2 urine samples and 3 stool samples), no comparison to patients in similar inflammatory state and meds but not infected by COVID, and no research on the food, drugs, or accidental ingestion of conotoxins, or a reproduction of this toxin in-vitro by infecting cells with SARS-COV-2 etc. that this toxin’s presence is curious. To me it seems like a false positive, but then again, it needs to be research to be prove or disproved.
Melatonin
It is true that pre-pubertal children have high levels of melatonin (list below).
18 months - 6 years: 60.8 +/- 100.58 pg/mL.
6-8 years: 35.54 +/- 9.17 pg/mL.
8-13 years: 25.28 +/- 7.16 pg/mL.
13-15 years: 31.14 +/- 8.29 pg/mL.
Adults can have 10-60 pg/mL
Reviewing the data above you will notice that children have higher levels of melatonin. These levels drop ay about 10-15% per decade. But, the difference within children’s groups is variable as well. But, COVID is not similarly variable in children.
I will think that melatonin is potentially helpful because it protects against mitochondrial damage caused by reactive oxygen species during inflammatory events. And, also because it helps restores cell’s aerobic breathing pattern. It is, however, incorrect to conclude that SARS-COV-2 is snake venom because melatonin can potentially help against the SARS-COV-2 infection and melatonin also potentially helps against the snake venom.
The writings I linked from my colleagues above have explained more inaccuracies in the snake venom hypothesis.
Suffice it to say that there is nothing slithering in the SARS-COV-2 but a virus that in itself has done more damage in two years than some of these animals we are talking about.
DrBeen you are the most gracious person I know.
An important question to answer - is a sequence found in venom (cobra?) also found in the sars-cov-2 genetic sequence. Is it correct to think that with all the sequencing of sars-cov-2 and all the research that has been done on venom that it would rather straight forward to make a detailed comparison?
If such a sequence is found then the obvious questions - natural vs lab recombination, and what part is it contributing in the process initiating the "allergic" type complication of covid that have been described.
early on in covid time, when I was downloading study after study and "searching" most of every day , I came upon 1 study stating that a sequence in sars-cov2 was identical to one in cobra venom. I may or may not have downloaded that study. shortly after I found an India study proposing to use a repurposed drug as an add on universal anti venom. then found a study proposing the use of that same drug for the treatment of covid. I have located these studies on a flash drive.
"The outworking of events." When 3 related events happen in close sequence I take note.