One feature amongst the AV community is their ability to illustrate the whole Dunning-Kruger Effect with real life example. If you are not familiar with the Dunning-Kruger effect, it is a cognitive bias initially reported by David Dunning and Justin Kruger, in which a person commonly overestimate or display an overconfidence on his/her knowledge on a topic but yet fails to master the topic in question, often living in a belief of superiority, in particular when challenging experts.
The average person on the Dunning-Kruger (DK) effect will make extraordinary claims while denigrating giving the credentials to experts, often arrogantly claiming they know more than an seasoned expert that spent his/her education and professional career on the topic.
Most of the time (>99%), AV experts are using and abusing credentials that don’t have. For instance, Avers claiming to be medical doctors only to be a doctor in chiropractic or naturopathy, or scientists whereas harboring at best a Bachelor’s degree. Amongst them is Ashley Everly.
1. Who is Ashley Everly?
Ashley loves to depict herself as a “toxicologist” and love to parade on social media as is. However, if you look a bit more attention to her LinkedIn profile, you will notice that she has a Bachelor degree in Environmental Toxicology from UC Davis, and some internship at the California EPA from 2007 to 2008. Then a 8 years gap, with suddenly posing as a toxicologist for “Health Freedom Idaho”, a notorious anti-vaccine group.
Let me be clear. In order to claim yourself as a “toxicologist”, you have to have a minimum a doctoral degree in toxicology from an accredited institution, have passed the peer-review amongst peers by showing evidence of publications in peer-reviewed journal and ideally hold a faculty position in that specialty.
At best, with a BSc you can claim the title of “lab technician” but nothing more. It also tells us the low-standard quality that “Health Freedom Idaho” stands and the quality of the science they must be using.
Ashley loves to parade as a peacock during mating season in the AV community as an expert, but once facing real experts quickly cave in and go into hiding. Let me show you some of my encounter with Ashley on Facebook a couple of months ago:
The PNAS study in question is this one (http://www.pnas.org/content/111/2/787?fbclid=IwAR1cwoO3monJZbDGvITilGMYBh7VRUFDs2lzyAexEaljdi6_69vhlGYDDpM) and as of today Ahsley was never seen again discussing on that topic. She quickly flounced and disappeared. So much for a “toxicologist” to refuse to address criticism from a peer and being completely clueless on interpreting a study she herself brought into.
Ashley, if you read that post, I hope that these last four months were enough for you to read and comprehend the PNAS paper and answer my question.
2. Vaccine Guide: Ingredients/Excipients/Contaminants
You will find below my rebuttal to the whole section, with the exception of reviews (because a review is a collection of studies picked from the literature and remains at the discretion of the author. I treat them as an opinion piece and I don’t discuss opinions. I discuss data and their interpretation). I maintained the sections and went through most of the “studies” present in her binder as published in May.
2.1. Aluminum Adjuvants:
Aluminum involvement in neurotoxicity
This is a study that is published in a potentially predatory journal (Hindawi), and you can feel the low-quality of the study presented by the sole figure making the paper (Figure 1).
The author main hypothesis is that aluminum is associated with neurological diseases and claim that chelation therapy (using IV infusion of EDTA) can help alleviate the patient.
The cohort of subjects are divided into several categories including a healthy, neurodegenerative diseases (ND, including MS, mislabeled as SM. An error that should have been labelled by reviewers but went through, Alzheimer=AD, Lou Gehrig/Amyotrophic Lateral Sclerosis (ALS) and Parkinson’s (PD), and non-ND (e.g. fibromyalgia group).
Here is the first problem: Why did the authors not provided blood/plasma levels of Al in patients? Blood levels would be a much better biomarker than urine, because it would indicate the systemic concentration of aluminum and pointed out that ND patient have abnormal Al load by default.
The second problem is the use of urine. It is interesting, but not as great than plasma samples. Especially because you have a high risk of variation in Al urine concentration based on the kidney function. Do these diseases affect the kidney function? I don’t know but showing an absence of difference in creatinine clearance between the patients would have really helped.
Third is the chelation method. By applying chelation therapy to these patients, they are forcing the pulling out of Al from their body, which can be highly variable and also an unreliable outcome for assessing heavy metal poisoning. Again, I repeat, blood sampling is the gold standard.
The fourth problem is putting different NDs together to try to show some statistics: that’s comparing apples to oranges. I am not even mentioning the error bars that are SEM instead of SD. SEM is equal to SD/square root of the sample size. It has little meaning in statistics. SD is a more appreciated parameters as it allows the assessment of the statistics (and verify the P-value calculated by the authors is correct or incorrect). Ideally, you would like to show the urine Al values for each individual as a dot-plot.
With honesty, a journal that is publishing studies based on solely one figure raises an important red flag about the quality of peer-review performed, and you can see that the important flaws in the methodology is unacceptable.
Contact allergy to aluminum induced by commonly used pediatric vaccines
It is interesting to see a comment taken as a “gotcha” moment by Ashley. Yes the authors reported a series of granuloma in Swedish children and note how Ashley highlighted only the pieces that were fitting her narrative, by willingly highlighting the final words of the authors.
“We want to point out that itching granulomas are benign and self-limiting and no cause to refrain from vaccination in consideration of the risk for a serious infectious disease. They are poorly known but easy to recognize once you are aware of them. They should be familiar to all health care staff working with children to avoid mistrust and anxiety in the parents and unnecessary investigations of the child.” The same authors reported that this is likely due to contact allergy and seems to improve over time as reported in their 2018 paper (https://www.ncbi.nlm.nih.gov/pubmed/29572857)
In conclusion: Yes, granuloma can happen in certain vaccinated children, it is mostly an allergy contact with aluminum and causes only minor effects (itching) that resolves over the year.
Aluminum hydroxide lead to motor deficits and motor neuron degeneration
Introduction: The whole hypothesis of the paper is to address the possible cause of the Gulf War Syndrome (GWS). GWS was a condition described in veterans of the first Gulf War (1990-1991) characterized by various neurological conditions. But for some reasons, Shaw is suspecting that GWS was correlating with cases of ALS with some veterans diagnosed with GWS. Shaw speculates that the anthrax vaccine (AVA) given to soldiers during the Gulf War (in anticipation of the use of anthrax-laden weaponry by Saddam Hussein) is the causative agent, and went up to nail to aluminum adjuvants to vaccines.
Using existing literature documenting high aluminum (Al) levels in mice following treatment at elephant dose (Table 1) and dubiously claiming these mice showed sign of ALS (spoiler: they just reported Al levels in tissues, no reported ALS phenotype in these mice), Shaw goes with big stretches to claim that the anthrax vaccines caused these to happen.
Methods: Shaw used CD-1 male mice, 3 months old (about 12-weeks old). That’s about young adults that matches the demographic of the military. Gender differences can be discussed but I would speculate the proportion of men serving the country back then was predominant.
The number of animals is about okay for a fair power of analysis (if you assume about 30% or more differences following treatment, with 10-15% variability, an optimum number would be 12). Note there are four groups: saline (PBS), squalene, aluminum hydroxide (AH) and AH+squalene.
The concerning part is that Shaw mentions the following: “The current study will report only on the aluminum treated and control groups from this experimental series. “. Why are you mentioning the squalene and AH+squalene group and not showing the data? Are you hiding something that your study is showing but contradicting your hypothesis? How did reviewers let that fly in the first instance? That’s already a big red flag you have not caught.
The Al dosing seems adequate but here is the problem: “In Experiment 1, we performed two injections of a suspension of aluminum hydroxide of (50 μg/kg) in a total volume of 200 μL sterile PBS (0.9%) spaced 2 weeks apart. The mice in this experiment would therefore have received 100 μg/kg versus a probable 68 μg/kg in humans. In Experiment 2, mice received six injections for a total of 300 μg/kg aluminum hydroxide over 2 weeks. Controls in both studies were injected with 200 μL PBS. “2 injections within two weeks or 6 injections within two weeks. What does the military say? Five doses injections at 0, 4 weeks, 24 weeks (6 months), 52 weeks (1 year) and 76 weeks (18 months) according to this site: https://www.health.mil/Military-Health-Topics/Health-Readiness/Immunization-Healthcare/Vaccine-Preventable-Diseases/Anthrax.
Remember, we are just talking about anthrax vaccine here. Under which rationale Shaw consider the fate of aluminum in a mouse body very different from a human body? Considering Al is mostly cleared by renal route and that mouse have physiologically a lower renal clearance level (based on creatine clearance) than humans, what we have here is basically a deliberate overdosing of mice with aluminum by running a complete irrational immunization schedule. He squeezed us a whole injection schedule that is spanned over a year and a half (76 weeks) within a 2 weeks period. A major an unacceptable methodological flaw that was repeated in the sheep studies by Lujan (the studies claiming vaccines in sheep caused ASIA).
How did you miss that Glenn? You had 24 hours to read that paper! And you were telling us PV how to design an experiment? This experimental design is so flawed, yet it flew under your nose.
I will give it to you, it also flew under the nose of reviewers, but I speculate either the reviewers were friendly to Shaw or had no expertise to review that paper at all.
Results: Let the fun begins with Figure 1. First thing here is Shaw is looking for signs of neuronal damage and spinal cord injury in his animals by immunocytochemistry. You can do that by staining tissue sections with antibodies. In ALS, motoneurons (the neurons controlling skeletal muscles) are the one affected by the disease and die. Motoneurons are localized in the ventral portion of the spinal cord in a region called the ventral horn. Motoneurons neurotransmitter of choice is acetylcholine, so you can label motoneurons with antibodies targeting an enzyme involved in acetylcholine biosynthesis (choline acetyltransferase or ChAT). Aside from neurons, you have glial cells that are here to support neurons. The major type is astrocytes. When astrocytes are injured or get wind of a bacterial information or injury, they become activated. One protein indicative of an astrocyte activation is glial fibrillary acidic protein (GFAP). Under physiological condition, GFAP is barely detected. Under injury (in my case, stroke injury), GFAP levels will go up, in particular in the region being injured. Iba-1 is a staining for activated microglia. Microglia are resident immune cells in the brain, sitting ducks waiting for an injury to happen. When an injury happens, microglial cells go berserk, will release tons of pro-inflammatory cytokine and press the RED ALERT button, activating both astrocytes and the BBB to let immune cells come inside the brain and induce neuroinflammation.
First flaw here is that Shaw never show us any representative tissue staining to let us appreciate his bar graphs with actual staining. That was unacceptable in 2009, it is still unacceptable in 2019. He also omitted to put all three spinal cord regions (cervical, thoracic and lumbar) for both ChAT, GFAP and Iba-1. Indeed, Shaw plays with the cherry-picking of both what he wants to show in terms of data and statistics.
Aluminum in cervical SC showed no differences in ChAT-positive neurons but has a higher number in the aluminum group. It is about 50-60% higher, yet Shaw conveniently brushed the statistics under the rug. How come he denotes us a statistical significance (P<0.05 as pointed by the * symbol) in 1C but not in 1B, despite showing similar difference and even smaller error bars? What about ChAT in the lumbar section?
This is not the first contradiction, how Shaw explains that in the thoracic region you have more reactive astrocytes in the cervical region, but less in the thoracic region? What about GFAP in the lumbar section?
Finally, same applies to Iba-1. Considering the huge variability observed between regions for ChAT and GFAP, how much credibility the Iba-1 lumbar section tells me. I bet he showed the opposite pattern in the cervical and thoracic regions and he brushed that off under the rug. How convenient it must be to brush off data not aligning with your hypothesis and only show the data that align with it, don’t you think? That’s called cherry-picking and that’s a no-no in science.
Figure 2: Shaw is trying to show us aluminum in the spinal cord using morin staining. Two things here. Shaw is showing us a spinal cord staining from control mice and you can see the high autofluorescence, but that does not stop him to claim there is no staining. Second, he is showing us blurbs of immunoreactivity. The problem is how do you sort real staining from garbage? The answer is you need to have a counter-staining, in particular a nucleus counterstaining. One would be the use of DAPI (that stains the DNA) and see if these blurbs are parts of cells and not just debris. You can also make things up by tuning in the exposure time. This, with the lousy quantification (how did he identify these are cells without DAPI? What is the sample area in micrometers2 or mm2?), is already sinking the boat of that paper. We are two figures and yet have to find any nuggets in that garbage dumpster.
Figure 3: He is trying to sell us a spinal cord section of its aluminum mice versus a brain cortical slice of a human (entorhinal cortex) suffering from Alzheimer’s’ to claim that aluminum is inducing Tau hyperphosphorylation. What is that garbage? First, Tau hyperphosphorylation is not associated with ALS, second Alzheimer’s is not ALS, third brain cortex is not spinal cord and finally human is not mice. And that isolated cell that is immunoreactive amongst a desert of empty staining, that screams out loud he cherry-picked a region of interest to show one single positive cell amongst thousands negative. What I am supposed to do with that?
I would have shown the following: control versus aluminum, spinal cord sections at three spinal cord regions (cervical, thoracic and lumbar), low-magnification and high-magnification to show the depletion of motoneurons and possibly the Tau hyperphosphorylation. But I would also show a Nissl staining to exclude the presence of amyloid plaques and neurofibrillary tangles in my spinal cord versus the cortex of human sample given here to show this Tau hyperphosphorylation was not associated with Alzheimer’s.
Figure 4: This is a statistical joke, you must be kidding me right? To tell me that he got a P<0.0001 with SEM bars big like that is a straight out lie, or he just found the obscure statistical test to make is so. You cannot run the statistics overall and conclude so, you have to do the test for each timepoint between the group. Also, why did he use a two-way ANOVA when he only has two groups? That is telling me he is as meticulous in his stats as his experimental design. The only time I would consider something happening (don’t forget we are overdosing our mice) is on Fig4G and H.
Figure 5: Finally, a water maze test to assess the ability of mice to memorize. The idea is you have mice submerged in a pool. In this pool, there is a platform that they can hold on and have a firm surface to stand. Over time, if you let them swim every day, they will become better at it and find the platform faster. The problem is the water is blurred out, so they have to remember where in the room and in the pool the platform is located. Also, here Shaw is remembering us something. Do you remember that?
“In Experiment 1, we performed two injections of a suspension of aluminum hydroxide of (50 μg/kg) in a total volume of 200 μL sterile PBS (0.9%) spaced 2 weeks apart. The mice in this experiment would therefore have received 100 μg/kg versus a probable 68 μg/kg in humans. In Experiment 2, mice received six injections for a total of 300 μg/kg aluminum hydroxide over 2 weeks. Controls in both studies were injected with 200 μL PBS.”
Here Shaw is telling us “This is the 6x mice”. What about the 2x mice? What about the previous figures? Which experiments were they? 2x?6x? Did he mix the 2x and 6x into the whole aluminum group? Sloppy as hell. And you have the audacity to tell me this study still worth something? Not even a kopeck!
Administration of aluminum to neonatal mice in vaccine-relevant amounts associated with adverse long-term neurological outcomes
Note: Chris Shaw must have a knack for publishing his paper in JIB, almost as if the editor in chief was complacent to his botched studies.
Introduction: Shaw continues on his hypothesis that aluminum in vaccines is bad and that he must be causing neurotoxic effects in infants brain, in particular he consider that aluminum in vaccines is associated to ASD, self-citing their study published also in JIB in 2011. Therefore, the aim of this study is to demonstrate that the current immunization schedule is bad because it induces an aluminum overload
Methodology: Here is the big flaw of the paper, that will be used and reused by other groups later. Shaw assumes that a mouse born (P0) is equal to a newborn (which is not, the literature is indicating that a P0 mouse is about a 7month of gestation fetus. A human newborn would be about a P7 or a 7-days old mouse). Considering that mouse puberty is about 5-6 weeks old, Shaw designed an experimental design that is about injecting mice every 2-3 days for 10 days with a final injection at P17. Noteworthy, the apparent shift in injection schedule of the saline group, that is never matching the US schedule (referred as high Al) or Scandinavian (referred as low Al). This is unacceptable. When you design an experiment, you want to be sure you align your control group to your treatment to remove the maximum number of variables.
The second problem here is a pharmacokinetic problem. We can argue that the 17-days schedule maybe reflective of a “0-2 years” schedule in humans. The problem is does Shaw (or anyone else) validated that this rapid schedule is respecting the pharmacokinetic pattern of aluminum adjuvants? He has not. Nobody has not either. That’s a huge mistake here. Aluminum adjuvants fate based on the Flarend data tells us that it has a two-phase: a rapid but mild peak concentration (that is about 2% of the injected dose) following IM injection (within 24 hours) followed by a progressive decrease at a rate estimated by 0.6%/day. In a human schedule (2 months interval), this allow to get rid of most of the aluminum. In a mouse schedule (2 days), you are basically overdosing mice with cumulative dose of aluminum and logically reach toxic levels (aluminum is neurotoxic, if you have a blood level of it at least 3x what we consider the normal level). Shaw never bothered to show Al levels in blood/plasma at day 17 to see if his schedule was making sense or not.
Results: Figure 1 and show weight. A decrease in weight is usually sign of mouse distress. Again, Shaw shows us Mean+SEM, making the assessment of the statistics useless and have you taken him on his words. Interestingly enough, the high Al showed higher weight gain than controls and low Al. I don’t know what to do about, but maybe the high Al load due to his botched Al overload is responsible for that.
Figure 2 and 3 show different behavioral testing, so I will not go through details much. High aluminum group is showing the worsened outcome at 22 weeks, but surprisingly only males. Why not females? I would not expect a difference in PK parameters between sex, but maybe some neuroprotection from the gonadal hormones in females.
No memory test done (swim test, Morris maze test), no social behavioral test done, no novelty test done. These are behavioral tests that are important and surely more relevant than the ones shown, especially if you consider the hypothesis “aluminum in vaccines cause autism in mice”. Did Shaw not performed the test because it was a neglection or did he hide the results of them in a drawer because it was not fitting the narrative?
That’s it for the results. No assessment of aluminum load in the brains, no Cresyl violet to show brain structure abnormality, no immunostaining to show some sort of damage or neuroinflammation. Shaw get a lofty free pass at JIB and use it conveniently.
Discussion and acknowledgment: Seems Shaw is not at all embarrassed to oversell the data, in particular as his main benefactor (the Dwoskin foundation,
Biopersistence and brain translocation of aluminum adjuvants of vaccines
This is a review from Romain Gherardi. The problem with a review is similar to an opiniated piece, you can make your case with basically anything that fits your narrative and you often end-up self-citing your papers and own papers. But that does not mean Gherardi is doing great science and I would easily debunk one of his studies anytime.
Aluminum in childhood vaccines is unsafe
This is a so-called study written by Neil Z. Miller. This is an example on assessing someone’s credential is important. Scroll at the end of the paper and read the following
“Neil Z. Miller is a medical research journalist. Contact:firstname.lastname@example.org.”
He has no credentials as a scientist, he has no affiliation with a research institute (with the rare time he points out to his PO Box in Santa Fe, NM) and he has absolutely no knowledge from what he is talking about (although he claimed the aliens talked to him and told him vaccines are bad). All of this published in JPANDS, the journal of the American Association of Physicians and Surgeons. This is a political (right-wing) organization that is anti-Medicare, anti-Government (they give tips to medical practitioners to tax dodge and reduce financial tracking) with a strong anti-abortion, anti-LGBT stances with dipping often with conspiracy theories (HIV denialism being one of them). Just Google Jane Orient (former president of the AAPS) and you will see a nebula of conspiracy theories promoted by her.
Neil is trying to sell the idea that aluminum is the new mercury, claiming levels went up as thimerosal was phased out. In Figure 2, Miller is giving the middle finger to basic pharmacokinetics claiming that an 18 months toddler holds almost 5’000microg of aluminum in his body from vaccines. The problem is that Neil omitted to count that such amount is mostly gone by that time, omitted a physiological function commonly referred as “pee-pee” (renal route represents 95% of the exit route for aluminum) and also omitted to count the exposure from food and water during that period. That’s sound like an awful lot of cherry-picking that only garbage journals would accept as valid papers. Of course, Neil cites the classical tropes and debunked studies from Shaw, Gherardi and Exley.
To make a point valid, someone has to show that the current CDC schedule 1) increases significantly Al blood levels during the first 24 hours of injection and 2) that the current schedule is translating into a cumulative increase in blood levels in infants. Both of these issues are never addressed by Neil, because Neil does not have the scientific baggage to answer these questions and conveniently ignored the literature that is not fitting his misconception.
2.2. Aborted Fetal Cell DNA
MRC-5 and WI-38 fibroblast ATCC technical data sheets
These are technical data sheets for these two cell lines. ATCC stands for American Tissue Cells Collection. It is a cell and tissue repository, a sort of giant cell culture database. If you are looking for a particular cell line and ATCC has it, it will provide you these cells (upon paying some $$$) so you can run your experiments. You can passage cells, in particular immortalized cells, as many times as the cells will accept. Some cells like HeLa and these two cell lines have been over 1000 passages easily, that’s is like 1000 generations of cells since the original isolation.
Ashley stupidity in plain sight:
“MRC-5 cell line………by J.P. Jacobs in September of 1966”. In other words, MRC-5 was created in 1966 and since the same cell line has been used to make vaccines. That’s should torpedo the claim of “they use aborted babies to make vaccines”. They used the same cells isolated from one aborted fetus sometime in 1965-1966 to produce billions of vaccines doses. One fetus.
The WI-38 is coming from the same period of time, produced by Plotkin in 1965. This is the original link to the study: https://jamanetwork.com/journals/jamapediatrics/fullarticle/501537. So what is Ashley trying to accomplish here? Stir the “aborted babies in vaccine” pot to scare people? These are cell lines coming from 2 babies, that are over 50 years old cells passaged at least 1000 times since their isolation. They are a far cry of the original product, yet they helped save the life of billions of babies worldwide. As Spock would quote “The need of many outweighs the need of few”.
Spontaneous Integration of human DNA fragments into Host Genome.
That’s a poster authored by Deisher. First, it is a poster. In other words, it has little or no value when it comes to publication. It is nice, but useless until it gets in its final form as a publication in a peer-reviewed journal. A poster is never peer-reviewed, at best it is reviewed by a scientist affiliated with a society meeting (for instance I review poster abstracts for the American Heart/Stroke Association for their International Stroke Conference meeting on regular basis) and give a “yeah/nay” for poster presentations. Poster presentation is usually the easiest form of communication that get an acceptance rate, it is not often you get rejected unless your abstract is poorly written or you are presenting something outside the field of interests of the meeting.
Ashley did a very poor job in cropping the poster making it difficult to read.
First, the author. Teresa Deisher. Deisher seems to have some experience in cardiac cell biology according to her PubMed profile, but her last relevant paper dates from 2010.
Deisher is back in publication by publishing three articles, all in Issues in Law Medicine. That does not sound a journal you would publish biomedical sciences, right? It is also unlikely that you will have the right experts to peer-review that studies.
The second issue is Deisher is not affiliated with any public institution. She is affiliated with Sound Choice Pharmaceutical Institute located in Seattle, WA. The use of “institute” is a common strategy of anti-science to pose as legitimate, but often these institute are mere than a basement in a suburb area or a hut located in a mountain. If you are unsure about an institute, just Google Map it. That’s how the so-called institute look like.
Does it look like the Broad Institute (this is what I would put at the top of molecular biology institute)? https://www.broadinstitute.org
In this “study” Deisher took some placental DNA (Cot1), labelled it with a fluorescent dye (Cy3, that fluoresce in the red range following excitation by a light source).
She lists few cells that took the dye (3 out of 7 cell lines) in her Table 2 with some dubious results. First, she is not showing all the data (in terms of genomic DNA incorporation), she is not validated the DNA uptake method (is she relying on fluorescence to determine the incorporation, did she use a PCR analysis or DNA sequencing to show the incorporation of that genomic DNA? No for any of these).
The rest is even more laughable if we move to the Figures. If you want to show that you have incorporation, you have to show each fluorescence by its own using a negative control.
A negative control is important to show, so people will accept that your fluorescent signal is real signal and not some noise background. A negative control should be either your untreated cells (because some cells can have autofluorescence), or cells treated with free fluorescent dye (to remove the non-specific uptake of free dye by the cells, which can lead to a false-positive).
More importantly, you have to show the fluorescence of each channels separately before showing a merged picture (example DAPI, Cy3 and brightfield separated and finally a merged picture).
Figure 1: What I am supposed to see here? Why is there a blue color in brightfield? How should I conclude that the red blobs I barely see is genuine signal and not background noise?
Figure 2: That’s the most laughable picture. Here Deisher treated the cells with saponin. Saponin will drill holes into your cells and let anything enter your cells. We use saponin to show the internalization of a protein normally located on the cell surface (to allow antibodies to enter and detect these proteins inside the cells). Deisher forced holes into the cells, treated them with her DNA fragment and low and behold see some red signals. No shit Sherlock!
Then with other figures, she used LPS instead and of course no controls. LPS is a lipopolysaccharide present in Gram-negative bacteria. When these bacteria explode following an immune response, this LPS is acting like a nuclear bomb in the body. It will induce a massive immune response that is commonly observed in the clinic as septic shock.
So what I am supposed to do with that data if I find DNA uptake in cells that were nuked by LPS but I have no idea if such DNA uptake even occur in non-treated cells? Why not using saponin as well?
Garbage in, garbage out. What you call a disgrace I call it a common practice in anti-science papers. Produce garbage, sell garbage as science. If I was the MJ Murdock foundation, I would ask for some explanation on why their grant money was spent on useless junk science.
Characteristics of a new human diploid cell line Walvax2 and its suitability as a candidate for vaccine production.
Ashley, based on her markups, seems to never read anything more than the title and the abstract of a paper. Past the introduction, and you will not find her yellow marker. So much for a “toxicologist” eh? Walvax-2 is a new cell line developed by Chinese scientists and assessing it as a possible alternative to the MRC-5 and WI-38 cell lines. Walvax-2 was isolated from an aborted fetus that was medically aborted. The mother had a uterine scar from a previous C-section. A uterine scar can break during pregnancy and can kill the mother (and the fetus) if ruptured. It was not a complacent abortion; it was a medical abortion and the chance of having this fetus to become a full-term newborn was almost null. Maybe Ashley should go back to school and learn some A&P courses before playing the scare and ignored the uterine scar.
For the lay person, this paper is not that interesting. It is mostly validation and characterization for the cell lines at different passages (P6, P14 and P20) and benchmark them versus MRC-5 in their ability to be infected with known pathogens.
Yet, there is still a long way to go for Walvax-2, as the authors mentioned “ Nevertheless, more research needs to be done to investigate the susceptibility of Walvax-2 cells to a greater variety of viruses, and to develop fully the potential of Walvax-2 cells as a cell substrate platform for producing viral vaccines for human use in China” (p. 1005)
Those that make the claim this cell line is already in use in China and used to produce vaccines anywhere in the world are lying liars that should be called out for spreading nonsense.
Effect of thimerosal, methylmercury and mercuric chloride on Jurkat T Cell Line
This is a paper that looked at the toxicity of mercury at different forms (EtHg, MeHg and HgCl2) in a rat T cell line, the Jurkat cell line. Cells were treated at different concentrations for 48 hours. Let’s assume this is a blood concentration and what these cells are exposed would be plasma concentration of mercury.
First, how much mercury do we receive in a vaccine injection? The closest thing I came come with is the Burbacher study (Env Health Persp.2005) that investigated the effect of multiple injection of EtHg versus MeHg (that one was given orally) at 20microg/kg, 4 injections spaced one week each (so it’s really aimed to overdose the baby monkey with it). The value of mercury is supposed to represent the value found in a vaccine. At the 4th week of injection, the value of Hg coming from thimerosal was 16ng/mL (MeHg via oral route peaked at 32-35ng/mL). That’s 16microg/L. The molecular weight of elemental mercury being about 200g/mol, that puts us about to 0.08micromoles/L (0.08microM).
It seems it did not bother at all Ashley that the 50 microM she cherry-picked (why not the 1microM? It has a statistical significance too, a value of P<0.05) was absolutely not a concentration even reached in a vaccine overdosing (no one get 1 injection/week for 4 weeks). We are talking about 312x the maximum amount observed in the overdose scenario. So, what should I care about a toxicity at a concentration never reached in the body at any condition? Worse, Ashley, despite her claims of being a toxicologist completely nixed the nature of methylmercury. Unlike thimerosal/ethylmercury, methylmercury has a nefarious feature to bioaccumulate and stay longer in the body. If you look at the Burbacher study, it takes about 3 more times to clear MeHg versus thimerosal. Yes, methylmercury maybe less bad if subjected to acute exposure, but his effects are much worse in terms of prolonged exposure to it.
Low-dose mercury exposure in early life relevance of theimerosal to fetuses newborns and infants
Ashley is not bothered to read papers, and she will take any abstracts aligning to her agenda as valid and will claim she read the paper. It is a paper from Dorea. This guy is not known for doing sound science and he is pretty goofy and even dishonest on how he sells his findings. I will skip that one as it is a review.
Thimerosal induces DNA breaks and cell death in cultured human neurons.
This paper is looking at the effect of thimerosal at different concentrations on DNA breaks and cell death in both fibroblasts and neurons. Again, Ashley took it, read it up to the intro and ran away with it.
Figure 1: They exposed neurons at different concentrations for 2, 4 and 6 hours at different concentrations. Since it is neurons, we have to see how much would reach the brain. This brings us to the Burbacher paper as she measured mercury clearance in the baby monkeys. She found by the end of her 4-weeks regimen that Hg levels in the brain of thimerosal-treated group was 40ng/g brain tissue. If we assume that the brain is 100% water, that would equal to 40microg/L or 0.2microM. What is the minimum concentration used in this study? 2microM, 10x the concentration you would have in the brain if you overdosed on vaccines.
They see an increase of DAPI-positive nuclei at 6 hours at 2microM (DAPI is a compound stacking within DNA and fluorescein in blue. It only enters cells that are dead). You would assume to be problematic but in the same time we don’t have an idea of how many cells (as counted by their nuclei were in the field). I would have expected the authors to take a picture before/after fixation or use a dual staining propidium iodide (red, dead cells)/DAPI (total cells after fixation) to be able to normalize. We cannot exclude that the authors could have cherry-picked the field to downplay the number of DAPI-positive cells in the control group.
Fibroblasts were more robust and stood up to 10microM (remember, we found that the Burbacher reported 0.08microM concentration in her monkeys).
In Figure 3, the authors looked at caspase-3 activity in neurons. Caspase-3 is the endpoint of the signaling cascade known as apoptosis. It is programmed cell death and result in a cell death comparable to euthanasia. Increase in caspase-3 activity was only measured at 10microM. That’s about 100x the amount found in the brain in the baby monkeys.
Finally they performed a TUNEL assay that will highlight damaged DNA (and indicative of cells undergoing apoptosis). You can see an increased TUNEL activity at 2microM, or 10x the maximum amount reported by Burbacher.
I don’t think we have to go through the end of this paper and concluded a minimum toxicity of 0.5microM after 24 hours in their neurons.
Again, Ashley brilliantly showed her credentials one more time by citing papers that are absolutely not supporting the claims made by her.
Review of neurotoxicity studies of low-dose thimerosal relevant to vaccines
Again, a Dorea review. You cannot do much with a review, especially coming from Dorea but would be more than happy to review a full-research article from our friend.
2.3. Polysorbate 80:
The blood-brain barrier: A bottleneck in brain drug development
Another review by Ashley but this time she cites a very good one. This one is written by Bill Pardridge back in 2005. Bill is a professor at UCLA specialist of drug delivery at the BBB. So, this is a very good review if you want to understand the BBB. My problem? Again, Ashley likely put that one in following her “research” that maybe not more than a Google search of “polysorbate 80 blood-brain barrier”. She is just highlighting blindly whatever she thinks is nice but obviously never read references 28 to 30. In particular reference 30. This is the JNS study that I used in my infographic about polysorbate 80 and the BBB. Of course, she did not read, otherwise she would have noted two things:
1. The administration route is by direct injection in the carotid artery. Since when are we giving vaccines by a shot in your carotid artery?
2. The second is the dose. Huge dose given. mg/kg range. That is almost 3000x doses given at once. Straight into the carotid artery……of a mouse. Not sure it was even shown to occur in humans. May I say that 25 years seems indicative that it fell short to work in humans?
Specific role of polysorbate 80 coating on the targeting of nanoparticles to the brain.
Ashley is again happy to just share an abstract but this time no yellowing, I guess she just put on the fly. This is a paper working on how to optimize the delivery of nanoparticles across the BBB. They are trying different combination of the nanoparticles, from the basic surfactant-free nanoparticles (SFNP), to the one coated with PS80 or other stuff as seen in Table 1.
It is a particle bound PS80, not some free-roaming PS80.
Overall, nothing really much interesting for those not into drug formulation, but I have to say I was not really convinced by the fluorescence pictures.
It seems that first the microscopy pictures were overexposed, suggesting a weak signal in the brain parenchyma. The only region that seems rich with fluorescence (bright) is what appears the vascular region (as we have something delineating as a tube). I guess the nanoparticles can enter the BBB but must remained trap inside it or in the perivascular space.
2.4. Fetal Bovine Serum
The use of fetal bovine serum: ethical or scientific problem
This is what seems a review about the use of FBS in cell culture medium. For those unfamiliar, FBS is an important component of mammalian cell culture. It provides the right amount of proteins to maintain what we call an oncotic pressure constant, as well as cell growth factors that we cannot completely reproduce in the lab due to the complex composition (number and amount of growth factors present).
This is a review written for a journal maintained by FRAME: Fund for the Replacement of Animals in Medical Experiments. This is something in biomedical sciences every scientist is working hard to achieve and commonly referred into the 3R guidelines: Reduce, Replace, Refine the use of animal in medical research. In vitro (cells in a Dish) models can help reduce or replace the need of animals for certain types of research, but it is only a viable option if you can have almost all reagents coming from animal-free origin. You can understand that fetal bovine serum is an ingredient that can be problematic. Usually, FBS is used at a final concentration of 10% (10mL of FBS for 100mL complete medium), with often reducing it down to 1% (as FBS can interfere with some experiments). Vaccine products (as well as biologics) are not used directly from the crude cell culture medium. There are a series of purifications and extraction processes that are aimed to obtain a pure product. This process brings it the presence of FBS to traces levels.
2.5. Propylene Glycol
Hyperosmolarity in small infants due to propylene glycol
Here we have Ashley winning the potato prize for the definition of parenteral!
She is defining parenteral as “intravenous, intramuscular, subcutaneous or intradermal administration”. No shit, Ashley! You just mentioned the major administration routes except the oral route and did not even took the time to read the article. So much for your professionalism, Ash! But this is not what parenteral means in this article. Usually, parenteral routes are used for administrating fluids and nutrients to patients uncapable to feed and drink.
This is a case report made on a premature newborn (27 weeks of gestation). She was put on a total parenteral nutrition (TPN). TPNs are always administered via IV route.
The source of propylene glycol was a multivitamin administration (named MVI-12) given in the final IV nutrition bag (10mL). Few days after the onset, the patient developed complications including hyperosmolarity that resulted in stopping the parenteral nutrition. This prompted the authors to screen other babies also put on the same multivitamins and noted an hyperosmolarity that was variable in extent. This let the authors to recommend restraining the use of any medical products containing a high amount of polyethylene glycol in their formulation.
But the last question we have: was this propylene glycol reaction due to vaccines?
Glyphosate pathways in modern diseases VI prions amyloidosis and autoimmune neurological diseases
Oh boy, what I have to say about that? That is a turd paper written by a computer scientist (Stephanie Seneff) that has ZERO, I repeat ZERO knowledge in biological sciences. Imagine, me as a BBB expert, writing an article about Linux operating system, claiming it is an utter piece of garbage, that its code is so degenerate that even penguins would write a better code. I would not sound credible right? Same here. Seneff makes extraordinary claims with ZERO evidence in her claims. Even critics of glyphosate such as Robin Mesnage and Michael Antoniou consider Seneff too kook to have her claims credible (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5705608/)
However, one thing is here laughable and that’s Table 4. Seneff claims that she can detect glyphosate at 3ppb. To reach such level of glyphosate, you need a very sensitive and quantitative method, usually used in analytical chemistry. Such methods are usually referred as liquid chromatography (LC) or gas chromatography (GC)-mass spectrometry (MS). The MS method allows to identify chemicals by their unique analytical fingerprints. We see such methods used in TV shows such as NCIS or CSI, but also at airports when the TSA has some suspicions of presence of prohibited products (the famous swipe test they perform). Here they use an ELISA. ELISA stands for Enzyme-Linked Immunosorbent Assay. It is a technique that uses antibody-antigen interactions to identify a chemical. The problem with ELISA? The very high risk of false positive. Do you want to have proof of the high variability? Check the LOD values given by two labs: 0.075ppb and 0.15ppb. That’s about a mean of 0.11ppb with a standard deviation of 0.053ppb. That’s a coefficient variation of 47%!!!!! The FDA tolerates a CV of 7.5% for compounds detection at 10ppm or less. 1ppm=1000ppb.
If we consider the 0.11ppb as a reference, that’s put us to 6.17nanomoles/L or 1microg/L limit of detection. The LC-MS method developed by McGuire and colleagues found their limit of detection to the same levels, and nothing was able to come significantly higher than that, whether the volunteers had a regular grocery based-diet or an organic-based diet. https://www.ncbi.nlm.nih.gov/pubmed/27030536
Unlike the McGuire study that is published and publicly accessible for the validation methodology, the ELISA is a well-kept secret kept by ABRAXIS that have been very mysterious on how their kit works. I have approached them for assessing glyphosate levels in cell cultures sample, and the impression left was a shroud of secrecy. Ask any analytical chemist, the gold standard for chemical analysis for organic molecules is the LC/GS-MS method. ELISA has so many variables involved and steps (I practice them routinely) that you cannot afford such variability in a rigorous analytical method.
3. Concluding remarks:
I had focused on this section because it was aligning on my expertise, and let others deal with the other sections. But here is the final conclusion I have, as a peer to Ashley: Ashley has ZERO credential as a scientist and as a toxicologist, and her “Vaccine Guide” perfectly illustrate that point. She does not know to read papers, she does not know how to face criticism but she knows to cherry-pick, she knows how to put irrelevant papers into a binder and pose as the next Nobel Prize contender.
Ashley is a hack, she is an impostor, and she is dangerous and therefore should be rightfully called on her lies.