Pharmacist-in-Hiding AAAB Continues to Ignore the Obvious

There is evidently another round of ignoring the obvious in the back-and-forth between AAAB, the Anonymous Aluminum Apologist Blogger (AAAB), who introduces themself thusly, and themselves:

“This article is by VaultDwellerSYR, a pseudonym used by a faculty member of a School of Pharmacy within a large medical school.”

Feigning fear of “attack” due to a “delicate time” in their career, this person appears to be afraid of losing a bid for career advancement in academia. For what? For engaging in open, rational discourse in the leaves of a peer-reviewed journal. Has part of academia fallen so low that bona fide publications on the question of aluminum toxicity, even in defense of its safety, have become taboo? If so, I am so very glad to be a truly independent research scientist.

AAAB pastes post-it notes of “victim” all over themself for my daring to call them out on their charades, and their mischaracterization of my criticism of them for failing to grasp at the real brass ring of honest, open dialog on issues that truly matter. But that’s all chatter, irrelevant to the points at hand.

In this latest retort, AAAB behaves less sophomorically than in his first tirade, realizing of course now that they are dealing with a true professional, a veteran of many, many academic engagements and research projects. The tone of the two articles is markedly shifted, which I take as me raising the standard of articles published at the website, Skeptical Raptor.

So let’s have a go at this latest rebuttal. First, I refute and negate that it is “my responsibility alone” to show that my null hypothesis – the curve outlined by Clark’s rule, is not “irrelevant”. It’s the only null hypothesis of a safe pediatric dose of aluminum ever published. AAAB side-stepped the challenge to come up with his own curve, pitching the challenge back to me.

I could, for the fourth time, throw down the guantlet to the FDA and ask What IS a the safe level pediatric dose curve for aluminum adjuvants in humans? I’m not the one who published so many recommendations of aluminum oxyhyroxide-containing vaccines; that was ACIP. I’m not the one who publishes a recommended schedule packed full of ACV’s; that’s CDC. I’m not the one who is eternally silent on a safe dose of aluminum for newborns, infants in the NICU, 1-year olds, 2-year olds and so on. My colleague Dr. Ricketson and I in 2018 proposed what might be – might be- a logical approach to addressing the pediatric safe dose limit, given that FDA has published limits per dose for adults, and we know roughly what adults weigh. So there’s our PDL for others to consider, to test; Science is, at its finest, a social enterprise: by all means, have it.

Does AAAB present new data on a new PDL refuting the hypothesis that Clark’s rule provided? No. Instead, AAAB carries on with the practice of obfuscation (of which FDA’s Mitkus paper is a glaring example), and thoroughly derails his own argument, again, of which I will shortly outline the shortcomings. But he does call upon me to test, with empirical data, the PDL implied by FDA’s 850 mcg per dose per adult body weight is, in fact, a correct estimate. Rest assured, AAAB, we are analyzing human subjects research data that seems likely to help us address that problem. We would expect, in a pediatric population, the rates of autoimmune conditions to be equivalent between children whose parents did not decline aluminum-containing vaccines and children whose parents did decline such vaccines. Please be patient, those data are in hand, but they are being written up right now.

We specifically undertook the studies we did because the FDA’s Mitkus study, and no other study, led to a PDL. AAAB would have his readers believe that because a multi-compartment model exists that is “complex, very complex”, Clark’s rule is irrelevant. That does not cut it for me. The mere existence of a complex multi-compartment model does not refute anything; it’s not robust empirical data, and it’s not based on rigorous empirical data for what it is.

(1) The study they cited would never lead to Clark’s rule, could never lead to Clark’s rule, and is unrelated to and thus does not falsify Clark’s rule whatsoever. Why? For one, it’s focused on plasma concentration first, which I already spelled out for AAAB is irrelevant to the known, i.e., published, mechanisms of action of aluminum toxicity.

(2) The study that AAAB thinks Weissman’s study validates (Flarend et al.) reported that 95% of aluminum hydroxide was still in the body of the rabbits after 28 days. That’s a big problem. Our concern (see point #1) is whole-body clearance, not plasma. The drop on plasma from high levels to low levels without evidence of body exit is a cause for grave concern, not a cause for reassurance. Perhaps an analog toxin would help. There are other toxins that have rapid plasma clearance, such as arsenic. Is arsenic safe due to rapid plasma clearance?

(3) [Added on 12/31, day 2 of this article] – The Weissner study deferred to the future for infant-to-2-year-old knowledge of the safety of aluminum adjuvants:

“With respect to children simple allometric dose scaling
is not adequate, in particular for infants below 2 years of
age due to complex age-related developmental changes (Lu
and Rosenbaum 2014). For that purpose, physiology-based
modeling is required as it is increasingly used in pediatric
drug development and toxicologic evaluations (Sharma and
McNeill 2009; Barrett et al. 2012).”

So AAAB’s appeal to Weissner is redundant, and his (and Orca’s) mispresentation that “all is well with aluminum dosing in infants” is disproven by his own source material. Weissner’s own model did not lead to a PDL, and she did not cite our PDL, published in 2018. [End section added on 12/31/2019].

AAAB teaches students how to use PK, using a trapezoidal model for estimating the area under the curve. Measurement alone does not ensure objectivity, even if it is quantitative. Thus, I’m not impressed: it really does not matter what tool you are measuring if you are measuring the wrong thing, or not able to interpret the significance of a 28-day retention of 95% of a toxin that is continuously, slowly being released over a long period. Thus, chronic toxicity.

The lack of fine-scale data is a bit bothersome for AAAB, and they surmise (guess) what would have been seen. They celebrate the horrific finding that plasma clearance is so fast it leads to measurements about the same as saline. So would arsenic. It’s problematic for aluminum safe dosing, evidently, because otherwise it would also clear from the body, which it does not, for quite some time. Time enough to interfere with brain development and balanced cellular development in the immune system. Aluminum kills cells via ER stress, and is released from those cells with oddly mishapen proteins: a recipe for autoimmunity if I ever heard one.

AAAB claims that I consider “my model” (i.e., the Clark’s rule-based PDL “valid”. Not quite. I don’t even consider the starting value of 850 mcg of aluminum for an adult “valid”. And I, and my co-authors, say so. I, and co-authors, also lament that the only safe level for aluminum that is body-weight based is the 4-5 mcg/kg/day limit for individuals with renal impairment. We propose that Clark’s rule might be useful for a liberal safe level, because, after all, infants have 20% glomular filtration rate at birth, and do not reach full adult capacity for two years. Aluminum is also a cause of renal impairment, so no, I don’t stand by Clark’s rule as “valid”. It would help if AAAB read our studies in detail to grasp our stance. Peer reviewers did. AAAB should not misrepresent our study nor position, for they risk setting up straw men, which we are not obligated to defend.

Nevertheless, nothing in our studies conflates IV administration with IM injection; we state clearly all of our concerns of the available studies that use IV administration. Our studies represent, and should be read as critique of the studies that came before ours, and include lamentations over the use of citrated forms, IV administration, adult instead of infant mice, oral forms instead of injected, etc, etc. AAAB would have their readers imagine that those criticisms apply to our study; they don’t, or rather, if they do, it’s because we, like Mitkus, used Priest’s flawed model. So our deconstuction is aided by these barbs aimed curiously only at our study, but those criticism are clearly already stated as limitations in our study, but they are not in Mitkus’ et al., nor sufficiently so in the Priest et al. study.

Our message is that Clark’s rule is evidently the best we can do toward an empirical regulation-based PDL that recognizes the limitations that AAAB acknowledges, which is why I am grateful for AAAB putting such a bright light on the flawed logic behind claims of safety of aluminum adjvants in doses as high as those found in the CDC’s pediatric vaccination schedule.

In the very, very complex model, I count ten compartments and twenty-seven transition parameters. Maybe twenty eight, but the missing parameter for which data are most relevant are data on the rate at which aluminum is exiting from the body. So let’s say there are thirty seven parameters, all estimated with error. I agree with AAAB that any study designed to grapple with estimation of so many parameters would have to be duly powered, and I agree with AAAB that the study AAAB cites is, likely, insufficiently powered. However, the model itself is irrelevant to the question posed by our research study unless it leads to an alternative, per-body weight, per day pedatric dose limit of aluminum hydroxide in humans – which it does not.

AAAB likes to falsely accuse me of not understanding different forms of chemicals, a canard that is irrelevant to whether studies have or have not been conducted to study the whole-body clearance of the forms of aluminum administered in the manner in which they are used in humans (that includes, once more, in infants, not adults). AAAB is clearly missing the larger picture, completely.

Neither I, nor my colleagues, ever claimed that aluminum release from the site of injection was rapid. The lengthy exposure from a granuloma may be reassuring to those who would see it as such – reassuring because it keeps plasma concentrations low. But that, too, is flawed thinking. In his own attack on our article, the primary focus by AAAB thus far has been on plasma clearance; whatever amount is there in the first few hours, and days, is reassuring to AAAB; it’s the net product of the inputs and the outputs; odd then that the clearance is a cause for concern for those who cite and acknowledge the published Science on specific, known mechanisms of pathophysiology (e.g., me) but it remains reassuring for those who do not (e.g., AAAB), even after it has been cited to them.

Long-release appears to not be a concern for AAAB, even though during that long release a patient may be exposed to other viruses and bacteria via infection, leading to increased likelihood of an adaptive immune response to such pathogens, which in a perfect world would be reassuring – a freebie vaccine, if you will. I have written extensively about the role of the oddly shaped proteins that are released due to the cellular death option of the adaptive unfolded protein response following genetic and environmental ER Stress. There is ample reason already to avoid a permanent state of being an overly adjuvanted person in a world of complex proteins. In world in which genetic variation exists among humans bringing some patient’s any-proteins one or two steps more similar in amino acid sequence or three-dimensional structure to a pathogen’s protein, the clinically unnecessary long-term duration of aluminum “in the body” (which includes, I remind AAAB, the bolus at the site of injection) logically then leads to the expectation of increased risk of autoimmunity through molecular mimicry. A second infection from a virus or bacteria could then cause cause a flare-up of an the autoimmune disorder.

For unknown reasons, AAAB cites (albeit obliquely) other’s representation of macrophage transportation of aluminum to the brain as well as descriptions of vaccine aluminum as nanoparticles. For the record, it is not questioned in mainstream aluminum toxicity whether aluminum can enter the brain, or not. An early published description (1985) of amyloid plaque cores (APCs) reports the non-proteinaceous part to be aluminum, part silica:

This reality should have been a source of dire concern for all since it was reported. There are many, many citations of findings of aluminum in the brain. The entire discussion on mechanisms of how aluminum enters the brain is obviated by its presence in the brain, and its known high brain persistance, all recorded in the scientific literature.

The issue of AAAB’s unfamiliarity of studies on the nature of aluminum brain toxicity can be rectified by further reading, such as the quote by Gherardi et al. (2015):

“…poorly biodegradable aluminum-coated particles injected into muscle are promptly phagocytosed in muscle and the draining lymph nodes, and can disseminate within phagocytic cells throughout the body and slowly accumulate in the brain” (Gherardi et al., 2015).

This citation and diverse many other references on aluminum neurotoxicity can be found here, especially Bondy (2015).

I also refer AAAB to this study that found intussesception and death due to aluminum-containing vaccines in guinea pigs:

https://www.ncbi.nlm.nih.gov/pubmed/31270308

It provides more data that shows that tissue-based toxicology is appropriate for aluminum, and that aluminum-containing vaccines are problematic. The study, “Incidental induction of secondary bowel disorders in guinea pigs during a batch safety test of veterinary vaccines”, reports:

“Histopathologically, the white nodules on the serous surface were granulomatous inflammatory foci that consisted of centrally located eosinophilic amorphous deposit, which were surrounded by macrophages, lymphocytes, and fibrin deposits. These granulomatous foci did not invade the muscular layer of intestine. The similar granulomatous inflammatory foci were detected within the sites of intussusception (Fig. 1b) and the focus of intestinal adhesion (Fig. 1c) in the symptomatic 7 guinea pigs. The eosinophilic amorphous deposits, which were found within the granulomatous foci, yielded partly positive response to aluminum staining…”

The relevant aluminum toxicity levels are in tissue, not plasma.

Tissue, not plasma. Thus, whole-body toxicity is relevant, and plasma levels are irrelevant.

AAAB gallantly excused me from offering an apology (for heavens knows what imagined slight I may have conducted for daring to defend my position). However, not that I’m even slightly interested in AAAB’s identity, but I would never apologize to an anonymous, random person on the web.

AAAB also said that they did not care to have a response from me, that they didn’t require one, which, as ostentatious as that sounds, I respond, I’m sorry. We now live in a world in which independent objective not-for-profit Science, funded by the people, conducted for the people, is a reality. So you will be hearing from me and my colleagues again, and again, and again as we reduce human pain and suffering through knowledge.

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