Aluminum Hydroxide Boehmite Crystals And Flarend’s Two Rabbits

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by SP

Summary of the Paucity of Safety Data on Aluminum Hydroxide Nanoparticles in Vaccines

For over 40 years it has been known that when total parenteral nutrition IV feeding solutions are given to premature human infants that inadvertent aluminum contamination from glass vials and tubing cause cognitive damage to their developing brains.  Great efforts have been invested to lower Al contamination of feedings.

In 1997, a study in NEJM was able to quantitate the neurologic damage done by Aluminum contaminants in IV solutions given to neonates.  Infants who received 45 micrograms/Kg/day were compared to 5 micrograms/Kg/day [ref #1]. The Baley Mental Development Index was used to measure cognitive development finding a reduction in cognitive development of 1 point per day of exposure.

Soluble aluminum is solidly established as a neurotoxin.

Professor Christopher Exley  aka “Mr. Aluminum”

Aluminum Kinetics:

Oral aluminum is very poorly absorbed and the great majority of ingested aluminum passes harmlessly into the stools without absorption into blood.   Only 0.3% of oral aluminum is absorbed into the blood stream.  The kidneys are quite efficient at eliminating soluble (dissolved) aluminum.

Studies where soluble (dissolved) aluminum is given IV to volunteers adults show a rapid elimination through the kidneys with >90% being eliminated in 24 hours.  A small percentage is deposited into bone, where it is eliminated very slowly over several years.  [Priest ref  #2 ]

Golub [ ref #3 ] fed mice food infused with dissolved aluminum citrate at several concentrations.  The low dose group did not show overt toxicity over the study period but the high dose group did.  From this study, the authors estimated how much aluminum can be tolerated without observable toxicity.  The Golub studies are the source of the commonly repeated number of 26 mg/kg/day as the No Observed Adverse Effects Level (NOAEL) for oral soluble aluminum, and, after a couple of fudge factors are calculated in, giving a human Minimum Risk Level (MRL) of 1 mg/kg/day.  This is the number used by the CDC when it reassures the public that the amount of aluminum in vaccines is safe.  This study is the basis of that reassurance.

However, a review article in 2018 by Masson’s group  [free full pdf here] critically dissects the basis of these  reassurances.   Prominent aluminum toxicity experts explain that this often quoted safety limit for Aluminum is faulty as adverse effects have been observed multiple times well beneath this “No Observable Adverse Effects Level” (NOAEL):

“Based on experimental data, oral MRL sets the safety curve too high. The MRL of 1 mg/kg/d [79] was determined based on a NOAEL of 26 mg/kg/day observed in mice in 2001 by Golub [85]. However, there are numerous reports of neurotoxic effects in mice and rats, confirmed by coherent neurobiological alterations, for oral doses of Al much less than 26 mg/kg/d: 6 mg/kg/d reported in 1993 [86], 5.6 mg/kg/d reported in 2008 and 2009 [87,88], 10 mg/kg/d reported in 2016 [89], 3.4 mg/kg/dreported in 2016 and 2017 [90,91], and even 1.5 mg/kg/d reported in 2017 [92].

However, the single most important aspect of vaccine aluminum safety is that the form of the aluminum used in vaccines is not in a dissolved (soluble) form, but in a particulate form, the Aluminum Hydroxide Nanoparticle.  And it is not taken orally, but bypasses the gut when the pediatric nurse injects these particles deep into muscle tissue of small children.

Aluminum hydroxide (AlOH) spontaneously forms a crystaline structure called a Boehmite.

These strands arrange in sheets, and then into 3D crystals.  Hydroxyl groups offer a place for biological material, the antigens to be used in the vaccine, to bond with the crystal.


These crystals form into linear fibers, then sheets, and then the sheet “agglomerate” into 3 dimensional Boehmite crystals referred to as Aluminum Adjunct Nanoparticles (AAN).  AANs are sized 2x4x10 nm under the electron microscope.   Biologic material from the outer coatings of bacteria and viruses (the antigen) are incubated with the AANs where the biological antigen binds to the surfaces of the crystals between layers and over its surfaces.

The AANs are given intramuscularly in a vaccination where they deposit and can persist in the muscle for years.  The AANs cause local inflammation and a reactive influx of macrophages which ingest the AAN essentially sequestering them.  Fibrous scar tissue is then laid down around the inflamed injection site causing a granuloma.

Picture:  Deltoid muscle biopsy from MMF patients taken 10 years after the vaccination showing intracellular AlOH crystals and surrounding fibrous granuloma.

The function of the AANs saturated with antigen is to cause a “persistent, synthetic pseudo-infection” giving a sustained, long-term stimulus to the immune system.

This stimulus is similar, but not identical, to the stimulus provided by an actual infection.

The two major types of aluminum adjuvant strongly potentiate the production of antibodies (humoral response by activation of CD4 + Th2 lymphocytes and B-cell priming) and not, or very little, production of cytotoxic T lymphocytes (CD8+) cells [and Memory Cells]. The mechanisms involved are still incompletely understood [From Masson, refs 47,48].

Lack of the cytotoxic T lymphocytes (CD8+) and Memory Cells induction are thought to be the prime differences between immunity induced by native infection compared to a vaccination.

So what is the fate of the AAN?  How are they eliminated?  What do we know about their safety for the brains of neonates?


Flarend and the Two Rabbits

PubMed Link:   and free pdf here ]


Flarend [ref #4] gave two rabbits IM injections of radioactively labeled AlOH and collected urine and stool to follow the elimination for a total of 28 days.  (The study also gave Al Phosphate to two rabbits and IV soluble aluminum to two more.)  But the most widely used adjuvant and the focus of this post, Al OH, was only tested on two rabbits.  These two rabbits are the total extent of the safety testing of Al hydroxide nanoparticles injected into the muscle of living mammals and is the basis of all of the reassurances given to the public for the safety of aluminum hydroxide in vaccines.   Two rabbits.  28 days only.  Flarend referred to his own paper as a “pilot study,” but no further testing has ever been done.

Flarend’s main findings:  At the end of the 28 day study period, 6% of the injected Aluminum had been excreted in urine.  The animals were sacrificed and organs sampled for residual aluminum.

Astute readers may notice that Flarend’s results leave 94% of the injected aluminum hydroxide unaccounted for at the end of the 28 day study period.

Much of the rest of this post is taken driectly from the discussions in the 2018 paper by Masson, Exley, Gherardi and others:  Critical analysis of reference studies on the toxicokinetics of aluminum based adjuvants [full free pdf here]

[First,] it should be noted that neurotoxic effects have been observed in mice injected with doses of Al hydroxide reproducing an equivalent of the American vaccination schedule from age 0 to 18 months [Shaw ref #6].

Masson then enumerates the three major errors in the traditional thinking on vaccine aluminum safety.  Vaccines do not contain soluble (dissolved) aluminum.  The particulate characteristic of Al OH nanocrystals used in vaccines profoundly alters the discussion in four ways.

1)  Persistence of Aluminum nanoparticles in human tissue for months to years.

2)  Migration of AANs carried by macrophages to distant organs including the brain, and,

3)  Stimulation of harmful immune activity by AANs, a process completely  independent of aluminum levels, per se.

1)  Masson explains the persistence issue.

The corollary of this over simplistic calculation [by Mitkas] is an underestimation of the bio-persistence time of Al in particulate form. Histological studies carried out after IM injection of Al hydroxide showed that particulate Al and the granulomas it induces, are still detectable in the injected muscle after monthsin animal studies [60,61] and several years (up to 12 years) in adult patients with chronic post-vaccine fatigue syndrome [Gherardi, ref #5 ].

2)  Migration:

Another limitation of the Mitkus study is that it does not take into account that the adjuvant can migrateaway from the muscle [injection site] in its particulate form [carried by macrophages]. Experimental studies have shown that the long intracellular bio-persistence of Al hydroxide relates to particles observed at the injection site as well as those transported to distant organs [70]. In mice Al hydroxide particles are indeed transported by cells of monocytic lineage (esp. macrophages and lymphocytes), first to the draining lymph nodes and then, probably via the thoracic duct, to the bloodstream, then reaching distant organs such as the spleen or even the brain, where slow and delayed accumulation can be observed in microglial cells and neurons [50,69]. After a single IM injection, cerebral penetration of the particles is low but increases considerably under the influence of Monocyte Chemoattractant Protein-1/Chemokine Ligand (MCP-1/CCL2) signaling.

3)  Immune activation

[Cerebral penetration of AAN across the blood-brain-barrier via the macrophage "Trojan horse” mechanism] is accompanied by cellular expression of Interleukin IL1beta, an expected effect of Al adjuvant-induced activation of the inflammasome [6[69]/p>

Professor Shoenfeld, Autoimmunity Center, Tel Aviv University.  From “Injecting Aluminum”

Vaccines and Autoimmunity

Shoenfeld and partners make a strong case that vaccines and adjuvants can trigger autoimmunity in susceptible people.  Understanding the metabolic and genetic risk factors for vaccine triggered autoimmunity is in its infancy.  For example, a multiple sclerosis type syndromes can be induced by vaccination of aluminum hydroxide containing vaccines in a mice model.

And Autism

Similarly, mitochondrial disease is a risk factor for vaccine triggered regressive autism in about 30% of cases according to trial deposition testimony of pediatric neurologists Dr Andrew Zimmerman and Dr Richard Kelley (Reported in JB Handley “How to End the Autism Epidemic,” Chapter 5).


[ [ #1 ]ishop NJ, Morley R, Day JP, Lucas A aluminum neurotoxicity in preterm infants receiving intravenous-feeding solutions. N. Eng. J Med 1997;336:1557-1561.

[#[#2 ]Priest, D. Newton, J.P. Day, R.J. Talbot, A.J. Warner, Human metabolism of aluminium-26 and gallium-67 injected as citrates, Hum. Exp. Toxicol. 14 (1995) 287–293. ] and Eickhoff, M. Myers, Workshop summary. Aluminum in vaccines, Vaccine 20 (Suppl. 3) (2002) S1–4.

[ [ #3 ]olub MS, Effects of Aluminum Ingestion on Spontaneous Motor activity in Mice.  Neurotox and Teratology11(1989) 231-235.    And,   Golub MS, Long-term consequences of developmental exposure to aluminum in a suboptimal diet for growth and behavior of Swiss Webster mice, Neurotoxicol. Teratol. 23 (2001) 365–372.

[ [ #4 ]larend R  In vivo absorption of aluminium containing vaccine adjuvants using 26 Al.  Vaccine 1997 Volume 15 Number 12/l 3

[ [ #5 ].K. Gherardi, H. Eidi, G. Crépeaux, F.J. Authier, J. Cadusseau, Biopersistence and brain translocation of aluminum adjuvants of vaccines, Front. Neurol. 6 (2015) 1-8,   (free full text pdf here ]

[#[#6 ].A. Shaw, Y. Li, L. Tomljenovic, Administration of aluminium to neonatal mice in vaccine-relevant amounts is associated with adverse long term neurological outcomes,  J. Inorg. Biochem. 128 (2013) 237–244,  [full free pdf here]p>

[M[Masson ref #50]. Eidi, M.-O. David, G. Crépeaux, L. Henry, V. Joshi, M.-H. Berger, M. Sennour, J. Cadusseau, R.K. Gherardi, P.A. Curmi, Fluorescent nanodiamonds as a relevanttag for the assessment of alum adjuvant particle biodisposition, BMC Med. 13 (2015),



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