BEWARE: Aluminum Nanoparticles Used in Vaccines Travel into the Brain

BEWARE: Aluminum Nanoparticles Used in Vaccines Travel into the Brain

Reposted from Vaccine Papers

Parents can be reassured that the trace quantities of aluminum in vaccines can’t possibly do harm.
-Dr Paul Offit: Vaccine promoter, vaccine patent licensor, and autism pundit, 2015

…the existing evidence on the toxicology and pharmacokinetics of Al adjuvants…altogether strongly implicate these compounds as contributors to the rising prevalence of neurobehavioural disorders in children.
-Dr Chris Shaw, Neuroscientist and aluminum researcher at University of British Columbia, 2013.

Click for list of papers in this post.

Many vaccines contain aluminum adjuvant, an ingredient necessary for stimulating a strong immune response and immunity. Aluminum adjuvant is typically made of Al hydroxide and/or Al phosphate nanoparticles.

Aluminum adjuvant has been used in vaccines since the 1920s. Despite this long history, aluminum adjuvant has not been studied much beyond its role in vaccine efficacy. Vaccine promoters cite studies of aluminum adjuvant safety (e.g. Jefferson 2004), but these only consider short term acute reactions, not long term effects on the brain. Vaccine promoters do not have evidence that aluminum adjuvants are safe with respect to neurological disorders (e.g. mental illnesses, autism, schizophrenia, anxiety, depression).

The present article is concerned with the unique way that aluminum adjuvant nanoparticles (AANs) are transported around the body. The movement (“kinetics”) of injected AANs is very different from the movement of ingested aluminum.

Ingested Aluminum Kinetics
Ingested aluminum enters the blood from the gut. Al is absorbed in a water-soluble ionic form, typically Al3+ or an aluminum complex*. This aluminum comprises individual Al atoms, like ordinary salt dissolved in water. Ionic aluminum is toxic, but at normal, natural levels of exposure it does not cause harm, for a few reasons:
1) absorption is low. Only about 0.3% enters the blood,
2) the blood-brain barrier (BBB) almost completely blocks Al3+ entry into the brain,
3) Al3+ is rapidly removed from the blood by the kidneys.

These defenses protect the body and brain from natural levels of aluminum ingestion.

Below is a diagram illustrating how ingested aluminum moves through the body.

Above: Ingested aluminum has low absorption (0.3%), is rapidly eliminated in the urine, and is (mostly) excluded from the brain by the blood brain barrier (BBB). These natural defenses are adequate to protect the brain from normal, natural levels of Al ingestion.

Based on this understanding of ingested aluminum transport, it was long assumed that AANs are eliminated in the same way as ingested aluminum. AANs cannot be filtered by the kidneys (they are too large). But it was assumed that the AANs dissolve rapidly in body fluids, and the resulting Al3+ is eliminated in urine, just like ingested aluminum. However, this simple model is wrong.

Below is a diagram illustrating this wrong understanding of what happens to aluminum adjuvants in the body.

Above: Vaccine promoters assume that Al adjuvant is safely eliminated by dissolution and urinary excretion. Thats why vaccine promoters believe only the blood concentration of Al3+ is important. We now know this is wrong. The Al adjuvant dissolves very slowly and so can remain in the body for many months or years. Also, its not just the dissolved Al3+ thats toxic; the Al adjuvant particles are also toxic. 

The above model is wrong. What actually happens is a type of immune cell called a macrophage (MF) ingests (called “phagocytosis”) the AANs. Eating foreign material is a primary function of MFs. When MFs detect bacteria or debris, the MFs eat it, and destroy it with enzymes.

The problem is that AANs are not digested by the MF enzymes. Consequently, the AANs remain inside the MFs for a long time. The AANs can persist for years. MFs that consume the AANs become highly contaminated with aluminum, and spread the aluminum wherever they go. And they go everywhere in the body.

The MFs travel across the blood brain barrier (BBB) when there is inflammation in the brain. The MFs, once loaded with AANs, act like a Trojan Horse and carry the AANs into the brain. This is harmful, because the brain is very sensitive to aluminum.

Below is a diagram illustrating how AANs travel around the body and into the brain.

Above: Before the Al adjuvant nanoparticles dissolve, they are eaten (“phagocytosed”) by MFs. The MFs then carry the Al nanoparticles around the body, including into the brain. MFs can pass through the BBB when inflammation is present. Aluminum at very low levels causes inflammation in the brain. Aluminum stimulates elevated production of the cytokine interleukin-6 (IL-6). Elevated IL-6 causes autism. 

Once inside the brain, the aluminum causes inflammation which attracts more MFs, some of which are loaded with still more aluminum. The result is a vicious cycle of inflammation and aluminum accumulation in the brain.

A Pinch Is All It Takes
The brain is extremely sensitive to aluminum. Concentrations of aluminum as low as 10-100 nano-molar can cause inflammation of brain tissue. 10 nano-molar is 270 nano-grams aluminum per liter. (nano = 1 billionth). Thats an amazingly low concentration.

10 nano-molar Al causes inflammation in human blood vessel cells (Alexandrov et al): Nanomolar aluminum induces expression of the inflammatory systemic biomarker C-reactive protein

100 nano-molar Al causes inflammation in human neurons (Lukiw et al):Nanomolar aluminum induces pro-inflammatory and pro-apoptotic gene expression in human brain cells in primary culture

A typical 1-year old infant has a brain weight of about 1000 grams. A 10 nano-molar concentration in 1000 grams contains 270 nano-grams (0.27 micrograms) of aluminum; a 100 nanomolar concentration in 1000 grams contains 2700 nano-grams (2.7 micrograms). This is extraordinary, because a single vaccine can contain 250 micrograms (250,000 nano-grams), and an infant can receive about 3,675 micrograms in the first 6 months. In other words, less than 0.01% of the aluminum in the first 6 months of vaccines can create a 10-nanomolar concentration in the brain, and 0.1% can create a 100-nanomolar concentration in the brain  (since 3,675 x 0.01% = 0.3675 micrograms, and 3,675 x 0.1% = 3.675 micrograms)). A single vaccine contains more than enough aluminum to inflame the brain.

Of course, this assumes uniform distribution of the aluminum in the brain, which is not the reality. Al concentration in the brain is highly nonuniform. However, the above calculation establishes plausibility. The amount of aluminum in vaccines greatly exceeds the amount necessary to cause brain inflammation.

The Scientific Evidence
The scientific evidence for this “Trojan Horse” mechanism is unequivocal and overwhelming. Every step has been proven by multiple studies from well-known universities and government-funded laboratories: the ingestion of AANs by MFs, the movement of MFs into the brain, and the observation that MFs carry nanoparticles into the brain. Also, the entire process has been demonstrated. AANs injected into experimental animals have been detected and imaged in the brain. The ability of MFs to transport particles into the brain has even been used to deliver therapeutic drugs (formulated as particles) into the brain. The Trojan Horse mechanism is well etablished and recognized. It is not theoretical.

First, there is the Flarend study, which shows that even after a month, only about 6% (of Al hydroxide) or 22% (of Al phosphate) is eliminated in urine. Most aluminum adjuvant was retained in the body 1 month after injection. The Flarend study also showed that the aluminum spread to numerous organs, including the brain.
Flarend: In vivo absorption of aluminium-containing vaccine adjuvants using 26Al

The Movsas study (published in 2013) used human infants and obtained similar results. Movsas looked for aluminum in urine and blood after routine vaccination with 1200mcg aluminum at the 2-month date. No change in urine or blood Al level was observed. Movsas states:

No significant change in levels of urinary or serum aluminum were seen after vaccination.

Movsas: Effect of Routine Vaccination on Aluminum and Essential Element Levels in Preterm Infants

Of course, these results contradict the claim by vaccine advocates that aluminum adjuvant dissolves in the blood and is removed by the kidneys. The reason why Movsas did not observe aluminum in blood or urine is because the aluminum is trapped in the MFs. MFs are are usually in a resting state (not traveling around), or if they are traveling, they travel via the lymphatic system (not the blood). MFs travel around the body in response to a specific inflammatory signal (MCP-1, explained below).

Aluminum Adjuvant Is Made Of Nanoparticles
Nanoparticles are typically defined as having at least one dimension of less than 100nm (0.1 microns). Vaccine promoters have argued that aluminum adjuvant particles are much larger, in the range of about 2-15 microns, and they cite optical  size measurements as proof. The optical measurements are misleading because they measure the size of particle agglomerates, which are loose, weakly-bound clumps of nanoparticles. All nanoparticles agglomerate to form larger particles. Agglomerated nanoparticles are still considered nanoparticles in the scientific literature. Agglomerates are defined as being held together by weak electrostatic forces, not chemical bonds, and that is the case with aluminum adjuvant. For example, nanoparticle agglomerates (including Al adjuvant) can be dispersed by gentle methods such as ultrasound.

Above: Electron microscope images of aluminum hydroxide adjuvant (brand name Alhydrogel, the most commonly used brand of aluminum adjuvant), after de-agglomeration by gentle ultrasonication. Scale bars in a, b, and c are 100nm; scale bar in d is 50nm. The particles are clearly smaller than 100nm. From Harris et al 2012. 

Paper (Harris et al 2012): Alhydrogel® adjuvant, ultrasonic dispersion and protein binding: A TEM and analytical study

Another study (Johnston 2002) determined primary particle size of 4.5 x 2.2 x 10 nm from  X-ray diffraction and water sorption measurements. Johnston 2002 states:

The X-ray diffraction pattern and the Scherrer equation were used to calculate the dimensions of the primary crystallites. The average calculated dimensions were 4.5 x 2.2 x 10 nm.

Paper (Johnston 2002): Measuring the Surface Area of Aluminum Hydroxide Adjuvant

MFs Eat AANs
Several studies show that MFs eat (“phagocytose”) the AANs in vaccines.

Paper (Mold et al): Unequivocal identification of intracellular aluminium adjuvant in a monocytic THP-1 cell line This study exposed a culture of “THP-1 monocytes” to Al adjuvant (aluminum hydroxide). Monocytes typically mature into macrophages, and, like macrophages, they eat debris such as nanoparticles. THP-1 cells are cancerous  (which makes them easy to grow and maintain in culture).


Above: Electron microscope images of aluminum adjuvant nanoparticles (AANs) inside monocytes exposed to Al adjuvant.  From Mold et al. 

Some have criticized the Mold et al experiment by arguing that THP-1 cells grown in culture may behave differently than normal macrophages inside the body. This argument is reasonable. To rebut it, I cite the papers below, which show that macrophages do indeed eat aluminum adjuvant.

Rimaniol et al, 2004:  Aluminum hydroxide adjuvant induces macrophage differentiation towards a specialized antigen-presenting cell type This paper reports that human macrophages become “loaded” with aluminum when exposed to AlOH adjuvant. The macrophages used in this experiment were isolated from fresh human blood samples taken from healthy subjects.

QUOTE: “As reported here, we found that aluminum-loaded macrophages differentiate into mature, specialized antigen-presenting cells…

QUOTE: “Following the injection of AlOOH-containing vaccine in vivo, muscle infiltrated macrophages bear crystalline inclusions of aluminum hydroxide. We assessed the presence of such inclusions in AlOOH-treated macrophages in vitro. By electron microscopy, we observed numerous, large crystalline inclusions in macrophages treated for 2 days with AlOOH (Fig. 2B and C), very similar to those observed in vivo. These crystalline inclusions were still observed in macrophages 7 days after the removal of AlOOH (Fig. 2D).

Eisenbarth et al., 2008: Crucial role for the Nalp3 inflammasome in the immunostimulatory properties of aluminum adjuvants This paper describes research on the inflammatory signals induced by Al adjuvants. It reported that macrophages eat the Al adjuvant. The paper used the generic term “endocytosis”, which refers to the intake of substances by a ell. Phagocytosis is a specific type of endocytosis.QUOTE:  “Aluminium particles of various aluminium adjuvants form insoluble particles that can aggregate, are readily phagocytosed by macrophages and have been shown to stimulate IL-1β and IL-18 production in vitro1215.
QUOTE: “...these data support a model of active endocytosis of alum by viable macrophages…

A study of macrophagic myofasciitis (MMF) patients observed AANs inside MFs at the location of intramuscular vaccine injections. Muscle tissue samples were obtained by biopsy 3 months to 8 years after vaccine injection (average: 36 months). Presence of aluminum inside MFs was confirmed by 3 different methods. Aluminum was present in MFs only, and not in muscle fibers.

Paper (Gherardi et al): Macrophagic myofasciitis lesions assess long-term persistence of vaccine-derived aluminum hydroxide in muscle.


Above: Electron microscope (top) and nuclear microprobe (bottom) images of thin sections of muscle taken from macrophagic myofasciitis (MMF) patients. This study showed that AANs remain inside macrophages (MFs) in muscle tissue for years after intramuscular injection. In one subject, Al adjuvant was still present 8 years after vaccination. Nuclear microprobe is also called proton-induced X-ray emission (PIXE), and it can identify chemical elements. Here, it is used to identify aluminum. From Gherardi et al. 2001.

Inflammation Causes Macrophage Movement
A 2009 study (D’Mello et al.) demonstrated that liver inflammation caused MFs to enter the brain and central nervous system (CNS). In this experiment the liver inflammation was induced by blocking a bile duct. The liver inflammation caused microglia (immune cells of the brain) in the CNS to become activated. The activated microglia released MCP-1, which attracted macrophages into the brain. When MCP-1 is produced by microglia, macrophages from around the body travel into the brain.  MCP-1 is described here: “MCP” stands for “macrophage chemoattractant protein”, which of course describes its primary function of summoning macrophages.   MCP-1 is also known as CCL2.

A key finding of the D’Mello study is that inflammation outside the CNS caused MFs to enter the CNS. D’Mello found that inflammation in the liver caused macrophages to travel into the brain. The MFs travel to the brain even if the original source of the inflammation is not in the brain! This fact suggests that a MFs may travel into the CNS in response to inflammation anywhere in the body. The inflammation must be the correct type, however (i.e., it must stimulate MCP-1).

Paper (D’Mello et al.): Cerebral Microglia Recruit Monocytes into the Brain in Response to Tumor Necrosis Factor Signaling during Peripheral Organ Inflammation

AANs Photographed in Mouse Brain
An impressive study by Khan et al. shows that AANs and other nanoparticles (e.g. latex particles) injected intramuscularly (into the leg) travel into the brain. AANs were detected in the brain and spleen, up to one year after injection. These results contradict the long-assumed “100% of adjuvant dissolves into the blood” and “aluminum adjuvant remains harmlessly at the injection site” myths believed by vaccine promoters.

Below is a page from the Khan paper showing that AANs traveled into the brain and spleen.

Paper (Khan et al.): Slow CCL2-dependent translocation of biopersistent particles from muscle to brain

Khan observed that transport of AANs depends on MCP-1, which indicates that the macrophages are responsible for transporting the nanoparticles. Al adjuvant detected in brain

Above: Images of aluminum adjuvant nanoparticles (AANs) in brain and spleen of mice. The AANs traveled into the brain from injection in a hind leg. AANs are not rapidly dissolved and excreted and do not remain at the injected site, as vaccine promoters claim. D21, D180, D365 indicate time (in days) between AAN injection, and detection of AANs in the brain. Images produced by nuclear microprobe, also known as proton-induced X-ray emission (PIXE). PIXE imaging can identify chemical elements; the yellow color in Fig. 1d (bottom) is aluminum. From Khan et al 2013.

The Khan et al. paper concludes with this statement:

…alum has high neurotoxic potential [49], and planning administration of continuously escalating doses of this poorly biodegradable adjuvant in the population should be carefully evaluated by regulatory agencies since the compound may be insidiously unsafe. It is likely that good tolerance to alum may be challenged by a variety of factors including overimmunization, BBB immaturity, individual susceptibility factors, and aging that may be associated with both subtle BBB alterations and a progressive increase of CCL2 production [50].” (Emphasis added)
BBB= blood-brain barrier
Note: CCL2 is another name for MCP-1

Brain Aluminum Content After Al Adjuvant Injection
An important new study (Crepeaux et al, 2017) reported that a dosage of 200mcg/Kg Al adjuvant (as 3 doses of 66 mcg/Kg), injected intramuscularly in the leg, caused a 50X increase in brain aluminum content. Brain aluminum was measured 6 months after the final injection. Of course, this result suggests that the Al adjuvant persists in the brain long-term. For the 200mcg/kg dosage, about 1.3% of the injected aluminum wound up in the brain (calculated from data provided by personal communication). The Al adjuvant injection also caused long term microglial activation (inflammation) in the brain. The Crepeaux 2017 paper is described in detail here:

Above: Al adjuvant dosage of 200mcg/Kg (as 3 doses of 66 mcg/Kg), injected intramuscularly, caused a 50X increase in brain aluminum content. Brain aluminum was measured 6 months after the final injection, which indicates that the aluminum persists in the brain long-term, and/or accumulates slowly over time. Of course, the large increase in brain aluminum definitively proves that the aluminum adjuvant travels into the brain. The higher dosages did not increase brain Al content because intense local inflammation (a granuloma) trapped the Al adjuvant at the injection site. From Crepeaux et al. 2017. 

MCP-1 production is stimulated by some types of immune activation. Hence, a vaccine that stimulates MCP-1 may cause AANs (e.g. from prior vaccines) to move into the brain. Some infections or toxins induce MCP-1. Interestingly, Al adjuvant induces MCP-1, suggesting that it may stimulate its own transport.

We can speculate that AANs from vaccines may remain “dormant” for years, until MCP-1 production is stimulated. The MCP-1 will cause macrophages containing AANs to mobilize and transport AANs into the brain and other sensitive tissues. This may explain some of the damage from the MMR vaccine. MMR is given at 15-18 months of age, which is after Al-containing vaccines are given (at 0, 2, 4, and 6 months). The measles vaccine can stimulate MCP-1 production (Citation: Therefore,  the MMR vaccine may stimulate the movement of AANs (received from prior vaccines) into the brain. This may explain how MMR could cause Al toxicity, even though it does not contain aluminum adjuvant.

Elevated MCP-1 in Autism
MCP-1 is elevated in the autistic brain and spinal fluid. This was one of the most significant findings of the 2005 Vargas study, the first to report chronic brain inflammation in autism. Note that Vargas mentions that MCP-1 causes movement of macrophages/monocytes into the brain. Vargas states:

The presence of MCP-1 is of particular interest, because it facilitates the infiltration and accumulation of monocytes and macrophages in inflammatory central nervous system disease.
MCP-1, a chemokine involved in innate immune reactions and important mediator for monocyte and T-cell activation and trafficking into areas of tissue injury, appeared to be one of the most relevant proteins found in cytokine protein array studies because it was significantly elevated in both brain tissues and cerebrospinal fluid.
The increased expression of MCP-1 has relevance to the pathogenesis of autism because we believe its elevation in the brain is linked to microglial activation and perhaps to the recruitment of monocytes/macrophages to areas of neurodegeneration…
monocytes= macrophages in an immature form

Vargas 2005:

A January 2017 paper confirms the finding of elevated MCP-1/CCL2 in autism (in blood serum). Levels in autistics were 182 pg/mL, compared to 142 pg/mL in normal children (statistically significant difference with p=0.03). Paper:

MCP-1 is elevated in newborns (24-48 hours after birth) that later become autistic. The babies with elevated MCP-1 will experience transport of Al adjuvant into the brain after vaccination. So, the fact that MCP-1 is elevated in babies later diagnosed with autism supports a causal link between Al adjuvant and autism. Paper:

Trojan Horse Technology Applications
The “Trojan Horse” mechanism is well established. For example, the Trojan Horse mechanism has been studied for therapeutic applications. Researchers have used MFs  to transport nanoparticles (e.g. containing serotonin, cancer drugs, or HIV drugs) through the BBB. This is useful for treating brain diseases because many drugs do not pass through the BBB. The papers below report using macrophages (or monocytes) to transport therapeutic drugs or nanoparticles into protected tissues such as the brain:

Choi et al, 2012: Delivery of nanoparticles to brain metastases of breast cancer using a cellular Trojan Horse
QUOTE: “More than two decades ago, Fidler and colleagues provided evidence that macrophages of blood monocyte origin can infiltrate experimental brain metastases while the blood–brain barrier is intact (Schackert et al. 1988).
QUOTE: “The use of monocyte/macrophages as delivery vehicles to the central nervous system has been investigated in situations other than malignancy. Afergan et al. demonstrated the delivery of serotonin to the brain by monocytes, which had phagocytosed nano-liposomes containing this otherwise brain impermeant drug (Afergan et al. 2008). Dou and colleagues utilized bone marrow derived macrophages as carriers of and depots for antiretroviral drugs to treat and attenuate the symptoms of HIV-associated neurocognitive disorder (Dou et al. 2009). Therefore, we hypothesized that nanoparticle-laden monocytes/macrophages would home in to intracranial metastatic deposits by crossing the blood–brain barrier following injection into the systemic circulation.

Batrakova et al, 2011: Cell-Mediated Drug Delivery  This is a review paper on using immune cells for delivering drugs to tissues and organs (like the brain) that are normally protected.
QUOTE: “This paper reviews how immunocytes laden with drugs can cross the blood brain or blood tumor barriers, to facilitate treatments for infectious diseases, injury, cancer, or inflammatory diseases.
QUOTE: “Immunocytes and stem cells exhibit an intrinsic homing property enabling them to migrate to sites of injury, inflammation, and tumor. In addition, they can act as Trojan horses carrying concealed drug cargoes while migrating across impermeable barriers (for example, the blood brain or blood tumor barriers) to sites of disease.
QUOTE: “Immunocytes (including mononuclear phagocytes (dendritic cells, monocytes and macrophages), neutrophils, and lymphocytes) are highly mobile; they can migrate across impermeable barriers and release their drug cargo at sites of infection or tissue injury.

Tong et al., 2016: Monocyte Trafficking, Engraftment, and Delivery of Nanoparticles and an Exogenous Gene into the Acutely Inflamed Brain Tissue  This study is particularly relevant because it showed that immune activation by lipopolysaccharide (LPS) simulated the movement of macrophages into the brain, and that the macrophages can be used to transport nanoparticles into the brain.
QUOTE: “This study was designed to fully establish an optimized cell-based delivery system using monocytes and MDM, by evaluating their homing efficiency, engraftment potential, as well as carriage and delivery ability to transport nano-scaled particles and exogenous genes into the brain…
QUOTE: “…recruitment of circulating monocytes to the diseased sites within the CNS were evident in numerous neurological disorders [61417]. Therefore, the use of monocytes and monocyte-derived macrophages for precise therapeutics delivery still holds great promises for combating many CNS disorders…

Brynskikh et al, 2010: Macrophage Delivery of Therapeutic Nanozymes in a Murine Model of Parkinsons Disease This paper demonstrated that macrophages can be used to deliver drugs into the brain in parkinsons disease.
QUOTE: “…we suggest the utilization of these cells [macrophages] as carriers of therapeutic formulations due to their ability to efficiently engulf particles, penetrate the BBB, and reach the site of neuropathology.

Pang et al 2016: Exploiting Macrophages as targeted Carrier to Guide nanoparticles into Glioma / This paper describes an experiment using macrophages to transport nanoparticles into the brain, for treating brain cancers (glioma).
QUOTE: “As with other inflammatory responses, inflammation in the brain is also characterized by extensive leukocytes infiltration into brain tissue by cell diapedesis and chemotaxis [1214]. Brynskikh et al. utilized macrophage as a drug vehicle to improve the delivery of redox enzymes into the brain for neuroprotection of dopaminergic neurons in a mouse model of Parkinson’s disease. Therapeutic efficacy of macrophages loaded with nanozyme was confirmed by twofold reductions in microgliosis and twofold increase in tyrosine hydroxylase-expressing dopaminergic neurons [15].”
QUOTE: “Inspired by these understandings, a novel strategy utilizing macrophage as a carrier to migrate across the BBB, BBTB and home into tumor sites is conceived. Importantly, macrophages are able to carry drugs into brain tumor…

Clearly, it is proven and accepted that macrophages can transport particles into the brain, and that transport is stimulated by inflammation.

It’s Proven
Every step has been proven: MFs eat Al adjuvant nanoparticles, MFs cross the BBB and MFs transport nanoparticles into the brain. All these steps have been experimentally demonstrated multiple times. And the entire process has been demonstrated with AANs in mice. AANs from an intramuscular injection were “photographed” in the brain by PIXE. Additionally, vaccine-relevant dosages of Al adjuvant increased brain Al content by 50X. These facts contradict the simplistic and wrong belief (preferred by vaccine promoters) that AAN toxicity is determined by the concentration of dissolved aluminum ions in the blood. The story is far more complicated and worrisome than that. The toxicity of aluminum adjuvant depends on the transport of Al adjuvant nanoparticles by macrophages. 

Since aluminum is a potent neurotoxin and strongly stimulates brain-injuring inflammation, transport of Al adjuvant into the brain is a serious concern for vaccine safety. After all, Al adjuvant is specifically designed to stimulate inflammation. Inflammation is what makes it effective as an adjuvant. Brain inflammation causes autism.

Transport of Al Adjuvant is Complicated
An important new paper (Crepeaux 2017) gives a more complete picture of Al adjuvant movement. It reports an inverted dose-toxicity relationship (low dosage more harmful than higher dosage!), because high dosage has reduced transport. Its an excellent study with fascinating results. Read about it here:

OLD Update from Nov 2015 (this is now old news, because of the Crepeaux 2017 paper. Read that instead, at link above). 

A new study of Al adjuvant injections in mice has revealed even more complexity to the issue of Al adjuvant transport. As expected, it showed that Al adjuvant transport depends on MCP-1; mice that produce more MCP-1 (due to genetics) suffer greater transport of AANs into the brain.

Surprisingly, it also showed:
1) Transport depends on injection location. Subcutaneous injection (i.e. under the skin) is necessary for brain transport, at least for the dosages used. Intramuscular injection does not produce brain transport. This may be due to the presence of more-mobile white blood cells (dendritic cells) in the skin compared to muscle.
2) Transport depends inversely on dosage. A dosage of 200mcg/kg resulted in brain transport (and behavioral changes) and dosage of 400mcg/kg did not result in brain transport (and showed no behavioral changes). This may be due to macrophage mobility being impaired by high dosage. For example, higher local inflammation at the injection site may cause reduced macrophage mobility.

There may also be an interaction between injection location and dosage. The dosage range that causes transport may be different for different tissues.

These phenomena may explain why the prior Al adjuvant injection experiments by the Shaw Laboratory (using 100, 300 and 550mcg/kg in divided doses) showed such strong adverse effects. Though aluminum adjuvant is harmful, in human infants the incidence of harmful effects is likely lower than what was observed in the prior mouse experiments. This has been a criticism made by vaccine advocates. Specifically, vaccine advocates have asserted that the Shaw Laboratory results were implausibly severe and therefore must be wrong. This new study may explain why adverse effects in human infants are less frequent than what was observed by the Shaw Laboratory.

The authors state:

In previously published studies, motor and behavioral impairments were observed following sc (behind the neck) Alhydrogel® injection to CD1 mice with doses of 100 and 300 μg Al/kg [17,41]. These effects were associated with Al deposits in the central nervous system (spinal cord) assessed by Morin stain. To examine if the route of exposure may represent an important factor for alum toxicity, a nested study was conducted herein, showing that alum particles may penetrate the brain at D45 after the sc (and not im) injection, performed at the dose of 200 μg Al/kg (and not at the dose of 400 μg Al/kg). A higher rate of brain translocation after sc injection may be explained by a much higher density of dendritic cells with high migrating properties, in the skin compared to the muscle. The fact that half dose resulted in brain translocation, which was not observed at higher dose, is reminiscent of the non-monotonic dose/response curves previously observed with environmental toxins, including particulate compounds [67]. In another study, we similarly observed neurobehavioral changes at 200 but not 400 μg Al/kg (Crépeaux et al., manuscript in preparation). The exact significance of such observations is unknown, but one may speculate that huge quantities of alum injected in the tissue may induce blockade of critical macrophage functions such as migration and xeno/autophagic disposition of particles, as previously reported for infectious particles [37].”

Although this study does show that the adverse effects of Al adjuvant are less frequent than observed by the earlier experiments, it is confirmation of the Shaw laboratory results. This study is further evidence that Al adjuvant can cause brain damage at dosages human infants receive from vaccines.

Clearly, there is much more to learn about the dangers of Al adjuvant. The risk of Al adjuvant depends on genetics, on dosage in a complicated way, and on which tissue receives the injection.

Another key finding from this study is the extreme biopersistence of Al adjuvant particles. The particles were observed in distant organs and tissues up to 270 days after injection, including in the brain, spleen and lymph nodes. This is confirmation of prior experiments that also found high persistence. Al adjuvant nanoparticles dissolve very slowly and travel extensively around the body.

The authors state:

The present study confirms that alum is extremely biopersistent [29, 37] and that alum biopersistence can be observed in both the injected muscle and distant organs, including dLNs and spleen. Regarding the strong immunostimulatory effects of alum and the unrequired depot formation for its adjuvant activity [36], long-term biopersistence of alum in lymphoid organs is clearly undesirable, and may cast doubts on the exact level of long-term safety of alum-adjuvanted vaccines [37].
dLNs = draining lymph nodes
alum = aluminum adjuvant

Full Paper (Crepeaux et al): Highly delayed systemic translocation of aluminum-based adjuvant in CD1 mice following intramuscular injections

Further reading: see this review paper by Dr Romain Gherardi (a co-author of the Khan et al paper): Biopersistence and brain translocation of aluminum adjuvants of vaccines



AANs: Aluminum adjuvant nanoparticles. Used in most vaccines.
BBB: Blood brain barrier. Protects brain from aluminum in normal conditions.
MF: Macrophage (same thing as monocyte). A type of white blood cell. Can travel through the BBB.
CNS: Central nervous system (brain + spinal cord).
CCL2/MCP-1: Macrophage chemoattractant protein. Immune system signaling substance that attracts MFs. Causes MFs to transport aluminum into the brain and around the body.

* Under physiologic conditions, some dissolved aluminum will not be in the Al3+ form, but rather AlOH4-. For the sake of this discussion, this is irrelevant, so we will use Al3+, even though this is not really correct. But AlOH4- arguably contains Al3+ in the center.

Monocytes and macrophages are basically the same thing. From “Macrophages (and their precursors, monocytes) are the ‘big eaters’ of the immune system. These cells reside in every tissue of the body, albeit in different guises — such as microglia (brain), Kupffer cells (liver) and osteoclasts (bone) — where they engulf apoptotic cells and pathogens and produce immune effector molecules. Upon tissue damage or infection, monocytes are rapidly recruited to the tissue, where they differentiate into tissue macrophages. Macrophages are remarkably plastic and can change their functional phenotype depending on the environmental cues they receive. Through their ability to clear pathogens and instruct other immune cells, these cells have a central role in protecting the host but also contribute to the pathogenesis of inflammatory and degenerative diseases.


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