Rebuttal to the “BBB Scientist”

Blogger ScientistAbe published a critical review of articles in April 2017:

I have received requests to respond. So here is my response.

First, a few general comments about ScientistAbe’s article:

ScientistAbe makes “straw man” arguments, i.e. he argues against things I did not say. He misunderstands or distorts my arguments. For example, ScientistAbe argues that I used scientific citations improperly, when in fact I did not use them in the way he alleges.
Definition of “straw man”: An intentionally misrepresented proposition that is set up because it is easier to defeat than an opponent’s real argument.

Scientist Abe cites no studies whatsoever (animal or human) demonstrating the neurological safety of aluminum adjuvant. Neurological injury is the primary safety concern with Al adjuvant. Studies of short-term, acute or local (i.e., injection-site) reactions to Al adjuvant are not relevant to concerns about neurological safety.

ScientistAbe cites no human studies on the long-term safety of aluminum adjuvant. In this context, “long term” preferably is at least one or a few years. Neurological and immune disorders are typically not observable until a child is a few years old. This is why long term follow up is necessary for establishing safety for these outcomes. Such studies have never been done.

Most of ScientistAbe’s article is copied below. Irrelevant sections are omitted for brevity. Key statements by ScientistAbe are numbered, shown in BOLD, and rebutted.

 April 15, 2017


This post constituted a direct response I had to the article posted by in February 10 2015 ( However, it recently got a recycling on the Collective-Evolution article (written by an author from VaccinesPapers) through this post:

I will not focus more on the first half of this article and I am just providing with some facts about it that I discussed earlier on Facebook.First paper (i exclude the CalTech thing since it is not peer-reviewed): They observed that mothers experiencing inflammation during pregnancy had higher risk of having offsprings with autism. Thats legit science. The senior author (Patterson) was (died in 2014) was a legit and recognized neuroscientist in the field of autism. This inflammation is either the result of some autoimmune disorder or infection. Thus the need to have mothers infection-free or avoid infectious diseases by keeping an updated vaccine schedule.
2. The second paper, again from the Patterson lab, show again the same conclusion, this time on rhesus monkey. It again emphasize the impact of infectious disorders on maternal gestation and the risk associated on the baby. Another good reasons for expecting mommies to keep their vaccines schedule up-to-date.
3. Now the China study show that if you increase interleukin-6 levels in the brain (IL-6, a well-known pro-inflammatory molecule), you can induce behavioral outcomes in mice that are considered representative of the ASD. It goes in the same direction that what Patterson showed and further underline the danger of having an “overactive/boosted” immune system and its ability to cause neuroinflammation. This is a growing field as we speculate that some psychiatric (depression) and neurological diseases other than multiple sclerosis (Alzheimers, stroke) maybe aggravated or induced by an inflammation and overactive immune system.…/pii/S0925443912000234. Then we have the slippery slope in which CE drank the Kool-Aid of BS by “ergo post hoc” fallacy. The false association fallacy: If cars run on petrol and because cars kill pedestrians, therefore petrol kill pedestrians”. This is the BS they are doing. 1) Since vaccination will induce a transient inflammation during the immune reaction and inflammation cause autism therefore vaccines cause autism”. Of course this was debunked but here they came back with the moving goalpost. 2) Since thiomersal did not cause an increase in number of autism, then the anti-vaxxers moved to “then it should be formaldehyde. No? Then it should be aluminum….”

To better debunk the bogus claim brought by the VaccinePapers post, I have written a long but detailed description on what is wrong with that post. Since I had initially written down into a Word documents with elements embedded in it, this may have been some formatting issues in this post. My sincere apologizes.

REBUTTAL (to BOLD text):
1) Inflammation from vaccines is not always transient. This fact is critical for linking autism and brain injuries. Aluminum adjuvant causes chronic, long term inflammation in the brain. Animal experiments show microglial activation 6 months after aluminum adjuvant injection. An experiment with hepatitis B vaccine in rats shows elevated IL-6 in the brain 8 weeks after vaccination. The chronic nature of brain inflammation caused by aluminum adjuvant is critical for linking it to autism and other brain disorders.

The Al adjuvant-autism hypothesis requires that Al adjuvant cause the right type of inflammation in the brain. These requirements are satisfied. IL-6 (a specific type of inflammation) causes autism.  Aluminum induces IL-6, and Al adjuvant (from Hep B vaccine) induces IL-6 in the brain. Al adjuvant causes inflammation in the brain.

2) The scientific method requires changing a hypothesis in response to scientific findings. Studies of thimerosal do not support a link, but Al adjuvant is increasingly implicated. So, shifting attention from thimerosal to Al adjuvant is a proper application of the scientific method.

ScientistAbe is arguing that studies of thimerosal can be used against the Al adjuvant-autism hypothesis. This is preposterous because thimerosal does not contain aluminum. Thimerosal studies therefore cannot be used as evidence for the safety of aluminum adjuvant. The argument is absurd and irrational. I am astonished that this argument is from a professional scientist. How depressing.


In this blog post, the author primarily focuses on the vaccine aluminum nanoparticles to enter and accumulate in the brain. Using several peer-reviewed articles, the author tries to convince that aluminum nanoparticles in the vaccines are uptaken by macrophages, such macrophages are capable to enter the brain and trigger neuroinflammation.

Therefore, the message of this post is clear: vaccines contain aluminum nanoparticles, aluminum is neurotoxic, and therefore vaccines are neurotoxic.  1) If you travel in time, back in the early 2000s, the same blog post title would have talked about ethylmercury (formulated as thiomersal) contained in some vaccines and would have cited the famous “Wakefield paper” that was just published (and will be retracted a couple of years later due to gross scientific misconduct).

1) This statement is not reality-based. did not exist in the early 2000s (VP launched in January, 2015). Also, it is presumptuous and bizarre to claim I am wrong because of things ScientistAbe thinks I would have said if I was transported back in time. It is also a straw man argument, because it is attacking something I did not say. The argument is idiotic.

I criticize the mercury hypothesis of autism causation. See:
I make two arguments regarding MMR and autism: 1) MMR-autism studies are wrong due to healthy user bias, and 2) MMR may increase Al adjuvant toxicity by stimulating transport into the brain, because MMR can induce MCP-1.


The blog website “Vaccine Papers” has the following slogan “an objective look at vaccine dangers”. Is it really an objective look or it is another anti-vaccine website distorting scientific studies to make fallacious claims in order to support an anti-vaccine agenda?

The goal of this article is to analyze, criticize and debunk claims made in this article and reveal the scientific fraud of this post and raise questions about the credibility of this website as a whole. In this post, we will explain why vaccines contain aluminum, which aluminum formulation has been used and is currently used in vaccines. Then we will refute the author’s arguments by directly citing passage of the post and provide a clear discussion about it.
How do vaccines work?[No rebuttals to this section, so is omitted for brevity]

Aluminum (symbol element “Al”) constitutes a particular potent class of adjuvant and have shown to have a potent stimulatory effect on the immune response for over 50 years with no particular side effects or increased risk observed (for review:

The primary safety concern with Al adjuvants is neurological/brain injury. Studies of Al adjuvant safety have never looked at long term or neurological outcomes. The cited paper (Lindblad 2004) does not mention neurological safety of Al adjuvants, and does not cite any studies supporting long term or neurological safety. Lindblad 2004 cites two studies (Refs 2 and 76) in support of Al adjuvant safety, but neither of these citations provides actual evidence:

Ref 2 (Edelman 1980, claims that Al adjuvant is safe, but does not provide evidence or data. Instead, Edelman cites a single 1969 paper to support the safety claim.  (Butler, 1969,   However, Butler 1969 also does not contain evidence for the long term or neurological safety of Al adjuvant! But it does have actual experimental results from an animal study. Butler 1969 reports a weight gain test with a 1 week follow-up (weight gain was reduced by Al adjuvant), and observation for “local or systemic reactions” for 30 days. Thats it. There was no behavioral testing, dissection, or brain analysis. No biochemical/histological studies. Just animal weights recorded, and observations for “reactions”, whatever that means. This data is completely inadequate as evidence for neurological safety. Its a joke. But thats all I found after digging through 3 layers of citations boasting about the enormous safety of aluminum adjuvant.

Ref 76 (Goldenthal 1993 includes this uncited assertion: “…extensive experience with this [aluminum] class of adjuvant for vaccine use has indicated that it is safe. Therefore, for vaccines with aluminum compound adjuvants, postinjection observation of the animal and the injection site is generally adequate from a preclinical safety standpoint without the need for a formal toxicology study
Goldenthal 1993 provides no safety evidence or citation supporting safety. And note that Goldenthal claims “formal toxicological studies” are not necessary!

Many times I have searched for the alleged safety evidence by following the citation trail. Every time, I find nothing useful. It always leads to a dead end or to studies totally inadequate for demonstrating long term or neurological safety. This is why I am confident in saying there are no studies supporting the long term or neurological safety of aluminum adjuvant.


The mechanism of action of aluminum as an adjuvant remains complex and unclear. It is the third most abundant element on Earth. It is considered as a metalloid, with its ionized form being Al3+. In contact with water, aluminum undergoes a chemical reaction resulting in the formation of aluminum hydroxide (AH): 2Al + 6H2O -> Al2(OH)3 + 3H2 (dihydrogen gas).

AH is classically used in adjuvants as it does not precipitate in solution, although an alternative form called aluminum phosphate (AP, AlPO4) is also used in certain vaccines formulation. This criteria is very important as chemicals used in injectable solutions have to be in an homogenous suspension. AH can organize and align themselves into crystalline structures, forming particles

Depending on how many AH are involved in these crystalline structures, these particles will have a particular sizes. In vaccines, AH particles distribution ranging from 2 to 10 micrometers, with a median size of 3 micrometer. In this post, the author refers to a particular type of aluminum, the aluminum adjuvant nanoparticles (AANs) without ever giving a bibliographical source or a definition to describe the nature of such term:

Aluminum adjuvant nanoparticles (AANs) are transported through the body differently than ingested aluminum. Most vaccines contain aluminum adjuvant, an ingredient necessary for stimulating a strong immune response and immunity. The aluminum is in the form of Al hydroxide and/or Al phosphate nanoparticles.

A request on search engine failed to provide us with a link on Pubmed and Sciencedirect databases with the term “aluminum adjuvant nanoparticles”, instead refers to “aluminum hydroxide nanoparticles (AHNs)” or “aluminum oxide nanoparticles (AONs)”. The usage of an uncommon term by the author is questionable and bring confusions on exactly what the author is referring to. However, the author later appears to refer to AH or AP nanoparticles, thus we speculate that AANs maybe an umbrella terms to refer to AH and APs and therefore we will refer on AHNs as AANs for the rest of this article.

1) The 2-10 micron size is from optical measurements, which measure the size of nanoparticle agglomerates. The agglomerates are made of many smaller “primary particles”, weakly held together by electrostatic interactions. Almost all nanoparticles form agglomerates in most solvents. The primary particles in AlOH adjuvant are about 10-100nm in size, which means they are nanoparticles. I created the term “aluminum adjuvant nanoparticles”. I am allowed to do that.
This paper has electron microscope images of Al adjuvant particles, showing they are about 10-100nm. See Figs 2 and 3.


Then the authors states the following: “Aluminum has been used in vaccines since the 1920s. Despite this long history, aluminum adjuvant was not studied much beyond its effect of making vaccines more effective. The safety of injected Al adjuvant was assumed, largely because aluminum is a normal (if unhealthy) component of many foods. Its one of the most common elements of the Earth’s crust. Its everywhere. So consideration of Al adjuvant safety was entirely based upon studies of ingested aluminum.” The author creates confusions for the reader as such sentences introduce a lots of concepts with few explanations and sounds more like a “word salad” than anything else.

As we have previously stated, aluminum is the third element in abundance in Earth’s crust ( 1) We can reasonably speculate that living organisms have been growing in an aluminum-rich environment since LUCA (last unicellular common ancestor) and therefore have adopted evolutionary traits to cope with such exposure to aluminum on the surface of Earth’s crust.

1) Aluminum is a common, toxic metal. Common occurrence does not necessarily imply safety. Safety can only be established empirically, via experiment. Aluminum is toxic to all life. All life seems to have protective adaptations for blocking Al absorption (in humans absorption is about 0.3%) and facilitating speedy elimination. Natural, evolutionary aluminum exposures involve only dissolved Al3+ ions, not persistent particles (of Al compounds) inside body tissues. Natural exposures (e.g. from ingestion) do not introduce solid particles of Al compounds into body tissues. Hence, there has been no evolutionary adaptation to solid particles of Al compounds in body tissues. The idea that evolution has selected for tolerance to injections of aluminum adjuvant is absolutely ridiculous. It is an incredibly stupid argument.


In this section, the author discussed and misused an important concept used in pharmacokinetics that will be discussed later: bioavailability. Bioavailability defines the amount of substance that reaches the systemic circulation (in other words the bloodstream) compared to the amount dispensed at the delivery site. It is a ratio of the amount measured in blood plasma following its delivery through an extravascular route (oral ingestion, intramuscular injection, dermal patch….) divided by the amount measured in blood plasma following a delivery through vascular route (most of the time an intravenous (IV) injection). When you inject a substance by IV route, this ratio is by definition 100%. Now if I re-use the example of the author, the bioavailability by oral route is 0.3%. If a patient swallows 100g of aluminum (Al), only 0.3g will make it inside the systemic circulation, thus giving us a bioavailability of 0.3%.

1) In the case of Al adjuvant, “bioavailability” (as defined by ScientistAbe) does not predict toxicity. Injected Al adjuvant does not rapidly enter the bloodstream, but this does not necessarily imply safety. Only the portion that dissolves enters the the blood, but it dissolves very slowly.  Al adjuvant remains in the body for months or years as particles. Transport of the particles to distant organs (e.g. brain, spleen, kidneys etc) occurs over months or years. Also, some transport of the particles occurs via the lymphatic system (not the blood) because macrophages often travel via the lymphatic system. The particles are biologically active and create inflammation. They are not benign or inert.

Al adjuvant produces exposure to two distinct substances: 1) Al3+ ions, dissolved in body fluids, and 2) solid, highly persistent particles of Al compounds. Both are toxic, but in different ways. Both travel around the body, but in different ways. Vaccine promoters and ScientistAbe only consider the Al3+, and ignore the particles. They erroneously and arbitrarily assume that Al adjuvant particles are inert or nontoxic. This is wrong for 3 reasons: 1) Al adjuvant particles induce inflammation, an essential property of an adjuvant, 2) particles can induce biological effects and toxicity via surface chemistry (this is particularly true of high-surface area nanoparticles), and 3) animal experiments with Al adjuvant show toxic effects too severe to be explained by Al3+ alone.


Although the author will cite an article by Flarend and colleagues ( later in his post, it failed to report the bioavailability reported by the same study. By courtesy, we introduce this study in this section to bring clarity. In this study, Flarend et al measured the pharmacokinetics of AH in rabbits, using radioactive aluminum (as radioactive-based analytical methods are the method of choice to quantify metals).   In this study, they injected two rabbits with an intramuscular injection of AH at a concentration of 13.24 mg/mL. In an equivalent dose, each rabbit got “vaccinated” with 0.85mg of AH. According to the FDA guidelines, the amount of AH present in vaccines sold in US have a maximal amount of 1.25mg/dose with a cumulative amount (total amount you will get from vaccines) estimated of 4.22 mg over the infant vaccination schedule (source: [UPDATE] 1) Keep in mind that such amount does not accumulate over time and we have a clearance of aluminum taking place over time. Because an intramuscular injection is not a vascular route, the bioavailability is below 100%. The authors here estimated the amount absorbed over 28 days to be 17%. What does it means? The amount absorbed is the amount that was able to diffuse through the epithelial barrier or from the connective tissue into the bloodstream (systemic circulation).  2) It also means that 82% of the Al is still present at the site of injection (take note, AVers: if it does not absorbed, it is not absorbed). So why is that? 3) Its all about solubility. This is the solubility equation:
Al(OH)3<-> Al3+ + 3OH-
It is an equilibrium equation, in which Al3+ is only soluble at its ionic form. Therefore, you need to deplete the Al3+ to dissolve the AH nanoparticles. At physiological pH, AH is practically insoluble. This drives the bioavailability of Al3+. If we consider the absorbed amount over 28 days, we can deduct that the bioavailability is about 0.6%, slightly higher than its absorption via GI tract.
Thus, AH releases its aluminum at a very slow pace but also at the very long time. This is why we have this biphasic curve after Cmax, with the second slope being more steady and explaining the long half-life of Al.

1) Flarend showed that 94% and 78% of AlOH and AlPO4 adjuvant (respectively) remained in the body after 28 days. Crepeaux 2017 showed that Al adjuvant remained in the brain (of mice) after 6 months). Crepeaux 2017:

2) In Flarend, the Al adjuvant remaining at 28 days was not confined to the injection site. Flarend (and recent studies) show that it travels into the brain and other organs. Both Al3+ and particles move around the body.  The claim that all undissolved Al adjuvant particles remain at the injection has been proven wrong by experiments in animals. ScientistAbe should provided a citation for the claim that all Al adjuvant particles remain at the injection site.

3) ScientistAbe assumes that Al3+ is responsible for all toxicity of Al adjuvant, and is the only thing that matters. This assumption is unstated and wrong. Today it is known that particles/nanoparticles per se have toxic properties. The toxicity of the particles can depend on surprising things, such as shape, surface roughness, surface charge etc.  Citation: “Toxicity of Nanomaterials”

The “Toxicity of Nanomaterials” paper states:

Particle size and surface area are crucial material characteristics from a toxicological point of view, as interactions between nanomaterials and biological organisms typically take place at the surface of the NP. As the particles’ size decreases, the surface area exponentially increases and a greater proportion of the particles’ atoms or molecules will be displayed on the surface rather than within the bulk of the material. Thus, the nanomaterial surface becomes more reactive toward itself or surrounding biological components with decreasing size, and the potential catalytic surface for chemical reactions increases.
“The nature of the interface between nanomaterials and biological systems affects the in vivo biocompatibility and toxicity of NPs.”
Particle shapes and aspect ratios are two additional key factors that determine the toxicity of NPs. Nanomaterials can have very different shapes including fibers, spheres, tubes, rings, and planes.”
Surface charge also plays a role in toxicity, as it influences the adsorption of ions and biomolecules that may change organism or cellular responses toward particles.”
NPs = nanoparticles


At baseline values (before injection), the amount of Al detected in plasma was about 30ng/mL. Upon injection of these four doses simultaneously, AH (black triangles) show a tmax (a time by which the concentration of aluminum peaked) at 10 hours, bringing a Cmax (maximal concentration) of 32ng/mL. In other means, a 6% increase in the amount of aluminum. Thats a bit of extra noise over noise. Not much a dramatic peak that would double up your exposure to aluminum. You don’t face an aluminum storm upon vaccine injection, but more a slight added noise over time. This is not a problem for healthy patients unless those with a kidney condition (we will discuss that later). [END UPDATE].
In the body, the authors estimated that AH mostly accumulated in the kidney, followed by the spleen and liver. This high retention is understandable as these organs are highly perfused with blood and therefore may accumulate more aluminum than other organs. These organs (liver and kidneys) are always monitored when drugs are developed as they can have serious toxic effects. However the amount accumulating is very negligible. The authors report an amount of 0.00001mg/g of tissue after 28 days. Put back into the context, at the time of injection, this tissue concentration may have peaked at 0.000283mg/g. Brain tissue, in contrast, have shown 100 times less accumulation than kidney. After 28 days, 3% of the initial aluminum injected remains in kidney, 1) we can therefore estimate only 0.03% of the initial amount is accumulating in the brain. Aluminum has a long half-life (time to eliminate 50% of a compound from your body), as it is estimated around 100 days.

1) Al adjuvant particles can continue to relocate to the brain and other distant organs long after 28 days. A recent study of Al adjuvant in mice reported that about 1.3% of injected Al adjuvant was found in the brain 6 months after injection, so ScientistAbe’s 0.03% figure is 43X too low.  Citation:


Because it takes some times to eliminate it, we can reasonably raise the question: what about the acute and chronic toxicity? The acute toxicity is defined by the toxicity obtained by a single injection, whereas the chronic toxicity is obtained from a continuous exposure.

An important concept in toxicology has been established in the 17th century by Paracelsus, the father of modern pharmacology and toxicology: “Every substance is poison, no substance is no poison. The dose and only the dose makes the substance the poison”.

It is not always true that only the dose makes a substance a poison. High doses can change transport or absorption, with surprising results. In the case of Al adjuvant, an injection site granuloma (caused by large doses) inhibits transport to distant organs, thereby reducing toxicity to the distant organs. Consequently, a low dose can be more toxic than a high dose. This study demonstrates this effect with Al adjuvant:

Toxicity can be affected by several factors, including: 1) dose, 2) transport mechanisms, 3) nutrient levels in the exposed organism, 4) genetics, and 5) composition of the microbiome. Its complicated!


It is all about how much you get exposed over time and about how long it takes to get it eliminated. A poison with a short half-life can see its toxic effect cleared very fast, whereas a poison that has a long half-live will accumulate if exposed continuously and show its toxicity after weeks if not years. This is often the case observed in poisoning with heavy metals (like lead, silver, mercury, arsenic). An historical example is Napoleon Bonaparte’s death by poisoning during his exile on the island of St. Helena. Because the amount of arsenic ingested was  low and did not alter taste, it did not raise suspicion of poisoning. However because arsenic half-life is high (12 days), it kept building up in the body until it reached a toxic level.

In a review published in 2007 by Krewski and colleagues (, non-occupational exposure to aluminum is mostly driven by food consumption, with a daily intake of 8.6 and 7.2mg/day for males and females respectively. The author of this post claim 0.3% oral bioavailabity in the following statement: “Ingested aluminum has a low absorption (about 0.3%), and when this low absorption is taken into account, there is good reason to expect vaccines to create aluminum toxicity. But that is not the subject of the present commentary. Commentary about the total amount of aluminum in vaccines can be found here:

[UPDATE] For our demonstration, we will rely on the data provided by the review, citing 0.1% of bioavailability. Based on this number, we can estimate males and females are exposed daily to 0.0086 and 0.0072mg/day (or 86 and 72 micrograms/day) (values were corrected for bioavailability). If we use the study from Flarend and colleagues, we should expect to add 0.21mg (or 210 micrograms) of AH per injection. Considering the 6% increase in Cmax  concentration observed in rabbits following injection, we are expecting about an extra 12.6 micrograms of aluminum added to the systemic circulation. Another review by Yokel & McNamara ( provides a more exhaustive comparison and sources for the amount of aluminum exposure summarized in the table below.

Now, we have more information available since I have written the first iteration of this post. We have an estimation of 0.07-0.4 micrograms/kg/day provided by vaccines. We will assume the more conservative number of 0.4 micrograms/kg/day. With the average weight of an infant (median weight at birth ~3.3kgs), we can assume a daily dose from vaccines of about 1.32 micrograms/day or about 237 micrograms over a 6-months period. These are plasma concentrations, therefore a better comparison would be to compare to the administration of aluminum via IV route as well.
As you can see in the chart, the most common medical procedure involving the IV infusion of aluminum is the total parenteral nutrition (TPN), or feeding directly via intravenous diffusion. The daily amount via TPN are much higher, we have values of 11-27micrograms/kg/day or for an infant getting a TPN at birth of about 36.3-89.1 micrograms/day. Therefore, the daily amount of aluminum obtained by vaccines is about 200 times less than the daily amount obtained by TPN route.
Now, this review came out before the FDA roundtable and risk assessment of aluminum in TPN bags. Following recommendation, the FDA consider an IV concentration of aluminum of 4-5micrograms/kg/day as possible neurotoxicity in premature and neonates connected to TPN bags.
Again, we have to compare to same scale. For an newborn, thats about 13.2 micrograms/day. Put the vaccine daily exposure, we are about 10% of this threshold value. Therefore, daily aluminum exposure in a vaccinated newborn infant is 10 times less the amount considered to have a possible neurotoxicity.
We have also to assume that the water and food intake does not apply to an infant and may bias our calculations. According to the Children Hospital of Philadelphia website (, they estimate the total aluminum intake in infants from vaccines during the first 6 months 4.4 miligrams (thats about 4000 micrograms). This have to put into contrast from the 7 milligrams (about 7000 micrograms) from breast milk and 38 milligrams (38’000 milligrams) from formula-fed.  At this point, the author is simply hand waving about the danger of aluminum by ignoring the fundamental concepts of pharmacology, pharmacokinetics and toxicology. Therefore, the question I would like to raise is why the author failed to mention the study of Flarend in this section? It constitutes the right place to discuss about it.

The above analysis is only applicable to Al3+. It ignores the toxicity and kinetics of Al adjuvant particles. The above analysis is similar to the analysis used in the Mitkus 2011 paper, which is debunked here:

However, even the Al3+ released by adjuvant is a safety concern. Al3+ released by Al adjuvant exceeds the safety threshold used in Mitkus 2011 (an FDA study), when the safety threshold is updated by new research. See argument #2 here:
The NOAEL used by Mitkus (26mg/kg/day Al) is too high; New research shows the NOAEL in fact is less than 3.4mg/kg/day.
NOAEL= no observed adverse effects level. This is the highest dosage that produces no observed harm in animals.

The Mitkus 2011 paper is the only citation used by the CDC and FDA to support the alleged safety of Al adjuvant. It is terribly bad research, with several fatal errors and wrong assumptions. The FDA boasts about it here:

Food intake of Al must be multiplied by the absorption rate of 0.3% to determine bioavailability. The ingested amount cannot be compared directly to the dose from vaccines.

Do the math:

Birth (Hep B): 74 mcg/kg (250 mcg for 3.4 kg infant)
2 month: 245 mcg/kg (1225 mcg for 5 kg infant)
4 month: 150 mcg/kg (975 mcg for 6.5 kg infant)
6 month: 153 mcg/kg (1225 mcg for 8 kg infant)

Total: 3675 mcg

Oral absorption of aluminum is 0.3%.

Over the first 6 months, a baby will absorb (these number are from CHOP):

From milk: 7mg x 0.3% = 21 micrograms (0.021 mg)
From formula: 38mg x 0.3% = 114 micrograms (0.114 mg)
From soy formula: 117mg x 0.3% = 351 micrograms (0.351mg)

Vaccine Al dose is 3675/21 = 175 times higher than human milk in the first 6 months.

Of course, this calculation does not distinguish between Al3 and Al adjuvant particles. I am aware that ScientistAbe may argue that the particles can be ignored, and that only Al3+ matters because the comparison is made to ingested Al, which introduces Al3+ only (no particles). This is actually a reasonable argument. However, the calculation illustrates that the total amount of Al from vaccines is very large compared to natural, ingested sources. The large amount of Al in vaccines, compared to ingested sources, supports plausibility of harm.

Now, does aluminum is harmless? Well it is all about the dose and the patients condition. Again, the review by Krewski and colleagues can bring us useful information. Al is excreted primary via kidney route, with about 95% of renal clearance. For a patient with normal kidney function, this is not a problem. For infants that receive injections on a monthly basis, this is not a problem either. The problem arises if you have a patient or a premature that have to be on a constant IV infusion, like patients on TPN bags. There is a risk of aluminum accumulation as the intake amount is much more important than the amount excreted. Such case in patients that display either immature kidneys or signs of renal failure. However, in such cases, such patients will have aluminum-depleted IV bags to avoid such accumulation. [END UPDATE]

  1. Aluminum and neurotoxicity

If there is a concern about aluminum toxicity, it is its possible effect on the central nervous system (we refer to it as aluminum neurotoxicity). A rapid review on Pubmed using “neurotoxicity aluminum” bring us a total number of 387 articles, including 73 reviews. A classical model to assess aluminum neurotoxicity is the model of aluminum chloride (88 articles) in rodents.

AlCl3 is not a vaccine adjuvant. It is highly water-soluble and is only relevant to Al3+ toxicity. Al3+ toxicity accounts for only a part of Al adjuvant toxicity (probably a small part). However, studies of soluble aluminum are relevant if they use dosages that are comparable to Al3+ exposure from adjuvant.


In these models, aluminum chloride (Al(Cl)3) is administered by oral route with concentration varying from 5mg/kg/day (, 50mg/kg/day (, with a maximal values of 200mg/kg/day as reported by Prakash and colleagues ( In all these studies, anatomical changes in the brain as well as motor and cognitive functions were reported. Now, it is important to relativise these amount to a 70kg body. At the minimal concentration of 5mg/kg of Al(Cl)3, the dose-equivalent needed to achieve these neurotoxic effects would be 350mg/kg/day. Thats about more than 43 times the daily dose of aluminum obtained with food intake. Every single day. With a chronic high exposure to aluminum, we would expect to reach such toxic level. However such model is not representative as Al(Cl)3 and AH (Al(OH)3) are distinct chemical entities and therefore do not share same physical and chemical features. But this did not stop the author from making false assumptions.

“Ingested aluminum enters the blood from the gut. In the blood, ingested aluminum is in a water-soluble ionic form, typically Al3+ or an aluminum complex*. This aluminum is separated into individual atoms, like ordinary salt dissolved in water. Ionic aluminum is toxic, but it is blocked from entering the brain by the blood-brain barrier (BBB), and it is rapidly filtered from the blood by the kidneys. Unless large amounts are consumed it does not cause a problem.”

1) A critic I have with his statement is how the author can exclude that Al3+ cannot cross the blood-brain barrier (BBB)? I will talk about the BBB later but I wanted to mention this logical fallacy. We just discussed about the neurotoxic effects of aluminum in the CNS, using Al(Cl)3.
 2) To better understand the difference, we have to compare the solubility of Al(Cl3) and Al(OH)3 (AH). To be soluble, a compound has to interact with water molecules and breakdown its chemical bonds to become an ion. Some can easily break their bonds (example H-Cl breaks into H+ or Cl-), some less (like H-O-H or water). Water is a polar solvent. The oxygen atom attract the electrons of the shared bonds more towards it, it then becomes electronegative. In the other hand, hydrogen discretely loses its electron and becomes slightly electropositive. Ions will mix very well because they counter the charges around. If a compound can ionize, it will dissolve in water. If it cannot ionize (like hydrocarbon chains found in oil and fat, because the carbon atom is not greedy for electrons), then it will not mix with water. That’s why oil and water never mix.

1) This criticism by ScientistAbe is correct. The BBB does allow some Al to enter the brain. Article has been updated to say aluminum entry into the brain is “mostly” blocked by the BBB. Thank you for the correction, ScientistAbe!

2) An analysis based on solubility incorrectly assumes that all toxicity of Al adjuvant is due to Al3+. In other words, the Al adjuvant particles are assumed to be completely inert and nontoxic. This assumption is absolutely wrong. Experiments with Al adjuvant are absolutely required for determining the toxicity of Al adjuvant, because Al3+ and particles are different.


According to Wikipedia, Al(Cl)3 solubility index is 43.9g/100 mL of water and AH is only 0.0001g/100mL. In other words, Al(Cl)3 in solution is under Al3+ and Cl- forms, whereas AH remains in its Al(OH)3 form. 1)How can the author explain the experimental studies that show the neurotoxic effects observed in animals treated with Al(Cl)3 if he claims Al3+ cannot cross the BBB?

In a section of his article, the author cites one study to disagree with it, the study of Movsas  ( published in JAMA Pediatrics.

The Movsas study (published in 2013) used human infants and obtained similar results. Movsas looked for aluminum in urine and blood before and after routine vaccination with 1200mcg aluminum at the 2-month date. No change in urine or blood levels was observed. Movsas states: “No significant change in levels of urinary or serum aluminum were seen after vaccination.“ Of course, these results contradict the claims by vaccine advocates that aluminum adjuvant dissolves and is removed by the kidneys.”

An important criteria when investigating journals is the impact factor. A high impact factor is usually associated with high-quality studies as the peer-review process in such journal has a higher expectation level. In the other hand of the spectrum, we have a new category of “predatory journals” (always based on fee for publications) that will publish studies with a weak or not peer-review process. JAMA Pediatrics impact factor is fairly good (7.13) to consider the study reliable. 2) The authors investigated the levels of aluminum before vaccination, about 11.1+/-10.3 ng/mL. Note the extreme variability of these levels among 15 pre-term babies. The author reported no changes in aluminum after vaccination and estimated to increase the concentration to 1% following the publication by Flarend (see previously). You have to remember Flarend used radioactive Al to measure the kinetics, whereas in this study, we measure aluminum using another analytical technique that may have less sensitivity. It also indicates that the aluminum contained in vaccines injection is not giving higher values than the basal aluminum level, thus you cannot distinguish the aluminum from the vaccine from the aluminum contained in food. 3) But this important point, the author failed to understand.

1) Al3+ does partially cross the BBB. Also Al3+ increases the permeability of the BBB.

2) Though not stated in the Movsas paper, the subjects almost certainly served as their own controls (i.e. before and after Al levels were compared per individual). Individual “self-controls” renders the large SD almost completely irrelevant for detecting a change in Al blood levels.

3) This statement is an irrelevant and ad hominem attack. The point about radioactive vs other measurement methods is not relevant to my article and I am aware of the issue. There is nothing in my article that suggests ignorance of this issue. This is a dishonest insult, not a reasoned, evidence-based argument.


Indeed, there is another study that tried to reproduce a model of vaccines injection using mice that the author surprisingly failed to cite in his report: the study of Shaw CA and Tomljenovic L published in 2013 in Journal of Inorganic Chemistry ( In this study the authors tried to develop a mouse model of newborn vaccine schedule and see the effect of such repetitive doses would impact on the neurological function.

However, the experimental design is inconsistent and raises question about the validity of the data. The author never explain why they change the experimental paradigm in the low AI group. A common sense in science is when you want to show a biological effect you change one parameter at the time. For instance, the dosing schedule should stay the same, only the dose be different (as presented 50% of the normal dose) and have the control (injection with saline solution only).  A poorly designed experimental setup can only to poor results and poor interpretations.

Based on this experimental setup, the authors observed an increase in weight in mice following the normal (or in this case, high) Al injections. No weight changes were observed in low AI or the control. 1) Because of the flaw in the experimental design, we cannot tell if this effect is due to stress (remember the mice received more frequent injections than the other groups) or due to the treatment. Because of the poor experimental design, this result is worthless and resulted in an unfair use of animals to get this data. Now things become very interesting, the authors use behavioral tests for all the experiments and determined that high Al showed a decrease in the number of successful tasks. There is also a sexual dimorphism as males showed statistical differences but not females. Again, there is the experimental flaw that do not let us know if it stress related or if it is due to aluminum.  In a behavioral test, you are observing your animal and try to count how many times your animal displays a movement of interest. For instance, in neurosciences, we can put a mouse into a Y-shaped maze and put a bit of cheese in one branch of the maze. Each day, you put the mouse in the bottom of the Y-maze and let the mouse find the right branch (the one containing the cheese). After 10 seconds, you will take out the mouse and score if it succeeded (1) or not (0). After scoring, you will put the mouse again in the maze and score again the mouse for 9 times, this everyday. After a few days, the mouse will remember where is the cheese and will achieve a perfect score. If the mouse has some memory problems, it will perform poorly and will maintain a low score. Now the problem is if the mouse is stuck between the two branches, do you count that as a success or a failure? That’s the problem of subjectivity. I may consider it as a success because the mouse faced the right branch, another experimenter may consider it a success only if the mouse reaches and touches the cheese.

1) The difference in timing between Al-exposed and control mice is a flaw in the study design, and it is unexplained. However, the minor differences in timing for the controls is not a reasonable explanation for the large effects observed. Also, there was a dose-response (larger Al dose produced larger effects), which is not attributable to the timing differences in the saline control injections. If the results were due to the saline control, and the Al adjuvant had no effect, then there would be no difference between the high and low dosage groups. Saying the results are “worthless” is hyperbolic and unreasonable, and not consistent with the observed dose-response.


There is also some concerns about the authors’ affiliations. Both researchers were faculty members from the University of British Columbia, Vancouver, BC (Canada) (Dept. of Ophthalmology and Visual Sciences), (Program in Experimental Medicine; Program in Neuroscience) until 2013. 1) Surprisingly one of the authors address displayed an unusual email for an academic researcher in a public institution ( but furthermore later publications saw a change in the affiliation (Neural Dynamics Research Group, 828 W. 10th Ave, Vancouver, BC, V5Z 1L8, Canada). 2) Firstly, I would question how a faculty researcher appointed in a department in which the mission is related to eye research has the expertise to study vaccines and toxicology.

Here is the website of Neural Dynamics and surprise, we find the same authors. What is interesting, is this page has been outdated for a while and it seems funding occurred for up to 2007. Are these authors still funded? Things become more and more murky when you see the name of Stephanie Seneff (a computer scientist at the MIT that claim autism is caused… glyphosate….in a journal called “Entropy”) as a co-author in one the publications (……in a predatory journal! Yes, that’s what I call entropic, sorry messy publication records. Orac from “Respectful Insolence” raised a red flag on this study published earlier on and it is worth a read ( How reliable is a peer-review from a journal aiming to publish inorganic chemistry, in assessing the validity of scientific claims that are aimed for experts in vaccines and neurotoxicology? As reliable to publish my work on the blood-brain barrier in a journal that studies plankton biology.

[UPDATE] The lab of Shaw and colleagues came again in the spotlight recently for a retracted study on the effect of HPV vaccine on behavioral issues in mice, as mentioned by Retraction Watch (source: The editor-in-chief of the journal (Vaccine) did not comment about the cause of the temporary retraction. 3) It is also worth noting that the WHO called this study on aluminum adjuvants “seriously flawed”. The full report on the WHO related to the study on the effect of aluminum adjuvant can be found here:


1) These arguments are absurd ad hominem attacks and innuendo. A gmail account indicates a problem? How does that work, exactly?

2) You have Dr Shaws email address. Rather than “questioning” or speculating, why dont you ask about his affilitation with opthamology? Dr Shaw is a neuroscientist by training. The eye is highly innervated, with dense networks of neurons so neuroscience is applicable to opthamology.

3) The WHO criticisms are baseless and not explained in enough detail to rebut. The WHO page is correct in stating “…ecological studies cannot be used to assert a causal association because they do not link exposure to outcome in individuals, and only make correlations of exposure and outcomes on population averages. Therefore their value is primarily for hypothesis generation”. Which is how the ecological study was used. Dr Shaw agrees with the inherent limits of ecological studies.

None of the papers criticized above are cited at So while some criticisms are valid (e.g. concerning the retracted paper, which did have errors), they are not directly relevant to content.


  1. Aluminum nanoparticles and macrophages

Later in the post, the author discussed about how aluminum nanoparticles (AANs) can enter into macrophages as citing the following: “This model is wrong because what actually happens is that a type of white blood cell called a macrophage (MF) engulfs or “eats” (process is called “phagocytosis”) the AANs before they can dissolve. Eating foreign material is normal behavior for MFs. When MFs detect bacteria or other pathogens, the MFs engulf the pathogens, and digest them with enzymes. They then tell other immune system cells about the pathogen and how to detect it. The problem with AANs is that they are not digested by the MF enzymes. And the AANs, once inside the MF, dissolve much more slowly. The AANs persist for a long time and cause the MFs to slowly leak aluminum. MFs that consume the AANs become highly contaminated with aluminum, and spread this aluminum around wherever they go.”

Again, 1) the author never identifies the nature of these AANs, bringing confusion to the reader. Because the author focuses on the vaccines, we speculate that he is referring to Al(OH)3 particles (AH). The author continues his explanation on why macrophages are the main cause of “MFs that consume the AANs become highly contaminated with aluminum, and spread this aluminum around wherever they go. And they go everywhere in the body.”  Now the author claims these AH enter macrophages (MF), then these macrophages enter the brain and deliver aluminum across the BBB. 2) Interestingly, after a search on Pubmed using the query “aluminum hydroxide AND macrophage”, I failed to find any relevant literature that demonstrated the inclusion of AH inside MF. Therefore the quote “Several studies show, with certainty, that MFs engulf AANs. In several studies, the AANs have been stained and photographed inside the MFs, and identified using several different methods. This is not surprising because it is well known that MFs will engulf nanoparticles just from being grown in a solution containing nanoparticles. The composition of the nanoparticles does not seem to matter“. 3) This statement is not only exaggerated (the authors failed to provide citations to support that claim) but also provocative and fraudulent. In biological sciences, we rarely use a bold statement such as “certainty”, only when you have millions of individual records.

Only pseudoscientists would take a single study as the absolute truth.

1) Nanoparticles are typically defined as having at least one dimension smaller than 100nm. This study of AlOH adjuvant shows that the primary particles are smaller than 100nm:

2) A single set of terms never provides a complete search. A good search requires using multiple terms and term combinations.

3) This criticism is reasonable. I should not have relied on a single citation for this claim. Supporting citations have been added to the “Adjuvant travels into the brain” article.

Studies show that macrophages phagocytose Al adjuvants:

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 uses the generic term “endocytosis”, which refers to many methods cells have for “eating” extracellular substances. Phagocytosis is a particular 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 vitro.
QUOTE: “...these data support a model of active endocytosis of alum by viable macrophages…


The only study that can bring some information is the study cited by the author of this post ( using THP-1 cells.  What are THP-1 cells? THP-1 cells are monocytes derived from a patient that suffered from an acute monocytic leukemia. As any other cell line isolated from patients, these cells are readily available through cell collections such as ATCC ( Technically, there are monocytes and not macrophages (see the schematics in chapter 1). Macrophages are derived from monocytes but in terms of biological identify these cells have distincts identity. It is like claiming my daughter is like my spouse. My daughter shares 50% of her DNA with my spouse and have the other 50% of mine, but she is different and unique. That simple concept appears not obvious for the author as at the end of his post cited: Monocytes and macrophages are basically the same thing.”. Such statement is simply wrong and raises some skepticism on the rationale the author will use this study to establish his claims.

Furthermore, we have to remember that THP-1 cells are by essence a cancer cell line, they came from a patient suffering from a certain form of leukemia. Cancer cells are known to have a complete different biology than normal cells, because they are cancer cells. This is where we can start to discuss and question the validity of the authors claim: why did he not cited a study using macrophages isolated from healthy patients. The problem is there is no study that have investigated the uptake of AH by normal macrophages and we can reasonably speculate that THP-1 may have an abnormal uptake activity, resulting in an abnormal accumulation of AH.

These criticisms are reasonable.  It is reasonable to speculate that THP-1 cells may have a different response to Al adjuvant than true macrophages, even though observations do not suggest differences  (i.e. the Al adjuvant goes intracellular in THP-1 cells and in macrophages).

Also, ScientistAbe is correct in that monocytes and macrophages are not identical. Monocytes are precursors to some types macrophages. In some literature the terms are used almost interchangeably. This is increasingly discouraged because monocytes and macrophages are different in some contexts.

Useful review paper on monocytes and macrophages:


[Section on MMF omitted for brevity]

If you inject a vaccine, you will expect an immune reaction to take place (that’s the goal of a vaccine). This translates into an inflammation stage that everyone experience few hours after injection: hot, red, swollen and painful. Inflammation also recruits a lot of macrophages (thus you would expect to see them under the microscope in your tissue samples) and you also expect  to see an important amount of aluminum in the site of injection, an amount that will take time to disappear (remember the half-life of aluminum? 100 days, it takes some time to get rid of it).  There is no biopsy samples from patients that have shown no side effects.

The half-life of Al adjuvant is not 100 days, but much longer (at least for AlOH, the most commonly used Al adjuvant). It has been observed to remain in humans years after vaccination. Apparently, ScientistAbe has again confused Al3+ and Al adjuvant. Citation is needed for the 100-day half life for AlOH. Perhaps the 100 day half life (for AlPO4 only) was derived from Flarend et al?


Most patients are identified in France. So there may be a rare autoimmune disease, that has a genetic background and that may be triggered by vaccines adjuvants following vaccinations. Because this condition appears only after vaccination, we may be tempted to claim vaccines caused this autoimmune disease. This conclusion is wrong as correlation is not causation. If adjuvant was causing autoimmune diseases,  we should see the same condition occurring in patients not carrying the genetic mutation, with a number of cases high enough to raise some epidemiological alert. Again remember, 600 cases in France, a country that count 60 millions inhabitants.

In conclusion, although the authors theory of macrophages loaded with aluminum nanoparticles may have some scientific basis, it still remains unclear as we have almost no studies to support its claim and have a rare disease that is only documented to one country (France) and mostly by one single group (Gerhardi group). To make a claim valid, you need a high number of studies (20 and more) coming from independent laboratories and described into different parts of the world. Therefore the macrophage-loaded theory raises some skepticism and clearly contradicts the claim of “certainty” posed by the author.

  1. Aluminum, macrophages and the blood-brain barrier

The author claims the blood-brain barrier protects the entrance of ionized aluminum (Al3+) but completely ignored the studies showing the toxic effects using Al(Cl)3. Indeed, the author come with one esoteric theory to explain the claims: “And they go everywhere in the body. The MFs are able to travel across the blood brain barrier (BBB). The MFs, once loaded with AANs, act like a Trojan Horse and carry the AANs into the brain. This is very harmful, because the brain is very sensitive to aluminum.” Before we can talk about this theory, we have first to understand the blood-brain barrier (BBB) and how aluminum may cross the BBB.

The BBB is a blood-brain interface separating the blood flow from the brain tissue (source: As other blood vessels, brain blood vessels are lined by endothelial cells separating the blood flow from the brain tissue. These endothelial cells (that we usually call brain endothelial cells) are unique: they are very tight, much tighter than other vessels. Such tightness is ensured by the presence of tight junctions between endothelial cells, that block exchange of molecules as small as water and ions between the blood and the brain. These tight junctions provide a “physical barrier”. In addition to such barrier, the BBB has another type of barrier: a “chemical barrier” .

As we mentioned, if you are a small water-soluble compound (a, like sucrose (table sugar) or water), your entrance into the brain is very limited. Now if you are a chemical compound that dissolves in oil (b, lipophilic), then you can diffuse across the BBB because cells have membranes made of fat (think about biological oil droplets). However, many of the compounds are still pumped out the brain because of presence of efflux pumps. These pumps block the diffusion of toxins and also drugs (such as cyclosporin A or AZT). Indeed, these pumps are responsible in the blockade of 95% of known chemicals, either natural or synthetic. This is one of the reasons why we fail to have effective treatments for brain cancer, because our current chemotherapy drugs are blocked by the BBB and we don’t have techniques to open this barrier.

If you have a bigger cargo to deliver (like protein), it is almost impossible to deliver it across unless you have a dedicated receptor (key lock) and you have the right key to unlock it (d, receptor-mediated transcytosis). We only know a few of them, among them are insulin (insulin receptor), transferrin (transferrin receptor) and low-density lipoprotein (LDL, LDL receptor). There is an important discussion about when the BBB appears during fetal development and when do we have a mature BBB that has the function of an adult. Up to ten years ago, we believed the BBB was immature in newborns based on studies using rat and mouse pups. However, with the recent development in modern biology techniques, it seems that indeed humans have a functional BBB that maybe are as mature as adults after full term pregnancy. This was firstly supported by Saunders and colleagues that demonstrated that BBB from the opossum, a small marsupial from the same family than kangaroos and koalas, have a tight barrier ( This observation was also observed on rat pups following stroke injury. During stroke, the BBB opens and lets water and ions enter inside the brain and causes brain damage by brain swelling. If the newborn BBB was more fragile than the adult one, the damage would be more devastating. Indeed it seems not and maybe the opposite. In a recent study, Vexler and colleagues demonstrated that rat pups better dealt with stroke injury than adult rats and showed lesser brain swelling (

Thus, the concept of the newborn BBB being more sensitive to vaccines than adults’ BBB maybe completely wrong. 2) If vaccines induced BBB disruption, we should have epidemiological data showing an increase in severe neurological disorders including cerebral palsy or epilepsies. As we mentioned in the previous section, aluminum is known to show neurotoxicity, based on the Al(Cl)3 model. In this model, we speculate that Al3+ is in free form. Al3+ can bind to transferrin (a protein that normally delivers iron to the brain), thus using the transferrin receptor as an entrance mechanism ( Indeed, there is little or no studies that investigated if Al(OH)3 can enter the BBB. One possible mechanism is that aluminum may disrupt the BBB, which in turn induce a BBB leakage and brain damage. 3) The only study found is from Wiesnieski and colleagues ( that investigated the effect of Al(Cl)3 and Al(OH)3 on rat BBB using radioactive sucrose to follow changes in the barrier tightness. The authors noted an increase in BBB leakage 2 and 4 hours after administration but did not show any differences after 24 hours. More interestingly, Al(Cl)3 triggered such leakage whereas Al(OH)3 showed no difference on the BBB. This study therefore refutes the idea that AH cross the BBB and/or induces BBB breakdown.

1) The discussion about adult vs immature BBB is a  straw man argument because I do not rely on the idea that the immature BBB is more permeable. That may be true, but its not an argument that I make, or that is necessary to demonstrate that vaccines cause brain injury. I intentionally do not make the “immature BBB” argument for strategic reasons (for example, its hard to prove from the science we have presently, and we dont have any data on this for Al adjuvant specifically). But maybe there are important citations I need to see? Contact me if you have relevant citations, please.

2) ScientistAbe wrongly assumes that “…we should have epidemiological data…”. Well, then ScientistAbe should find it and cite it. It is wrong to make an argument based on data “we should have.”  The data ScientistAbe assumes is available, is not. Al adjuvant has never been studied in relation to neurological disorders or mental illnesses. Of course, its tough to prove a negative (i.e. non-existence of such studies), so contact me if you (including ScientistAbe!) have citations on this.

3) The main citation ( was a study that lasted 24 hours.  It takes much longer than that for AlOH adjuvant to travel around the body. Also it is not claimed that Al adjuvant “induced BBB breakdown”; thats a straw man. Rather, the claim is that Al adjuvant causes inflammation in the brain when it is transported there by macrophages.

However, the author believes in the AH-loaded macrophages theory and made the following claim: “The MFs are able to travel across the blood brain barrier (BBB). The MFs, once loaded with AANs, act like a Trojan Horse and carry the AANs into the brain. This is very harmful, because the brain is very sensitive to aluminum.”
This claim is fairly outrageous for the BBB expert that I am, for different reasons. Firstly, the author simply ignores the notion of “immune privilege” organ such as the brain (for review: In the difference of other organs, the brain has no immune cells residing inside healthy patients. Only one type of cells, microglial cells (derived from monocytes), is the only immune cell residing inside the brain. Immune cells (including lymphocytes and macrophages) cannot enter the brain because they don’t have the right keys to open the BBB.  Immune cells only cross the BBB following certain neurological disorders such as stroke or multiple sclerosis. In such diseases, brain endothelial cells undergo a phenomenon called “endothelial cell activation”, resulting in the expression of cell adhesion molecules (for review:

The brain is not “immune-privileged” in the sense of blocking entry of immune cells. Macrophages enter the brain in response to inflammation. Inflammation is not a state of health. Inflammation anywhere in the body (in the brain or periphery) can cause macrophages to enter the brain.  ScientistAbe makes a straw man argument by considering only healthy people. I do not argue that macrophages enter the brain in a normal state of health. They enter the brain when there is inflammation occurring.

Six citations (in rebuttal below) prove that macrophages can enter the brain in response to inflammation. Further, these citations prove that macrophages can carry substances (e.g., drugs, nanoparticles) into the brain.

Following this activation, now immune cells (also known as leukocytes), have anchor points to anchor at the surface of the BBB as displayed in the schematics below. Leukocytes get anchored, undergo a complicated tango dance with the activated endothelial cells, squeeze through the endothelial cells (by diapedesis) and finally enters inside the brain. Because the brain is an “immune-privileged system”, these immune cells identify antigens present in the brain as foreign agents and triggers an neuroinflammation. A poster child of such neuroinflammation is multiple sclerosis. Therefore macrophages can only enter the brain, if you have have an activation of the BBB that will allow these cells to bind to the endothelial cell surface.

To support the claim that Al-loaded MFs are causing a neuroinflammation, the author goes again with another study from Gherardi again (remember the previous article missing the proper controls?). This time, he uses another study looking at the effect of fluorescent latex beads surface-coated with AH and published in BMC Medicine (IF~7) ( [this is the Khan paper]. Before we further investigate this paper, it is important to note that BMC has been recently caught in a massive fraud scale involving fake peer-reviews and the subsequent retraction of 43 papers (

This argument is a straw man. I did not cite the Khan/Gherardi 2013  paper for the purpose of demonstrating brain inflammation. The Khan study did not measure brain inflammation. Rather, I cited Khan because it shows that Al adjuvant travels into the brain. The Khan paper proved that the transport is dependent on MCP-1/CCL2, which means macrophages do the transporting.

The Khan paper was not cited for its experiments with flourescent beads (which was just one small part of the paper). I cited it for the experiments with Al adjuvant.

The author used the following image figure to claim the presence of aluminum inside the brain section. What appears disturbing is the inconsistency of the panel presented. On panel a, the author show a muscle biopsy tissue sample using hematoxylin-eosin staining, a common mixture of chemical dyes to observe tissue samples under a light microscope. Then for the spleen and the brain, the author show fluorescence tissue sections. Why did the authors switch from technique to another? Then we have the pseudo-colored pictures showing aluminum deposition. For the injected muscle, we can see some accumulation of aluminum consistent with the macrophages (deep purple) staining. But we cannot associate the aluminum deposition with the tissue sections of spleen and brain. Therefore nothing proves to me that the aluminum deposition observed in the spleen and brain are consistent with the presence of macrophages in that region. Also the aluminum analysis fails to show a proper scale bar. I cannot tell if panel b, c and d used the same magnification. For a manuscript of such caliber, it is unacceptable. Finally, the bar graph on the bottom right is not annotated properly. What tissue are we measuring aluminum levels over time? Muscle? Spleen? Brain?

This is the figure annotation: “Aluminum deposits in tissues following injection of alum-containing vaccine in the TA muscle. a) Granuloma composed of PAS+ cells is formed in the injected muscle envelope; b) PIXE mapping shows muscle Al deposits in pseudocolors, with confirmatory Al emission spectrum (d21); c) Section of spleen tissue (left panel) displays the large 500 × 500 μm and restricted 100 × 100 μm protonized fields corresponding to the PIXE maps (middle and right panel, respectively) enclosing eligible Al spots (d21); d) Section of brain tissue (left left panel) displays the restricted 100 × 100 μm protonized field corresponding to the PIXE map (middle panel) enclosing eligible Al spot (d21); the number of fields containing one or more Al spots was increased at all tested time points compared to unvaccinated (right panel) mice. (bars: 100 μm). d, day; PIXE, particle induced X-ray emission, TA tibialis anterior.

We have been just at figure 1 and we have already the same botched and neglected experimental paradigm that not only make the results inconclusive but also a complete waste of animals for the experiment. A complete opposition to the author’s claim as “In an impressive study in mice, AANs and other nanoparticles (e.g. latex) were injected intramuscularly into mice”. It is not impressive; it is a deeply flawed study that anyone holding a Ph.D. degree would be outraged to read. An important point to note: I never found information on how many mice have been used for the study. The minimum required to perform statistical analysis in animal models is 8 mice per group or treatment. Therefore, I call this study as “n=1” or a single mouse study. A single individual study has no scientific value unless it is a clinical case report (however, a case report remains the lowest level in the pyramid of scientific evidence).

In the next part of this study, things become even murkier. The authors now use fluorescent latex beads (FLB) to model alum agglomerates. This is something very important. Latex and AH are completely two different chemicals. Latex is a natural polymer made of number of cis-isoprene repeats ( It is basically a series of repeat of a molecule made of carbon and hydrogens atoms. These are two distinct structures and FLB cannot model AH. Furthermore, why did the authors not inject AH-loaded macrophages? even AH-loaded THP-1? So instead of investigating AH accumulation in the brain, we are now having a paper that investigates the accumulation of latex particles inside the brain. Latex is a natural product that is biodegradable. Such degradation is ensured by micro-organisms ( Animals do not have the enzymatic toolkit to degrade latex. Latex beads will accumulate in our body. The information in Figure 2 is basically telling us we are accumulating latex beads in the site of injection and because latex is not synthesized by our cells, it is recognized as a foreign agent and macrophages will try to clear these beads from the injection sites by swallowing them.

we are accumulating latex beads in the site of injection and because latex is not synthesized by our cells, it is recognized as a foreign agent and macrophages will try to clear these beads from the injection sites by swallowing them.

In Figure 3, we are seeing the accumulation of FLB inside the brain. 1) This is a natural consequence of injecting a substance that cannot be degraded. Because of the systemic circulation, these beads will reach the circulation from the site of injection and being spread in all areas perfused by the circulatory system. At the BBB, you will expect some non-specific uptake occurring. It is called pinocytosis, as endothelial cells will form some small sacks trapping liquid from the blood side and deliver this content to the other side. This event is rare but that happens. We can also speculate that because these animals are undergoing an important inflammation, such inflammation may be sufficient to activate brain endothelial cells and to allow FLB-loaded macrophages to enter the brain parenchyma.

Now, the onset of inflammatory response at the site of injection maybe what drives the opening at the BBB. If you look at figure 6, the intravenous injection of FLB did not trigger the infiltration of the BBB, simply because you need to have macrophages to swallow these beads in order to trigger an inflammatory signal. Macrophages are rarely circulating and mostly located in tissues. Following inflammation, macrophages will migrate to the inflammatory site. Thus explaining the absence of FLB infiltration inside the brain once injected by intravenous route. Now if you have a compromised BBB (like in mdx mice), you can see an important increase of FLB detected in brain sections from mdx mice.

2) To conclude, this story fails to directly demonstrate that AH triggers an inflammation in healthy mice, the authors using a complete different material (latex) to make a scientific claim that has no scientific values. You cannot claim that if I observe an allergic reaction following the ingestion of apples, it can be reproduced by ingesting oranges instead. I cannot show data using oranges and claim that these results reflect what happens when you have apples

1) Al adjuvant particles cannot be degraded (or are very slowly degraded). So, this comment  reveals 1) he is not aware that Al adjuvant comprises persistent, non-or-slowly degradable particles, and 2) ScientistAbe agrees that persistent particles should be expected to travel into the brain.
2) This is another straw man argument . The Khan paper was not used to make the link to inflammation. The Khan study did not measure inflammation.

Rather, the three papers below are used to link Al adjuvant to brain inflammation. These papers show brain inflammation from Al adjuvant (Or Hep B vaccine, which contains Al adjuvant), at vaccine dosages. Specifically, these papers show Al adjuvant cause microglial activation (# 1-2) and that Hep B vaccine causes elevated IL-6 expression in the brain (#3).

#2 (See Fig 1E)


In addition to this study, the author also cited a study that used gold silica-loaded macrophages to target brain metastasis originated from metastatic breast cancer using a study from Clare and colleagues and published in Cancer Nanotechnologies (no impact factor as it is an open-access journal) ( The authors showed they can load gold-silica nanoparticles inside macrophages directly obtained from whole blood samples of their institution Blood Center. Silica is a different entity than aluminum. It is formed by silicium (Si) that can ionize into Si2+. Like AH, silicium can bind hydroxyde and form Si(OH)2 that can crystallize and form particles. Why didn’t Gherardi and colleagues perform the same approach?

Again, this is a form of cherry-picking data, because the author tries to make the analogy between AH (Al(OH)3) and silica (Si(OH)2) – remember that these are completely two different chemical entities. Second Gherardi paper, second poor experimental designed study, second misleading conclusion. Not only did the author just drank the “Kool-Aid” without questioning it, he is also clueless on whether the Kool-Aid was genuine or tainted.

  1. Aluminum, autism and inflammation

Until now, we have been able to breakdown and debunk one piece at the time all these studies and showed that either their data were cherry-picked by the author to support its claim or the papers are of questionable quality that let us wonder how such papers went through the peer-review process without rejection. In the last piece, the author uses a study from Vargas and colleagues ( published in Annals of Neurology, a journal with a good impact factor (IF=9.97).

It is important to note, this study is not investigating if aluminum or vaccines are causing autism. It is investigating what anatomical and biological changes can be observed between autistic brains and healthy brains. The authors used brain tissue samples from 11 autistic patients characterized by an IQ less than 70. Normal IQ score ranges from 90 to 110, so we can consider these patients as borderline. They have intelligence below average but not showing severe mental retardation. There is also an association of with epileptic seizure, with ~30% of autistic patients were epilepsy-positive. This study is legitimate and fairly well designed. We have proper controls and autistic patients. Interestingly, there is an increase in GFAP (activated astrocytes) astrocytes  and HLA-DR (a cellular marker expressed in antigen-presenting cells such as macrophages, dendritic cells or B-cells) in brain samples from autistic patients. This suggests the presence of brain inflammation in these patients compared to controls. The authors further investigated and measured changes in cytokines extracted from brain tissue homogenates and cerebrospinal fluid (CSF). The brain homogenates will tell us if cells produce (and maybe releases) these cytokines, whereas the CSF (a fluid in which our brain is soaked) will tell us if these cytokines are freely circulating. Cytokine measurements were done by antibody array using cell extract and patients CSF. It measures the cytokines by trapping them on a surface and then are detected by chemical reaction resulting in the formation of a dark spot. The darker and bigger the spot is, higher is the amount of cytokine. This method has the advantage to provide some information, although a more absolute method for quantification would have been a 2-D gel electrophoresis that directly identify these cytokines by their chemical structure and count the exact amount present.

You get interesting information from this table that compares the levels of various cytokines detected in the CSF from autistic versus controls.

We can clearly see very high levels of cytokines known to promote inflammation (such as IFN-gamma, MCP-1) but there are also other cytokines known to promote BBB leakage (VEGF) and other cytokines with a biological function that remains unclear (TGF-beta2, FGF-9). This is some serious study that is supported by another research group, as published by Croen and colleagues (

These studies tell us that there is an inflammatory component in a certain form of autism, with experimental data that are robust and reliable. 1) Yet, these studies is not telling us autism is caused by inflammation or if autism causes brain inflammation. Furthermore, this study do not tell us if AH causes autism or if vaccines causes autism. However, by citing such articles at the end of this tortuous and fallacious pseudo demonstration, 2) the authors want us to follow in the following fallacy: “Vaccines contains aluminum. Aluminum induces inflammation and get swallowed by macrophages. Macrophages causes brain inflammation. Inflammation is causing autism. Therefore vaccines causes autism”. You can see that such construction is invalid, flawed and completely irrational. Correlation IS NOT causation.

1) Scientist Abe makes another straw man argument here .Observational studies of humans (such as Pardo 2005) can never establish causation. I do not cite observational human studies as evidence of causation. That’s what animal experiments are for. There are hundreds of animal experiments (including monkey studies) proving beyond reasonable doubt that early-life immune activation causes autism, neurological disorders, and mental illnesses (seizure disorders, schizophrenia etc). For example, IL-6 (and IL-17) cause autism and IL-6+IL-1B in combination cause seizure disorders. Autism causation by immune activation and cytokines is well established by the animal models.

The immune activation animal models are widely accepted as valid models of human autism and mental illnesses generally. They satisfy all the criteria required of an animal model. An autism researcher at UC Davis recently wrote:

These MIA (maternal immune activation) animal models meet all of the criteria required for validity for a disease model: They mimic a known disease-related risk factor (construct validity), they exhibit a wide range of disease-related symptoms (face validity), and they can be used to predict the efficacy of treatments (predictive validity).
–Dr Kimberley McAllister, UC Davis MIND Institute, Science, August 2016 (i.e. this paper: )

2) Thats not my causal chain, so this argument is a straw man. For example, macrophages do not cause brain inflammation; the Al adjuvant does that. Macrophages are attracted to the inflammation.  The causal chain I assert is:

1) Al adjuvant injection and phagocytosis by macrophages, then
2) Macrophages transport Al adjuvant to the brain, then
3) Al adjuvant induces chronic brain inflammation, stimulating IL-6 in the brain, then
4) The IL-6 (and downstream signals like IL-17) cause autism.

Also, causation is proven by controlled animal experiments with immune activation and aluminum adjuvant. These experiments prove 1) that brain inflammation during early development causes autism (and epilepsy, mental illnesses etc), and 2) that Al adjuvant travels into the brain and causes brain inflammation. Critically, aluminum causes the specific type of inflammation (IL-6) that causes autism. Causality (IL-6 >> autism, and Al >> IL-6) is proven by animal experiments.

The purpose of animal experiments is to establish causality, because 1) it is illegal to conduct tests of injury causality on humans (such research is unethical!), and 2) observational studies in humans cannot establish causality. 


[ADDED SECTION] 7. Aluminum, the blood-brain barrier and neurotoxicity

As I have mentioned, 1) the claim that macrophages loaded with aluminum leave the injection site and migrate to the brain via the lymphatic system and enter the brain via the BBB is unfounded and not back by science. Does it mean that aluminum does not cross the BBB?
The answer is no, aluminum can cross the BBB and therefore exert a neurotoxicity. This is why the presence of aluminum from external sources such as TPN bags can be problematic for patients that have either immature kidneys (premature newborns) or present some kidney malfunction (kidney failure, patients needing dialysis).
If I have to cite an expert in aluminum and neurotoxicity, the name of Pr. Robert Yokel (University of Kentucky) comes in mind ( He has an impressive track-record in terms of peer-reviewed articles (145 publications) and other documentations. You can find his studies in Pubmed (
Aluminum can enter the BBB via various mechanisms. 2) Because aluminum is an ion, it cannot diffuse through the BBB per se, it requires the use of carriers to piggyback on. According to a study by Yokel and colleagues, the monocarboxylate transporter 1 (MCT1) might be one of these carrier (
Another study speculate the possible use of zinc-transporter (ZnT) as Song and colleagues ( described a protective effect of zinc on aluminum-induced disruption of the BBB following co-administration with zinc. We can speculate a possible competition between Zn and Al for the uptake at the BBB or we can speculate a competition for the site of action. Keep in mind that such study noted a disruption of the BBB following intraperitoneal (IP route, considered similar to IV route in terms of pharmakonetics) injection that were 5 and 10mg/kg, a value 1000x and 2000x higher than the value considered by the FDA to display neurotoxic effects (5microg/kg/day).
Another name that comes in the aluminum and neurotoxicity is the name of Chris Exley from Keele University (Staffordshire, UK, you can see his profile here:  He has a legitimate expertise in alumium research in chemistry, but his positions and claims on aluminum neurotoxicity are not very accurate (the link between Al and Alzheimer’s Disease is mostly based on a case report from occupational exposure:, fallacious (calling on the risk of aluminum as adjuvants in vaccines without providing direct evidence for the claims:, if not simply borderline conspiracy theory (
One of the most fascinating yet skeptical claim is the ability of silicon-rich water to “clear out the brain from aluminum”, according to his clinical trial  published in 2013 ( and promoted by “woo” website and UK tabloid (in his case, The Daily Mail) as here (, citing brands like Fiji water and Volvic (French mineral water)
I don’t know what he calls “silicon-rich water” (in other words, silicium dioxide (SiO2) the same chemical that make sand and your electronic chips) but I am highly skeptical how this highly polarized molecule can cross the GI barrier and the BBB, trap the Al inside the brain and clear it out.
To refute his claim, I would use the data from a study by Che and colleagues that looked at the effect of chronic exposure (13-weeks) to various dioxide via oral administration in rats (;jsessionid=57E87335BDC127B06DAB5E9DAE7BF815.f04t01).
One figure worth a thousand words, the one about brain distribution of SiO2 in the brain of males and females.

Note the dose given (mg/kg) and the dose measured in the brain (ug/g). Even by literary eating silicon (245mg/kg/day), only a bare fraction make it inside the brain (0.28% to be precise). But foremost, even at the highest amount (almost 1g/L), there is no difference between the background noise (see the control values). I would be curious how does the silicon contained in Fiji water (95mg/L) and Volvic (32mg/L) will show higher SiO2 levels when concentration 2 to 7 fold higher cannot do better than background noise. Should we assume Exley is profiteering from Big Mineral Water?

1) ScienceAbe is absolutely wrong here. Overwhelming evidence shows 1) that Al adjuvant is eaten or taken up (phagocytosed) by macrophages, and 2) that macrophages travel into the brain in response to inflammation. ScienceAbe is either ignorant of the scientific research on these topics, or does not understand it. This is surprising in view of his claim to be a “BBB Scientist”.

Evidence that macrophages phagocytose/uptake Al adjuvant is cited above.

Evidence that macrophages enter the brain in response to inflammation (i.e. MCP-1 specifically), and can transport nanoparticles or other substances includes:

Khan et al., 2012:  Slow CCL2-dependent translocation of biopersistent particles from muscle to brain

Pardo et al., 2005:   which states the following about MCP-1 in autism:
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…

Mello et al, 2009:
QUOTE: “In conclusion, we have observed that in the setting of peripheral organ-centered inflammation there is a directed recruitment of activated monocytes into the central nervous system, which occurs as a result of an initial activation of cerebral microglia to produce MCP-1/ CCL2.” (Mello et al use “monocyte” in the broad sense, encompassing macrophages). An important aspect of this paper is that it shows that inflammation outside the nervous system is sufficient to induce monocyte movement into 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 monocyte-derived macrophages, 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 []. 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 []. 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 [].”
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…

Finally, Crepeaux 2017 measured aluminum content in the brain 6 months after Al adjuvant injections. The results unequivocally prove that the aluminum adjuvant winds up in the brain.

Above: Measurements of brain aluminum content 6 months after injection with 200, 400 or 800 mcg/kg Al adjuvant. The 200mcg/kg dosage caused a huge increase in brain aluminum content. From Crepeaux et al 2017.
Article on this paper is here:

2) Aluminum in Al adjuvant is not a free ion. Al adjuvant comprises solid, persistent particles, which very slowly release Al3+ ions as they dissolve over months and years. This statement by ScienceAbe is another example of his wrong understanding of the nature of Al adjuvant in the body.


[Section on papers by Dorea is omitted for brevity]

Papers by Dorea are not cited at


Concluding remarks

In this article, we investigated, analyzed and criticized the blog post that questioned the safety of aluminum in vaccines, with an ending clearly pointed to associate autism with vaccines. The same logic can be applied to thiomersal, an adjuvant containing mercury [Correction: One reader noted the inaccuracy of this claim and I make an apology for this mistake. The retracted Wakefield paper made an association between children displaying autistic traits with MMR vaccinations (see Table 2). However, the origin (manufacturer) of such MMR vaccines was not reported and therefore such study could not pinpoint which agent contained in those vaccines was the cause of such condition. Neither such study mentioned which MMR vaccines contained thiomersal. End of correction]. Of course, the Wakefield study scientific fraud has been raised and resulted in the retraction of it. Thiomersal has been removed but anti-vaccinationists now turn to another component: aluminum hydroxide, despite the clear evidence of no association between autism and vaccines (

ScientistAbe cites the well-known Taylor 2014 meta-analysis of MMR and thimerosal studies. Taylor 2014 is completely irrelevant to Al adjuvant safety because it is limited to MMR and thimerosal. MMR and thimerosal do not contain aluminum. Studies of MMR or thimerosal cannot be used as evidence for the safety of Al adjuvant.

Taylor 2014 cannot be used to support statements about vaccines in general, since it covers only MMR and thimerosal. So, ScientistAbe has misused/falsely characterized the Taylor 2014 paper.

Here is a list of the 10 studies included in Taylor 2014. See the rows outlined in red. 6 of 10 studies looked at MMR, and 4 looked at thimerosal/Hg. None are relevant to aluminum.


Early on, we demonstrated the confusion brought by the authors. The author creates confusion by introducing the terms “aluminum adjuvants nanoparticles”. There is two class of aluminum adjuvants used in vaccines: aluminum hydroxide (AH) and aluminum phosphate.  For the clarity of this article we focused on the AH nanoparticles. Unlike some websites making claims without providing any source for primary literature to support their claim, we indeed observed a smart strategic move from the author to use primary literature as sources but never showing the real data or discussing the main information coming from these studies. I call such move as a “hijack” method in which a legitimate study is used as a decoy making the claims supported by scientific evidence. A neophyte will accept this claim for granted but a more scientifically alert person will access the primary source to ensure what have been claimed on the website is in agreement with the original study. This strategy has been applied by pseudoscience websites such as “Natural-News” or “Collective-Evolution” that will have legitimate references listed to make their claims appear credible.

Data and quotes from cited papers are provided in all articles at Also, full text papers or links to the papers are provided. The statement about “never showing the real data” is a lie.


[Omitted ranting by ScientistAbe]

Based on the current literature, 1) there is no evidence that AH incorporate into macrophages, such macrophages cannot enter the healthy BBB and therefore the neurotoxic effects of aluminum due to vaccines is unproven. The house of cards built by the authors just crumbled under an intense and scientific scrutiny.

In my final words, I would say to 2) anyone trying to argue with conspiracy theorists is the same than with wrestling with a pig: you will end up exhausted, covered with mud and the pig will feel happy.

1) Citations above show that Al adjuvant is phagocytosed by macrophages. This is commonly accepted.

Macrophages do not enter a healthy brain. They enter an inflamed brain, and thats what matters. Specifically, they enter the brain in response to the inflammation signal MCP-1, which is highly elevated in the autistic brain, and elevated in infants that later become autistic. Autism is caused by brain inflammation. Also, autistics have chronic brain inflammation.

2) I do not allege any conspiracy theories. I am not a conspiracy theorist.  The “conspiracy theorist” statement by ScientistAbe is a dishonest smear and straw man.
See my debunking of the idiotic chemtrails conspiracy theory, for example:





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