Source: True Activist
By: Jeff Roberts/Collective Evolution *This article is a summary of a larger article put together by J.B. Handley at Healthcare in America. It is a conglomeration of a wide body of recent research pieced together by a growing group of concerned scientists. For more information, please visit the website, vaccinepapers.org.
A study out of China is the first to test the effects of immune activation by vaccination (hep B/BCG) on brain development in rats. Results indicate vaccines containing an aluminum adjuvant (i.e., hep B) spike cytokine levels in the hippocampus region of the brain, in particular, the cytokine interleukin-6 (IL-6), the key cytokine known for its dysregulating effect on neuronal circuitry and the key cytokine implicated in autism.
History of research into immune activation and autism
Before we get into the China study, it’s important to understand all of the previous research leading up to it.
In 2006, late Caltech scientist Dr. Paul Patterson and his colleagues were among the first to discover the implications of maternal immune activation and brain development in offspring.
In an article published in the Engineering & Science journal, titled “Pregnancy, Immunity, Schizophrenia, and Autism,” Patterson wrote that “brain-immune conversation actually starts during the development of the embryo, where the state of the mother’s immune system can alter the growth of cells in the fetal brain.”
Patterson and his team built on the work led by Carlos Pardo at Johns Hopkins, which discovered “neural inflammation” in postmortem examination of brains of patients with autism. Strangely, these autistic patients did not die due to any infections that would have caused the inflammation.
This research was the first to suggest “an ongoing, permanent immune-system activation in the brains of autistic people.”
In 2007 Patterson took this research further, publishing a study that found the culprit of this chronic brain inflammation — cytokine interleukin-6 (IL-6).
Cytokines are cell signaling molecules that aid cell to cell communication, stimulating the movement of cells toward sites of inflammation, infection, and trauma.
Patterson found that IL-6 was critical for mediating the behavioral and transcriptional changes in the neurology of the rat offspring.
This study was replicated by Patterson in 2012, which was more autism-specific, and reached the same conclusion: “These results indicate that [maternal immune activation] MIA yields male offspring with deficient social and communicative behavior, as well as high levels of repetitive behaviors, all of which are hallmarks of autism.”
In 2014, the M.I.N.D. Institute at UC-Davis replicated Dr. Patterson’s work in rhesus monkeys and found the same results.
Another 2012 study from Neuroscience agreed with Patterson — Brain IL-6 elevation causes neuronal circuitry imbalances and mediates autism-like behaviors.
The next question, then, was what causes immune activation that would lead to increased levels of IL-6 in the brain?
Aluminum bioaccumulates in the brain
Aluminum compounds (Al hydroxide and Al phosphate) are currently used in the hepatitis A, hepatitis B, diphtheria-tetanus-pertussis (DTaP, Tdap), Haemophilus influenza type b (Hib), human papillomavirus (HPV), and pneumococcus (PCV) vaccines.
Aluminum adjuvant “activates” the immune system, which induces long-term immunity to antigens in the vaccine.
Dr. Chris Shaw at the University of British Columbia did extensive research on injected aluminum in 2007 and 2009 and found “the results reported mirror previous work that has clearly demonstrated that aluminum, in both oral and injected forms, can be neurotoxic. Potential toxic mechanisms of action for aluminum may include enhancement of inflammation.”
Concerns about the limited understanding of aluminum toxicity were further questioned by Dr. Lucija Tomljenovic in this 2012 paper.
It is somewhat surprising to find that in spite of over 80 years of use, the safety of Al adjuvants continues to rest on assumptions rather than scientific evidence. For example, nothing is known about the toxicology and pharmacokinetics of Al adjuvants in infants and children.9 On the other hand, in adult humans, long-term persistence of Al vaccine adjuvants can lead to cognitive dysfunction and autoimmunity.6,10 Yet, in spite of these observations children continue regularly to be exposed to much higher levels of Al adjuvants than adults, via routine childhood vaccination programmes.
In 2013, French scientists demonstrated that aluminum adjuvant, when injected into the body of a mouse, ended up in the brain one year later.
In 2015, another study from Université Paris Est Créteil (UPEC) in France further supported this new view of aluminum adjuvant, showing that Al makes its way to the brain slowly, where it stays there, possibly forever.
Last fall, results published in the journal Toxicology sealed the deal on Al adjuvant, revealing that low, consistent doses of Al were most dangerous of all for neurotoxic effects. Larger doses produced granulomas at injection sites, which prevented the Al from spreading. Smaller doses did not produce this effect, causing changes in the brain and behavior.
The study authors stated that “the present study may suggest that aluminum adjuvant toxicokinetics and safety require reevaluation.”