by The Vaccine Reaction

A recent small study out of Tufts University Medical Center in Boston, Massachusetts has concluded that, “inflammation may be the main driver behind autism.”​¹

As reported in the Proceedings of the National Academy of Sciences, the researchers compared the brains of 16 deceased male, Caucasian children between the ages of three and 14.

Eight of the children had autism spectrum disorder (ASD) and eight did not. The study determined that the children with ASD all had increased levels of Interleukin-18 (IL-18), a protein known to trigger a severe inflammatory response.

The areas of the brain most prominently affected were the amygdala, responsible for processing emotions such as fear, anger, and pleasure;​ and the dorsolateral prefrontal cortex, which is plays a role in a number of cognitive functions of the brain including memory maintenance, attention, behavior modification, and evaluation of rewards.

Damage to this area of the brain can result in deficits in social cognition, impulse control and multi-sensory integration.​^{2 3}

The researchers also found increased levels of the anti-inflammatory protein IL-37 in the ASD children compared with the control group, though the differences were not as dramatic as those for the inflammatory proteins. The researchers stated that,

“ASD does not have a distinct pathogenesis or effective treatment. Increasing evidence supports the presence of immune dysfunction and inflammation in the brains of children with ASD.”

They speculated that treatment with drugs that target IL-37 may be a promising therapeutic approach to decreasing the amount of IL-18 in the brain.​⁴

Immune Response Targeting Brain Cells in Autism

In another study published in Annals of Neurology on Oct. 8, 2019, researchers at Beth Israel Deaconess Medical Center examining brains donated to Autism BrainNet, a non-profit tissue bank, reported finding evidence suggesting that an immune response targeting specialized cells in the brain resulted in chronic inflammation in two thirds of autistic brains analyzed postmortem.

The researchers speculated that autism, like multiple sclerosis, might be an autoimmune disorder that involves an abnormal immune response targeting brain cells.⁵ Explaining the purpose of their study, the researchers said:

Autism spectrum disorder (ASD) affects 1 in 59 children yet, except for rare genetic causes, the etiology in most ASD remains unknown. In the ASD brain, inflammatory cytokine and transcript profiling show increased expression of genes encoding mediators of the innate immune response. We evaluated post mortem brain tissue for adaptive immune cells and immune cell-mediated cytotoxic damage that could drive this innate immune response in the ASD brain.⁶

They concluded that:

Consistent with multifocal immune cell-mediated injury at perivascular CSF-brain barriers, a subset of white matter vessels have increased perivascular space (with jagged contours) and collagen in ASD compared to control brains. CSF-brain barrier pathology is also evident at cerebral cortex pial and ventricular ependymal surfaces in ASD… These findings suggest dysregulated cellular immunity damages astrocytes at foci along the CSF-brain barrier in ASD.⁶

Chronic Inflammation Is a Long-Recognized Hallmark of ASD

The concept that chronic inflammation is one of the hallmarks of ASD is not new. In 2013, the Journal of Neuroinflammation published an article stated that, “Increasing evidence indicates that brain inflammation is involved in the pathogenesis of neuropsychiatric diseases,” including ASD.​⁷ 

Pointing out that many children with ASD “regress at about age 3 years, often after a specific event such as reaction to vaccination, infection, trauma, toxic exposures, or stress,” the authors of that article go on to discuss increasing evidence of immune dysfunction/inflammation in ASD and to detail multiple markers of inflammation in the brains and cerebral spinal fluid of children with ASD.

Other evidence of the link between chronic inflammation and ASD is presented in a collaborative study between Johns Hopkins and the University of Alabama that was published in 2014.⁸​

Researchers conducting that study questioned whether brain inflammation was a “root cause” or a “downstream consequence” of ASD. They did observe that in autistic brains the microglial cells, “which police the brain for pathogens and other threats… appeared to be perpetually activated, with their genes for inflammation responses turned on.”

Gut and Brain Inflammation Go Hand in Hand

More recently, scientists have reported that, “Although the precise pathophysiologies underlying ASD are unclear, growing evidence supports a role for dysregulated neuroinflammation.”⁹​ Noting that research into the role played by inflammation in ASD also extends to the potential interplay between the gut and the brain:

[T]he gut-brain axis involving microbial-immune-neuronal cross talk is also a growing area of neuroinflammation research. Greater understanding of these interactions under patho/physiological conditions and the identification of consistent immune profile abnormalities can potentially lead to more reliable diagnostic measures and treatments in ASD.⁹

The relationship between gut inflammation and ASD has long been recognized. According to one recent large-scale study, children with ASD are 67 percent more likely to be diagnosed with inflammatory bowel disease (IBD) than their peers without ASD.

Those researchers suggest that genetic variables and disruptions in gut microbiome might be a common factor in both ASD and IBD, and concluded that the possibility that both disorders share biological underpinnings merits exploration.​¹⁰

Teasing out the precise connections between chronic inflammation and the development of ASD is challenging, but a plethora of data support that inflammation is a major player. Multiple factors can lead to inflammation of the brain and gut.

Brain inflammation can be linked to encephalitis following vaccination, defective placenta or maternal immune response to infection, immature blood-brain barrier, premature birth and environmental toxins.

Inflammation of the gut can be caused by an imbalance in the microbiome caused by factors such as Caesarian birth or an abnormal maternal microbiome, infant formula or processed foods, among many others.¹¹​

Vaccine Induced Brain Inflammation and Autism First Reported in 1985

The association between vaccination and autism was first reported by medical historian Harris L. Coulter and Barbara Loe Fisher, co-founder of the National Vaccine Information Center, in their 1985 book DPT: A Shot in the Dark (Harcourt Brace Jovanovich).

Among the case history descriptions of DPT vaccine injury and death were cases of healthy children who suffered brain inflammation and brain damage after DPT vaccinations and were diagnosed with autism.

In the year 2000, Loe Fisher wrote a special report for The Vaccine Reaction newsletter published by the National Vaccine Information Center (NVIC). She stated:

The incidence of autism, like that of learning disabilities, attention deficit hyperactivity disorder (ADHD), asthma, diabetes, arthritis, chronic fatigue syndrome, inflammatory bowel disease and other autoimmune and neurological disorders, has risen dramatically in the U.S. and other technologically advanced countries, while high vaccination rates have caused the incidence of childhood infectious diseases to fall just as dramatically in these countries. Instead of epidemics of infectious disease, there are now epidemics of chronic disease.¹²​

In 2008, Loe Fisher published Vaccines, Autism and Chronic Inflammation: The New Epidemic,which provided an analysis and summary of studies in the medical literature documenting complications of infectious diseases and vaccinations that produce chronic inflammation in the body. She observed:

A review of more than a century of medical literature reveals ample evidence that neurological and immune system dysfunction caused by infectious diseases are often identical to neurological and immune system dysfunction caused by vaccines created using the same viruses and bacteria.

A host/disease or host/vaccine interaction causes inflammation, which is acute at first, and becomes chronic rather than resolving and leaving the host with good health. In both cases, the end result is unresolved inflammation leading to immune mediated brain dysfunction of varying degrees of severity, which is the same profile many have observed in children with autism spectrum disorders.¹³​

Read the full article at thevaccinereaction.org.

References

¹ Kekatos M. Inflammation May Be Main Driver Of Autism, Find Scientists Who
Studied The Brains Of Eight Children On The Spectrum Who Had Died. Daily Mail
Oct. 7, 2019.
² Bailey R. Amygdala’s Location and Function. ThoughtCo. July 17, 2019.
³ Voytek B. Neuroanatomy: What Are The Primary Functions Of The Dorsolateral Prefrontal Cortex? Quora. Dec. 11, 2013.
⁴ Tsilioni I, Patel AB et al. IL-37 Is Increased In Brains Of Children With Autism Spectrum Disorder And Inhibits Human Microglia Stimulated By Neurotensin. PNAS. Oct. 7, 2019.
⁵ Beth Israel Deaconess Hospital Medical Center. Study: First Evidence of immune response targeting brain cells in autism. Medical Daily Journal Oct. 18, 2019.
⁶ DeStasio MD, Nagakura I et al. T-lymphocytes and Cytotoxic Astrocyte Blebs Correlate Across Autism Brains. Ann Neurol 2019.
⁷ Theoharides T, et al. Focal Brain Inflammation and Autism. J. Neuroinflammation. Apr 9, 2013.
⁸ Brain Inflammation A Hallmark Of Autism, Large-Scale Analysis Shows. Johns Hopkins Medicine Dec. 10, 2014.
⁹ Matta SM, et al. The influence of Neuroinflammation in Autism Spectrum Disorder. Brain, Behavior & Immunity July 2019.
¹⁰ Zeliadt N. Large Study Ties Gut Issues In Autism To Inflammation. Spectrum. Jan. 8, 2018.
¹¹ Mercola J. Research Confirms Gut-Brain Connection In Autism. Mercola Newsletter June 27, 2019.
¹² Fisher BL. Autism & Vaccines: A New Look At An Old Story. The Vaccine Reaction Summer 2000 (Special Report).
¹³ Fisher BL. Vaccines, Autism & Chronic Inflammation: The New Epidemic. National Vaccine Information Center 2008.

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