Towards understanding the rise in autism

December 29, 2018


David Glenn

Zenith News


There has been a significant increase in reported cases of autism—from 1 in 2,000 back in the ’70s and ’80s, to 1 in 150 today. Better diagnosis and reporting cannot account for so many new cases, especially within subsections of the population with zero family history.


Vaccines have been thoroughly debunked as the cause of the autism increase. If vaccines play a role at all, it’s so peripheral that any trauma could tip the scales—the flu, poison ivy, Yoko Ono records.


Issac Newton, Nikola Tesla, and to a lesser degree Albert Einstein all showed signs of Autism Spectrum Disorder (ASD) long before the practice of inoculating people against pathogens.


Not to mention, if vaccines were the cause, the explosion in autism rates would have occurred during the Baby Boomer and Gen X developmental years.


While there is no consensus—there are as many autism hypotheses as there are researchers writing grant proposals—the latest research suggests that ASD results from a series of mutations, errors, breakdowns, and missteps in the developmental process, influenced heavily by the environment.  


This being the age of fast and cheap genetic sequencing, many researchers have sought to identify which mutations might be responsible. There seems to be a more-than-chance genetic correlation, as suggested in the much-referenced British twin studies and the higher prevalence of autism in families of engineers and scientists.


But even though there is a strong genetic component, there is still only a 90 percent chance that identical twins will share the disease. So an identical genetic profile and gestational environment is not a guarantee that the disorder will develop.


There are radical differences between the genes affected in autistic individuals. One may have one or two mutated genes, while another has a totally different set of mutated markers. Multiple mutations build on one another and are often seen in those with more severe forms of the disorder.


Beyond impaired social cognition and the repetitive behaviors that are the hallmarks of autism, it is often diagnosed alongside other conditions including epilepsy, mood disorders, synesthesia, eczema, diarrhea/constipation, colitis, food allergies, etc.


Many of these are “proinflammatory autoimmune disorders,” and some experts have classified autism as such as well. Researchers are pursuing alternative causes and contributors including abnormal neurological, immune, and gastrointestinal factors.  


Brain scans of autistic people show abnormal neural connectivity between and within the regions associated with language, aggression, memory, and social skills. Researchers discovered an over-abundance of synaptic connections within the amygdala, cerebellum, and frontal lobe, and a shortage of routing pathways between regions and hemispheres.  


During early development, an overabundance of synaptic connections are formed between neurons that prime the pump for fast-track experiential learning. This process is known as “exuberant synaptogenesis.”


At about three years of age, the under-used and unneeded circuits are pared down through synaptic pruning. Coincidentally, this is the same age that children begin showing signs of disorders related to conceptual language and social development.


The cells responsible for pruning the synapses are “microglia.” Due to the blood-brain barrier preventing the body’s other defenses, microglia act as the brain’s sole defense. Their job is to engulf damaged neurons, infectious agents, and rarely used synapses.


Higher levels of gene activity are observed in boys during gestation, which might account for why autism is up to four times more prevalent in men. If abnormal synaptic connectivity and microglia are at fault, then hat causes the microglia to malfunction?


While mutations in the genes associated with microglial expression and activation have been implicated in some ASD patients, once again, enough are missing these markers to warrant an investigation into possible epigenetic and environmental influences.


A few researchers have proposed a connection between maternal inflammation during pregnancy and offspring microglia disregulation. This is thought to occur when cytokines (messaging proteins responsible for tagging damaged or infected cells) cross from the mother to the fetus. These proteins set up an overactive inflammatory response made worse by postnatal environmental conditions, e.g., allergens.


Wonder where this is going, or think you already have an idea? Pick up the Zenith next month as this series further explores inflammation’s role in autism, the environmental and epigenetic factors, as well as Minnesota’s role in autism research. 

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