Exploring the role of inflammation in autism

January 17, 2019


David Glenn

Zenith News


Last month, we explored the neurology of autism as well as genetic influences that might drive its development. We also touched on the role of malfunctioning microglial misdirecting the synaptic pruning process in the brain, as well as the comorbidity of other disorders associated with autism and the possible role maternal inflammation during pregnancy.


We continue our journey down the rabbit hole by examining inflammation and its effects on the body.


Inflammation is part of the body’s response to damage or infection. Its role is to identify, isolate, neutralize, and dispose of malfunctioning or dead cells and pathogens. This is accomplished through the use of messaging proteins like cytokines, chemokines, and MDA5, which flag unwanted biological material for containment and disposal by macrophages, killer T-cells, etc.


Mutations, as well as exposure to inflammatory stimuli, can cause this system to start attacking the host’s own cells. This is known as an autoimmune disorder, and its subset of diseases have seen the same sharp rise in reported cases as Autism Spectrum Disorders (ASD).


Something as simple as gum disease can provide the sort of long-term irritation that, when coupled with genetic and environmental factors, leads to the development of more serious disorders. An association between inflammation and depression has been reported in the scientific literature since the early '60s.


Non-steroidal anti-inflammatory drugs, such as aspirin and ibuprofen have been used to reduce and regulate inflammation and synaptic pruning in those suffering from ASD, depression, and geriatric dementia. It is worth taking the time to compare the recent proliferation of autoimmune diseases, of which autism is one, against what would be expected as a result of mutated genes propagating throughout the population via vertical transmission (i.e., genetic inheritance).


Typical inherited genetic disorders, such as Huntington’s Disease or cystic fibrosis, spread through the transfer of dominant/recessive alleles from one or both parents. While there is a higher incidence of autism in families where both parents are employed as engineers or scientists, this is not the case in those groups experiencing exponential growth in the number of children diagnosed with ASD. Patients with zero family history are routinely diagnosed and treated for disorders like autism, arthritis, celiac disease, and diabetes.


Research has shown that older males have a greater chance of producing sons who develop ASD symptoms. This “aging of the germline” hypothesis might explain some occurrences—but not all.


What it does add to the argument is a case for epigenetic factors, which can be thought of as an outside agent altering the expression of specific genes. In this case, the agent of influence is the inevitable copying errors that creep in as time progresses.


But this still does not explain the explosion in autism and other autoimmune diseases resulting from “de novo” (new or original) genetic mutations. That almost requires an unidentified environmental agent. The most logical place to look for this causative factor would be in a group experiencing higher than average rates of autoimmune dysfunction. Unfortunately, there are more than a handful of such groups.


Oft-cited studies performed in Sweden in 2008 of autistic children born to Somali immigrants found that the rate of ASD was three to five times higher than the general population. What's even more mysterious is that autism is almost non-existent in Somalia and other developing countries, as are most autoimmune disorders.


Minnesota’s Somali community has a disproportionately higher rate of autism. The similarities in climate between Sweden and Minnesota has led some to propose a vitamin D deficiency as a significant factor in the abnormal neural development seen in autistic children.


Vitamin D has been shown to play a part in DNA repair and the prevention of oxidative stress, which leads to genetic damage. Environmental contaminants, such as lead, mercury, and pesticides, are more prevalent in industrialized countries and have also been implicated.


Vitamin deficiency and increased exposure to mutagenic chemicals are not the only threats faced by immigrants from developing countries. Western culture and diet may also contribute to the epigenetic onset of a variety of diseases. Rates of obesity and diabetes within Minnesota’s Hmong, Latino, and Somali communities are six times higher than the state average.


So what changes when immigrants arrive in post-industrial countries? Two significant changes are diet and a more antiseptic lifestyle.


A recent study by University of Minnesota researcher Dan Knights has identified significant changes in the intestinal microbiota in these groups. Their once diverse population of gut microflora fell below measurable levels just days after setting foot on American soil.


Loss of microbiome diversity in obese immigrant adults was 15 percent, while their children experienced an additional five to ten percent deficit. Drastic changes in the ratio of microbial species populating the gut have been linked to obesity and Type II diabetes.


Wonder where this is going or think you already have an idea? Pick up the Zenith next month as this series explores the role of gastrointestinal abnormalities, diet, and the microbiome in ASD development.




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