In 1944, the American psychiatrist Dr. Leo Kanner was curious as to why 20 children had an affective disorder along the same lines as those recorded some 35 years earlier by the Swiss psychiatrist Eugen Bleuler. Both men considered the condition to be autistic, meaning, as Kanner wrote:
"an individual disregards, ignores, shuts out
anything that comes to the child from the outside."
Since Kanner's discovery of what is now known as autism or autism spectrum disorder, there has been a significant effort by research to find out exactly what causes this change in behaviour and whether it can either be prevented or cured.
The problem, however, was that until the 1970s, the information was scattered between two divergent sciences, biology and psychiatry. That all changed in 1973 when researchers, including the notable Dr. Edward Ornitz of the University of California, decided to aggregate all the information and form a more complete picture of the problem. What they found was a common denominator to all known cases: neurological dysfunction. Unfortunately, at the time, they didn't know what was causing the damage.
Others sought to link vaccination with autism but that also has been dispelled. Genetic links -- such as Fragile X Syndrome -- have also been found for some but not all patients; Fragile X can only be found in 30 per cent of autistic individuals.
In the end, the real culprit for the onset may well be a normal bodily function that is common to us all and is usually helpful in keeping us healthy: the immune response.
The initial evidence in the 1980s suggested that there was some type of immune dysfunction in brains of autistic children. This was confirmed several times over the years and in the 1990s was thought to be an autoimmunity. Yet this postulate was not accepted by all; autoimmunity did not simply arise out of the blue. There had to be a reason although at the turn of the millennium, no one quite knew what.
In 2002, a collaboration of over 20 American researchers found a possible answer although at first glance, it seemed ludicrous. The team looked at the bacteria in the gut of both normal and autistic children in the hopes of identifying any changes. Indeed, there were. Those with autism appeared to have a form of dysbiosis meaning that the population had shifted from good germs to bad. This in turn would have caused the inflammation and led to the neurological problems. It wasn't entirely welcomed yet it opened up the door to a new direction in autism research: the microbiome.
Over the coming years, other studies all supported the microbiome link to autism leaving many to consider whether the bacteria themselves were actually controlling the disorder. Yet even with the knowledge that the gut is the "second brain" finding a link between a gut microbe and a brain disorder was a huge hurdle.
Last year, Dr. Derrick MacFabe at the University of Western Ontario suggested a mechanism that would inevitably lead to the dysfunction. Some of the by-products of bacteria are short chain fatty acids.
These have been shown to not only trigger but also at times control the immune response. According to MacFabe, a series of genetic and environmental factors could lead to dysbiosis and the inevitable change in SCFAs from healthy to harmful. He also suggested that if there was a way to change the chemical nature of the gut, then there may be a chance to not only prevent but also treat the disorder.
Perhaps the best way to accomplish this change is to change the gut microbiome through the introduction of good germs, better known as probiotics. While the idea had been proposed earlier there had been no real definitive research to show whether or not this was valid.
This week, a group of researchers led by the California Institute of Technology took the first step to show that probiotics may indeed offer an answer. They published a paper in which they tested the impact of a probiotic bacterium, Bacteroides fragilis on mice that exhibit similar profiles to those suffering from autism. What they found was a complex cascade that involved the gut, the immune system, and a short-chain fatty acid-like chemical known as 4-ethylphenylsulfate, or 4EPS.
The picture formed from the data was fascinating. When there were no probiotics present, there was an increase in gut abnormalities triggering both inflammation and production of the fatty acid ultimately leading to psychological abnormalities. When the probiotics were added, the gut returned to normal, inflammation was decreased and 4EPS levels were reduced. The overall outcome was calmer mice and improved symptoms. In essence, the team had found a potential natural therapeutic.
The study is a pioneer for the future of both autism treatment as well as prevention. There will be no doubt future studies involving mice and eventually human clinical trials will proceed. If the data from this and other studies reveal to be true, the benefit of probiotics should be conclusive in autism by 2020.
In the meantime, while research continues to do its best to keep up with society, taking probiotics now for general gastrointestinal health is a good idea. If there are other benefits, whether proven by research or not, then that can be considered as an added bonus.