Society has constantly been searching for ways to compartmentalize individuals into groups based on levels of normalcy. Any variation from the narrow definition of “normal” is often regarded with a negative connotation. Scientists have found ways to further isolate humans into said subgroups through the development of new diagnoses. The turning point of this marginalization began in 1908, when psychiatrist Eugen Bleuler used the term “autism” to describe 11 of his patients that seemed to “withdraw into [their] own world” under several circumstances. From this point on, “autism” was utilized to distinguish individuals who fell outside the bounds of “normal” behavior.
Once autism was deemed a “disorder” in 1943 by Leo Kanner, an intense need to “diagnose” and find causal relationships for this newfound “obscurity” arose within the scientific field. The initial theory of causation was popularized by Bruno Bettelheim, who hypothesized that “refrigerator mothers” provoked autism by not loving their children enough. The fact that Bettelheim’s claim was merely considered as a possible cause of autism is not only baffling and upsetting, but also not scientifically substantiated.
Over the past several decades, scientists have theorized a multitude of causes for autism beyond Bettelheim’s initial hypothesis. In 1998, a British researcher suggested that immunization shots may have a negative effect on the development of a child’s brain. This began the quest to find a link between vaccines and autism spectrum disorder (ASD). Countless studies commissioned by the British department of health confirmed that there is no concrete evidence of a connection between vaccines and autism. Yet again, scientists were back at square one.
Autism spectrum disorder continues to be a conundrum for scientists across the globe. The causes are elusive and research remains indeterminate. After behavioral and environmental factors were ruled out, scientists turned to potential prenatal causes. Prenatal exposure to certain variables are currently a topic of interest in the quest for a cause of ASD, but truly it is a shot in the dark. In a study conducted by Croen, Grether and Yoshida, antidepressant use during pregnancy was analyzed to discover if there was a correlation to the development of ASD.
Children born at the Kaiser Permanente Medical Care Program in Northern Carolina were evaluated through the review of their mother’s mental health records and prescriptions consumed in the year before delivery. Throughout each pregnancy, four exposure times to selective serotonin reuptake inhibitors (SSRIs), commonly referred to as antidepressants, were defined as follows: preconception, first trimester, second trimester, and third trimester. Using statistical models, it was found that there is an increased risk of ASD associated with treatment for mental health disorders when medications were consumed during the first trimester of pregnancy.
Unfortunately, the results show a very minimal link between the two variables, considering only 6.7% of children with autism and 3.3% of children without ASD had been exposed prenatally to SSRIs. This poses the question of how conclusive the evidence may be. It may also be difficult to ascertain if the risk factor for ASD is due to the actual drug exposure or the underlying mental health condition of the mother that inevitably led to treatment.
Similar case-control studies have shown weak and inconsistent associations, further decreasing the efficacy of this particular study. Another study administered by Childhood Autism Risks from Genetics and the Environment (CHARGE), revealed contradictory results. Exposure to SSRIs was found to be strongest in the third trimester of pregnancy. Again, however, the difference in the prevalence of SSRI exposure varied extremely slightly among children diagnosed with ASD versus children not diagnosed.
After prenatal drug consumption was deemed an obsolete factor, mode of delivery was used to discover an association with developmental disorders. A third study which took place at the Irish Center for Fetal and Neonatal Translational Research (INFANT), attempted to evaluate long term effects of Caesarean section (CS) births and induced labor on a child’s development. Despite the fact that mode of delivery was categorized into six distinct groups, there was still a non-significant link between the two variables. To no surprise, Ireland’s primary prenatal research center was unable to reach a definitive result in regards to risk factors for ASD.
The American Journal of Epidemiology posted a study that sought to prove that heredity and early fetal development provide an explanation for causes of autism. Children born in Denmark between the 1970s and 1990s were scrutinized based upon perinatal, or during pregnancy, factors, parental psychiatric backgrounds, and parental socioeconomic status. Analyses of parental psychiatric history showed a statistical increase in the risk of autism when mental health status became more severe. The dissection of socioeconomic factors made autism a politicized issue, as class and wealth status were related to a mental health disorder.
While some studies show a potential link to autism and hereditary factors, such as psychological disorders, findings need to be replicated multiple times in order to achieve more consistent results that can be applicable in the scientific field in the future. As of now, there are unmeasured variables that could be related to diagnoses of autism, so studies are full of ambiguity. It appears as if scientists may be dedicating time and resources to research that is not necessary in the first place.
ASD has been stigmatized for far too long, and those with developmental disorders have been marginalized without good reason. Autism cannot be “treated” or “fixed”; there is no cure. Thus, it is a waste of time to find a cause when the likelihood of a solution is impossible. Instead, society must look for ways to be accommodating and accepting of others that stray from the popular conception of normal. After all, some of the most successful and bright figures have been diagnosed with “disabilities.” Alan Turing was on the spectrum for ASD, yet without his cryptography skills, the German Enigma code would not have been broken, and World War II may have ended much differently.
It is time to stop attempting to improve flaws or inconsistencies in those that think differently than the mainstream. Rather, such individuals should be treasured and valued for their notable strengths that can allow society to progress and grow in a bevy of ways. The stigma of autism ends here. Scientific research to find causation must be abandoned. The diagnosis of ASD is a blessing, not a curse.
by: M. Srochi
References
Croen LA, Grether JK, Yoshida CK, Odouli R, Hendrick V. Antidepressant Use During Pregnancy and Childhood Autism Spectrum Disorders. Arch Gen Psychiatry. 2011, 68(11):1104–1112. doi:10.1001/archgenpsychiatry.2011.73.
Eileen A. Curran, John F. Cryan, Louise C. Kenny, Timothy G. Dinan, Patricia M. Kearney, Ali S. Khashan, Obstetrical Mode of Delivery and Childhood Behavior and Psychological Development in a British Cohort, Journal of Autism and Developmental Disorders, 2016, 46(2): 603.
Heidi Jeanet Larsson, William W. Eaton, Kreesten Meldgaard Madsen, Mogens Vestergaard, Anne Vingaard Olesen, Esben Agerbo, Diana Schendel, Poul Thorsen, Preben Bo Mortensen; Risk Factors for Autism: Perinatal Factors, Parental Psychiatric History, and Socioeconomic Status, American Journal of Epidemiology, 15 May 2005, 161(10): 916–925. https://doi.org/10.1093/aje/kwi123.
Rebecca A. Harrington, Li-Ching Lee, Rosa M. Crum, Andrew W. Zimmerman, Irva Hertz-Picciotto Pediatrics May 2014, 133(5) e1241-e1248; doi:10.1542/peds.2013-3406.