Initially, vaccines were blamed for the surge in autism rates. This argument gained traction when the parents of Hannah Polling won a lawsuit in a federal court, claiming that their daughter’s autism was caused by vaccines (Wallice, 2006). In this unique case, Polling’s symptoms were reported to have increased dramatically after receiving a large dose of a variety of vaccines. Expert witnesses testified and indeed were victorious in showing that Polling’s autism symptoms were either caused or increased significantly after receiving vaccinations.

Following this case, many families worried that their child’s symptoms could be due to vaccines as well. One reason for this belief is that some symptoms of autism may not be evident until immediately following the vaccines administered at the 1-year or 2-year check-up. This sudden increase may be due to the fact that there are some regressive forms of autism where symptoms do tend to show around the second year of life which coincides with the timing of vaccines. Another rationale for the symptom increase during this phase of life is that many developmental language milestones tend to become more evident during that time and the absence of delay of speech is often a characteristic of autism. That is, it is possible that many of the signs of autism go unnoticed in infancy; however, when a child is not gesturing, sharing enjoyment, talking, or responding to his name at 2 years of age, parents and clinicians take notice. Thus, there may be a correlation between the timing of the symptoms surfacing and the shots being administered; however, this correlation does not necessarily indicate a causal relationship.

Although the potential relationship between vaccines and autism has been sensationalized in the media, researchers have repeatedly concluded that there is no clear relationship between vaccines and autism. The original research linking the MMR shot to autism was rejected when multiple flaws were uncovered, revealing their results were exaggerated and statistically unsubstantiated (Kaye, del Mar Melero-Montes, & Jick, 2001). Salzberg (2015) indicates, “We’re still spending vast amounts of time and money trying to counter the ill effects of a discredited, retracted paper from 1998 that claimed to find a link between the MMR (measles, mumps and rubella) vaccine and autism” (p. 1). Adding to this skepticism in the medical community is the fact that the allegedly dangerous preservatives in the MMR shot have been removed, and autism prevalence continues to be on the rise. Further problems with the vaccine argument were uncovered when a relatively sizable percentage of Americans stopped vaccinating their children, which might predict a co-occurring reduction in autism rates (Rosenberry Conference, 2010). Unfortunately, autism rates continued to skyrocket, thus further calling into question the plausibility of the relationship between autism and vaccines. Taken together, the medical community does not believe that vaccines cause autism. Salzberg lashes out against the hype around vaccines, “So: once again we have a large, carefully conducted study showing that the MMR vaccine does not cause autism… Let’s hope this study helps to end the anti-vax movement, so that we can soon stop spending time and money trying to refute their long-discredited hypotheses and instead focus on trying to understand the true cause ” (p. 1). Many also warn that the authors of the original study linking autism to vaccines have seriously endangered public health by creating fear around vaccines that could potentially have prevented a myriad of serious illnesses.

The belief that autism could be born from a combination of genetic and environmental causes is well-founded (D’Amelio et al., 2005; Demark, n.d.; Horvath et al., 1999; McCandless, 2002/2009; Nash, 2002; Reid, 2004; O’Hara & Szakacs, 2008; Wallis, 2006). Scientists believe that children are generally born with autism; however, is it possible that certain risk factors in pregnancy and early life are also implicated in development of the disorder. Preliminary research on the risk factors for autism includes parental age, maternal exposure to environmental toxins, and frequent illnesses in utero or in early infancy. Studies have shown a significantly high number of children with autism who are born to mothers who are obese or have metabolic conditions (Harmon, 2012; Krakowiak, et al., 2012). Paternal and maternal age is known to be an additional risk factor. There is a high correlation between older fathers and increased numbers of sons born with autism. That is, paternal age over 30 is linked with 50 % higher risk of having a child born with autism; age over 40 with a 500 % higher risk; age over 50 with a 900 % higher risk (Hnida, 2006; Deer, 2009). Harmon (2012) identified that the increased risk with paternal age may be due to the continual sperm division process which happens throughout a man’s life and the resultant higher risk of mutation during continual DNA replications (Harmon, 2012; Schubert, 2008; Willard, 2013). There is also an increased risk of other developmental disorders associated with increased parental age, so this genetic variance is not necessarily unique.

Autism is a complex disorder for which many models blending genetic and external factors have been proposed. Epigenetics research investigates the mechanism by which genes are expressed in individuals and by which gene expression is passed on through generations. Specifically, epigenetics considers environmental influences on gene expression (Lahiri et al., 2013). Although autism has a high heritability, the cause of autism is made ever more complicated by the fact that siblings and even twins do not always show signs of autism to the same degree. The science of epigenetics has been associated with autism as an additional mechanism to explain how genetics and environment interact and alter phenotypic expression. Epigenetics may provide some explanation as to why many children who are exposed to the same toxins do not develop autism; whereas some cases of autism seem to show a clear link to environmental or health insults.

Day and Sweatt (2011) explain how environmental conditions impact gene expression thusly, “we consider how aberrant epigenetic modifications may lead to cognitive disorders that affect learning and memory, and we review the therapeutic potential of epigenetic treatments for amelioration of these conditions” (Day & Sweatt, 2011, p. 813). This research points to the fact that the brain is plastic, as is our genetic expression of our brain’s capacity, and both can be affected; either positively or negatively, by environmental factors. Pennington (2002) puts forth that the familial phenotype may be dimensional and that certain epigenetic factors can lead to expression of symptoms or traits. Even though a child may have the genetic “code” for autism, he may appear healthy and typical as a young child. Later, after exposure to certain toxins, the child may start showing symptoms. It is possible then, that it may appear the child’s autism was “caused” by the environmental trigger. Could it be that children who are medically fragile or genetically vulnerable to certain viruses or toxins suddenly show symptoms after being exposed to toxins? Possibly; research has not provided clear conclusions. A whole book could be written on the science of epigenetics and whether or not autism symptoms could indeed be expressed (or not expressed) due to an epigenetic mechanism. It does stand to reason that understanding the complex epigenetic interaction of genes and environment may allow researchers to comb through and untangle the reasons why some children’s symptoms emerge in response to environmental triggers while others do not.