Patterns of ASD-Onset and Parents' Beliefs about Causes

Background: Researchers traditionally have described two types of onset for autism spectrum disorders (ASD): early onset, which refers to delays/aberrant development during the first several months of life, and regressive, which characterizes children who exhibited seemingly typical development, then lost previously acquired skills. Recent investigations have expanded these categories to include plateau (no loss, but halted acquisition of new skills) and early onset plus regression (delays with loss of skills also observed) (e.g., Kalb et al., 2010; Shumway et al., 2011). Understanding the nature and prevalence of ASD onset is valuable because different developmental courses may imply different etiological mechanisms. Parental report of regression in their children also has been shown to color parents’ beliefs about causes of ASD (Goin-Kochel & Myers, 2005), which has further implications for the types of treatments that parents choose to pursue.

Objectives: (a) To provide descriptive information about ASD-onset types among a large, well-characterized sample; (b) To determine whether parents’ beliefs about causes of ASD are associated with their reports of how ASD manifested in their children.

Methods: Data will be analyzed for children with ASD (probands; N = 2755; M age = 9 years, SD = 3.6 years, range = 4—17.9 years) who participated in the Simons Simplex Collection (SSC). Type of ASD onset will be categorized using data from the Autism Diagnostic Interview—Revised (ADI-R), according to the system used in Shumway et al. (2011). A subset of these families (n = 68) participated in an additional project that used an ASD-adapted version of the Revised Illness Perception Questionnaire (IPQ; Moss-Morris, et al., 2002) to query parents’ level of agreement with 21 possible causes of ASD. Frequencies of ASD-onset types will be presented for the entire SSC sample as a partial replication of Shumway et al. Frequencies of etiological beliefs about ASD have been calculated for the subset of families who completed the IPQ. Chi-square tests of homogeneity will be computed with data from the IPQ subsample to assess possible relationships between ASD-onset type and causal beliefs about ASD.

Results: The largest proportions of families agreed with 4 possible causes for ASD: genetics (75.8%), child’s brain structure (59.7%), will of God (46.3%), and toxins found in vaccines/immunizations (41.8%). Disagreement was espoused by the largest percentages (52.2—93.9%) for all remaining possible causes (e.g., germ/virus, my partner’s age, stress at birth), with the exception of “environmental pollution,” which was espoused in relatively equal proportions (37.4% = agree; 28.4% = neutral; 34.3% = disagree). Results regarding ASD-onset patterns and their potential associations with beliefs about causes for ASD are forthcoming.

Conclusions: Most parents disagreed with a greater number of potential causes than agreed with them (16 vs. 4 causes). A larger proportion espoused vaccines as causing ASD than in prior work (~42% vs. 33%). This is surprising, given that the SSC was marketed largely as a genetic-factors study of ASD. Additional findings regarding prevalence of ASD-onset types in the SSC and their relations to etiological beliefs about ASD will be discussed.