Participants were recruited from the community and area mental health clinics (via fliers, Internet postings, etc.), on the basis of symptoms of anxiety and depression. In keeping with the aims of RDoC, we did not use a cutoff to demarcate between normal and abnormal levels of internalizing symptoms (Cuthbert, 2014 (link); Cuthbert & Insel, 2013 (link)). Instead, we used minimal symptom-based inclusion and exclusion criteria, and aimed to recruit a sample with a broad range of internalizing symptomatology. However, to ensure the clinical relevance of the sample, we also oversampled from individuals with severe psychopathology. Thus, the goal was to recruit a sample with normally distributed internalizing symptoms but with a mean more severe than the mean of the general population. Prior to their involvement in the study, participants were screened via telephone using the Depression, Anxiety, and Stress Scale (DASS; Lovibond & Lovibond, 1995 ), a brief (21-item) measure of broad internalizing psychopathology (the measure was used to ensure that the sample had the above-mentioned distribution on internalizing symptoms). As manic and psychotic symptoms have been shown to be separable from internalizing disorders (Watson, 2005 (link)), probands and siblings were excluded during screening if they had a personal or 1st degree family history of a manic/hypomanic episode or psychotic symptoms, assessed via items from the Structured Clinical Interview for DSM–IV (SCID; First, Spitzer, Gibbon, & Williams, 1996). Participants were also excluded if they were unable to read or write English, had a history of head trauma with loss of consciousness, or were left-handed. Potential participants were not excluded based on current psychotropic medication use, or current substance use.
Participants were eligible for the study if they were between the ages of 18 and 30, and had a full sibling between the ages of 18 and 30 who was also interested in participating. We opted to recruit siblings rather than other relatives because this approach allowed us to have siblings and probands matched on mean age. We restricted the age of the probands and siblings to 18-30 because we were interested in risk for internalizing psychopathology. It was therefore critical that ‘healthy’ (or low symptom) siblings were not out of the peak risk period for internalizing disorders (through age 45; Kessler et al., 2005 (link)). The premise of examining whether healthy or low-symptom siblings of symptomatic probands have abnormal neural responses is that even though siblings have not developed significant symptoms, they still may carry the vulnerability marker (Zubin & Spring, 1977 (link)). However, if a low symptom sibling was significantly past the peak risk period (e.g., age 50) and still had not developed symptoms, they may be less likely to carry the vulnerability marker, or may even be characterized by some resilience process that counteracted their vulnerability.
Participants were only included in the analyses that follow if complete ERP and self-report data were available from both members of the sibling pair (n = 160). Of these, 10 individuals (from 10 families) were excluded as a result of excessive noise in the ERP data, leaving a final sample of n = 140 individuals, from 70 sibling pairs. The final sample was 59% female, and was racially diverse (43.5% Caucasian-American, 28% Hispanic, 13.4% African-American, 7% Asian, 3.7 % Middle Eastern, 2.4% “Other”, and 2.4 % Mixed Race), well-educated (48.7% had completed at least some college education; 21.5% had completed four years of college) and relatively young (Age M = 22.54, SD = 3.15). All procedures were approved by the University of Illinois–Chicago Institutional Review Board.
Participants were eligible for the study if they were between the ages of 18 and 30, and had a full sibling between the ages of 18 and 30 who was also interested in participating. We opted to recruit siblings rather than other relatives because this approach allowed us to have siblings and probands matched on mean age. We restricted the age of the probands and siblings to 18-30 because we were interested in risk for internalizing psychopathology. It was therefore critical that ‘healthy’ (or low symptom) siblings were not out of the peak risk period for internalizing disorders (through age 45; Kessler et al., 2005 (link)). The premise of examining whether healthy or low-symptom siblings of symptomatic probands have abnormal neural responses is that even though siblings have not developed significant symptoms, they still may carry the vulnerability marker (Zubin & Spring, 1977 (link)). However, if a low symptom sibling was significantly past the peak risk period (e.g., age 50) and still had not developed symptoms, they may be less likely to carry the vulnerability marker, or may even be characterized by some resilience process that counteracted their vulnerability.
Participants were only included in the analyses that follow if complete ERP and self-report data were available from both members of the sibling pair (n = 160). Of these, 10 individuals (from 10 families) were excluded as a result of excessive noise in the ERP data, leaving a final sample of n = 140 individuals, from 70 sibling pairs. The final sample was 59% female, and was racially diverse (43.5% Caucasian-American, 28% Hispanic, 13.4% African-American, 7% Asian, 3.7 % Middle Eastern, 2.4% “Other”, and 2.4 % Mixed Race), well-educated (48.7% had completed at least some college education; 21.5% had completed four years of college) and relatively young (Age M = 22.54, SD = 3.15). All procedures were approved by the University of Illinois–Chicago Institutional Review Board.
