In this study, we examined the hypothesis that childhood SAD confers an increased risk for the development of internalizing disorders in young adulthood and a decreased risk for externalizing disorders (ie, alcoholism and substance abuse) in a community sample. Additionally, we assessed the extent to which SAD increases risk for mental disorders during early adulthood compared with other childhood/adolescent disorders. Our results were consistent with our hypothesis that even when controlling for the occurrence of other psychological disorders through age 19, SAD contributed a unique degree of increased risk for the occurrence of certain subsequent mental disorders between 19 and 30. Specifically, children with SAD were more likely to develop panic disorder and depressive disorders, but not other anxiety disorders or substance use disorders by age 30, than those without SAD. This study improves upon many previous SAD studies in that it initially (at T1) obtained retrospective reports of child psychopathology, but then followed participants prospectively through the age of 30. Furthermore, its diagnoses were based on structured diagnostic interviews and DSM criteria.
Having experienced an episode of SAD emerged as a major risk for future psychopathology, as 73.5% of the SADs (almost all of whom had recovered from the SAD by age 19) developed an episode of psychopathology during young adulthood. Previous researchers have debated whether childhood SAD is uniquely related to the development of panic disorder in adulthood, and as indicated earlier, there have been conflicting findings reported in the literature. Our results supported those of Biederman et al.22-24
and Gittleman and Klein15
, suggesting that childhood SAD is linked to subsequent panic disorder. Our results also suggested that childhood SAD confers a vulnerability for subsequent depression, with 75% of the subjects with childhood SAD experiencing an episode of depression during young adulthood. This is consistent with the findings reported by Orvaschel et al.11
Similarly, Warner et al42
also argued that anxiety symptoms are the earliest manifestations of psychiatric disorders and that early anxiety symptoms increase the risk for subsequent MDD. Other findings in the literature also indicate that anxiety disorders usually precede depressive disorders.43
Given the preponderance of evidence that SAD creates a substantially elevated risk for future mental disorder, a child who develops SAD should not only receive treatment for the SAD but also be a candidate for preventive efforts aimed to minimize the chances of future psychopathology—especially depression and panic disorder. It remains for future research to ascertain whether successful treatment for SAD during childhood/adolescence and provision of preventative interventions reduce the likelihood of future psychopathology. The self-limiting nature of SAD may make it difficult for parents (and children) to accept treatment for SAD, but the long duration of SAD episodes and increased likelihood of subsequent panic disorder and/or depressive disorders should help to persuade parents and children of the importance of SAD treatment.
Despite the fact that our data suggest an association between SAD and future pathology, they do not allow for comments about causality. Although it is possible that SAD is a causal agent for subsequent psychopathology, it is also possible that childhood SAD and adult depressive and panic pathology may be caused by a common, underlying vulnerability. If the latter is true, it may also be that SAD is a marker for severity of the underlying vulnerability.
This study should be evaluated in light of its strengths and weaknesses. A strength of our study is that the presence of the symptoms of SAD were obtained during adolescence, ie, in relatively close temporal proximity to the SAD episode. The majority of previous studies examining the relationship between childhood SAD and subsequent psychopathology have relied upon retrospective reports of childhood SAD obtained during adulthood, and concerns about the accuracy of long-term retrospective self-reporting can be raised. Another strength of our study is that our data were collected from a large community sample. Thus, our conclusions may be more generalizable to the population at large but perhaps not to clinical samples.
A limitation of our study is that we were unable to examine whether childhood SAD predicted the development of future Axis II disorders. It is reasonable that individuals affected early in life by SAD might be at an increased risk for the development of certain personality disorders like dependent personality disorder. This possibility seems plausible given the similarity between certain symptoms (eg, feeling intensely fearful with the thought of being left alone without a primary caretaker).44
Relatedly, we were unable to examine whether SAD predicts an increased future occurrence of certain Axis I disorders, including eating disorders and psychotic disorders, due to the small number of individuals in our sample who developed these disorders.
An additional concern with our data is that they were solely based on participant self-report. Previous researchers have raised important questions about the degree to which one can rely on child reports for information about SAD diagnosis.45
In this regard, it is fortunate that mother's report of children's SAD symptoms were collected in a subset of the participants in this study but only fair concordance rates were observed (ICC[3,1] = .46).46
Because maternal reports were only available for a subset of participants, and because the ICC was low, we relied solely upon adolescent reports of SAD symptoms. However, the study would have been strengthened by the inclusion of maternal and paternal interviews regarding childhood SAD symptoms in the entire sample. An additional limitation is that because parental psychopathology was not assessed in this sample, and given that both pure SAD and comorbid SAD have been found to be associated with parental anxiety disorder, it is unclear whether the association between SAD and panic and depression are affected by parental psychopathology.
Finally, we did not collect data on the presence of adult SAD as proposed by Manicavasagar et al.47,48
These investigators have suggested a possible continuity between child SAD and adult SAD. If future researchers are able to assess this question in a prospective design that assessed SAD symptoms beyond adolescence, our understanding of Manicavasagar and colleagues' proposal would be enhanced.