Cognitive reserve has been proposed as an important etiologic factor in the development and severity of neuropsychiatric disorders (1
). The construct of cognitive reserve refers to individual differences in brain structure (e.g., density of neuronal synapses) and function (e.g., processing efficiency) thought to buffer the effects of neuropathology. Evidence has emerged from the rapidly evolving field of cognitive epidemiology (2
) showing that IQ, a marker of cognitive reserve, is inversely related to risk of total psychiatric illness (3
). However, with the exception of research on schizophrenia (4
), surprisingly few studies have examined the relation between IQ early in life and the risk of other specific adult psychiatric disorders. Among those studies that have examined other disorders, the results have been inconclusive. We report a longitudinal study of the 20-year predictive association between childhood IQ and adult mental disorders among members of the Dunedin, New Zealand, birth cohort.
In the earlier studies, low IQ at military entry increased the risk of hospitalization for depression in male Swedish conscripts (5
) but not male Danish conscripts (6
). Studies of bipolar disorder have largely shown no association with premorbid IQ (5
), but one study of U.S. Army recruits found elevated IQ scores in bipolar patients (9
). Low IQ has been associated with increased risk of substance use disorders in some study groups (6
) but not in others (11
). In one cohort, the association between low childhood IQ and increased risk of any anxiety disorder was attenuated to nonsignificance once other covariates were included (11
). An inverse association between premorbid IQ and posttraumatic stress disorder (PTSD) has been consistently documented in military (14
) and civilian samples, including our Dunedin birth cohort (15
). However, with the exception of one report showing that lower IQ increased the risk of generalized anxiety disorder (16
), the association between premorbid IQ and other specific anxiety diagnoses has not been studied.
Understanding of the potential role of cognitive reserve in the etiology of neuropsychiatric disorders is constrained by five methodological limitations of extant research. First, many studies have relied on IQ at military induction as a marker of cognitive reserve (5
). Such studies cannot rule out the possibility that low IQ at induction is the consequence of prior juvenile disorder or an early prodromal disease process, rather than antecedent to disorder. Prospective studies using IQ measured in childhood provide a more rigorous test of whether lower premorbid IQ increases the risk of subsequent disorder. Second, most prior studies have considered either a single or limited number of disorders, making it difficult to determine whether low IQ is a general risk factor for all psychiatric disorders or a specific risk factor for select disorders with a neurodevelopmental etiology (e.g., schizophrenia). Third, studies including a range of diagnoses have tended to rely on hospitalization records for their psychiatric outcome data (5
), which may introduce ascertainment biases. Only individuals with the most severe forms of nonpsychotic disorders are hospitalized, and thus hospitalized patients do not represent nonpsychotic disorders in the population. If low IQ increases the likelihood of hospitalization, the association between premorbid IQ and psychiatric disorders would be inflated. Fourth, several of the most rigorous studies have used male samples (5
). Studies in cohorts representing both sexes are needed. Fifth, prior studies have predicted the presence of either lifetime disorder or disorder at the time of assessment. However, the cognitive reserve model proposes that low IQ should be associated with the severity of psychopathology, not merely the presence versus absence of a diagnosis. Indicators of disorder severity, such as comorbidity and persistence, should be studied.
In order to test the cognitive reserve model for psychiatric disorders, we examined whether childhood IQ predicted psychiatric disorders at the most recent follow-up of the Dunedin birth cohort, at age 32. Focusing on age 32 allowed greater confidence in the validity of certain diagnoses, such as substance dependence and schizophrenia, which can be difficult to make at earlier ages in cohort studies. To allow comparison with prior reports of the association between IQ and adult disorder at one time point, we report this association between childhood IQ and past-year disorder assessed at age 32. However, we also capitalized on the longitudinal design of our study and report the relationship between childhood IQ and the persistence of disorder across repeated assessments carried out from age 18 to 32. This study overcomes several methodological limitations by using a birth cohort of both men and women who had prospective data on childhood IQ and potential confounders and who were diagnosed with specific mental disorders by means of structured clinical interview rather than hospital records. In addition, it is one of the first studies to examine the relation between IQ and indicators of disorder severity.