The joint impact of cognitive performance in adolescence and familial cognitive aptitude on risk for major psychiatric disorders: a delineation of four potential pathways to illness

Abstract

How do joint measures of premorbid cognitive ability and familial cognitive aptitude (FCA) reflect risk for a diversity of psychiatric and substance use disorders? To address this question, we examined, using Cox models, the predictive effects of school achievement (SA) measured at age 16 and FCA-assessed from SA in siblings and cousins, and educational attainment in parents-on risk for 12 major psychiatric syndromes in 1 140 608 Swedes born 1972-1990. Four developmental patterns emerged. In the first, risk was predicted jointly by low levels of SA and high levels of FCA-that is a level of SA lower than would be predicted from the FCA. This pattern was strongest in autism spectrum disorders and schizophrenia, and weakest in bipolar illness. In these disorders, a pathologic process seems to have caused cognitive functioning to fall substantially short of familial potential. In the second pattern, seen in the internalizing conditions of major depression and anxiety disorders, risk was associated with low SA but was unrelated to FCA. Externalizing disorders-drug abuse and alcohol use disorders-demonstrated the third pattern, in which risk was predicted jointly by low SA and low FCA. The fourth pattern, seen in eating disorders, was directly opposite of that observed in externalizing disorders with risk associated with high SA and high FCA. When measured together, adolescent cognitive ability and FCA identified four developmental patterns leading to diverse psychiatric disorders. The value of cognitive assessments in psychiatric research can be substantially increased by also evaluating familial cognitive potential.

Figure 1

(a) The hazard ratio (and 95% confidence intervals) for first registration for six neurodevelopmental psychiatric disorders (ASD, autism spectrum disorder; SZ, schizophrenia, ONAP, other non-affective psychoses; OCD, obsessive compulsive disorder; ADHD, attention deficit hyperactive disorder; BP, bipolar disorder) in 1 140 608 Swedish individuals born 1972–1990 as a function of their school achievement at age 16 and their familial cognitive aptitude calculated from school achievement in full siblings and cousins and educational status in parents. s.d.—standard deviation. The X-axis reflects the familial cognitive aptitude divided into five groups: very low (− 2 s.d. below the mean), low (−1 s.d. below the mean), average, high (+1 s.d. above the mean) and very high (+2 s.d. above the mean). The Y-axis reflects the school achievement levels, in s.d. units, of individuals within each family type. Not all possible combinations are presented because some potential groups (e.g. familial cognitive aptitude of +2 s.d. and school achievement of −1 or − 2 s.d.) were too rare to calculate with confidence. (b) The hazard ratio (and 95% confidence intervals) for first registration for two internalizing psychiatric disorders (MD—major depression and Anx Dis—anxiety disorders) in 1 140 608 Swedish individuals born 1972–1990 as a function of their school achievement at age 16 and their familial cognitive aptitude. For further details, see legend to (a). (c) The hazard ratio (and 95% confidence intervals) for first registration for two externalizing psychiatric disorders (DA—drug abuse and AUD—alcohol use disorders) in 1 140 608 Swedish individuals born 1972–1990 as a function of their school achievement at age 16 and their familial cognitive aptitude. For further details, see legend to (a). (d) The hazard ratio (and 95% confidence intervals) for first registration for two eating disorders (Ano—anorexia nervosa, Bul—bulimia nervosa) in 1 140 608 Swedish individuals born 1972–1990 as a function of their school achievement at age 16 and their familial cognitive aptitude. For further details, see legend to (a).

Figure 1

(a) The hazard ratio (and 95% confidence intervals) for first registration for six neurodevelopmental psychiatric disorders (ASD, autism spectrum disorder; SZ, schizophrenia, ONAP, other non-affective psychoses; OCD, obsessive compulsive disorder; ADHD, attention deficit hyperactive disorder; BP, bipolar disorder) in 1 140 608 Swedish individuals born 1972–1990 as a function of their school achievement at age 16 and their familial cognitive aptitude calculated from school achievement in full siblings and cousins and educational status in parents. s.d.—standard deviation. The X-axis reflects the familial cognitive aptitude divided into five groups: very low (− 2 s.d. below the mean), low (−1 s.d. below the mean), average, high (+1 s.d. above the mean) and very high (+2 s.d. above the mean). The Y-axis reflects the school achievement levels, in s.d. units, of individuals within each family type. Not all possible combinations are presented because some potential groups (e.g. familial cognitive aptitude of +2 s.d. and school achievement of −1 or − 2 s.d.) were too rare to calculate with confidence. (b) The hazard ratio (and 95% confidence intervals) for first registration for two internalizing psychiatric disorders (MD—major depression and Anx Dis—anxiety disorders) in 1 140 608 Swedish individuals born 1972–1990 as a function of their school achievement at age 16 and their familial cognitive aptitude. For further details, see legend to (a). (c) The hazard ratio (and 95% confidence intervals) for first registration for two externalizing psychiatric disorders (DA—drug abuse and AUD—alcohol use disorders) in 1 140 608 Swedish individuals born 1972–1990 as a function of their school achievement at age 16 and their familial cognitive aptitude. For further details, see legend to (a). (d) The hazard ratio (and 95% confidence intervals) for first registration for two eating disorders (Ano—anorexia nervosa, Bul—bulimia nervosa) in 1 140 608 Swedish individuals born 1972–1990 as a function of their school achievement at age 16 and their familial cognitive aptitude. For further details, see legend to (a).