In the Journals

Childhood infection linked to lower IQ, higher risk for psychosis in Swedish men

Golam Khandaker
Golam M. Khandaker
 

Research published in JAMA Psychiatry demonstrated that exposure to infections during the first year of life was associated with lower IQ and higher risk for nonaffective psychosis in adulthood.

“Prospective birth cohort studies suggest that childhood infections are associated with increased risk of schizophrenia in adulthood and with abnormal neurodevelopment in childhood/adolescence as measured by school grade or neurological soft signs; however, studies using IQ tests in a general population sample are rare,” Golam M. Khandaker, PhD, department of psychiatry, University of Cambridge, and colleagues wrote. “It is unclear whether lower IQ mediates or moderates the association between childhood infection and adult psychosis.”

Using population-based, longitudinal cohort study data from Sweden, researchers examined the relationship of infection during childhood with IQ and adult nonaffective psychosis. They also assessed whether shared familial confounding explains the infection-nonaffective psychosis and IQ-nonaffective psychosis relationships, and whether IQ alters the childhood infection-psychosis link. They included 647,515 Swedish men born between 1973 and 1992 in the analysis who were hospitalized with any infection from birth to age 13 years. They measured hospitalization for diagnosed nonaffective psychosis until the end of 2011, and IQ at age 18 years.

Khandaker and colleagues found that participants who were exposed to infections, especially in early childhood, were more likely to have lower IQ (adjusted mean difference for infection at birth to age 1 year = –1.61; 95% CI, –1.74 to –1.47) and increased risk for nonaffective psychosis in adulthood (adjusted HR = 1.19; 95% CI, 1.06-1.33). In addition, analysis showed a linear association between lower premorbid IQ and adult psychosis (adjusted HR per 1-point increase in IQ = 0.976; 95% CI, 0.974-0.978). Furthermore, IQ mediated (P<.001) and moderated (multiplicative; P=.02 and additive; P=.001) the relationship between childhood infection and nonaffective psychosis. Participants with lower IQ saw a greater link between childhood infection and risk for adult psychosis compared with those with higher IQ.

The association between IQ and nonaffective psychosis did not significantly differ in the general population and in relative pairs with discrepant IQs, indicating that shared familial factors probably do not completely explain this association, according to the researchers, and also suggesting that lower premorbid IQ in those with psychosis may come from unique environmental factors, such as infection in early life.

“We present evidence that early childhood is a sensitive period for the effects of infection on IQ and risk of [nonaffective psychosis],” Khandaker and colleagues wrote. “Childhood infection may increase risk of adult [nonaffective psychosis] by affecting neurodevelopment and by exaggerating the effects of cognitive vulnerability to psychosis.” – by Savannah Demko

Disclosures: The authors report no relevant financial disclosures.

Golam Khandaker
Golam M. Khandaker
 

Research published in JAMA Psychiatry demonstrated that exposure to infections during the first year of life was associated with lower IQ and higher risk for nonaffective psychosis in adulthood.

“Prospective birth cohort studies suggest that childhood infections are associated with increased risk of schizophrenia in adulthood and with abnormal neurodevelopment in childhood/adolescence as measured by school grade or neurological soft signs; however, studies using IQ tests in a general population sample are rare,” Golam M. Khandaker, PhD, department of psychiatry, University of Cambridge, and colleagues wrote. “It is unclear whether lower IQ mediates or moderates the association between childhood infection and adult psychosis.”

Using population-based, longitudinal cohort study data from Sweden, researchers examined the relationship of infection during childhood with IQ and adult nonaffective psychosis. They also assessed whether shared familial confounding explains the infection-nonaffective psychosis and IQ-nonaffective psychosis relationships, and whether IQ alters the childhood infection-psychosis link. They included 647,515 Swedish men born between 1973 and 1992 in the analysis who were hospitalized with any infection from birth to age 13 years. They measured hospitalization for diagnosed nonaffective psychosis until the end of 2011, and IQ at age 18 years.

Khandaker and colleagues found that participants who were exposed to infections, especially in early childhood, were more likely to have lower IQ (adjusted mean difference for infection at birth to age 1 year = –1.61; 95% CI, –1.74 to –1.47) and increased risk for nonaffective psychosis in adulthood (adjusted HR = 1.19; 95% CI, 1.06-1.33). In addition, analysis showed a linear association between lower premorbid IQ and adult psychosis (adjusted HR per 1-point increase in IQ = 0.976; 95% CI, 0.974-0.978). Furthermore, IQ mediated (P<.001) and moderated (multiplicative; P=.02 and additive; P=.001) the relationship between childhood infection and nonaffective psychosis. Participants with lower IQ saw a greater link between childhood infection and risk for adult psychosis compared with those with higher IQ.

The association between IQ and nonaffective psychosis did not significantly differ in the general population and in relative pairs with discrepant IQs, indicating that shared familial factors probably do not completely explain this association, according to the researchers, and also suggesting that lower premorbid IQ in those with psychosis may come from unique environmental factors, such as infection in early life.

“We present evidence that early childhood is a sensitive period for the effects of infection on IQ and risk of [nonaffective psychosis],” Khandaker and colleagues wrote. “Childhood infection may increase risk of adult [nonaffective psychosis] by affecting neurodevelopment and by exaggerating the effects of cognitive vulnerability to psychosis.” – by Savannah Demko

Disclosures: The authors report no relevant financial disclosures.