Inflammation in Childhood May Cause Depression, Psychosis in Adulthood

Study data showed that increased levels of infection, inflammation, and metabolic alterations frequently observed in people with depression and psychosis may be a cause rather than a consequence of these disorders.

Early-life infection, inflammation, and metabolic changes may play a key role in the development of certain psychiatric disorders, according to a growing body of research. During critical periods of brain development, data have demonstrated that immunometabolic risk factors may potentially contribute to the development of depression, psychiatric disorders, and schizophrenia in particular, later in life.1,2

Published in a special issue of the Harvard Review of Psychiatry, the study authors presented data from this line of research that they noted could provide new approaches to the treatment of depression and psychosis in adults. Further, this research may lead to the prevention of these disorders using methods that target immunometabolic risk factors in early life.1,2

"This special issue of the Harvard Review of Psychiatry tackles this intriguing topic of psychoimmunology from various perspectives reflecting the interdisciplinary nature of the problem at hand," writes guest editor Paulo Lizano, MD, PhD, of Harvard Medical School and Beth Israel Deaconess Medical Center, in an introduction to the issue.1

Study findings presented in the article demonstrated linear dose-response associations connecting high concentrations of circulating inflammatory markers, such as the inflammatory cytokine interleukin 6 marker, during patients’ early life with an increased risk for depression and psychosis later in life.2

Additionally, the study authors found that the results suggest inflammation has a causal relationship with a subset of psychiatric disorders outside of the common categorization detailed in the Diagnostic and Statistical Manual of Mental Disorders, which is the standard resource in the field for the diagnosis of mental disorders.1,2

In prior research, data have demonstrated that maternal and childhood infections may be correlated with the psychiatric diagnoses later in life, and in particular, a schizophrenia diagnosis. Additionally, other research has also found associations present between inflammation markers in children and adolescents and increased rates of depression and psychosis in adulthood. However, the correlations observed were complex, with specific markers of inflammation in early life found to be associated with specific symptoms in adulthood.1,2

The study authors noted that the results of their analysis suggest that increased levels of infection, inflammation, and metabolic alterations that have been frequently observed in people with depression and psychosis, although previously thought to be a consequence of these disorders are, in fact, more clearly linked to being their potential cause.1

"Despite these many advances, much still remains unknown, and further research is needed to enhance the clinical applicability of these findings," Lizano wrote in the issue’s introduction.1

Additionally, Lizano noted some points requiring further analysis based on the results of the research presented, including the identification of "inflammatory subtypes" associated with psychiatric disorders to aid in the development of treatments for those disorders, which may help to address not only their symptoms but also their cause. Further, Lizano explained that investigation into strategies to help with early recognition and treatment in children and adolescents may help to prevent low-grade inflammation in the brain during critical stages of its development.1,2

REFERENCE

  1. Could childhood inflammation or infection be a cause of depression and psychosis? Wolters Kluwer Health; Jan 11, 2022. Accessed Jan 12, 2022. https://www.eurekalert.org/news-releases/939841
  2. Kappelmann N, Perry BI, Khandaker GM. Prenatal and Childhood Immuno-Metabolic Risk Factors for Adult Depression and Psychosis. Harvard Review of Psychiatry. 2022;30(1):8-23. doi: 10.1097/HRP.0000000000000322