Maternal Infection, Inflammation during Pregnancy Linked to Baby's Risk for Schizophrenia

Sarah Canetta, Ph.D. - Brain and behavior research expert on schizophrenia
Sarah Canetta, Ph.D.

Researchers have long known that women who get an infection such as the flu while pregnant have a slightly increased chance that their baby will develop schizophrenia in adulthood. However, because so many different types of infections, from bacteria to viruses to parasites, all increase the offspring's risk of schizophrenia, researchers think that activation of the immune system in general—rather than the specific pathogen causing the infection—is responsible. A new study, based on a large sample of people in Finland and published online June 27th in The American Journal of Psychiatry, strengthens this idea, and adds to the ever-growing pile of evidence implicating the immune system in schizophrenia.

The results are the latest findings from the Finnish Prenatal Studies, a large project that collected blood samples from all pregnant women who gave birth in Finland from 1983-1998, and followed the health of the infants all the way into adulthood. A team of researchers from Columbia University including 2013 NARSAD Young Investigator Grantee Sarah E. Canetta, Ph.D., and former NARSAD Grantees Christoph Kellendonk, Ph.D., (2002 and 2008) and Andre Leif Sourander, M.D., (2008) has tapped into this wealth of data to investigate the link between inflammation and schizophrenia.

The researchers found that, compared to the blood from moms whose offspring did not develop schizophrenia, the blood from the women whose progeny were later diagnosed with schizophrenia had higher levels of an inflammatory protein. Although not definitive proof, these results strongly suggest that higher levels of maternal inflammation during pregnancy are somehow involved in the development of some cases of schizophrenia, and may have implications for treatment and prevention of the illness.

Read more about this research on the Schizophrenia Research Forum.

Read the abstract for this research paper.

Article comments

Interesting. I've read there are virtually no cases I'd rheumatoid arthritis among schizophrenics. One don has schizoaffective disorder with a strong immune system and the other son has ankylosing spondylitis and asthma with no mental illness. Wonder about the connection or inversion of the same gene ....?

Will this be offered again? Or, archived?

. There are increasing evidences that favor the prenatal beginning of schizophrenia. These evidences point toward intra-uterine environmental factors that act specifically during the second pregnancy trimester producing a direct damage of the brain of the fetus. The current available technology doesn't allow observing what is happening at cellular level since the human brain it is not exposed to a direct analysis in that stage of the life. In 1977 we began a direct electron microscopic research of the brain of fetuses of schizophrenic mothers in order to finding differences at cellular level in relation to controls. In these studies we have observed within the nuclei of neurons the presence of complete and incomplete viral particles that reacted in positive form with antibodies to herpes simplex hominis type I [HSV1] virus, and mitochondria alterations. The importance of these findings can have practical applications in the prevention of the illness keeping in mind its direct relation to the aetiology and physiopathology of schizophrenia. A study of amniotic fluid cells in women at risk of having a schizophrenic offspring is considered. Of being observed the same alterations that those observed previously in the cells of the brain of the studied foetuses, it would intend to these women in risk of having a schizophrenia descendant, previous information of the results, the voluntary medical interruption of the pregnancy or an early anti HSV1 viral treatment as preventive measure of the later development of the illness.

when trying to breast feed my first born child my breasts became infected and I was treated with antibiotics. I was pregnant with my second child during that time. My second child at the age of 15 was diagnosed with schizophrenia. She now is dual diagnosed as schizoeffective I have been told I have a problem with how my blood metabolizes protein. The skin of my feet have a purplish color and blotchy. Could this be a correlation?

Schizophrenic monozygotic twins concordance is of only 45% although both twins share 100% of the derived genoma of a single zygote for what the discordance in monozygotic twins is related to the influence of prenatal environmental factors independently of genetic factors. These prenatal environmental factors are related to the alterations in the brain and the skin more frequently observed in patients since both tissues are derived from the embryonic ectoderm. This fact explains the anomalies of the nervous system together with anomalies of the hair, face, hands and feet more frequently observed in schizophrenics discordant twin than in the normal population. Among the environmental factors virus occupies a more and more excellent position for the results obtained in clinical observations in human and in experimental animals. A virus acting in this first phase of development, especially during the 2do. pregnancy trimester can explain the anomalies observed in both structures derived of the embryonic ectoderm in the affected twin. In our works the results obtained in an ultrastructural study are exposed in samples of the brain of two monozygotic twin fetuses with strong antecedents of schizophrenia in their family. The obtained findings indicate an infection for the virus herpes simplex hominis type I [HSV1] in the brain of one of the twins and mitochondria alterations. The obtained results can explain the discordance of the illness found in the postnatal clinical and epidemiologic studies. It should be considered their relation to the viral etiology to be the first direct evidence of virus in the brain of a fetus from a schizophrenic mother with important biological load of family schizophrenia.

Very interesting the results obtained by Sarah Canetta related to prenatal studies in schizophrenia that indicate a relation of maternal prenatal inflamatory findings and the develop of schizophrenia in the offsprings. In this sense The neurodevelopmental theory in the aetiology of schizophrenia is considered one of the most consistent at present. Evidence from epidemiological and neuropathological studies indicates that the pathogenic process that culminate in the development of schizophrenia are initiated early in life and has been associated with a variety of prenatal environmental insults to the developing brain, including infection. Although the infectious agents have been proposed as one of the risk factors for schizophrenia the data on the association of a specific infectious agent with prenatal brain evidence is absent. Understanding of the structural abnormalities would allow a better identification of neurodevelopmental processes that contribute to risk for schizophrenia. We have hypothesized that at ultra high-risk fetuses would have alterations at cellular level that would let us differentiate them to the comparison subjects. A reappraisal of our ultrastructural studies carried out in samples of the left temporal lobe of foetuses at ultra high risk of developing schizophrenia was published. The findings obtained are compatible with an active infection of the central nervous system by herpes simplex hominis type I [HSV1] virus. The present results are the first direct evidence that demonstrate the presence of this virus in the central nervous system of foetuses from schizophrenic mothers in the critical period of foetal development. The importance of this finding can have practical applications in the prevention of the illness keeping in mind its direct relation to the aetiology and physiopathology of schizophrenia.

Hypothesis: We have considered the hypothesis that the brains of fetuses from schizophrenic mothers would have alterations at cellular level that would allow to differing them of healthy controls. Unfortunately the human brain is not exposed to a direct observation in that stage of the life. Only an eventual circumstance as it is the interruption of a pregnancy for medical reasons that would allow us to observe possible alterations at cellular level. The magnitude of the obtained results depends on the resolution of the technique that is used. The only direct studies of the brain of fetuses from schizophrenic mothers with electron microscopic techniques carried out in the world up to where we know were carried out by us. The results obtained related to the blood from the women whose progeny were later diagnosed with schizophrenia that had higher levels of an inflammatory protein is according our results related to the presence of viral particles in the brain of fetuses from schizophrenic mothers. WHEN AN INFECTIOUS AGENT IS OBSERVED IN AN ILLNESS OF UNKNOWN ETIOLOGY IT HAS BEEN ALWAYS CONSIDERED: IF THE DISCOVERED AGENT IS ETIOLOGICALLY RELATED OR NOT WITH THE ILLNESS IN QUESTION. RELATED TO OUR RESULTS: lead to the question whether prenatal exposure to the virus observed is a risk factor for suffering schizophrenia later on. We must consider:
1. It can be a viral infection in the patients that affected the fetuses and not related with the etiology of the illness.
2. It can be a viral infection in the fetuses and the patients related with the etiology of the illness. In this sense several favorable circumstances converge:
A. Second pregnancy trimester
B. Family antecedents of schizophrenia and of severe neurodevelopmental disturbances
C. Presence of an incomplete viral form
D. Affectation of the neurons and of the nucleus mainly
E. Discordance of infection in monozygotic twins
F. Ultra high risk. Familial aggregation of schizophrenia. Mother and grandmother schizophrenics and two schizophrenic’s aunts in twins. Congenital malformations in two uncles.
G. None signs or clinical symptoms of infection were observed in the mothers neither in the fetuses
H. Not inflammatory reaction in the brain tissue
I. Similar previous findings in adult schizophrenics and in experimental animals
J. Samples from the tip of the left temporal lobe
K. Relationship with the herpes simplex hominis type 1 virus
L. Similar findings in other fetuses from schizophrenic mothers not in controls
M. Similar findings in the placenta in one study

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