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Running head: FEVER IN, SCHIZOPHRENIA OUT RESEARCH

Fever In, Schizophrenia Out

Márcio Padilha

Lewis-Clark State College

PSYC 226 – Ravet

Fall/2010

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Fever In, Schizophrenia Out Research

Schizophrenia is “a disabling mental disorder characterized by the loss of contact

with reality and by disturbances in perception, emotion, cognition, and motor behavior”

(Klein & Thorne, 2007). In light of its commonality and debilitating effects to sufferers and

their families, scientists have researched it extensively trying to understand how genetics

factors affect the sufferer’s predisposition to develop the condition in adulthood (Klein &

Thorne, 2007).

Amongst the different studies conducted, J. R. Minkel reports that scientists had

suspected that exposure to influenza during pregnancy raises risk of offspring developing

schizophrenia later in life” (Minkel, 2004). In order to further explore this venue, the first

study comprehended a maternal serologic analysis where the primary exposure measure

was influenza infection, which, in accordance with the results of the validity study, was

defined as the first occurrence during pregnancy of an influenza antibody titer of 1:20 or

greater. This was a “nested case-control study of a large birth cohort, born from 1959

through 1966, and followed up for psychiatric disorders 30 to 38 years later.” Cases were

64 birth cohort members diagnosed as having schizophrenia spectrum disorders (mostly

schizophrenia and schizoaffective disorder). Controls were 125 members of the birth

cohort, had not been diagnosed as having a schizophrenia spectrum or major affective

disorder, and were matched to cases on date of birth, sex, length of time in the cohort, and

availability of maternal serum. The findings of this study represent the first serologic

evidence that prenatal influenza plays a role in schizophrenia which, if confirmed, may

have implications for the prevention of schizophrenia and for unraveling pathogenic

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mechanisms of the disorder. Although the study analogically addressed brain structure and

function in mice, it does not per se specifically address human brain structure and function

(Brown, et al., 2004). Nevertheless, relevance and congruence is established in that

“postmortem examinations of the brains of people with schizophrenia have revealed

differences in specific neural structures when compared with normal individuals without

schizophrenia and those with other mental disorders” and that such differences comprise

larger spaces which suggest “less brain matter” as “enlarged ventricles have been

attributed to smaller-than-normal neurons and increased neuronal density and the loss of

neurons in structures near the ventricles such as the amygdala and hippocampus” (Klein &

Thorne, 2007).

The “Serologic Evidence of Prenatal Influenza in the Etiology of Schizophrenia” does

point out that the serologic material analyzed possessed great integrity. Nevertheless, it

also mentioned that “ecologic studies have demonstrated associations between

schizophrenia and prenatal exposure to polio, varicella-zoster, and measles” and that

“study also did not include data on family history of schizophrenia, which would have

permitted the adjustment for possible confounding by this factor, and the examination of

interaction between prenatal influenza exposure and genetic susceptibility to

schizophrenia”, which has great potential for tainting of actual results. Furthermore, as per

Minkel, the number of subjects studied does not have statistical expression and further

independent replication is needed for validity reaffirmation.

The risk of schizophrenia was increased 7-fold for influenza exposure during the

first trimester. There was no increased risk of schizophrenia with influenza during the

second or third trimester. With the use of a broader gestational period of influenza

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exposure — early to mid-pregnancy — the risk of schizophrenia was increased 3-fold. The

findings persisted after adjustment for potential confounders. These findings represent the

first serologic evidence that prenatal influenza plays a role in schizophrenia. If confirmed,

the results may have implications for the prevention of schizophrenia and for unraveling

pathogenic mechanisms of the disorder (Brown, et al., 2004)

Therefore, in light of all presented evidence in the literature at hand, I would infer

that the presence of prenatal influenza infection is not necessarily a unique predisposing

element for the onset of schizophrenia in the adulthood as it has been further evidenced

that other prenatal infections may precipitate such outcome in similar fashion.

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Works Cited

Brown, A. S., Begg, M. D., Gravenste, S., Schaefer, C. A., Wyatt, R. J., Bresnahan, M., et al. (2004). Serologic Evidence of Prenatal Influenza in the Etiology of Schizophrenia. Arch Gen Psychiatry , 61:774-780.

Klein, S. B., & Thorne, B. M. (2007). Biological Psychology. New York: Worth Publishers.

Minkel, J. R. (2004). Fever In, Schezophrenia Out. Scientific American , p. 38.