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Published Online: 1 February 2015

Maternal C-Reactive Protein and Schizophrenia

To the Editor: In their article published in the September 2014 issue of the Journal, Sarah Canetta, Ph.D., et al. (1) report that increasing maternal C-reactive protein levels, classified as a continuous variable, were significantly associated with schizophrenia in offspring (adjusted odds ratio reported in the abstract=1.31; 95% confidence interval [CI]=1.10–1.56; adjusted odds ratio reported in the results=1.28; 95% CI=1.07–1.54). The authors interpret this finding from Finland as evidence that maternal inflammation plays a role in this disorder and claim that this inflammation may be due to infections during pregnancy.
Surprisingly, the authors do not mention the possibility that the increased C-reactive protein levels were caused by maternal smoking. Levels of C-reactive protein are increased in smokers and remain elevated up to 5 years after cessation (2, 3). This is important because schizophrenia patients are more likely to have a mother who smoked during pregnancy (4). Moreover, smoking during pregnancy is relatively common in Finland. An investigation in 1997 found high prevalence rates among single (30%) and less educated (25%) pregnant women (5). Thus, the increase in maternal C-reactive protein levels may be due, at least in part, to smoking. The same considerations apply to the association, reported by the same research group, between maternal C-reactive protein and autism (6).
Finally, it is worth remembering that the results of studies on the relationship between prenatal infection and schizophrenia are not entirely consistent. Birth during the 9-month period after the 1957 influenza pandemic, which produced infection rates of about 50%, was not a risk factor for schizophrenia (7).

References

1.
Canetta S, Sourander A, Surcel HM, et al: Elevated maternal C-reactive protein and increased risk of schizophrenia in a national birth cohort. Am J Psychiatry 2014; 171:960–968
2.
Bazzano LA, He J, Muntner P, et al: Relationship between cigarette smoking and novel risk factors for cardiovascular disease in the United States. Ann Intern Med 2003; 138:891–897
3.
Hastie CE, Haw S, Pell JP: Impact of smoking cessation and lifetime exposure on C-reactive protein. Nicotine Tob Res 2008; 10:637–642
4.
Stathopoulou A, Beratis IN, Beratis S: Prenatal tobacco smoke exposure, risk of schizophrenia, and severity of positive/negative symptoms. Schizophr Res 2013; 148:105–110
5.
Jaakkola N, Jaakkola MS, Gissler M, et al: Smoking during pregnancy in Finland: determinants and trends, 1987–1997. Am J Public Health 2001; 91:284–286
6.
Brown AS, Sourander A, Hinkka-Yli-Salomäki S, et al: Elevated maternal C-reactive protein and autism in a national birth cohort. Mol Psychiatry 2014; 19:259–264
7.
Selten JP, Frissen A, Lensvelt-Mulders G, et al: Schizophrenia and 1957 pandemic of influenza: meta-analysis. Schizophr Bull 2010; 36:219–228

Information & Authors

Information

Published In

Go to American Journal of Psychiatry
Go to American Journal of Psychiatry
American Journal of Psychiatry
Pages: 200
PubMed: 25640933

History

Accepted: November 2014
Published online: 1 February 2015
Published in print: February 01, 2015

Authors

Affiliations

Jean-Paul Selten, M.D., Ph.D.
From the Department of Psychiatry and Psychology, Maastricht University Medical Centre, Maastricht, the Netherlands; and the Department of Psychosis Studies, King’s College London, King’s Health Partners, London.
Jim van Os, M.D., Ph.D.
From the Department of Psychiatry and Psychology, Maastricht University Medical Centre, Maastricht, the Netherlands; and the Department of Psychosis Studies, King’s College London, King’s Health Partners, London.

Funding Information

The authors report no financial relationships with commercial interests.

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