One fifth of schizophrenia cases linked to Toxoplasma gondii?

"The PAF [population attributable fraction] for schizophrenia in those exposed to T. gondii is tentatively 21.4%". That was the headline conclusion made by Prof. Gary Smith [1] in his modelling analysis estimating what percentage of cases of schizophrenia might involve the protozoan Toxoplasma gondii. Some of the accompanying media about this potentially very important finding can be found here and here.

You don't need to study scaring, you just do it.

Although no expert on the PAF - defined as [2]: "the proportional reduction in average disease risk over a specified time interval that would be achieved by eliminating the exposure(s) of interest from the population while distributions of other risk factors in the population remain unchanged" - the author seems to have undertaken some nifty statistical analysis to calculate how many cases of schizophrenia might not occur if T. gondii infection wasn't present.

For those who might not be up to speed with this area, there is quite a bit of evidence to suggest that T. gondii infection (or history of infection) may well tie into the presentation of schizophrenia [3]. The evidence is not altogether straight-forward in this area [4] including some potential involvement for food (see a previous post), but there is certainly something more to see in this area of investigation and perhaps further in psychiatry. As I write this post, yet another study has found evidence of a possible link with schizophrenia in mind [5] and a meta-analysis [6]  has reported: "An increased seroprevalence of T. gondii IgM in patients with acute psychosis". I'll be coming back to that last paper in a subsequent post.

Prof. Smith has quite sensibly called for quite a bit more inspection of the possible connection between T. gondii infection and schizophrenia over and above just "ridiculing the idea of a connection". In the press release about his study he notes: "In other words, we ask, if you could stop infections with this parasite, how many cases could you prevent?” Smith said. “Over a lifetime, we found that you could prevent one-fifth of all cases. That, to me, is significant."

Knowing what we are starting to know about schizophrenia, it's direct and indirect impact on a person and the all-important possibility of plurality issues, I would have to agree that some priority be given to this line of thought albeit in conjunction with other factors undoubtedly moderating any relationship.

And since we're on the topic of organisms potentially affecting human behaviour, I'll draw your attention to a recent paper by Robert Yolken and colleagues [7] (a veteran of the T. gondii - schizophrenia research correlation) on Chlorovirus ATCV-1 and cognitive functions...

Music to close: Marina and the Diamonds with Primadonna.

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[1] Smith G. Estimating the population attributable fraction for schizophrenia when Toxoplasma gondii is assumed absent in human populations. Preventive Veterinary Medicine. 2014. October 23.

[2] Rockhill B. et al. Use and misuse of population attributable fractions. Am J Public Health. 1998 January; 88(1): 15–19.

[3] Torrey EF. et al. Toxoplasma gondii and other risk factors for schizophrenia: an update. Schizophr Bull. 2012 May;38(3):642-7.

[4] Li Y. et al. Association between antibodies to multiple infectious and food antigens and new onset schizophrenia among US military personnel. Schizophr Res. 2013 Dec;151(1-3):36-42.

[5] Khademvatan S. et al. Toxoplasma gondii Exposure and the Risk of Schizophrenia. Jundishapur Journal of Microbiology. 2014 November; 7(11): e12776.

[6] Monroe JM. et al. Meta-Analysis of Anti-Toxoplasma gondii IgM Antibodies in Acute Psychosis. Schizophr Bull. 2014 Nov 9. pii: sbu159.

[7] Yolken RH. et al. Chlorovirus ATCV-1 is part of the human oropharyngeal virome and is associated with changes in cognitive functions in humans and mice. Proc Natl Acad Sci U S A. 2014 Oct 27. pii: 201418895.

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Smith, G. (2014). Estimating the population attributable fraction for schizophrenia when Toxoplasma gondii is assumed absent in human populations Preventive Veterinary Medicine DOI: 10.1016/j.prevetmed.2014.10.009