Anyway, I commerate the day with this post on schizophrena and an old friend.
This is not the first time that the topic of Toxoplasma gondii has graced this blog and probably won't be the last time either. What is perhaps so fascinating about this parasitic protozoa is its single-minded drive to survive (and replicate) and, as a result, its ability to affect animal behaviour by whatever mechanism.
Fine if you are a rodent I hear you cry. But when it comes to human beings, much of the recent chatter about T.gondii has been on its speculated links to conditions like psychosis, mood disorders and, in extreme cases, suicide. Presentation of schizophrenia spectrum conditions and the risks associated with T.gondii infection have also figured fairly prominently in the various discussions as a result of studies like this one and this one from Faith Dickerson and colleagues. A recent study by Pedersen and colleagues* published in the American Journal of Psychiatry has confirmed an association between T.gondii infection and risk of schizophrenia. Association is one thing; causation is another. I note that Dr Emily Deans over at Evolutionary Psychiatry has just posted about this study also.
The facts and figures:
- IgG-antibodies specific to T.gondii were measured in over 45,000 women in Denmark giving birth between 1992 and 1995.
- Women were followed up until 2008 for the presence of a schizophrenia spectrum condition.
- A positive association between T.gondii antibody level and risk of schizophrenia was found; with risk varying according to the strength of the antibody response. The overall risk was 1.68, although where antibody levels were highest, that rose to 1.73.
There are some interesting points to take from the cumulative research on T.gondii. Not everyone who is infected with this little scoundrel will go on to develop schizophrenia or other conditions. Obviously there are other factors also at work. The immune system is the first place to look; how our bodies handle such infections, viruses, bacteria and how genes and environment might interact either in a protective or facilitative fashion. I touched upon this briefly with my post on the C4B null allele in relation to autism and a few other conditions. I note also this recent publication from Whitmarsh and colleagues** published in the journal Cell Host & Microbe which suggested that knockout mice (is this the right term?) might more frequently succumb to T.gondii infection when specific cytokine signalling molecules are absent; one factor probably among many. It is not as straight-forward as to say this molecule does this and this one does this; more likely a combination of multiple factors coupled with a cascade effect confer protection or not.
So there you have it, more evidence for the influencing factor of environment on our behaviour. Makes you wonder whether we should be looking more closely at some of the treatments for T.gondii and any potential onward effects for psychological symptoms? Or do we already have our treatment measures?
* Pedersen MG. et al. Toxoplasma infection and later development of schizophrenia in mothers. Am J Psychiatry. August 2011.
** Whitmarsh RJ. et al. A critical role for SOCS3 in innate resistance to Toxoplasma gondii. Cell Host & Microbe. September 2011.
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