Showing posts with label population attributable fraction (PAF). Show all posts
Showing posts with label population attributable fraction (PAF). Show all posts

Friday, 28 December 2018

"Psychotic experiences are important clinical markers of risk for future suicidal behavior"

The quote titling this post - "Psychotic experiences are important clinical markers of risk for future suicidal behavior" - comes from the systematic review and meta-analysis findings reported by Kathryn Yates and colleagues [1].

Authors posed the research question: "Are psychotic experiences associated with an increased risk of later suicidal ideation, suicide attempt, and/or suicide death?" and looked to the existing peer-reviewed research literature to try and answer it. Based on the combined results from ten studies that "reported on 84 285 participants from 12 different samples and 23 countries" and met the inclusion criteria of their review, Yates et al made some important conclusions.

"Individuals who reported psychotic experiences had an increase in the odds of future suicidal ideation (5 articles; n = 56 191; odds ratio [OR], 2.39 [95% CI,1.62-3.51]), future suicide attempt (8 articles; n = 66 967; OR, 3.15 [95% CI, 2.23-4.45]), and future suicide death (1 article; n = 15 049; OR, 4.39 [95% CI, 1.63-11.78])." These are important statistics. They translate into some important details insofar as "individuals who reported PEs [psychotic experiences] had 2-fold increased odds of subsequent suicidal ideation, 3-fold increased odds of subsequent suicide attempt, and 4-fold increased odds of subsequent suicide death." Some further nifty statistical analysis from the authors looking into something called the population-attributable fraction (PAF), defined as "the proportion of incidents in the population that are attributable to the risk factor", suggested that the percentage figure for "PEs for suicide attempts and suicide deaths combined was 24.7%." That is also something rather important.

Should anyone be surprised by these results? Well, yes and no. Yes, because the magnitude of the association between PEs and suicidal behaviours was probably a lot more pronounced than many would have perhaps expected. No, because other literature has talked about psychosis in depression for example, as being potentially important to the development and presentation of suicidal behaviour (see here). Having said all that, I will reiterate that suicidal behaviours are very complicated.

Aside from the important issue of potentially expanding screening for suicidal behaviours when PEs are present, there are other factors to consider. Not least that: "The mechanisms explaining the association between PEs and suicidal behavior are potentially manifold." I was particularly interested in one theory put forward by the authors, suggesting that: "In the context of high stress and poorer communication skills, this might adversely affect the individual’s ability to formulate logical plans to manage perceived challenges and instead increase the likelihood of turning to suicide." Such an idea is based on other findings observing that there may be cognitive 'challenges' accompanying PEs that may impair problem-solving skills. Y'know, not having the skills to stop molehills from turning into mountains? Perhaps further research in this area might also turn to looking at some of the underlying biology behind such issues as well as the psychology. How, for example, inflammatory processes and the immune system *might* show some important involvement (see here and see here) for at least some people? One future avenue of research attention at least.

The data from Yates and colleagues is particularly poignant at the time of writing this post as the US CDC release figures suggesting that suicide mortality in the United States has climbed and climbed and climbed over the past few decades (see here). Again, the reasons are probably going to be complicated but that shouldn't stop people from continually asking 'why?' and 'what can we do about them?'

I close this post with some important contact details should anyone need someone to talk to (see here)...

----------

[1] Yates K. et al. Association of Psychotic Experiences With Subsequent Risk of Suicidal Ideation, Suicide Attempts, and Suicide Deaths. JAMA Psychiatry. 2018. Nov 28.

----------

Friday, 14 November 2014

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.

----------

[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.

----------

ResearchBlogging.org 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