Friday, 27 March 2015

Inflammation impairs social cognitive processing

A quote to begin: "acute inflammation can lead to decreases in the ability to accurately and reliably comprehend emotional information from others."

It comes from the article published by Mona Moieni and colleagues [1] who examined a concept familiar to many people with a connection to autism either personally or professionally: Theory of Mind (ToM). Rather interestingly, Moieni et al "examined whether exposure to an experimental inflammatory challenge led to changes in ToM." Inflammatory challenge refers to the artificial induction of a state of inflammation via the use of something called endotoxin, something I've covered under another name previously on this blog (see here).

As part of a larger research project on inflammation-induced depressed mood (see here) researchers set about looking at social cognition under inflammatory-inducing and placebo conditions specifically based on the "Reading the Mind in the Eyes (RME) test". The RME test has quite a firm foundation in autism research [2]. Their results indicated that using the RME test as a sort of measure of ToM "endotoxin (vs. placebo) led to decreases in performance on the RME test from baseline to the peak of inflammatory response, indicating that acute inflammation can lead to decreases in the ability to accurately and reliably comprehend emotional information from others."

With the caveats that (a) this wasn't a study of people with autism (or at least not those diagnosed with autism) and (b) acute inflammation may not be the same as chronic inflammation, these are intriguing results potentially overlaying onto several other research areas. Autism and inflammation is something that I'm quite interested in on this blog as per the idea that physiology and psychology might not be some far apart in certain cases/types of autism (see here). That other somatic manifestations might also be linked to inflammatory processes with autism in mind (see here) is something else to mention.

I hold back from saying that all those with autism who 'fail' ToM tasks are somehow in a state of inflammation given that this is a complicated area (see here). As per my previous ramblings, I'm also not necessarily the greatest fan of the sweeping generalisations made about ToM when it comes to autism (see here). Particularly when one looks at the way that ToM is examined in relation to autism [3] and how ToM issues cross quite a few different labels [4] some of which might overlap with autism (see here).

Still, if there is the remotest possibility that the physiological state of acute inflammation might correlate with issues with mentalising or completing mentalising tasks, I'd be minded to suggest that future work on ToM might be minded to take this into account. Likewise, in all those studies looking at inflammatory processes linked to something like autism, measuring ToM before and after could represent an interesting parameter when looking at potential interventions...

Some music then... The Wedding Present and My Favourite Dress.

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[1] Moieni M. et al. Inflammation impairs social cognitive processing: A randomized controlled trial of endotoxin. Brain, Behavior, and Immunity. 2015. May 10.

[2] Baron-Cohen S. et al. The "Reading the Mind in the Eyes" Test revised version: a study with normal adults, and adults with Asperger syndrome or high-functioning autism. J Child Psychol Psychiatry. 2001 Feb;42(2):241-51.

[3] Iao LS. & Leekam SR. Nonspecificity and theory of mind: new evidence from a nonverbal false-sign task and children with autism spectrum disorders. J Exp Child Psychol. 2014 Jun;122:1-20.

[4] Chung YS. et al. A meta-analysis of mentalizing impairments in adults with schizophrenia and autism spectrum disorder. Schizophr Bull. 2014 May;40(3):602-16.

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ResearchBlogging.org Moieni M, Irwin MR, Jevtic I, Breen EC, & Eisenberger NI (2015). Inflammation impairs social cognitive processing: a randomized controlled trial of endotoxin. Brain, behavior, and immunity PMID: 25770082

Thursday, 26 March 2015

Autism increases risk of nonaffective psychotic disorder and bipolar disorder

Published at the same time and in the same journal as the 'MoBa does bowel issues in autism' paper from Bresnahan and colleagues [1], the study results from Jean-Paul Selten et al [2] reporting that "A diagnosis of ASD [autism spectrum disorder] is associated with a substantially increased risk for NAPD [nonaffective psychotic disorder] and BD [bipolar disorder]" has, at the time of writing this post, received little or no press attention in comparison despite being pretty important findings.

Continuing an important theme that a diagnosis of autism is in no way protective against the development of mental health issues (see here), the Selten results suggest that quite a bit more diagnostic vigilance might be required in order to ensure that further health inequalities do not appear for those on the autism spectrum.

Containing a familiar author name - Cecilia Magnusson, who is no stranger to autism research - the authors set about analysing data from the Stockholm Youth Cohort [3] and specifically "included cohort members ever diagnosed as having ASD (n = 9062) and their full siblings never diagnosed as having ASD." Cases were matched 10 to 1 with controls of the same sex and born in the same month/year. Researchers looked for diagnoses of NAPD and BD and importantly "adjusted for age, sex, population density of place of birth, personal or parental history of migration, hearing impairment, parental age, parental income, parental educational level, and parental history of psychiatric disorder."

Results: distinguishing between cases of autism with intellectual (learning) disability and those without, those diagnosed with autism without intellectual disability (ID) were calculated to show "a substantially increased risk for NAPD and BD" compared with controls. Depending on whether ASD was "registered before age 16 or 28 years" also seemed to play a role in the risk (odds ratios, ORs) statistics. Those "non-ID ASD registered before age 28 years" presented with ORs of 12.3 and 8.5 respectively for NAPD and BD. Those "non-ID ASD registered before age 16 years" presented with ORs of 5.6 and 5.8 respectively. The comparative statistics for full siblings of those with ASD for NAPD and BD were also elevated (ORs: 1.8 and 1.7 respectively) but nothing like to the degree noted for those with a diagnosis of ASD.

As I've mentioned, these are important findings. I've talked a few times on this blog about conditions like psychosis being diagnosed alongside cases of autism (see here and see here). The data from Khandaker and colleagues [4] (see here) reporting on a "Higher risk of PEs [psychotic experiences] in early adolescence among individuals with childhood ND [neurodevelopmental disorders]" adds to the evidence that there may be shared mechanisms at work when it comes to something like autism and schizophrenia for example (see here). This might also mean that our views about autism across the lifespan should more thoroughly incorporate the higher risk of mental health issues potentially being noted. Anyone who follows this blog and my ramblings about the health inequalities associated with something like schizophrenia (see here for example) will know what this might mean for some on the autism spectrum too.

Insofar as the findings on bipolar disorder potentially being more frequently noted when autism is mentioned, I'm not at all surprised. 'Bipolar disorder is frequent in adult Asperger syndrome' was a post I previously wrote on this topic and how, based on research like that from Vannucchi and colleagues [5], anywhere between 6-20% of those with Asperger syndrome (AS) can potentially expect to be diagnosed with BD at some stage. Actually I'd probably suggest the rate might be higher than those statistics suggest given the assertion that BD in autism/AS is: "often characterized by atypical presentation, making its correct identification particularly difficult."

Need I say any more?

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[1] Bresnahan M. et al. Association of Maternal Report of Infant and Toddler Gastrointestinal Symptoms With Autism Evidence From a Prospective Birth Cohort. JAMA Psychiatry. 2015. March 25.

[2] Selten JP. et al. Risks for Nonaffective Psychotic Disorder and Bipolar Disorder in Young People With Autism Spectrum Disorder: A Population-Based Study. JAMA Psychiatry. 2015 Mar 25.

[3] Idring S. et al. Autism spectrum disorders in the Stockholm Youth Cohort: design, prevalence and validity. PLoS One. 2012;7(7):e41280.

[4] Khandaker GM. et al. A population-based longitudinal study of childhood neurodevelopmental disorders, IQ and subsequent risk of psychotic experiences in adolescence. Psychol Med. 2014 Nov;44(15):3229-38.

[5] Vannucchi G. et al. Bipolar disorder in adults with Asperger׳s Syndrome: A systematic review. J Affect Disord. 2014 Jul 8;168C:151-160.

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ResearchBlogging.org Selten JP, Lundberg M, Rai D, & Magnusson C (2015). Risks for Nonaffective Psychotic Disorder and Bipolar Disorder in Young People With Autism Spectrum Disorder: A Population-Based Study. JAMA Psychiatry PMID: 25806797

Wednesday, 25 March 2015

MoBa does bowel issues in autism

'MoBa' in the title of this post, refers to the Norwegian Mother and Child Cohort Study and a handy resource which has already impacted on autism research (see here for example).

Now MoBa has turned its epidemiological clout to an issue which less and less is encountering scientific resistance: are gastrointestinal (GI) symptoms over-represented when it comes to a diagnosis of autism? Further, when do such bowel issues start to present?

The answer, shown in the paper by Michaeline Bresnaha and colleagues [1] is yes, functional bowel symptoms are seemingly more frequently reported when it comes to autism as per the results of quite a few other studies. To quote from the authors: "maternally reported GI symptoms are more common and more often persistent during the first 3 years of life in children with ASD [autism spectrum disorder] than in children with TD [typical development] or DD [developmental delay]." Said symptoms also seemed to present pretty early on; quite a bit before many children are diagnosed with autism. Some further coverage of these findings can be seen here and here.

Including a couple of giants in research terms on the authorship list - Mady Hornig and Ian Lipkin - who also continue to push the research boundaries in relation to another diagnosis which crops up on this blog (CFS/ME or SEID as it may well be eventually known) - MoBa was put to use.

Authors "defined 3 groups of children: children with ASD (n = 195), children with DD and delayed language and/or motor development (n = 4636), and children with TD (n = 40 295)." Maternal reports garnered prospectively covering various GI symptoms including "constipation, diarrhea, and food allergy/intolerance" were analysed across the groups covering children at 6, 18 and 36 months of age.

The results suggested that constipation and food allergy/intolerance were more likely to be reported in children with autism during the 6-18 month old age range compared with typically developing controls. Diarrhoea and food allergy/intolerance were also more likely to be reported in children with autism in the 18-36 month age range again, compared with TD controls. Children with autism/ASD were also more likely to present with "1 or more GI symptom in either the 6- to 18-month or the 18- to 36-month-old age period and more than twice as likely to report at least 1 GI symptom in both age periods compared with mothers of children with TD or DD." Some might quibble about the use of maternal report in discussing the presentation of bowel issues in children but I'm not one of them (see here) as the Gorrindo findings [2] drift back into my consciousness.

The press release attached to this study also contains an intriguing quote from Mady Hornig: "Although the connection of GI disturbances to autism remains unclear, the presence of GI symptoms in early life may not only help to identify a subset of children with autism who require clinical input for their GI issues, it may also open new avenues for determining the underlying nature of the disorder in that subgroup." The implication being that (a) GI symptoms, early GI symptoms, are not a universal (or exclusive) feature of autism, but are present in quite a few infants, and (b) among the increasingly pluralised view of autism (see here), the idea that said GI symptoms might represent something quite fundamental to some cases of autism offers something of an opportunity to perhaps intervene and treat/manage both bowel symptoms and potentially impact on behavioural features linked to autism. On this point I'm drawn back to some of the research from Micah Mazurek and colleagues talking about sensory issues and anxiety completing a triad with bowel issues with autism in mind (see here).

I'm probably repeating myself here but quite a bit more research is required on the relationship between autism and the presentation of GI issues. I'd be inclined to suggest that a few research areas might be useful to explore: (a) the link between functional bowel issues and more pathological bowel states (see here), (b) the link between inflammation / inflammatory markers and bowel issues (see here) taking into account the work of people like Harumi Jyonouchi for example (see here), (c) the possibility that bowel issues might have some connection back to the gut microbiota as per other work by Hornig/Lipkin (see here), and (d) how said GI issues might impact on issues such as pharmacotherapy in terms of drug availability and absorption issues (see here). This isn't an exhaustive list, just a few ideas to play around with.

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[1] Bresnahan M. et al. Association of Maternal Report of Infant and Toddler Gastrointestinal Symptoms With Autism Evidence From a Prospective Birth Cohort. JAMA Psychiatry. 2015. March 25.

[2] Gorrindo P. et al. Gastrointestinal dysfunction in autism: parental report, clinical evaluation, and associated factors. Autism Res. 2012 Apr;5(2):101-8.

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ResearchBlogging.org Bresnahan, M., Hornig, M., Schultz, A., Gunnes, N., Hirtz, D., Lie, K., Magnus, P., Reichborn-Kjennerud, T., Roth, C., Schjølberg, S., Stoltenberg, C., Surén, P., Susser, E., & Lipkin, W. (2015). Association of Maternal Report of Infant and Toddler Gastrointestinal Symptoms With Autism JAMA Psychiatry DOI: 10.1001/jamapsychiatry.2014.3034

Autism and depression: interlinked?

"A possible implication is that interventions aimed at either autism symptoms or symptoms of depression may improve the other."

That was the intriguing statement made by Per Normann Andersen and colleagues [1] who "investigated the course of and association among changes in autism symptoms, depression symptoms and executive functions (EF) in children with high-functioning autism (HFA)." Aside from frowning a little at the mention of the concept of 'high-functioning' I assume to denote those who have "relatively mild symptoms which, despite their mildness, are significant enough to merit an autism spectrum diagnosis" according to one description (see here), I was interesting in the Andersen findings. Specifically, the idea that the spectrum of depression (depressive illness if you will) might be something rather more integral to the presentation of autism at least for some people.

I've talked before about depression as one of several mental health issues/problems perhaps over-represented following a diagnosis of autism (see here). The paper by Vannucchi and colleagues [2] covered in a previous post (see here) did particularly well bringing into sharp focus the fact that bipolar disorder may very well be a frequent comorbidity in cases of Asperger syndrome albeit "often characterized by atypical presentation, making its correct identification particularly difficult."

Of course this is not the first time that something of a rather intimate relationship has been reported when considering depression and autism together. Takara & Kondo [3] (open-access) reported that: "Depressed adults with comorbid atypical autistic traits are at higher risk for suicide attempts and may engage in methods that are more lethal" based on their case-control study. This is perhaps one of the more extreme outcomes potentially associated with depression but also highlights something of a growing realisation that suicide ideation may not be an uncommon issues reported by some on the autism spectrum (see here) and may to some extent tie into the presentation of depression.

Further work is required to better categorise depression comorbid to a diagnosis on the autism spectrum as per the the findings from Gotham and colleagues [4]. Additional work is also required on the best way(s) to tackle depression in cases of autism whether based on pharmacotherapy or other more psychological approaches. I might also advance the case that several other potentially important variables be also examined, such as vitamin D (see here) in light of the evidence related to autism in this area and the various anti-inflammatory strategies (see here) also tentatively put forward as management options for depression. Inflammation and autism, as some readers might know, is a topic in the research ascendancy (see here). There may be other areas slightly outside of the mainstream that might also be considered as research targets too.

Without any medical advice given or intended, I'm also going to link you to the case study (stress: case study) presented by Philip Bird [5] (open-access) talking about the use of the anti-epileptic phenytoin with a young man with autism. Aside from some interesting positive effects recorded on autism presentation, Bird also noted that: "Post-treatment, there was robust change in all domains, with an absence of depressive symptoms and with both anxiety and stress being recorded as moderate." I'm not saying that this will be for everyone (personalised medicine and all that). Merely that there may be many different ways of tackling such issues when combined and some thinking 'outside of the box' might be required.

The next questions: how does depression combine with something like anxiety with autism in mind, and what happens to depressive and other symptoms when anxiety is 'treated'? Further, given the connection between depression and other diagnoses such as schizophrenia [6] and acknowledging that a diagnosis of autism is seemingly not protective against developing schizophrenia (see here), are there other lessons that could be learned about the relationship(s) between various diagnostic labels?

More research is indicated...

So: Black Grape - Reverend Black Grape.

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[1] Andersen PN. et al. Associations Among Symptoms of Autism, Symptoms of Depression and Executive Functions in Children with High-Functioning Autism: A 2 Year Follow-Up Study. J Autism Dev Disord. 2015 Mar 13.

[2] Vannucchi G. et al. Bipolar disorder in adults with Asperger׳s Syndrome: A systematic review. J Affect Disord. 2014 Jul 8;168C:151-160.

[3] Takara K. & Kondo T. Comorbid atypical autistic traits as a potential risk factor for suicide attempts among adult depressed patients: a case-control study. Ann Gen Psychiatry. 2014 Oct 16;13(1):33.

[4] Gotham K. et al. Depression and its measurement in verbal adolescents and adults with autism spectrum disorder. Autism. 2014 Jun 10. pii: 1362361314536625.

[5] Bird PD. The treatment of autism with low-dose phenytoin: a case report. J Med Case Rep. 2015 Jan 16;9:8.

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ResearchBlogging.org Andersen PN, Skogli EW, Hovik KT, Egeland J, & Øie M (2015). Associations Among Symptoms of Autism, Symptoms of Depression and Executive Functions in Children with High-Functioning Autism: A 2 Year Follow-Up Study. Journal of autism and developmental disorders PMID: 25763986

Tuesday, 24 March 2015

More extremes of a limiting diet and autism

In a previous post a while back, I discussed some examples in the peer-reviewed literature of where a self-limiting diet in the extreme can lead to with autism in mind. Today, I'm adding a further example of what food faddism might mean, to further forward the point that "a low threshold for vitamin level testing should be undertaken in autistic spectrum disorder cases, highlighting the importance of enquiring about dietary habits."

That last quote comes from the paper in question by Emma Duignan and colleagues [1] (open-access available here) who describe two case reports of teenagers with autism "with a background of moderate autistic spectrum disorder who were diagnosed with a multivitamin deficiency, including vitamin A." Said nutritional deficiency manifested as ophthalmic issues - relating to the physiology of the eye - that importantly seemed to abate following vitamin supplementation.

Aside from the idea that several factors might align to bring a person diagnosed with autism to a deficiency state, I was interested in the Duignan results for a few other reasons. I've talked about vitamin and mineral deficiencies a few times on this blog; more generally as per the results from Jim Adams and colleagues back in 2011 (see here) following the publication of their double-blind, placebo-controlled trial of supplementation through to more specific issues with something like the vitamin-of-the-hour, vitamin D (see here) or even the scurvy-preventer that is vitamin C (see here). There is quite a bit of literature out there to suggest that particularly in cases where dietary issues are noted to accompany a diagnosis of autism or autism spectrum disorder (ASD), one perhaps should expect nutritional deficiencies to follow.

The other thing that struck me about the Duignan results was the focus on ophthalmic issues as manifestations of those vitamin deficiency issues. It's not new news that among the various effects linked to something like vitamin A deficiency for example, vision and eye health may suffer. Although still in need of quite a bit of research, issues related to the eyes and knock-on effects for things like visual perception are no stranger to autism research as per my ramblings about the findings reported by Ikeda and colleagues [2]. The paper from Pineles and colleagues [3] on optic neuropathy due to vitamin B12 deficiency in cases of autism is also worth mentioning at this point and the question of whether at least some of the visual perceptual issues discussed with autism in mind might have a nutritional link?

We don't currently know how widespread nutritional deficiencies are when a diagnosis of autism is received because, at the moment, this is not something that is routinely tested for. On the basis of the Duignan and other results, I'd be minded to repeat my suggestion that where dietary issues are present for people on the autism spectrum, modern medicine could do a lot worse than find out whether there may be biological effects to come from a limited or restricted diet save any further charges of health inequality being levelled...

Music to close. Paul Simon - Me and Julio Down by the Schoolyard.

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[1] Duignan E. et al. Ophthalmic manifestations of vitamin a and d deficiency in two autistic teenagers: case reports and a review of the literature. Case Rep Ophthalmol. 2015 Jan 24;6(1):24-9.

[2] Ikeda J. et al. Brief report: incidence of ophthalmologic disorders in children with autism. J Autism Dev Disord. 2013 Jun;43(6):1447-51.

[3] Pineles SL. et al. Vitamin B12 optic neuropathy in autism. Pediatrics. 2010 Oct;126(4):e967-70.

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ResearchBlogging.org Duignan, E., Kenna, P., Watson, R., Fitzsimon, S., & Brosnahan, D. (2015). Ophthalmic Manifestations of Vitamin A and D Deficiency in Two Autistic Teenagers: Case Reports and a Review of the Literature Case Reports in Ophthalmology, 6 (1), 24-29 DOI: 10.1159/000373921

Monday, 23 March 2015

Early life probiotics reducing the risk of subsequent neuropsychiatric disorder?

With my continued interest in all-things gut microbiome on this blog (see here for example) it is little wonder that I was taken to blog about the study findings from Anna Pärtty and colleagues [1] reporting that: "Probiotic supplementation early in life may reduce the risk of neuropsychiatric disorder development later in childhood." Probiotic by the way, refers to various 'live' organisms (bacteria, yeasts) thought to confer some positive effect on health and/or wellbeing.

Not only does such a conclusion weigh into the increasingly vocal debate about the gut-brain axis (whereby the gut and it's contents may play quite an important role outside of just digesting food and providing fuel for the body) but also the idea that supplementation during early infancy with Lactobacillus rhamnosus GG (ATCC 53103) might actually offset risk of diagnoses such as attention deficit hyperactivity disorder (ADHD) and/or Asperger syndrome (AS) being received up to 13 years later is potentially pretty important. Potentially.

At the time of first tweeting about the paper by Pärtty et al, one of the first replies concerned another sentence in the paper abstract: "At the age of 13 years ADHD or AS was diagnosed in 6/35 (17.1%) children in the placebo and none in the probiotic group (p=0.008)." Not only was no-one diagnosed with AS or ADHD in the probiotic group, but a whopping 17% of those in the control group subsequently received a diagnosis "by a child neurologist or psychiatrist were based on ICD-10 diagnostic criteria". Accepting the small participant groups included for study, that figure of 17% far exceeds anything that I'm aware of when it comes to the population estimates for AS and/or ADHD. The pediatric ADHD estimates normally come in at between 5-8% (see a post I wrote about this here) and although reliable figures for AS are few and far between outside of the umbrella 'autism spectrum disorder' I don't think the rate [2] is going to be anything like that reported by Pärtty et al. I say this accepting that in the latest version of DSM (DSM-5) AS does not exist as a specific categorical label any more.

A few further details about the Pärtty study might be in order:


Obviously one has to be a little cautious about accepting the Pärtty results at face value in terms of modifying the risks of ADHD or AS (or anything else). As much as some people would like to think that the gut microbiome is the be-all-and-end-all of autism research, it is more likely to be one part of a very complicated picture for some. The paper by Daniel McDonald and colleagues [5] (open-access) talks about the journey still required for gut microbiome research with autism in mind.

I might also direct you to the findings reported by Rinne and colleagues [6] talking about how probiotic supplementation "administered for 6 months postnatally" did not seem to have as much of an effect on "long-term composition or quantity of gut microbiota" as one might think. Whether this ties into the sentiments from Pärtty et al when they talked about "mechanisms not limited to gut microbiota composition" to account for their results is a question open to some debate. One could conceivably assume that there may be some critical period during early infancy when gut bacteria may modify (directly or peripherally) biological mechanisms pertinent to risk of neuropsychiatric disorder. But evidence of such an effect is fairly thin on the ground at present outside of the various reports of early and repeated antibiotic administration (which would impact on the gut microbiome) being talked about in the histories of some people who went on to receive a diagnosis (see here). Oh and the idea of psychobacteriomics too (see here).

Still, I'd be minded to suggest that the recent results should be inviting a lot more inquiry into the area of the gut and psychology/behaviour as not being as distant as one might first imagine [7].

Music: Eric B. & Rakim - Paid In Full.

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[1] Pärtty A. et al. A possible link between early probiotic intervention and the risk of neuropsychiatric disorders later in childhood - a randomized trial. Pediatr Res. 2015 Mar 11.

[2] Suzuki Y. & Saito K. Epidemiology of Asperger's syndrome. Nihon Rinsho. Japanese Journal of Clinical Medicine. 2007; 65: 419-423.

[3] Pärtty A. et al. Infant distress and development of functional gastrointestinal disorders in childhood: is there a connection? JAMA Pediatr. 2013 Oct;167(10):977-8.

[4] Pärtty A. et al. Effects of early prebiotic and probiotic supplementation on development of gut microbiota and fussing and crying in preterm infants: a randomized, double-blind, placebo-controlled trial. J Pediatr. 2013 Nov;163(5):1272-7.e1-2.

[5] McDonald D. et al. Towards large-cohort comparative studies to define the factors influencing the gut microbial community structure of ASD patients. Microbial Ecology in Health & Disease 2015; 26: 26555.

[6] Rinne M. et al. Probiotic intervention in the first months of life: short-term effects on gastrointestinal symptoms and long-term effects on gut microbiota. J Pediatr Gastroenterol Nutr. 2006 Aug;43(2):200-5.

[7] Severance EG. et al. Gastroenterology Issues in Schizophrenia: Why the Gut Matters. Current Psychiatry Reports. 2015; 17: 27.

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ResearchBlogging.org Pärtty A, Kalliomäki M, Wacklin P, Salminen S, & Isolauri E (2015). A possible link between early probiotic intervention and the risk of neuropsychiatric disorders later in childhood - a randomized trial. Pediatric research PMID: 25760553

Saturday, 21 March 2015

Toxoplasma gondii and schizophrenia (again and again)

The findings reported by Ainsah Omar and colleagues [1] (open-access available here) adding further weight to the notion of a "strong association between the active Tg [Toxoplasma gondii] infection and schizophrenia" are set out for your reading consumption today.

Continuing a research topic that has already enjoyed quite a bit of air time on this blog (see here and see here) whereby the parasite T. gondii known to cause the condition toxoplasmosis might also be implicated in at least some cases of schizophrenia, Omar et al report some pretty stark differences in rates of seropositivity between cases of schizophrenia (n=101) and asymptomatic controls (n=55).

"The serofrequency of Tg IgG antibodies (51.5%, 52/101) and DNA (32.67%, 33/101) among patients with schizophrenia was significantly higher than IgG (18.2%, 10/55) and DNA (3.64%, 2/55) of the controls." IgG antibodies refers to immune status with regards to a particular agent with the focus on past or recent exposure to said pathogen. In this respect, the results suggest that over half of participants with schizophrenia had met with T. gondii at some point compared with nearly 20% of controls. Insofar as active infection measured by IgM antibodies to T. gondii, the authors reported no significant difference in rates between the groups. DNA, as in measurement for the presence of T. gondii DNA as evidence of infection, also showed some interesting differences between the groups in favour of the schizophrenia group.

"In our study, the OR [odds ratios] of having schizophrenia among those with positive Tg DNA (OR=12.9) was much higher than those with positive Tg IgG antibody (OR=4.8)." This sentence in particular hints at some of the novelty behind the results from Omar et al with their focus on both antibody response to T. gondii infection and their more direct method of looking for T. gondii DNA.

"Although there was significant difference in the seropositivity of Tg IgG and Tg DNA between the 2 groups, however, there was no significant difference between the serointensity of Tg IgG antibody and DNA between schizophrenia patients and controls. These could possibly be due to the effects of antipsychotic medications which caused the reduction in the level of Tg IgG antibody and DNA by inhibiting the replication of Tg." I've talked before on this blog about how a wide variety of the medicines we use in modern times may have so many more 'effects' than those listed on the package insert. Certain antipsychotic drugs are known to possess "anti-toxoplasmic activity" [2] and one might entertain the fact that when used for some with schizophrenia there is the potential for some effect mediated via this pathway. I would like to see a lot more medicines tested for their anti-parasitic effects [3] that's for sure.

Of course one has to be a little cautious not to make too many generalisations from the findings from Omar and other research groups [4] (several other research groups [5]) about the idea that T. gondii might be linked to cases of schizophrenia. But as part of a wider research strategy [6] and accepting the moves towards the possible pluralisation of schizophrenia (see here), I believe there is quite a bit more to see in this area...

Music: The Cure - Pictures Of You.

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[1] Omar A. et al. Seropositivity and Serointensity of Toxoplasma gondii Antibodies and DNA among Patients with Schizophrenia. Korean J Parasitol. 2015 Feb;53(1):29-34.

[2] Fond G. et al. Comparative analysis of anti-toxoplasmic activity of antipsychotic drugs and valproate. Eur Arch Psychiatry Clin Neurosci. 2014 Mar;264(2):179-83.

[3] Fond G. et al. Treatment with anti-toxoplasmic activity (TATA) for toxoplasma positive patients with bipolar disorders or schizophrenia: A cross-sectional study. J Psychiatr Res. 2015 Feb 24. pii: S0022-3956(15)00043-6.

[4] Cevizci S. et al. Seroprevalence of anti-Toxoplasma gondii and anti-Borrelia species antibodies in patients with schizophrenia: a case-control study from western Turkey. World J Biol Psychiatry. 2015 Mar 16:1-7.

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

[6] Severance EG. et al. Gastroenterology Issues in Schizophrenia: Why the Gut Matters. Current Psychiatry Reports. 2015; 17: 27.

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ResearchBlogging.org Omar A, Bakar OC, Adam NF, Osman H, Osman A, Suleiman AH, Manaf MR, & Selamat MI (2015). Seropositivity and Serointensity of Toxoplasma gondii Antibodies and DNA among Patients with Schizophrenia. The Korean journal of parasitology, 53 (1), 29-34 PMID: 25748706