Friday, 19 December 2014

Uric acid and bipolar disorder

Bipolar disorder appearing again on this blog this week? It's just the way that the papers fall...

With a title like: 'Increased uric acid levels in bipolar disorder subjects during different phases of illness' I was hardly likely to pass up the opportunity to discuss the paper by Umberto Albert and colleagues [1] and their suggestion that there may be a lot more to see when it comes to "a purinergic dysfunction associated with BD [bipolar disorder]".
I lost the defuser gun when I misplaced the invisible car.

Based on the analysis of serum uric acid (UA) levels in 150 participants formally diagnosed with BD compared with "150 age- and gender-matched subjects with MDD [major depressive disorder], OCD [obsessive compulsive disorder], or Schizophrenia", researchers reported that: "Mean serum UA levels (5.06±1.45 vs. 4.17±1.05mg/dL) and rates of hyperuricaemia (30.7% vs. 6.7%) were significantly higher in the bipolar than in the control group." The authors pointed out the limitations of their study: "Our study suffers from the lack of a healthy comparison group; moreover, longitudinal data are missing" so no need for me to say anything further in that respect.

Uric acid, more commonly associated with a condition like gout, has been getting quite a bit of research attention when it comes to behaviour and psychiatry down the years. I've talked previously on this blog about the intriguing work suggestive of a possible connection between levels of uric acid and impulsivity (see here) highlighting a possible biology - trait connection. As per the Albert findings - "No differences were detected between bipolars in different phases of illness, with all three groups (manic, depressive and euthymic bipolars) showing significantly higher UA levels as compared to controls" - other research has hinted that the relationship between uric acid and BD is quite a bit more than just one related to trait [2]. I'm open to accepting that this might however change as more research is done on this topic.

Mechanism of effect for uric acid in BD? A very good question. Unfortunately I don't have a good answer at the moment, aside from reiterating the Albert suggestion "of a purinergic dysfunction associated with BD". Going all the way back to the 1921 book by Emil Kraeplin where the connection between uric acid and "manic symptoms" was discussed, there is quite a long history attached to this area. Even further back, the paper by Sutherland (1892) [3] talked about uric acid diathesis in children exemplified by: "keen precocious minds, and small restless bodies; they are excitable, nervous, bright and amusing at one time, and greatly depressed at another". Lithium salts were the treatment of choice for the 'gouty diseases' [4] and perhaps might offer some further explanation for the mechanism of effect in BD.

Other than that I can say no more, aside from pointing out that if one considers uric acid to be an agent of inflammation [5] and associated with other inflammatory responses [6], one might entertain some possible association between elevated levels of the stuff and other potentially important work in the area of BD...

And to close: White Coats by Foxes.


[1] Albert U. et al. Increased uric acid levels in bipolar disorder subjects during different phases of illness. J Affect Disord. 2014 Nov 15;173C:170-175.

[2] Kesebir S. et al. Increased uric acid levels in bipolar disorder: is it trait or state? J Biol Regul Homeost Agents. 2013 Oct-Dec;27(4):981-8.

[3] Sutherland GA. On some Symptoms Associated with the Uric Acid Diathesis in Children. Br Med J. 1892 Apr 23;1(1634):856-8.

[4] Amdisen A. & Hildebrandt J. Use of lithium in the medically ill. Psychother Psychosom. 1988;49(2):103-19.

[5] Shi Y. Caught red-handed: uric acid is an agent of inflammation. The Journal of Clinical Investigation 2010;120(6):1809-1811. doi:10.1172/JCI43132.

[6] Lyngdoh T. et al. Elevated serum uric acid is associated with high circulating inflammatory cytokines in the population-based Colaus study. PLoS One. 2011;6(5):e19901.

---------- Albert U, De Cori D, Aguglia A, Barbaro F, Bogetto F, & Maina G (2014). Increased uric acid levels in bipolar disorder subjects during different phases of illness. Journal of affective disorders, 173C, 170-175 PMID: 25462413

Thursday, 18 December 2014

Autistic traits in adults with epilepsy

"Increased autistic characteristics found in adults with epilepsy without an ASD [autism spectrum disorder] diagnosis suggest that epilepsy syndromes may incorporate behavioral aspects of autism in the absence of some of its core cognitive features."
Contrariwise, if you think we're alive you ought to speak to us.

That was the intriguing finding reported by Sally Ann Wakeford and colleagues [1] who examined test performance on the Autism Spectrum Quotient (AQ) and "systemizing and empathizing abilities" in a small-ish sample of adults with epilepsy compared with those without epilepsy. They found that: "Significantly more autistic behavioral traits, as measured by the AQ, were related to having epilepsy" but those systemising (UK spelling) and empathising abilities did not differ between the groups. The AQ, as I've indicated in previous posts, is a self-report measure and not necessarily autism-specific in terms of the features being described, so one has to be slightly cautious from this angle. But please don't let that detract from the interesting suggestion being reported...

Autism and epilepsy is an association which goes back quite a few years. Not only is epilepsy one of the more frequently reported comorbidities suggested to follow at least some diagnoses of autism (see here), epilepsy and autism co-occurring in certain situations, also provides some of the strongest evidence yet that the plural autisms might be a better definition than the catch-all categorisation that we currently use (see here). Dare I even direct you also to the preliminary research talking about joint intervention for autism and epilepsy too?

Insofar as the connection between autism and epilepsy, the Wakeford results might also imply that the genetics and biology of autism (some autism) and epilepsy (some epilepsy) might also show some kind of interplay with one and another. From me, this could imply that the research by Ong and colleagues [2] talking about a heightened risk of epilepsy in those with autoimmune disorders (see here for my take), might also extend into autism as per quite the increasing body of peer-reviewed literature talking about autoimmunity and [some] autism.

I'm also minded to suggest that despite the lack of a relationship between epilepsy and the core cognitive features of autism, I wouldn't yet rule out more subtle presentation as uniting the two diagnostic concepts [3].

Music then... Pharrell Williams - Gust of Wind.


[1] Wakeford S. et al. Autistic characteristics in adults with epilepsy. Epilepsy Behav. 2014 Oct 30;41C:203-207.

[2] Ong MS. et al. Population-level evidence for an autoimmune etiology of epilepsy. JAMA Neurol. 2014 May;71(5):569-74.

[3] Kavanaugh BC. et al. Parent-rated emotional–behavioral and executive functioning in childhood epilepsy. Epilepsy & Behavior. 2015; 42: 22-28.

---------- Wakeford S, Hinvest N, Ring H, & Brosnan M (2014). Autistic characteristics in adults with epilepsy. Epilepsy & behavior : E&B, 41C, 203-207 PMID: 25461216

Wednesday, 17 December 2014

Folate receptor autoantibodies and (some) schizophrenia

I am the league's director, Silas Ramsbottom.
Upon reading the paper published by Ramaekers and colleagues [1] talking about the use of folinic acid in cases of schizophrenia as a function of the presence of "Auto-antibodies against folate receptor alpha (FRα)", I raised a little smile. Not only because the authors suggested that there may be quite a lot more to see in this area on top of some already interesting discussions about the folate cycle and schizophrenia, but also because of the 'overlap' with some autism findings which have been previously discussed on this blog (see here). Indeed, if readers would like quite a nice summary of this area of investigation - folate receptor autoantibodies - I'm minded to direct them to the paper by Richard Frye and colleagues [2] (open-access) which initially presented the idea of cerebral folate receptor autoantibodies occurring in autism to the world and was the source material for that previous blog post.

Quoting from the Ramaekers study text: "Fifteen of 18 patients (83.3%) had positive serum FR auto-antibodies compared to only 1 in 30 controls". This was a study of those described as having "schizophrenia unresponsive to conventional treatment" and alongside the presence of those autoantibodies, researchers also assessed what some of the metabolic knock-on effects might have been in terms of analysis of spinal fluid levels of "MTHF [5,10-Methylenetetrahydrofolate] and the metabolites of pterins, dopamine and serotonin". It appears that FR autoantibodies may indeed affect levels of said compounds alongside "intermediates linked to metabolic processes affecting homocysteine levels... [and] synthesis of tetrahydrobiopterin". Homocysteine and tetrahydrobiopterin (BH4) in schizophrenia y'say?

"Administration of folinic acid (0.3-1mg/kg/day) to 7 participating patients during at least six months resulted in clinical improvement." Without wishing to provide any medical or clinical advice on the utility of folinic acid for schizophrenia or anything else, these are interesting findings. This is not the first time that folinic acid has been discussed in the research literature with schizophrenia in mind as per the case report by Wang and colleagues [3]. In that single case, authors described the presence of the MTHFR mutation - "665C>T homozygous mutations in the MTHFR gene" - as the reason for secondary cerebral folate deficiency. Other authors have discussed more pertinent cases [4]. Obviously one would like to see more formal clinical trials on the use of folinic acid as potentially being appropriate for at least some of the [plural] schizophrenias. The important thing to take from the Ramaekers and other studies is that a panel of tests might be able to spot who might be best responders to this kind of intervention...

Music to close, and Peter Griffin sings the opening tune to Indiana Jones and The Last Crusade? Why not.


[1] Ramaekers VT. et al. Folinic acid treatment for schizophrenia associated with folate receptor autoantibodies. Mol Genet Metab. 2014 Oct 12. pii: S1096-7192(14)00311-4.

[2] Frye RE. et al. Cerebral folate receptor autoantibodies in autism spectrum disorder. Molecular Psychiatry 2013;18(3):369-381. doi:10.1038/mp.2011.175.

[3] Wang Q. et al. Methylenetetrahydrofolate reductase deficiency-induced schizophrenia in a school-age boy. Zhongguo Dang Dai Er Ke Za Zhi. 2014 Jan;16(1):62-6.

[4] Ho A. et al. Cerebral folate deficiency presenting as adolescent catatonic schizophrenia: a case report. J Child Neurol. 2010 Jul;25(7):898-900.

---------- Ramaekers VT, Thöny B, Sequeira JM, Ansseau M, Philippe P, Boemer F, Bours V, & Quadros EV (2014). Folinic acid treatment for schizophrenia associated with folate receptor autoantibodies. Molecular genetics and metabolism PMID: 25456743

Tuesday, 16 December 2014

Thioredoxin... a new 'diagnosis indicator' for autism?

My name's Buttercup. You've
met Baron von Shush.
"Our study demonstrated that serum TRX [thioredoxin] levels were associated with ASD [autism spectrum disorder], and elevated levels could be considered as a novel, independent diagnosis indicator of ASD." So was the conclusion reported by Qing-biao Zhang and colleagues [1] looking at serum levels of TRX in 80 children diagnosed with an ASD compared against "100 sex and age matched typically developing children".

I'll freely admit that I was not even aware of thioredoxin (TRX) before reading this study; although a quick trawl through some of the research literature on this protein that "act as antioxidants by facilitating the reduction of other proteins by cysteine thiol-disulfide exchange" (thank you Wikipedia) hints that I should have been. Quite a good [peer-reviewed] overview of TRX can be found in the paper by Arnér & Holmgren [2] and in particular, describing their role in the process of reducing oxidative stress similar to another compound of interest to this blog: glutathione.

Zhang and colleagues reported significantly higher median serum levels of TRX in their participants with autism compared to asymptomatic controls. Further, that the severity of autism  - as measured using the CARS - might also be linked to TRX levels, and "the optimal cut-off value of serum TRX levels as an indicator for auxiliary diagnosis of autism was projected to be 10.6ng/ml". I might add that such results should not be translated as serum levels of TRX higher than 10.6 ng/ml = autism exclusively, as per other research looking at elevated levels of TRX in other conditions [3].

This is not the first time however that TRX has been studied with autism in mind. The paper by Yusra A Al-Yafee and colleagues [4] (open-access) looking at "sulfur-dependent detoxification mechanisms" in relation to the autism spectrum noted that alongside aberrant values for glutathione (yes, quite consistently so) in their autistic cohort, elevated levels of TRX and related thioredoxin reductase (TrxR) were also detected compared with controls. They stated: "the recorded raised levels of Trx, TrxR and Prxs [peroxidoxins] of the present study could be related to... previous work... which they proved that Saudi autistic children are under H2O2 stress due to over expression of SOD and a slightly lower activity of catalase." Interestingly, this group also suggested that TRX and glutathione parameters might also have some legs when it comes to their usefulness "as diagnostic biomarkers of autism."

Oxidative stress and autism is a research area in the ascendancy. With links being made to the gastrointestinal (GI) issues quite commonly reported alongside a diagnosis of autism (see here) and some really quite interesting work talking about oxidative stress potentially inducing mitochondrial issues in autism (see here), some important correlations are being made. My recent discussions including the paper by Main and colleagues [5] (open-access) suggesting that: "children with autism are more sensitive to necrosis caused by oxidative and nitrosative stress than their non-autistic siblings" adds to the intrigue, as does a little study about broccoli extracts recently...

Of course, quite a lot more replicative work is required, also including more focus on the hows and whys of issues with redox regulation related to autism. But more and more, oxidative stress is taking a place among quite a few other issues detected in at least some cases of autism [6].

Music to close: Queenie Eye by Paul McCartney.


[1] Zhang QB. et al. Thioredoxin: A novel, independent diagnosis marker in children with autism. Int J Dev Neurosci. 2014 Nov 26. pii: S0736-5748(14)00191-9.

[2] Arnér ES. & Holmgren A. Physiological functions of thioredoxin and thioredoxin reductase. Eur J Biochem. 2000 Oct;267(20):6102-9.

[3] Yamada Y. et al. Elevated serum levels of thioredoxin in patients with acute exacerbation of asthma. Immunol Lett. 2003 Apr 3;86(2):199-205.

[4] Al-Yafee YA. et al. Novel metabolic biomarkers related to sulfur-dependent detoxification pathways in autistic patients of Saudi Arabia. BMC Neurol. 2011 Nov 4;11:139.

[5] Main PA. et al. Necrosis is increased in lymphoblastoid cell lines from children with autism compared with their non-autistic siblings under conditions of oxidative and nitrosative stress. Mutagenesis. 2013 Jul;28(4):475-84.

[6] Rossignol DA, Frye RE. Evidence linking oxidative stress, mitochondrial dysfunction, and inflammation in the brain of individuals with autism. Frontiers in Physiology 2014;5:150. doi:10.3389/fphys.2014.00150.

---------- Zhang QB, Gao SJ, & Zhao HX (2014). Thioredoxin: A novel, independent diagnosis marker in children with autism. International journal of developmental neuroscience : the official journal of the International Society for Developmental Neuroscience PMID: 25433158

Monday, 15 December 2014

Rates of medical illnesses in bipolar disorder

I've mentioned a few times on this blog that a diagnosis of autism or autism spectrum disorder (ASD) is by no means protective against any other diagnosis being received, be it based on a somatic illness or condition, or something more behaviourally defined.

Reading through the paper by Liz Forty and colleagues [1] (open-access) it appears that a similar scenario might also pertain to other behaviourally-defined conditions as per the example of bipolar disorder (BD) and their conclusion: "Bipolar disorder is associated with high rates of medical illness."

If I had a world of my own, everything would be nonsense
I was drawn to discuss this paper for a few reasons. First and foremost is the idea that a psychiatric diagnosis may actually place a person 'at risk' of a few important comorbidities above and beyond the presentation of their behavioural symptoms. We seem to be in an unfortunate situation these days that receipt of a psychiatric diagnosis seems to lead to a severe lack of appreciation that other symptoms or ailments of a more physical nature can also be present. Take for example the health inequalities which seem to be springing up as and when a diagnosis of schizophrenia is received (see here) and coincidentally in the same journal as the Forty paper, the study results from Mike Crawford and colleagues [2] concluding: "Assessment and treatment of common physical health problems in people with schizophrenia falls well below acceptable standards." Another reason I want to talk about the Forty paper is the fact that bipolar disorder (previously referred to as manic depression) has been described as occurring 'quite frequently' with regards to at least one part of the autism spectrum (see here). What this might suggest is that a co-occurrence of BD and something like Asperger syndrome might mean that said medical illness/conditions reported to be raised in BD would also be raised in BP + Asperger syndrome.

The Forty paper is open-access but a few pointers might be useful...

  • Based on quite an impressive participant number (N=1720) diagnosed with bipolar disorder, lifetime rates of self-reported medical illnesses were compared with data derived from participants diagnosed with unipolar depression (N=1737) and asymptomatic controls (N=1340) (both previously described in other work from some of the authors [3]).
  • Participants were quizzed - yes, no or uncertain - over whether any of 20 health conditions had been diagnosed by a health professional including: "asthma, cancer, diabetes type 1, diabetes type 2, elevated lipids/high cholesterol, epilepsy, gastric ulcers, heart disease, hypertension, kidney disease, liver disease, memory loss/dementia, migraine headaches, multiple sclerosis, osteoarthritis, osteoporosis, Parkinson’s disease, rheumatoid arthritis, stroke, thyroid disease." All the 'uncertain' codings were "excluded from analyses for that medical illness".
  • Results: "The most prevalent medical conditions in the bipolar sample were migraine headache (23.7%), asthma (19.2%), elevated lipids (19.2%), hypertension (15%), thyroid disease (12.9%) and osteoarthritis (10.8%)." Quite a few of these conditions were significantly more frequently reported in cases of BD over control groups (see Figure 1 here). I'll in particular highlight the findings for asthma and thyroid disease as being more commonly reported in the BD group.
  • Authors also divided the BD group up into subgroups (BD1 and BD2) based on the severity of manic episodes, and reported that: "The rates of gastric ulcers, heart disease, Parkinson’s disease and rheumatoid arthritis were significantly higher in the bipolar II group." They also found that several variables seemed to be linked to an increased medical illness burden including: "a longer illness duration, a typically acute onset of mood episodes, a greater number of psychiatric in-patient admissions, deterioration in functioning, increased rates of anxiety disorder, suicide attempt, rapid cycling, and treatment with anxiolytics, mood stabilisers and electroconvulsive therapy (ECT)." Some of these variables also predicted the high medical illness burden group too.

Reiterating the authors' sentiments about the need for such medical comorbidity to be taken into account by healthcare professionals "in order to improve outcomes for patients with bipolar disorder" these are important results. Assuming that there may be shared/overlapping genetic or biological mechanisms at work which influence risk of BD and also such medical comorbidity, one might think that future work would take this into account when looking at the possible underlying aetiology of BD. Such work might also accept the heterogeneity noted in BD as per similar sentiments when it comes to conditions like 'the autisms' (see here) and 'the schizophrenias' (see here).

Asthma has been highlighted from the Forty results on the basis of the condition already showing something of an interesting 'link' with conditions like autism and attention-deficit hyperactivity disorder, ADHD (see here). Indeed, data from Taiwan (yes, further interrogation of the Taiwan National Health Insurance Research Database) concluded that a diagnosis of asthma might increase the risk of subsequent mood disorders (including BD) later in life [4]. Forty et al suggested that of the possible reasons why asthma might be more frequently present in BD "carbon dioxide hypersensitivity and corticosteroid therapy may partly explain this association." I'd be perhaps inclined to add that other [speculative] work looking at the link between autism and asthma for example, might also offer another potential explanation [5].

Thyroid disease was also plucked out from the Forty data. The reason: some interesting data previously covered on this blog talking about autoimmune thyroiditis and various types of depression (see here). I'm not by the way saying that every case of thyroid disease in BD is due to such an autoimmune pathology, but as per other discussions, there might be quite a bit more to see when it comes to immune system function and behavioural and/or psychiatric diagnoses. At the very least, testing for said autoimmune issues might be considered for some.

There is little more for me to say on this subject matter. This is by no means the first time that medical comorbidity has been linked to BD [6] and even more widely depression [7] and I very much doubt it will be the last. If there are lessons to be learned from this area of investigation, the primary one must be to look at mind and body when it comes to diagnosing and managing psychiatric issues such as bipolar disorder as per other examples.

Oh, and I wonder if this would be a good time to introduce the findings from Almeida and colleagues [8] again published in the same journal as Forty and colleagues, concluding: "B vitamins did not increase the 12-week efficacy of antidepressant treatment, but enhanced and sustained antidepressant response over 1 year." Food for thought?

Music: Janis Joplin and Piece of my heart.


[1] Forty L. et al. Comorbid medical illness in bipolar disorder. Br J Psychiatry. 2014. October 30.

[2] Crawford MJ. et al. Assessment and treatment of physical health problems among people with schizophrenia: national cross-sectional study. Br J Psychiatry. 2014. October 16.

[3] Farmer A. et al. Medical disorders in people with recurrent depression. Br J Psychiatry. 2008 May;192(5):351-5.

[4] Chen MH. et al. Higher risk of developing major depression and bipolar disorder in later life among adolescents with asthma: a nationwide prospective study. J Psychiatr Res. 2014 Feb;49:25-30.

[5] Becker KG. Autism, asthma, inflammation, and the hygiene hypothesis. Med Hypotheses. 2007;69(4):731-40.

[6] Sylvia LG. et al. Medical burden in bipolar disorder: findings from the Clinical and Health Outcomes Initiative in Comparative Effectiveness for Bipolar Disorder study (Bipolar CHOICE). Bipolar Disord. 2014 Aug 16. doi: 10.1111/bdi.12243.

[7] Smith DJ. et al. Depression and multimorbidity: a cross-sectional study of 1,751,841 patients in primary care. J Clin Psychiatry. 2014 Nov;75(11):1202-1208.

[8] Almedia OP. et al. B vitamins to enhance treatment response to antidepressants in middle-aged and older adults: results from the B-VITAGE randomised, double-blind, placebo-controlled trial. Br J Psychiatry. 2014. September 25.

---------- Forty L, Ulanova A, Jones L, Jones I, Gordon-Smith K, Fraser C, Farmer A, McGuffin P, Lewis CM, Hosang GM, Rivera M, & Craddock N (2014). Comorbid medical illness in bipolar disorder. The British journal of psychiatry : the journal of mental science PMID: 25359927

Sunday, 14 December 2014

Beware the inflated science related press release!

I'm not normally minded to post on a Sunday (day of rest and all that) but I did want to bring your attention to the results presented by Petroc Sumner and colleagues [1] (open-access) concluding that: "Exaggeration in news is strongly associated with exaggeration in press releases" when it comes to the media reporting of [some] health-related science news.

The idea behind this particular study - which has been summarised pretty well in some of the accompanying media and in an editorial in the publishing journal [2] - was to look at the contribution of the press release (the 'look at me' part of some science publishing) to those sometimes 'inflated' health science headlines which we all encounter on a day-to-day basis. The results suggested that whilst [some] journalists and editors might need a refresher course on some of the basics of science (including the concept of probability and risk), academic press offices and even the very academics behind said research might also have to shoulder some responsibility (bearing in mind correlation is not the same as causation!) So when for example, a mouse study correlating the presence of compound X with improvement in the [mouse] condition Y is interpreted as meaning that compound X is the elixir of life for Homo sapiens and that we should instantly rush out and buy as much of it as we can afford, look to the press release before blaming the newspaper. I exaggerate of course with that example.

So as not to keep you from your Sunday breakfast or that magnificent Sunday lunch you no doubt have planned/are eating, I'm not going to say much more about this topic aside from making two additional points:

(a) Post-publication peer-review is mentioned somewhere in one of the texts. Although this is traditionally meant to imply that researchers who have a beef about some study or interpretation of results send a letter to the publishing (or other) journal outlining their issues, there are quite a few other mediums these days which seem to get the job done just as well. You are reading one of those mediums - yes, bloggers of the world unite - and how on occasion, blog entries have talked about press releases and peer-reviewed results not quite tallying together. I dare say someone somewhere might eventually start a blog titled something like: 'pressing ahead: press release vs. actual results' if it hasn't already been done. Other social media might also play an important role in highlighting discrepancies.

(b) Although interesting, the Sumner results perhaps leave out one very important variable in this scientific producer - consumer relationship: the consumer. You might well scoff that anyone without a PhD or related qualification 'doesn't understand science' but I would say that you are wrong. Although there are people out there who actually believe the term 'scientifically proven', as if God himself endorsed the product, I'd suggest that there are enough people who don't believe every headline they read and are vocal enough to say so. Search engines such as Google do a pretty good job of ensuring that anyone researching a scientific claim important to them (which most people do these days) quickly get both sides of the story. In that respect, an inflated press release (which are also generally detectable on the web) will probably not stay inflated for too long. Probably less so, after this and other research [3] starts to percolate through the web...

Without further ado, I'll leave you to finish of your 'super-food' packed Sunday lunch. And just in case anyone is interested, a few things to bear in mind when reading and interpreting science...


[1] Sumner P. et al. The association between exaggeration in health related science news and academic press releases: retrospective observational study. BMJ 2014; 349: g7015.

[2] Goldacre B. Preventing bad reporting on health research. BMJ 2014; 349: g7465.

[3] Woloshin S. et al. Press releases by academic medical centers: not so academic? Ann Intern Med. 2009 May 5;150(9):613-8.

---------- Sumner, P., Vivian-Griffiths, S., Boivin, J., Williams, A., Venetis, C., Davies, A., Ogden, J., Whelan, L., Hughes, B., Dalton, B., Boy, F., & Chambers, C. (2014). The association between exaggeration in health related science news and academic press releases: retrospective observational study BMJ, 349 (dec09 7) DOI: 10.1136/bmj.g7015

Saturday, 13 December 2014

Social communication disorder (SCD) reviewed

Sometimes I believe in as many as
six impossible things before breakfast.
A micropost if you will, for today, and a link to a potentially very important paper by Lauren Swineford and colleagues [1] (open-access) talking about the diagnostic concept: social (pragmatic) communication disorder (SCD) and it's various crossings with language impairments and autism spectrum disorder (ASD).

SCD, as I've indicated in other posts (see here and see here) is something that the autism community in particular, is going to be hearing a lot more about in the coming years, derived from the latest DSM-5 schedule.

Just one choice quote to offer from the Swineford paper: "Evidence of SCD was provided in the DSM-5 field trials, which indicated that a decrease in DSM-IV ASD diagnoses was accounted for by movement to SCD diagnostic category." Yes, it appears that this is already happening...

Some music then... Johnny Marr - Getting Away With It.


[1] Swineford LB. et al. Social (pragmatic) communication disorder: a research review of this new DSM-5 diagnostic category. Journal of Neurodevelopmental Disorders 2014, 6:41.

---------- Swineford, L., Thurm, A., Baird, G., Wetherby, A., & Swedo, S. (2014). Social (pragmatic) communication disorder: a research review of this new DSM-5 diagnostic category Journal of Neurodevelopmental Disorders, 6 (1) DOI: 10.1186/1866-1955-6-41