The move of the Australian government to measure the impact of university research on society introduces many new challenges that were not previously relevant when evaluation focused solely on academic merit. … Read More →... Read more »
Gunn, A., & Mintrom, M. (2016) Higher Education Policy Change in Europe: Academic Research Funding and the Impact Agenda. European Education, 48(4), 241-257. DOI: 10.1080/10564934.2016.1237703
Morris ZS, Wooding S, & Grant J. (2011) The answer is 17 years, what is the question: understanding time lags in translational research. Journal of the Royal Society of Medicine, 104(12), 510-20. PMID: 22179294
"Rates of ASD [autism spectrum disorder] and ASD traits are elevated in a psychosis population."The paper by Debbie Kincaid and colleagues  provides yet more [short] blogging material pertinent to the increasing interest in how psychosis may be yet another comorbidity over-represented when it comes to autism (see here) and vice-versa. I know this is another topic that has to be treated with some caution in terms of concepts like stigma but more discussions - science discussions - are needed to ensure that appropriate screening, diagnosis and also management is available to those who might need it.A systematic review was the name of the research game for Kincaid et al as seven studies "reporting prevalence rates of Autistic-like Traits (ALTs) and ASD in populations with a diagnosis of schizophrenia or other psychotic disorder" were included. The results weren't exactly precise in terms of what was reported as anywhere between 9-61% of those diagnosed with psychosis presented with those ALTs and between 1-52% of those with psychosis were also diagnosed with an autism spectrum disorder (ASD). The authors however are correct when they point out that the "prevalence rates of ALTs and ASD in psychosis populations are much higher than in the general population." Quite a bit higher if one looks at the top end of those prevalence stats.I'll leave it at that for now.---------- Kincaid DL. et al. What is the prevalence of Autism Spectrum Disorder and ASD traits in psychosis? A systematic review. Psychiatry Research. 2017. Jan 6.----------Kincaid, D., Doris, M., Shannon, C., & Mulholland, C. (2017). What is the prevalence of Autism Spectrum Disorder and ASD traits in psychosis? A systematic review Psychiatry Research DOI: 10.1016/j.psychres.2017.01.017... Read more »
Kincaid, D., Doris, M., Shannon, C., & Mulholland, C. (2017) What is the prevalence of Autism Spectrum Disorder and ASD traits in psychosis? A systematic review. Psychiatry Research. DOI: 10.1016/j.psychres.2017.01.017
The bacterium, Deinococcus radiodurans, is thought to be discovered as a contaminant in radiation-sterilized cans in 1960s. The name of the bacterium comes from the Ancient Greek, i.e. deinos and kokkos meaning “terrible grain/berry”, and the Latin language, i.e. radius and durare, meaning “radiation surviving”. The bacterium is also known as Conan the Bacterium.
Deinococcus radiodurans is a comparatively larger bacterium having spherical shape. It is a red-pigmented bacterium that does not cause diseases. The bacterium also possesses a highly efficient DNA repair system that is thought to be responsible for the unbelievable survival strategies.
It is considered as the toughest bacterium in the world as it is highly resistant to radiations, i.e. it can resist thousand times more radiation as compared to a normal person. The bacterium also has a strong ability to survive in conditions of cold, vacuum, dehydration, and acid. Therefore, it is also known as polyextremophile.
Deinococcus radiodurans in a dish (Source: science.nasa.gov)
Deinococcus radiodurans in a dish (Source: science.nasa.gov)
Deinococcus radiodurans has also been used by scientists for the consumption and digestion of solvents as well as heavy metals. It is also thought to have an ability to store information that can survive even after huge catastrophes.
Data stored in multiplying bacteria – https://www.newscientist.com/article/dn3243-data-stored-in-multiplying-bacteria/
Genome News Network – http://www.genomenewsnetwork.org/articles/07_02/deinococcus.shtml
The Possible Mechanisms Involved in the Protection Strategies against Radiation-Induced Cellular Damage by Carnitines – http://file.scirp.org/Html/1-2101023_53873.htm
Krisko, A., & Radman, M. (2013). Biology of Extreme Radiation Resistance: The Way of Deinococcus radiodurans Cold Spring Harbor Perspectives in Biology, 5 (7) DOI: 10.1101/cshperspect.a012765
Meet Conan the Bacterium – https://science.nasa.gov/science-news/science-at-nasa/1999/ast14dec99_1... Read more »
Krisko, A., & Radman, M. (2013) Biology of Extreme Radiation Resistance: The Way of Deinococcus radiodurans. Cold Spring Harbor Perspectives in Biology, 5(7). DOI: 10.1101/cshperspect.a012765
"As compared with 54 typically developing controls, we found no evidence of differences in the blood profile of immune mediators supportive of active systemic inflammation mechanisms in participants with autism."That was the unexpected research bottom-line published by Carlos Pardo and colleagues  (open-access) examining whether various immune-related chemicals - "cytokines, chemokines, or growth factors in serum and cerebrospinal fluid" - might be linked to autism following longitudinal assessment. By longitudinal I mean that: "Up to four serum samples and up to two CSF samples were obtained from participants, at intervals ranging from 9–24 months, and stored until simultaneous laboratory analysis.""Participants were drawn from a longitudinal study of autism" we are told, the aim of which was 'to learn more about autism and its subtypes'. Indeed, some of the research attached to this cohort has been previously discussed on this blog (see here) and for example, the suggestion that the horror that is a gluten- and/or casein-free diet used in the context of autism might not be as horrible as many people might think . This time around serum samples were available for over 100 children diagnosed with autism and some 54 not-autism controls. Sixty-seven of the children with autism also provided a cerebrospinal fluid (CSF) sample taken via a lumbar puncture. The authors note: "Ethical constraints prevented lumbar punctures in the TYP [control] group" so make of that what you will.Bearing in mind that no participants had a history of immunodeficiency or autoimmune disorder (important concepts to some autism) but that "Food, environmental, and seasonal allergies were present in a minority of participants, but were more common in AUT [participants with autism]" the results are interesting. First, when comparing results based on the analysis of CSF samples and serum samples researchers noted that there were "striking differences in the expression of selected cytokines, immune-related growth factors, and chemokines in the CSF compartment compared to the circulating bloodstream compartment." So basically what goes on in serum might not necessarily be the same as that going on in CSF in a biochemical sense.Next and as per the title and headline of this post: "we found no evidence for major differences in the expression of circulating cytokines and chemokines between children with autism and typically developing controls." This contrasts with quite a bit of other research in the area of immune-related compounds and autism (see here for example) but one has to be a little careful with the wording here, specifically the term 'major differences'. I say that because the authors do report that EGF - epidermal growth factor - did come out as 'different' between the groups (greater in the autism group) for example. EGF has been mentioned before in the context of autism but levels of the stuff have tended to be lower in autism not higher (see here). Puzzling.This is important work not least because of the cautions highlighted by the authors: "about the lack of relationship between central and peripheral immune markers, signaling that caution should be taken when interpreting the available studies implicating current immune dysfunction in the phenomenology of ASD [autism spectrum disorder], as few have included direct measures of CNS [central nervous system] status." Bearing in mind that there were no CFS comparison samples from controls included in this study (quite a big research flaw by all accounts) it is something else to suggest that if one really wants to see what is going on with immune function and autism, one needs to be looking to a far more invasive sample media. That some of this research group have some 'form' when it comes to the immune system potentially being linked to autism  and even more invasive tissue types is also worth noting as further investigations are very carefully merited...The immune system and autism continues to intrigue.---------- Pardo CA. et al. Serum and cerebrospinal fluid immune mediators in children with autistic disorder: a longitudinal study. Molecular Autism. 2017. 8: 1. Graf-Myles J. et al. Dietary adequacy of children with autism compared with controls and the impact of restricted diet. J Dev Behav Pediatr. 2013 Sep;34(7):449-59. Vargas DL. et al. Neuroglial activation and neuroinflammation in the brain of patients with autism. Ann Neurol. 2005 Jan;57(1):67-81.----------Pardo, C., Farmer, C., Thurm, A., Shebl, F., Ilieva, J., Kalra, S., & Swedo, S. (2017). Serum and cerebrospinal fluid immune mediators in children with autistic disorder: a longitudinal study Molecular Autism, 8 (1) DOI: 10.1186/s13229-016-0115-7... Read more »
Pardo, C., Farmer, C., Thurm, A., Shebl, F., Ilieva, J., Kalra, S., & Swedo, S. (2017) Serum and cerebrospinal fluid immune mediators in children with autistic disorder: a longitudinal study. Molecular Autism, 8(1). DOI: 10.1186/s13229-016-0115-7
Birt-Hogg-Dubé (BHD) syndrome is a rare disorder caused by mutations in FLCN and associated with increased risk of kidney cancer. It has been shown that FLCN-interacting protein 1 and 2 (FNIP1 and FNIP2) double knockout mice, like the FLCN knockout mice, develop renal carcinoma (Hasumi et al., 2015). However, the molecular mechanisms linking FNIP and FLCN remain unknown. In their new study, Nagashima et al. (2016) show that FNIP2 undergoes proteasome-dependent degradation via β-TRCP and Casein Kinase 1 (CK1)-directed ubiquitination in a nutrition-dependent manner. Degradation of FNIP2 leads to lysosomal dissociation of FLCN and association of mTOR, which promotes the proliferation of renal cancer cells.... Read more »
Nagashima K, Fukushima H, Shimizu K, Yamada A, Hidaka M, Hasumi H, Ikebe T, Fukumoto S, Okabe K, & Inuzuka H. (2016) Nutrient-induced FNIP degradation by SCFβ-TRCP regulates FLCN complex localization and promotes renal cancer progression. Oncotarget. PMID: 28039480
"Our data suggest that exercise is more effective than control at reducing anxiety symptoms."So said the meta-analysis published by Brendan Stubbs and colleagues  who surveyed the peer-reviewed literature "investigating the benefits of exercise compared to usual treatment or control conditions in people with an anxiety and/or stress-related disorders." From the 6 randomised, controlled trials found "from inception until December 2015" exercise (various types of exercise regime) did seem to have something of an effect on anxiety symptoms in adults compared to control conditions.I'm not going to labour too much on these findings because they really speak for themselves bearing in mind control conditions may not be the same as pitting exercise against something rather more proactive when it comes to tackling anxiety. Allied to the idea that exercise is basically medicine when it comes to various psychological/psychiatric labels as well as more somatic ones (see here) and is one of the more cost-effective interventions proposed (and typically side-effect free), the questions that remain are: (a) what are the mechanisms of effect? and (b) are there specific types of exercise that might be more suited to specific diagnostic labels? At least one of those questions has been touched upon in other papers  whereby low to moderate intensity exercise seems to be the way forward for at least some forms of anxiety. I assume that means activities such as walking, swimming and non-competitive cycling might be something to consider for example. A quick trawl of some of the other literature in this area also suggest that activities such as yoga might be useful for trait anxiety when attached to other diagnoses  but please, do not read this as medical or clinical advice in any intended form. Speak to your medical physician if you're unsure.Finally, given my previous discussions on how various types of anxiety disorder seem to be over-represented among many parts of the autism spectrum (see here for example), I can't help but wonder whether the chatter about behavioural outcomes following exercise with autism in mind (see here) might also come into play here. If for example, one accepts that anxiety can not only be an utterly disabling state to exist in but might also 'interact' with more 'core' presentation of autism (see here), future studies may be minded to look at how exercise might impact on both autistic and anxiety-related traits for the benefit of the individual...And finally, for the 'weekend [exercise] warriors' out there, some good news...---------- Stubbs B. et al. An examination of the anxiolytic effects of exercise for people with anxiety and stress-related disorders: A meta-analysis. Psychiatry Research. 2017. Jan 6. Takács J. & Stauder A. The role of regular physical activity in the prevention and intervention of symptoms of anxiety and anxiety disorders. Psychiatr Hung. 2016;31(4):327-337. Buffart LM. et al. Physical and psychosocial benefits of yoga in cancer patients and survivors, a systematic review and meta-analysis of randomized controlled trials. BMC Cancer. 2012 Nov 27;12:559.----------Stubbs, B., Vancampfort, D., Rosenbaum, S., Firth, J., Cosco, T., Veronese, N., Salum, G., & Schuch, F. (2017). An examination of the anxiolytic effects of exercise for people with anxiety and stress-related disorders: A meta-analysis Psychiatry Research DOI: 10.1016/j.psychres.2016.12.020... Read more »
Stubbs, B., Vancampfort, D., Rosenbaum, S., Firth, J., Cosco, T., Veronese, N., Salum, G., & Schuch, F. (2017) An examination of the anxiolytic effects of exercise for people with anxiety and stress-related disorders: A meta-analysis. Psychiatry Research. DOI: 10.1016/j.psychres.2016.12.020
"However, patients admitted on five day/number combinations were 20-30% more likely to survive at 13 years. These findings could be explained by subgroup analysis inflation of the type I error, although supernatural causes merit further investigation."
No. Supernatural causes do not merit further investigation, at least, not based on anything in this paper.
The authors used Friday the 13th as their "normal" date for comparison with every other date, but the outcomes from Friday the 13th are not the true statistical mean. The outcomes on Friday the 13th were just chosen because of the superstition being investigated. Friday the 13th is so close to the statistical mean that this mistake is easy to make.... Read more »
Protty, M., Jaafar, M., Hannoodee, S., & Freeman, P. (2016) Acute coronary syndrome on Friday the 13th: a case for re-organising services?. The Medical Journal of Australia, 205(11), 523-525. DOI: 10.5694/mja16.00870
"Fifteen studies suggest a higher prevalence rate of ASDs [autism spectrum disorder] among children of immigrants in comparison to native children."Those fifteen studies formed a large part of the seventeen studies included in the review by Rafal Kawa and colleagues  who set out to look at the collected peer-reviewed literature on the topic of the "prevalence and risk for ASD in Europe among immigrants and ethnic minorities." Carried out as part of a European Union (EU) initiative titled 'Enhancing the Scientific Study of Early Autism' the Kawa review was a sort of first step to looking at whether the racial/ethnic disparities noted in autism rates in the United States for example, might also hold true for Europe. Evidently they did.This is a topic covered before on this blog (see here for example) and so the results come as little surprise. One does have to be slightly cautious about how such data is interpreted, particularly in light of recent European history but outside of any politics there are some intriguing scientific questions posed by such data and some potentially important 'connections' with other independent datasets that could benefit autism research more generally (see here and see here). Given also some emerging research suggesting that autism may not be the only diagnostic label where risk is heightened according to immigrant status (see here), there are some further studies to be undertaken on this topic, in these days of overlapping labels (see here).---------- Kawa R. et al. European studies on prevalence and risk of autism spectrum disorders according to immigrant status-a review. Eur J Public Health. 2016 Dec 24. pii: ckw206.----------Kawa R, Saemundsen E, Lóa Jónsdóttir S, Hellendoorn A, Lemcke S, Canal-Bedia R, García-Primo P, & Moilanen I (2016). European studies on prevalence and risk of autism spectrum disorders according to immigrant status-a review. European journal of public health PMID: 28013245... Read more »
Kawa R, Saemundsen E, Lóa Jónsdóttir S, Hellendoorn A, Lemcke S, Canal-Bedia R, García-Primo P, & Moilanen I. (2016) European studies on prevalence and risk of autism spectrum disorders according to immigrant status-a review. European journal of public health. PMID: 28013245
The placenta is a unique organ as it is an extra-embryonic tissue primarily regulated by the fetal genome and shared between mother and fetus. However, it is a transient organ that is only needed throughout pregnancy and gestation and then is discarded after delivery. The essential role of the placenta in pregnancy is unquestionable but, surprisingly, as highlighted by the NIH NICHD Human Placenta Project (https://www.nichd.nih.gov/research/HPP/Pages/default.aspx), it is the human organ we know least about. Due to its unique features, the epigenetic mechanisms that regulate placental gene expression may not be under the same constraints as for other organs. We have recently reviewed the literature on DNA methylation in the placenta1 and highlighted the fact that this tissue is the most hypomethylated in the body when compared to other healthy tissues.2, 3 However, the reasons for this relative DNA hypomethylation are unknown. We do know that DNA methylation within the placenta increases across gestation.3-5 In addition, DNA methylation patterns in the placenta are characterized by large partially methylated domains in which the genes in these domains are repressed.6... Read more »
Mayne BT, Leemaqz SY, Smith AK, Breen J, Roberts CT, & Bianco-Miotto T. (2016) Accelerated placental aging in early onset preeclampsia pregnancies identified by DNA methylation. Epigenomics. PMID: 27894195
Bianco-Miotto T, Mayne BT, Buckberry S, Breen J, Rodriguez Lopez CM, & Roberts CT. (2016) Recent progress towards understanding the role of DNA methylation in human placental development. Reproduction (Cambridge, England), 152(1). PMID: 27026712
Ehrlich M, Gama-Sosa MA, Huang LH, Midgett RM, Kuo KC, McCune RA, & Gehrke C. (1982) Amount and distribution of 5-methylcytosine in human DNA from different types of tissues of cells. Nucleic acids research, 10(8), 2709-21. PMID: 7079182
Fuke C, Shimabukuro M, Petronis A, Sugimoto J, Oda T, Miura K, Miyazaki T, Ogura C, Okazaki Y, & Jinno Y. (2004) Age related changes in 5-methylcytosine content in human peripheral leukocytes and placentas: an HPLC-based study. Annals of human genetics, 68(Pt 3), 196-204. PMID: 15180700
Novakovic B, Yuen RK, Gordon L, Penaherrera MS, Sharkey A, Moffett A, Craig JM, Robinson WP, & Saffery R. (2011) Evidence for widespread changes in promoter methylation profile in human placenta in response to increasing gestational age and environmental/stochastic factors. BMC genomics, 529. PMID: 22032438
Price EM, Cotton AM, Peñaherrera MS, McFadden DE, Kobor MS, & Robinson W. (2012) Different measures of "genome-wide" DNA methylation exhibit unique properties in placental and somatic tissues. Epigenetics, 7(6), 652-63. PMID: 22531475
Schroeder DI, Blair JD, Lott P, Yu HO, Hong D, Crary F, Ashwood P, Walker C, Korf I, Robinson WP.... (2013) The human placenta methylome. Proceedings of the National Academy of Sciences of the United States of America, 110(15), 6037-42. PMID: 23530188
Fogarty NM, Burton GJ, & Ferguson-Smith AC. (2015) Different epigenetic states define syncytiotrophoblast and cytotrophoblast nuclei in the trophoblast of the human placenta. Placenta, 36(8), 796-802. PMID: 26008948
Marioni RE, Shah S, McRae AF, Chen BH, Colicino E, Harris SE, Gibson J, Henders AK, Redmond P, Cox SR.... (2015) DNA methylation age of blood predicts all-cause mortality in later life. Genome biology, 25. PMID: 25633388
There is limited evidence that poor movement quality is associated with a greater risk of lower extremity injury in athletic and military/first-responder populations.... Read more »
Whittaker JL, Booysen N, de la Motte S, Dennett L, Lewis CL, Wilson D, McKay C, Warner M, Padua D, Emery CA.... (2016) Predicting sport and occupational lower extremity injury risk through movement quality screening: a systematic review. British journal of sports medicine. PMID: 27935483
The quote making up the title of this post comes from the case report described by Albino J Oliveira-Maia and colleagues  talking yet again about how coeliac disease - the archetypal autoimmune condition where dietary gluten is the baddie - may have effects well beyond just the physical.Describing the experiences of a woman who was admitted to a psychiatry inpatient unit on the basis of "suicidal behaviours" who also "developed an agitated catatonic state", a mix of "antidepressants, anxiolytics, antipsychotics and electroconvulsive therapy" seemingly did very little to her state at/during admission we are told. Further, some diagnostic work-up beyond just her psychiatric features "allowed for the diagnosis of coeliac disease" and instigation of a gluten-free diet - the primary management option for coeliac disease - seemed to have something of a 'significant' effect on her psychiatric well-being as per that opening quote.Am I particularly surprised by all of this? No. Regular readers will know that I've previously talked about gluten and psychiatry quite a few times on this blog (see here and see here for example) and there is other research out there in the peer-reviewed domain pertinent to discussions . Without trying to over-generalise a case report to anything further, there are a number of notable peer-reviewed papers that have suggested that diet can affect psychiatry and this addition merely adds to the haul.If I did perhaps have to go into further detail on how something like suicidal behaviours might link into gluten and coeliac disease (CD) I would perhaps draw your attention to how gluten does seem to be a 'mood affector' when it comes to at least some cases of CD (see here) and the link between something like depression and suicidality. I'm sure however that this is not the final word on any such link and please, don't generalise with any sweeping suggestions about how all depression is somehow caused solely by gluten. Depression is a very complicated entity.More research is of course indicated but I do wonder how many more case reports on previously unidentified coeliac disease (or non-coeliac gluten sensitivity even?) and similar psychiatric symptoms there may be out there? Time for more screening of vulnerable populations perhaps...---------- Oliveira-Maia AJ. et al. Case of coeliac disease presenting in the psychiatry ward. BMJ Case Rep. 2016 Dec 21;2016. pii: bcr2016216825. Ludvigsson JF. et al. Increased suicide risk in coeliac disease--a Swedish nationwide cohort study. Dig Liver Dis. 2011 Aug;43(8):616-22.----------Oliveira-Maia AJ, Andrade I, & Barahona-Corrêa JB (2016). Case of coeliac disease presenting in the psychiatry ward. BMJ case reports, 2016 PMID: 28003229... Read more »
Oliveira-Maia AJ, Andrade I, & Barahona-Corrêa JB. (2016) Case of coeliac disease presenting in the psychiatry ward. BMJ case reports. PMID: 28003229
Mechanisms of antibiotic resistance... Read more »
The germline FLCN missense mutations H255Y (Hasumi et al., 2009) and K508R (Toro et al., 2008) have been identified in patients with bilateral multifocal (BMF) kidney tumours and other clinical symptoms of Birt-Hogg-Dube (BHD) syndrome, or with BMF kidney tumours as the only manifestation. Building on their previous work identifying the H255Y mutation in human BHD kidney tumour, Hasumi et al. (2016) investigated whether these mutations have an impact on FLCN function. The authors evaluated the FLCN missense mutations, H255Y and K508R in genetically engineered mice, and demonstrated that they both are pathogenic mutations that promote aberrant kidney cell proliferation to different degrees, with the potential for malignancy. In addition, the phenotypic effect of the Flcn K508R mutant expression in mice with wild-type Flcn by expressing the Flcn K508R mutant transgene in heterozygous Flcn knockout mice was examined.... Read more »
Hasumi H, Hasumi Y, Baba M, Nishi H, Furuya M, Vocke CD, Lang M, Irie N, Esumi C, Merino MJ.... (2016) H255Y and K508R missense mutations in tumour suppressor folliculin (FLCN) promote kidney cell proliferation. Human molecular genetics. PMID: 28007907
It's been a while since I've talked about Toxoplasma gondii on this blog; the parasite that more than most, has been linked with all-manner of different psychiatric labels (see here for example). Although still the topic of some discussion, I'm swayed towards the possibility that there may be some important *associations* to be seen when it comes to this survivor and human behaviour(s) outside of just making rats attracted to cat urine (see here) to improve reproduction chances.Indeed, in that context I offer up the findings reported by Flegr & Horáček  who presented results pertinent to "earlier reports of the association between toxoplasmosis and OCD [obsessive compulsive disorder]." OK, the first thing to note about this study is that: "Examined subjects provided the information about their toxoplasmosis and OCD statuses themselves, which could result in underrating the strength of observed associations." Most people probably wouldn't falsely admit to being toxoplasmosis positive but I can imagine that a few people might not want to share such sensitive information for various reasons.Researchers examined data from over 7400 volunteers (participants), asking about their toxoplasmosis status and also whether they had been diagnosed with OCD, a condition characterised by obsessive thoughts and compulsive behaviours, or one or more of a variety of other neuropsychiatric labels. The symptoms of OCD were also characterised on the basis of the use of the Obsessive-Compulsive Inventory-Revised (OCI-R) (self-completed).They observed the incidence of OCD to be present in approximately 2% of their cohort. They also observed that where toxoplasmosis was reported, these participants were quite a bit more likely to also report being diagnosed with OCD. A similar relationship also held when it came to the presence of a learning (intellectual) disability too. When researchers also took into account those self-report scores on the OCI-R, they noted that in those with toxoplasmosis "even the OCD-free subjects, scored higher on the OCI-R." Ergo, something of a relationship between T. gondii and OCD (diagnosed or symptoms) may exist.Accepting the methodological failings of the Flegr / Horáček study, their data do indeed seem to tally with other independent study  in this area, albeit still quite limited in quality and amount. Such research also potentially ties into other investigations on other behavioural/psychiatric labels where the gondii has been implicated (see here for example) that might overlap with cases of OCD. There are however still questions to answer, not least which came first, psychiatric presentation or infection with the gondii? Could a behavioural or psychiatric diagnosis increase the risk that someone is more likely to become infected by the gondii? I suppose given what OCD encompasses - "fear of contamination by disease, infection or an unpleasant substance" - one could argue that OCD is not exactly a great template for coming into contact with T. gondii and becoming infected. But before I, or anyone else, jumps to conclusions, more investigation(s) are implied on the nature of the relationship and onward any pertinent biological mechanisms...---------- Flegr J. & Horáček J. Toxoplasma-infected subjects report an Obsessive-Compulsive Disorder diagnosis more often and score higher in Obsessive-Compulsive Inventory. Eur Psychiatry. 2016 Dec 16;40:82-87. Miman O. et al. Is there any role of Toxoplasma gondii in the etiology of obsessive-compulsive disorder? Psychiatry Res. 2010 May 15;177(1-2):263-5----------Flegr J, & Horáček J (2016). Toxoplasma-infected subjects report an Obsessive-Compulsive Disorder diagnosis more often and score higher in Obsessive-Compulsive Inventory. European psychiatry : the journal of the Association of European Psychiatrists, 40, 82-87 PMID: 27992837... Read more »
Flegr J, & Horáček J. (2016) Toxoplasma-infected subjects report an Obsessive-Compulsive Disorder diagnosis more often and score higher in Obsessive-Compulsive Inventory. European psychiatry : the journal of the Association of European Psychiatrists, 82-87. PMID: 27992837
"ADHD [attention-deficit hyperactivity disorder] patients were overrepresented in the group with low levels of some vitamins, possibly indicative of inadequate dietary intake of these micronutrients in a subgroup of patients. It is important to identify these patients in dietary intervention trials of ADHD."So said the study findings reported by Elisabeth Toverud Landaas and colleagues  (open-access) providing some potentially important data on how nutritional factors might intersect with the diagnosis of ADHD. So: "Owing to the important and neurologically relevant functions of vitamins and the lack of studies exploring this topic in ADHD, we measured serum levels of the major vitamin classes in a sample of adult ADHD patients and controls to determine whether vitamin levels are associated with ADHD diagnosis and psychiatric symptoms." Said participants (n=133) were young adults and most were listed as having ADHD according to a "Norwegian national registry of adult ADHD patients." Vitamin levels were assessed from blood samples and compared with results for 131 control participants as per other studies on this cohort from this authorship group . It's worth pointing out that samples were in deep freeze storage for between 2-9 years between collection and thawing for analysis.Various vitamins were measured in those samples (vitamins A, B6, , B9, B12 and D to name a few) alongside levels of cotinine "to assess [tobacco] smoking status." The analytical assay(s) of choice was, in the most part, a familiar one to this blog: liquid- or gas chromatography-tandem mass spectrometry.Results: "The concentrations of vitamins B2, B6 and B9 were all significantly lower in the ADHD group." When results were analysed according to percentiles based on blood levels of the various vitamins results similarly showed that those with ADHD were 'over-represented' in the lower levels bandings of those previously described vitamins. Smokers, as defined by a "widely used cut-off of 80 nmol/L" of blood cotinine, were also over-represented in the ADHD group (66%) compared with control participants' samples (12%). The authors reported that: "vitamin B6 and B9 levels were significantly higher in non-smoking ADHD patients compared with smokers" suggesting that lifestyle choices may play a role in some of the results obtained. Finally, when it came to looking at any possible association(s) between measured vitamin levels and behaviours pertinent to ADHD (derived from responses to the Adult ADHD Self-report Scale (ASRS), the authors report some preliminary observations but I'd like to see a little more data before anything further is made of this.These are interesting results (aren't they always!). I note that the authors make reference to the findings reported by Julia Rucklidge and colleagues on a vitamin-mineral mix for ADHD (see here) and the idea that correcting vitamin deficiencies might have effects beyond just the somatic. There are however caveats to the latest results: "The reason why we observed association between lower levels of some vitamins and ADHD is uncertain and probably multifactorial. Regrettably, we do not have information on lifestyle and nutrient intake from the participants to help in the interpretation of our observations. It is reasonable to think that differences in dietary factors may partly be responsible for the differences." Indeed.There is also one final observation to touch upon in the Landaas results concerning the vitamin/hormone of the hour: vitamin D. Although there was no overall difference in vitamin D concentrations in the ADHD and not-ADHD group samples, the authors did observe that: "for vitamin D, ADHD patients were significantly overrepresented both in the lowest and highest 10th percentile groups." Bearing in mind past research has suggested that ADHD might be yet another diagnosis/label where vitamin D deficiency might be a feature (see here) it is pertinent that the authors suggest: "One reason for the overabundance of ADHD patients in the highest 10th percentiles of vitamin D may thus be that relatively more ADHD patients take vitamin D supplements, either as part of an experimental treatment of symptoms or as a consequence of a diagnosed vitamin D deficiency."Finally: "It is possible that low levels of certain vitamins may contribute to ADHD symptoms. Dietary intervention trials have shown promising effects in ADHD. Thus, identification and correction of low vitamin levels could be beneficial in treatment of ADHD. Further studies are warranted for replication and for examination of the underlying mechanisms."---------- Landaas ET. et al. Vitamin levels in adults with ADHD. BJPsych Open. 2016 Dec 13;2(6):377-384. Aarsland TI. et al. Serum concentrations of kynurenines in adult patients with attention-deficit hyperactivity disorder (ADHD): a case-control study. Behav Brain Funct. 2015 Nov 5;11(1):36.----------Landaas ET, Aarsland TI, Ulvik A, Halmøy A, Ueland PM, & Haavik J (2016). Vitamin levels in adults with ADHD. BJPsych open, 2 (6), 377-384 PMID: 27990293... Read more »
"To conclude, the evidence from the studies allows us to conclude that there is an association between PM [particulate matter] exposure and ASD [autism spectrum disorder] whose strength varies according to the particle size studied with the association with PM2.5 and diesel PM being stronger."Although probably not great sentence structure to begin a post with a conclusion, the 'bottom line' reported by María Morales-Suárez-Varela and colleagues  summarises the current research looking at particulate matter (a.k.a pollution) and risk of autism. Surveying the current research literature - well, a window "from November 2015 up to January 2016" - authors reported finding a majority of studies showing "positive associations restricted to specific exposure windows which however do not reach statistical significance at times." This adds to other reviews of the research in this area .I don't want to dwell too much on this paper and topic because it's something that has already received quite a bit of attention on this blog (see here and see here for examples). As with most research areas focused on autism, there is evidence for and evidence against any association/correlation between air pollution exposure and risk of autism. Given the various factors included under the heading of pollution (type, particle size, how exposure is measured) it's perhaps not surprising that there is not yet any 'smoking gun' (pardon the pun) when it comes to any possible association.I however, am taken by the ideas that (a) genes probably play a hand in translating air pollution exposure to a heightened risk of [offspring] autism and (b) other conditions linked to air pollution such as asthma might also feature in any connection (see here for example). Indeed, in these times of seemingly ever-increasing air pollution (see here) and lots of possible connections, further investigations are very much indicated.---------- Morales-Suárez-Varela M. et al. Systematic review of the association between particulate matter exposure and autism spectrum disorders. Environ Res. 2016 Dec 13;153:150-160. Lam J. et al. A Systematic Review and Meta-Analysis of Multiple Airborne Pollutants and Autism Spectrum Disorder. PLoS One. 2016 Sep 21;11(9):e0161851.----------Morales-Suárez-Varela M, Peraita-Costa I, & Llopis-González A (2016). Systematic review of the association between particulate matter exposure and autism spectrum disorders. Environmental research, 153, 150-160 PMID: 27984759... Read more »
Morales-Suárez-Varela M, Peraita-Costa I, & Llopis-González A. (2016) Systematic review of the association between particulate matter exposure and autism spectrum disorders. Environmental research, 150-160. PMID: 27984759
"Our data show there may be a specific subtype of ASD [autism spectrum disorder] linked to comorbid psychosis. The results support findings that psychosis in people with ASD is often atypical, particularly regarding affective disturbance."So said the findings reported by Felicity Larson and colleagues  (open-access available here) who bring an important topic into view that has recently been raised in the media too (see here). I appreciate that to talk about yet more comorbidity potentially following an autism diagnosis is not exactly great news. If however, one accepts that various comorbid conditions can actually be pretty disabling for many on the autism spectrum, identifying, screening and managing/treating said comorbidity then actually becomes pretty important.Researchers set about looking to "describe autistic and psychotic phenomenology in a group of individuals with comorbid ASD and psychosis (ASD–P) and compare this group with populations affected by either, alone." Their group comprised of adults aged 16 and over diagnosed with an ASD and comorbid psychosis (N=116). This was an opportunistic cohort insofar as being recruited between January 2010 and June 2013. Eligibility was determined by a formal diagnosis of autism at referral and meeting "criteria on the Autism Diagnostic Observation Schedule (ADOS)... at the time of involvement in the study, or... meet criteria on the Autism Diagnostic Interview-Revised (ADI-R)... for a lifetime diagnosis." Psychotic illness determination was a 2-stage affair. First, inclusion was based on "a prior clinical diagnosis of psychotic illness or gave an account of an episode that was clearly psychotic" followed by evidence of psychotic symptoms being elicited using one or more questionnaires onward to the presentation of 'research-significant psychosis'.Results: "What is clear from this research is that individuals who experience concurrent ASD and psychotic illness exist and are treated in mental health services." I don't think there is anything too earth-shattering about that statement but it does need to be said in the context of the label of autism rarely/not existing in some sort of diagnostic vacuum (see here). Next: "Mental health services in the UK are yet to be fully equipped to support people with both psychotic illness and ASD." Again, nothing new; following a trend of resources not being available or 'ready' to accommodate people on the autism spectrum and the health inequalities that inevitably follow. Insofar as the idea that psychosis presentation may at times be 'atypical' when it comes to autism, this also follows an important trend noted in other comorbidity research (e.g. when it comes to bipolar disorder for example).The other data presented by Larson and colleagues on the profile of autistic symptoms potentially being slightly different when compared to a 'control group' of those diagnosed with autism but without evidence of psychosis - "the ASD–no psychosis (ASD–NP) group" (n=69) - is interesting but requires quite a bit more follow-up work. I might at this point drop in the paper by the wonderfully named Robustelli and colleagues  talking about how "youth at high-risk of developing psychosis have fewer and poorer quality social relationships" as being potentially relevant and indeed, how social functioning can be affected long-term when it comes to psychosis. Further investigation is also required around the observation that: "Individuals with ASD–P had lower rates of schizophrenia and higher rates of psychosis-NOS" in light of other work talking about spectrums (autism and schizophrenia) colliding (see here). Although not part of this study, the name of one co-author on this paper being linked to the Autism-Spectrum Quotient (AQ) is also potentially relevant, given other work asking whether the AQ might actually be picking up signs and symptoms of something like schizophrenia too (see here).There is also the question of possible overlapping mechanisms potentially at work when it comes to autism and psychosis. In light of recent chatter about an immune system 'feature' to some psychosis (see here) and the myriad of immune related findings linked to autism, I'd suggest that this could be one area for further research inspection. The idea also that vitamin D for example, shows some relationship to some autism (see here for example) is another area for joint investigation given some chatter about levels of the sunshine vitamin/hormone and cases of psychosis . There will no doubt, be other areas of overlap potentially pertinent too...There is quite a bit more to do in this increasingly important area of research.---------- Larson FV. et al. Psychosis in autism: comparison of the features of both conditions in a dually affected cohort. Br J Psychiatry. 2016 Dec 15. pii: bjp.bp.116.187682. Robustelli BL. et al. Social relationships in young adults at ultra high risk for psychosis. Psychiatry Res. 2016 Dec 7;247:345-351. Suetani S. et al. Prevalence and correlates of suboptimal vitamin D status in people living with psychotic disorders: Data from the Australian Survey of High Impact Psychosis. Australian & New Zealand Journal of Psychiatry. 2016. Dec 21.----------Larson, F., Wagner, A., Jones, P., Tantam, D., Lai, M., Baron-Cohen, S., & Holland, A. (2016). Psychosis in autism: comparison of the features of both conditions in a dually affected cohort The British Journal of Psychiatry DOI: 10.1192/bjp.bp.116.187682... Read more »
Larson, F., Wagner, A., Jones, P., Tantam, D., Lai, M., Baron-Cohen, S., & Holland, A. (2016) Psychosis in autism: comparison of the features of both conditions in a dually affected cohort. The British Journal of Psychiatry. DOI: 10.1192/bjp.bp.116.187682
"Our findings identify distinctive mucosal microbial signatures in ASD [autism spectrum disorder] children with FGID [functional gastrointestinal disorders] that correlate with cytokine and tryptophan homeostasis."So said the study results published by Ruth Ann Luna and colleagues  who "compared mucosa-associated microbial communities in children with ASD to previous reports characterizing stool in this population" among other things. If you are eating breakfast/lunch/dinner at the time of reading this post, maybe give it a few minutes before reading on...So rectal biopsies and blood specimens were the samples under investigation and the focus was very much on those children on and off the autism spectrum who also presented with various functional bowel issues. Just before anyone starts to question the ethics of taking biopsies and the like, the authors expand by reporting that participants were "undergoing a lower endoscopy for one of the following symptoms: abdominal pain, altered stool patterns, or painless bright red blood per rectum." In these days of health inequality attached to the label of autism (see here for an example), these were children who were being investigated for their bowel issues and not being unnecessarily subjected to such invasive techniques just for the sake of science.The various analyses undertaken on those blood and biopsy samples were pretty wide-ranging. Bacterial species present in mucosal samples and their supernatants were included but so researchers also looked at cytokines (various chemical markers linked to immune function among other things) in blood samples and supernatants and levels of "serotonergic metabolites" (chemicals related to the aromatic amino acid tryptophan) pertinent to their "microbiome-neuroimmune signatures" hypothesis testing. Bear in mind that when it comes to the neurotransmitter called serotonin (5-HT), the gut truly is the second brain.Results: taking into account the relatively small participant numbers included for study - "ASD children with functional GI disorders (ASD-FGID, n=14), as compared to neurotypical (NT) children with (NT-FGID, n=15) and without abdominal pain (NT, n=6)" - there were some interesting, if not unexpected, results to be seen. "Principal component analysis showed clear separation between the ASD-FGID group and the NT-FGID and NT groups" on the basis of the bacterial communities present in those mucosal samples. In the autism group, several mucosa-associated Clostridiales species were predominant as per that noted in other independent findings (see here). Interestingly authors also observed "marked decreases in Dorea and Blautia, as well as Sutterella" species perhaps contrasting with other research in this area (see here). I'll let readers trawl through the other bacterial families talked about in the paper including those potentially linked to the presence of specific functional bowel states derived from questionnaire data from participants.Looking at any potential associations between mucosal bacterial communities, cytokines and those tryptophan metabolites, researchers also reported some important, if preliminary, observations. So: "Group comparisons revealed that IL-6 [interleukin 6] and tryptophan release by mucosal biopsies was highest in ASD children with abdominal pain, whereas serotonergic metabolites were generally elevated in children with FGIDs." I'd like to see these findings replicated in larger groups before I make anymore of what their potential significance could be but it is intriguing that pain might play some hand in immune signalling and the production of amino acid metabolites. More so when one considers other related research .On the back of a recent post talking about blood-based 'biomarkers' pertinent to more pathological bowel states occurring alongside cases of autism (see here) it is good to see that autism + GI issues is starting to receive a little more scientific attention. It shows that science has moved on from the question 'are bowel symptoms over-represented when it comes to autism?' (answer: yes) and actually started to look at the questions of 'why? and 'how?' The focus on gut bacteria is a worthy cause (see here) and if replicated and found to be important, opens up various intervention options derived from work in other areas of medicine (see here). Indeed, there is a 'watch this space' call for investigations looking at probiotics and autism for example (see here) with the promise of more to come . Oh, and don't forget the good old 'gut-brain axis' when it comes to a possible tie-up between bowel and brain with at least some autism in mind.But for now, autism, gut disorder, gut bacterial composition, mucosal immune function and little old tryptophan and its metabolites get some well deserved combined research attention...---------- Luna RA. et al. Distinct microbiome-neuroimmune signatures correlate with functional abdominal pain in children with autism spectrum disorder. CMGH Cellular and Molecular Gastroenterology and Hepatology. 2016. Dec 11. Ahmad SF. et al. Imbalance between the anti- and pro-inflammatory milieu in blood leukocytes of autistic children. Mol Immunol. 2016 Dec 24;82:57-65. Navarro F. et al. Can probiotics benefit children with autism spectrum disorders? World J Gastroenterol. 2016 Dec 14;22(46):10093-10102.----------Luna, R., Oezguen, N., Balderas, M., Venkatachalam, A., Runge, J., Versalovic, J., Veenstra-VanderWeele, J., Anderson, G., Savidge, T., & Williams, K. (2016). Distinct microbiome-neuroimmune signatures correlate with functional abdominal pain in children with autism spectrum disorder CMGH Cellular and Molecular Gastroenterology and Hepatology DOI: 10.1016/j.jcmgh.2016.11.008... Read more »
Luna, R., Oezguen, N., Balderas, M., Venkatachalam, A., Runge, J., Versalovic, J., Veenstra-VanderWeele, J., Anderson, G., Savidge, T., & Williams, K. (2016) Distinct microbiome-neuroimmune signatures correlate with functional abdominal pain in children with autism spectrum disorder. CMGH Cellular and Molecular Gastroenterology and Hepatology. DOI: 10.1016/j.jcmgh.2016.11.008
Viscosupplementation at the time of partial meniscectomy failed to provide better outcomes than surgery alone. ... Read more »
Filardo, G., Di Matteo, B., Tentoni, F., Cavicchioli, A., Di Martino, A., Lo Presti, M., Iacono, F., Kon, E., & Marcacci, M. (2016) No Effects of Early Viscosupplementation After Arthroscopic Partial Meniscectomy: A Randomized Controlled Trial. The American Journal of Sports Medicine, 44(12), 3119-3125. DOI: 10.1177/0363546516660070
"Consistent with the previous findings, [the] rate of suicidality is higher in individuals with ASD [autism spectrum disorder]."That was one of the conclusions reported in the paper by Sevcan Karakoç Demirkaya and colleagues  (open-access) yet again touching on a most important topic when it comes to autism, particularly the part of the autism spectrum labelled as 'high-functioning'. Personally, I'm not a great fan of the 'functioning' description typically added to autism to somehow denote can from can't do. As science is starting to realise, high-functioning does not automatically imply 'can function' across the board just as the even worse description 'low-functioning' does not necessarily generalise to mean 'can't function'. I know it's the best we have at the moment but...Anyhow, Karakoç Demirkaya et al report results following a review of medical charts for some 55 adolescents (mostly boys) aged between 7 and 20 years of age. All were diagnosed with an ASD and all had "capability of reading, writing and speaking" and were deemed to have cognitive abilities in the typical range (i.e. no learning disability). Included in the data examined were responses to the Eskin’s Suicide Screening Questionnaire; specifically answers to 5 questions on thoughts of (suicidality) and actual attempts at suicide.Results: "Suicidality was observed in 16 individuals in our group which accounts for a rate of suicide of 29%. Among the suicidal ones, seven individuals had the diagnosis of AD [autistic disorder], eight had AS [Asperger syndrome], and an individual had PDD-NOS [pervasive developmental disorders - not otherwise specified]." Because no 'not autism' control group was included in this specific study, authors draw attention to how their figure compared with "the result of previous studies implemented on a typically developing adolescent population in our country" (Turkey) and suggest that their figure was slightly higher (29% vs 25%). I have to say that I'm pretty shocked by the suicidality figures reported in both the autism and not-autism groups.On the issue of actual suicide attempts, Karakoç Demirkaya and colleagues report that about 12% of their small-ish cohort had some history of this type of behaviour. Again, this contrasted with data from other independent studies where around 4-5% of adolescents were reporting such a history. Worrying figures again.Further: "Rates of comorbid psychiatric disorders such as mood disorders, anxiety disorders and disruptive behaviors were 23.6%, 43.6% and 65.4% respectively. Groups with the psychotic features, positive family history for suicidal behaviors and completed suicide showed more suicidality than the non-suicidal group." This is an important part of the results obtained. It implies that when we say suicidality (thoughts and/or behaviours) is 'elevated' when it comes to the autism spectrum, we can't at the present time, tease autism apart from other comorbidities that may also have an important bearing on this type of behaviour. It's a point that has been raised in relation to suicidality accompanying other labels too (see here).I'm gonna leave it at that with the Karakoç Demirkaya findings save any charges of 'going beyond the data'. As I seem to do quite a lot these days, the primary message is that screening - preferential screening - should be an important part of the continued 'management' of autism (see here). Alongside other media headlines illustrating how for example, psychosis can be (a) present and (b) can sometimes exert a powerful effect on some people on the autism spectrum, further investigation(s) on the role of such issues (minus any stigma) in relation to suicidality and autism is also indicated.---------- Karakoç Demirkaya S. et al. Assessment of suicidality in children and adolescents with diagnosis of high functioning autism spectrum disorder in a Turkish clinical sample. Neuropsychiatr Dis Treat. 2016 Nov 11;12:2921-2926.----------Karakoç Demirkaya, S., Tutkunkardaş, M., & Mukaddes, N. (2016). Assessment of suicidality in children and adolescents with diagnosis of high functioning autism spectrum disorder in a Turkish clinical sample Neuropsychiatric Disease and Treatment, Volume 12, 2921-2926 DOI: 10.2147/NDT.S118304... Read more »
Karakoç Demirkaya, S., Tutkunkardaş, M., & Mukaddes, N. (2016) Assessment of suicidality in children and adolescents with diagnosis of high functioning autism spectrum disorder in a Turkish clinical sample. Neuropsychiatric Disease and Treatment, 2921-2926. DOI: 10.2147/NDT.S118304
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