"In a population of children diagnosed with ASD [autism spectrum disorder], the rate of ADHD [attention-deficit hyperactivity disorder] + ASD was 42% and the rate of ADHD + ASD + ID [intellectual disability] was 17%, resulting in a 59% total comorbidity rate of ADHD and ASD."That was one of the important findings reported by Tara Stevens and colleagues  who using data from the Survey of Pathways to Diagnosis and Services (Pathways), a US initiative that has previously been discussed on this blog (see here), threw their research hat into an increasingly important part of the autism research and practice landscape.I mentioned the percentage figure of 76% in the title of this post with reference to other, smaller scale, findings previously talked about on this blog (see here) based on the work published by Joshi and colleagues  and their observation of a: "high rate of comorbidity with ADHD... in psychiatrically referred youth with ASD, with a clinical presentation typical of the disorder."The Stevens data is based on a larger sample cohort and whilst not necessarily carrying the same sort of diagnostic clout as the Joshi data ("Diagnostic interviews were administered by highly trained and closely supervised psychometricians with bachelor’s or master’s degrees in psychology or a related field") does benefit from those larger numbers included and indeed, the more naturalistic setting of data collection. That Stevens et al report that: "Average age at diagnosis was over 6 years for children with ASD + ADHD but close to 2.5 years for children with ASD only" also provides some welcome information about the experiences of a dual diagnosis of autism plus ADHD.In these days of autism plus  (ESSENCE even) further focus on the idea that the label of autism rarely exists in some sort of diagnostic vacuum (see here) represents an important step towards offering appropriate - preferential - screening when autism is mentioned and also focusing minds on how comorbidity can in some cases be even more disabling than the core diagnosis of autism (see here). Although one has to be quite careful not to 'big up' the relationship between autism and ADHD, particularly in these days where a very vocal group of people talk about over-diagnosis of ADHD, I'd be minded to suggest that as per the example with other comorbidity over-represented when it comes to autism, tackling something like ADHD when it is present/diagnosed might have some important repercussions for the presentation of core autism itself and its impact on quality of life...---------- Stevens T. et al. The comorbidity of ADHD in children diagnosed with autism spectrum disorder. Research in Autism Spectrum Disorders. 2016; 31: 11–18. Joshi G. et al. Symptom Profile of ADHD in Youth With High-Functioning Autism Spectrum Disorder: A Comparative Study in Psychiatrically Referred Populations. J Atten Disord. 2014 Aug 1. pii: 1087054714543368. Gillberg C. & Fernell E. Autism plus versus autism pure. J Autism Dev Disord. 2014 Dec;44(12):3274-6.----------Stevens, T., Peng, L., & Barnard-Brak, L. (2016). The comorbidity of ADHD in children diagnosed with autism spectrum disorder Research in Autism Spectrum Disorders, 31, 11-18 DOI: 10.1016/j.rasd.2016.07.003... Read more »
Stevens, T., Peng, L., & Barnard-Brak, L. (2016) The comorbidity of ADHD in children diagnosed with autism spectrum disorder. Research in Autism Spectrum Disorders, 11-18. DOI: 10.1016/j.rasd.2016.07.003
A new study suggests that given the choice, many dogs prefer praise from their owners over food. The study is one of the first to combine brain-imaging data with behavioral experiments to explore canine reward preferences.
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Cook, P., Prichard, A., Spivak, M., & Berns, G. (2016) Awake Canine fMRI Predicts Dogs’ Preference for Praise Versus Food. Social Cognitive and Affective Neuroscience. DOI: 10.1093/scan/nsw102
There they go again. Taiwan and their 'big data' publishing, yet again, some rather interesting population-based research trends derived from data from the National Health Insurance Research Database (NHIRD).This time around it is the paper by Han-Cheng Wang and colleagues  and the hypothesis to evaluate the "association between group A streptococcal (GAS) infections and the risks of developing tic disorders, obsessive-compulsive disorder (OCD), and attention-deficit/hyperactivity disorder (ADHD)." For those in the know, the relationship between Strep infection and those neuropsychiatric labels brings us into the realm of PANDAS and PANS (and no, not the fluffy black-and-white kind of panda either).Based on a not insignificant participant number - "2,596 patients and 25,960 controls" - researchers set about looking at under-18 year olds newly diagnosed with a GAS infection and their subsequent risk of receiving one or more of those neuropsychiatric labels.Compared to controls, the incidence of neuropsychiatric disorder in the GAS group was higher (60.42 per 10,000 person-years vs. 49.32 per 10,000 person-years) particularly when it came to the presentation of a tic disorder. If said GAS infection was serious enough to put someone in hospital, the risk of neuropsychiatric disorder was even higher compared with than those who did not have a GAS infection. The authors conclude: "Our results confirmed an association between previous group A streptococcal infection and neuropsychiatric disorders."Set within the growing research base suggesting that various infections can very much lead to behavioural outcomes (see here for another example) as well as physical ones, there is some interesting science still to be done on the hows and whys. Whether said infection meets us during the nine months that made us (see here) or some time after provides some intriguing insights on how timing and infection type might show differential effects for a person. The question of whether (a) we can prevent certain infections or (b) offset their primary effects via the use of agents affecting immune function or immune response perhaps represent some of the more important avenues for further investigations in this area.---------- Wang HC. et al. Group A Streptococcal Infections Are Associated With Increased Risk of Pediatric Neuropsychiatric Disorders: A Taiwanese Population-Based Cohort Study. J Clin Psychiatry. 2016 Jul;77(7):e848-54.----------Wang, H., Lau, C., Lin, C., Chang, A., & Kao, C. (2016). Group A Streptococcal Infections Are Associated With Increased Risk of Pediatric Neuropsychiatric Disorders The Journal of Clinical Psychiatry DOI: 10.4088/JCP.14m09728... Read more »
Wang, H., Lau, C., Lin, C., Chang, A., & Kao, C. (2016) Group A Streptococcal Infections Are Associated With Increased Risk of Pediatric Neuropsychiatric Disorders. The Journal of Clinical Psychiatry. DOI: 10.4088/JCP.14m09728
"Although some associations between ADHD [attention-deficit hyperactivity disorder] and offending may be accounted for by co-morbidity with substance use disorders, early onset of offending and repeated violent offending appear to be directly related to ADHD."That was the conclusion reached by Jan Román-Ithier and colleagues  reporting on their study designed to "examine correlates of childhood ADHD symptoms among prisoners." Based on a sample adult prison population (N=1179) where self-reported "retrospective measures of ADHD and a diagnostic interview for substance use disorders" were coupled with data on offending behaviour(s), researchers reported that there may be more to see when it comes to self-reported ADHD and offending behaviour not necessarily just due to substance abuse. Indeed: "Self-reported ADHD was associated with age of first arrest, a number of violent and non-violent offences and re-offending."Of course you'd be right if you highlighted a few methodological issues with the current data insofar as the use of self-report and indeed, retrospective self-report when it comes to ADHD or ADHD-type symptoms. I might even throw in the idea that feigning ADHD is not something unheard of in the peer-reviewed literature either (see here) bearing in mind one might expect some special treatment or accommodation for prisoners who might meet diagnostic thresholds. There is more [controlled] research to be done in this area for sure.But set within the idea that there may be something of an over-representation of ADHD in the prison population (see here), the Román-Ithier results add further weight to the idea that screening (including preferential screening for some) and treating ADHD early in life might be something to seriously think about from a population health and wellbeing perspective. Yes, one has to be careful about sweeping generalisations when it comes to ADHD and 'adverse outcomes' (see here) including the idea that ADHD persistence might not be uniform  and I don't doubt that some might be slightly adverse to the idea of some of the currently indicated treatment measure for ADHD when it comes to medication for example (see here). But as with many things in life, the pros and cons of tackling such issues need to be weighed up on an individual basis assuming for example, that a life of offending and re-offending is probably not to be helpful to anyone. I might also throw the findings by Chorniya & Kitashimab  into this post and how substance abuse disorder and other 'risky behaviours' might also decline as and when ADHD is appropriately managed.And outside of just pharmacotherapy for ADHD, there are other management options to potentially consider (see here and see here and see here for example)...To close, fair-dos to Gary Lineker...---------- Román-Ithier JC. et al. Attention deficit hyperactivity disorder symptoms, type of offending and recidivism in a prison population: The role of substance dependence. Crim Behav Ment Health. 2016 Jul 26. McAuley T. et al. Clinical, Sociobiological, and Cognitive Predictors of ADHD Persistence in Children Followed Prospectively Over Time. J Abnorm Child Psychol. 2016 Jul 29. Chorniya A. & Kitashimab L. Sex, drugs, and ADHD: The effects of ADHD pharmacological treatment on teens' risky behaviors. Labour Economics. 2016. July 5.----------Román-Ithier, J., González, R., Vélez-Pastrana, M., González-Tejera, G., & Albizu-García, C. (2016). Attention deficit hyperactivity disorder symptoms, type of offending and recidivism in a prison population: The role of substance dependence Criminal Behaviour and Mental Health DOI: 10.1002/cbm.2009... Read more »
Román-Ithier, J., González, R., Vélez-Pastrana, M., González-Tejera, G., & Albizu-García, C. (2016) Attention deficit hyperactivity disorder symptoms, type of offending and recidivism in a prison population: The role of substance dependence. Criminal Behaviour and Mental Health. DOI: 10.1002/cbm.2009
Aerobic exercise can significantly help people coping with the long-term mental health condition schizophrenia, according to a new study. Through combining data from 10 independent clinical trials with a total of 385 patients with schizophrenia, Joseph Firth found that around 12 weeks of aerobic exercise training can significant improve patients' brain functioning.
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Firth, J., Stubbs, B., Rosenbaum, S., Vancampfort, D., Malchow, B., Schuch, F., Elliott, R., Nuechterlein, K., & Yung, A. (2016) Aerobic Exercise Improves Cognitive Functioning in People With Schizophrenia: A Systematic Review and Meta-Analysis. Schizophrenia Bulletin. DOI: 10.1093/schbul/sbw115
Intestinal flora has multiple influences on human health, but researchers have revealed that it is also likely to have an effect on the body's response to drugs. Recent research suggests that changes in the intestinal flora, caused by antibacterial and antibiotic drugs or individual differences between people, may have an effect on a person's response to drugs including side effects. The research focused on the changes in proteins due to the condition of intestinal flora that affect the response to drugs in the liver and kidneys.
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Kuno, T., Hirayama-Kurogi, M., Ito, S., & Ohtsuki, S. (2016) Effect of Intestinal Flora on Protein Expression of Drug-Metabolizing Enzymes and Transporters in the Liver and Kidney of Germ-Free and Antibiotics-Treated Mice. Molecular Pharmaceutics, 13(8), 2691-2701. DOI: 10.1021/acs.molpharmaceut.6b00259
Although mostly trying to avoid any politics-talk on this blog I am going to make some reference to it in this post set in the context of the Persian Gulf War otherwise known at the First Iraq War.The recent publication of the Chilcot report describing the case for the UK's involvement in the 2003 Iraq War (the second Iraq War) has further lit up an already illuminating year in British politics, by perhaps adding fuel to the notion that 'finishing the job' might have been an important link between the two conflicts...Operation Desert Storm - the combat phase of the First Gulf War (1991) - described by some as 'the most toxic war in history' left a mark not just on the region where it was fought and its people but also on many of the returning service personnel, some of whom came back in a pretty poor state of health. Their various symptoms known collectively as Gulf War Syndrome or Illness, are still the topic of discussions and debate to this day despite increasing evidence that they are 'real' symptoms (see here) and not just some psychosomatic manifestation of combat stress for example, as advocated by some quite prominent figures. The possible reasons for illness are varied (see here) but when one uses the words 'sarin' in the context of potential exposures for example you get a flavour for what might have been involved  and their potential contributions to health or rather ill-health.The paper by Gerhard Johnson and colleagues  (open-access) adds further credence to the idea that Gulf War Illness (GWI) is indeed a real phenomenon and specifically: "that inflammation is a component of the pathobiology of GWI." Based on the examination of a relatively small number of veterans (85 out of 500 deployed veterans who were invited to participate), researchers undertook a "structured interview" that "assessed their health status, and blood samples were obtained." They managed to divide veterans up into GWI+ (n=57) and GWI- (n=28) groupings dependent on whether or not they reached the Fukuda criteria  for a "a chronic multisymptom condition" linked to deployment to the Gulf War.Results: over 80 specific analytes were assayed for from the blood samples provided by participants. Many compounds had an immunological slant in terms of being cytokines or being other markers of immune system (specifically inflammatory) 'activation'. "The results of the current study provide evidence of alterations in a number of blood parameters that are readily measurable in routine clinical laboratories" was the headline as six specific compounds, all with inflammation in mind, were ripe for further independent study: plasma C-reactive protein (CRP), leptin, brain-derived neurotrophic factor (BDNF), and matrix metalloproteinase-9 (MMP-9) = higher in the GWI+ group. Heart-type fatty acid binding protein (H-FABP) and matrix metalloproteinase-2 (MMP-2) = lower in the blood of GWI+ subjects. Alongside "the distributions of peripheral blood lymphocyte, monocyte, neutrophil, and platelet counts were higher in GWI+ subjects" compared with GWI- participant data leading researchers to observe that "a model utilizing three readily measurable biomarkers [lymphocytes, monocytes, and C reactive protein]... appears to significantly augment the symptom-based case definition of GWI.""The limitations of the study include small sample size, restricted geographic, ethnic, and sex composition of the study subjects, assay of blood parameters only once, some plasma protein assays, including cytokines, considered inevaluable due to a high percentage of assays below the level of detection, overlap of biomarker distributions within the normal range, absence of correction for multiple comparisons, a limited number of blood proteins found to be positively related to GWI+ status, and the absence of a confirmation cohort study." Apologies for just grafting a large chunk of text from the Johnson paper into this post, but when it comes to the limitations of their work, the authors do a pretty good job of cautioning against any over-hype and providing a roadmap to 'where next?'And as part of that 'where next?' it appears that we might be talking quite soon about some findings if an associated ClinicalTrials.gov entry is anything to go by (see here) on the use of 'delayed-release prednisone' with this group. I say this without making any value judgements or providing anything that looks, sounds or smells like medical or clinical advice.We wait and see.And to close: "all is as the Force wills it" apparently...---------- Proctor SP. et al. Effects of sarin and cyclosarin exposure during the 1991 Gulf War on neurobehavioral functioning in US army veterans. Neurotoxicology. 2006 Dec;27(6):931-9. Johnson GJ. et al. Blood Biomarkers of Chronic Inflammation in Gulf War Illness. PLoS ONE 11(6): e0157855. Fukuda K. et al. Chronic multisymptom illness affecting Air Force veterans of the Gulf War. JAMA. 1998 Sep 16;280(11):981-8.----------Johnson GJ, Slater BC, Leis LA, Rector TS, & Bach RR (2016). Blood Biomarkers of Chronic Inflammation in Gulf War Illness. PloS one, 11 (6) PMID: 27352030... Read more »
Johnson GJ, Slater BC, Leis LA, Rector TS, & Bach RR. (2016) Blood Biomarkers of Chronic Inflammation in Gulf War Illness. PloS one, 11(6). PMID: 27352030
Researchers have discovered that our brain actively takes sugar from the blood. Prior to this, researchers around the world had assumed that this was a purely passive process. An international team reports that transportation of sugar into the brain is regulated by so-called glial cells that react to hormones such as insulin or leptin; previously it was thought that this was only possible for neurons.
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García-Cáceres, C., Quarta, C., Varela, L., Gao, Y., Gruber, T., Legutko, B., Jastroch, M., Johansson, P., Ninkovic, J., Yi, C.... (2016) Astrocytic Insulin Signaling Couples Brain Glucose Uptake with Nutrient Availability. Cell, 166(4), 867-880. DOI: 10.1016/j.cell.2016.07.028
by Piter Kehoma Boll Certainly the most widespread, adaptable and well-known honey-producing bee is Apis melifera, commonly known as honeybee for obvious reasons. But there are a lot of other honey makers all over the world. Today I’m going to present … Continue reading →... Read more »
Miorin, P., Levy Junior, N., Custodio, A., Bretz, W., & Marcucci, M. (2003) Antibacterial activity of honey and propolis from Apis mellifera and Tetragonisca angustula against Staphylococcus aureus. Journal of Applied Microbiology, 95(5), 913-920. DOI: 10.1046/j.1365-2672.2003.02050.x
Sawaya, A., Cunha, I., Marcucci, M., de Oliveira Rodrigues, R., & Eberlin, M. (2006) Brazilian Propolis of Tetragonisca angustula and Apis mellifera. Apidologie, 37(3), 398-407. DOI: 10.1051/apido:2006011
Germline mutations of the folliculin gene are normally responsible for Birt–Hogg–Dubé (BHD) syndrome. The 3D structure of the C-terminal domain of folliculin (FLCN), folliculin-CT, has been previously determined (Nookala et al., 2012). FLCN is a tumor suppressor and a guanine nucleotide exchange factor (GEF) for Rab35. GEF activity of FLCN towards its GTPase might be essential for cellular processes. Most of the reported FLCN mutations lead to the BHD phenotype (Lim et al., 2010) and to loss of GEF activity which triggers carcinogenesis (Nookala et al., 2012). A new study by Verma et al. (2016) examines the effect of FLCN mutations on the protein conformation and in loss of function. Authors performed molecular dynamics (MD) simulation on mutated protein variants to predict the protein conformation which is associated with BHD phenotype.... Read more »
Verma S, Tyagi C, Goyal S, Pandey B, Jamal S, Singh A, & Grover A. (2016) Mutations induce conformational changes in folliculin C-terminal domain: possible cause of loss of guanine exchange factor activity and Birt-Hogg-Dubé syndrome. Journal of biomolecular structure , 1-6. PMID: 27484154
A bit of a lazy post for you today with lots of quotes based on the findings reported by Ragnar Nesvåg and colleagues  asking some important questions about 'off-label' use of antipsychotics.Drawing on population-based data from Norway concerning "which substances, and for which mental disorder diagnoses, antipsychotic drugs were prescribed to 0–18-year-old boys and girls" the conclusions drawn make for some interesting reading.So: "In total, 0.18% of Norwegian children and adolescents were prescribed antipsychotic drugs during 2010." I found this to be quite a reassuring figure insofar as antipsychotic use not to be at 'epidemic proportions' or at least not as high as other psychoactive meds.Next: "The most common mental disorder diagnoses among male users were hyperkinetic (49.9%) and autism spectrum disorder (27.1%), while anxiety disorders (41.5%) and depressive illness (33.6%) were most common among female users." These data are a little more worrying. Granted, certain antipsychotics have received license elsewhere in the world when it comes to aspects of labels such as autism (see here) but importantly, this doesn't yet include the 'core symptoms' of autism, or at least not here in Blighty (see here). This hasn't however seemingly stopped many from receiving such prescriptions it seems (see here).Finally: "These results demonstrate that children and adolescents who use antipsychotic drugs are predominantly diagnosed with non-psychotic mental disorders such as hyperkinetic disorder among boys and anxiety disorder or depressive illness among girls." Accepting that diagnoses and labels are sometimes not the starting point for the use of antipsychotic medication (physicians normally treat symptoms not labels) and that there is often significant overlap between various psychiatric and behavioural diagnoses, these findings are challenging. Not least because although very good at treating symptoms experienced b y many people, antipsychotics are not without their side effects (see here and see here for example).The implication from the Nesvåg data is that antipsychotic use may be very much moving outside of the realms of just treating psychosis...---------- Nesvåg R. et al. Mental disorder diagnoses among children and adolescents who use antipsychotic drugs. European Neuropsychopharmacology. 2016. July 21.----------Nesvåg, R., Hartz, I., Bramness, J., Hjellvik, V., Handal, M., & Skurtveit, S. (2016). Mental disorder diagnoses among children and adolescents who use antipsychotic drugs European Neuropsychopharmacology DOI: 10.1016/j.euroneuro.2016.07.001... Read more »
Nesvåg, R., Hartz, I., Bramness, J., Hjellvik, V., Handal, M., & Skurtveit, S. (2016) Mental disorder diagnoses among children and adolescents who use antipsychotic drugs. European Neuropsychopharmacology. DOI: 10.1016/j.euroneuro.2016.07.001
There's a reason it's called a gut feeling. The brain and the gut are connected by intricate neural networks that signal hunger and satiety, love and fear, even safety and danger. These networks employ myriad chemical signals that include dopamine, a powerful neurotransmitter most famous for its role in reward and addiction.
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Xiou Cao, & Alejandro Aballay. (2016) Neural inhibition of dopaminergic signaling enhances immunity in a cell non-autonomous manner. Current Biology. info:/http://dx.doi.org/10.1016/j.cub.2016.06.036
There was always that nagging feeling of not being accepted, of whispers behind his back. They pretended to be open-minded, but in reality not belonging to the group of professionals was reason enough to dismiss his work and findings. In their eyes, he was just a solicitor. A hobbyist. He was tolerated, but their derision […]... Read more »
De Groote, I., Flink, L., Abbas, R., Bello, S., Burgia, L., Buck, L., Dean, C., Freyne, A., Higham, T., Jones, C.... (2016) New genetic and morphological evidence suggests a single hoaxer created ‘Piltdown man’. Royal Society Open Science, 3(8), 160328. DOI: 10.1098/rsos.160328
"In this nationwide sample of live births we observed no association between induction of labor and offspring ASD [autism spectrum disorder] within sibling comparison. Our findings suggest that concern for ASD should not factor into the clinical decision about whether to induce labor."So said the findings reported by Anna Sara Oberg and colleagues  supposedly providing some reassurance to mums-to-be and other groups around the likelihood of offspring autism when birth or labour has to be induced. Based on the analysis of one of those oh-so important Scandinavian health registries, researchers followed all the live births recorded in Sweden between 1992 and 2005 looking for signs that labour was induced. As per some media discussion of the study: "Methods to induce labor include rupturing of membranes, mechanical or pharmacological ripening of the cervix, and administration of oxytocin, either used alone or in combination." They also followed the cohort, numbering above a million offspring, looking for recorded diagnoses of ASD in children and, taking into account "a wide range of measured confounders" examined whether induced labour might elevate the risk of offspring ASD.The headlines suggesting 'no link' between induced labour and offspring autism don't however actually tell the full story of these findings. When taking into account the full cohort - "1 362 950 births"- there did seem to be a slight increased risk of offspring autism associated with labour induction. This association persisted "after adjustment for measured potential confounders" albeit to an even lesser degree. The 'no link' headlines seemed to have focused on further analysis where siblings, one who was induced, one who was not, were compared with regards to autism rates: "thus accounting for all environmental and genetic factors shared by siblings, labor induction was no longer associated with offspring ASD."I've talked about labour induction and autism risk before on this blog (see here) based on findings  that Oberg et al were knowledgeable about and that had reported something of an increased risk based on the analysis of over half a million births in a part of the United States. Personally, I do think there is a little more to see in this area than has hitherto been uncovered. The reasons for induction is something to focus on as per the observations that issues such as pre-eclampsia and gestational diabetes are mentioned and the body of research linking such factors to offspring autism risk (see here and see here for examples). That induction also might mean use of oxytocin (the cuddle hormone!) is something else that perhaps require further investigations too. Without trying to scaremonger, I do wonder whether further thought might be needed based on the findings reported by Leffa and colleagues  with oxytocin in mind.The take-away message: induced labour is pretty unlikely to 'cause' offspring autism but beware of sweeping generalisations and media headlines...---------- Oberg AS. et al. Association of Labor Induction With Offspring Risk of Autism Spectrum Disorders. JAMA Pediatr. 2016. 25 July. Gregory SG. et al. Association of autism with induced or augmented childbirth in North Carolina Birth Record (1990-1998) and Education Research (1997-2007) databases. JAMA Pediatr. 2013 Oct;167(10):959-66. Leffa DD. et al. DNA damage after chronic oxytocin administration in rats: a safety yellow light? Metab Brain Dis. 2016 Aug 3.----------Oberg, A., D’Onofrio, B., Rickert, M., Hernandez-Diaz, S., Ecker, J., Almqvist, C., Larsson, H., Lichtenstein, P., & Bateman, B. (2016). Association of Labor Induction With Offspring Risk of Autism Spectrum Disorders JAMA Pediatrics DOI: 10.1001/jamapediatrics.2016.0965... Read more »
Oberg, A., D’Onofrio, B., Rickert, M., Hernandez-Diaz, S., Ecker, J., Almqvist, C., Larsson, H., Lichtenstein, P., & Bateman, B. (2016) Association of Labor Induction With Offspring Risk of Autism Spectrum Disorders. JAMA Pediatrics. DOI: 10.1001/jamapediatrics.2016.0965
Last week, I discussed how male quality in birds may be related to their song. How do males evaluate females in return? The answer may lie in their nests.... Read more »
Cantarero, A., López-Arrabé, J., Plaza, M., Saavedra-Garcés, I., & Moreno, J. (2016) Males feed their mates more and take more risks for nestlings with larger female-built nests: an experimental study in the Nuthatch Sitta europaea. Behavioral Ecology and Sociobiology, 70(8), 1141-1150. DOI: 10.1007/s00265-016-2122-2
If you read my blog often, it's no surprise I suffer from PTSD, depression, and anxiety issues. Maybe it's from my military service, but maybe it's my father's, or his father's, maybe it's an insidious family legacy that was just never noticed. This is because having both parents and grandparents with major depressive disorder (MDD) was associated with higher risk of MDD for grandchildren, which could help identify those who may benefit from early intervention.
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Myrna M. Weissman, PhD, Obianuju O. Berry, MD, MPH, Virginia Warner, DrPH, Marc J. Gameroff, PhD, Jamie Skipper, MS, Ardesheer Talati, PhD, Daniel J. Pilowsky, MD, MPH, & Priya Wickramaratne, PhD. (2016) A 30-Year Study of 3 Generations at High Risk and Low Risk for Depression. JAMA Psychiatry . info:/10.1001/jamapsychiatry.2016.1586
One cannot over estimate the ways that water affects life on Earth. Beyond its chemical properties, some animals have evolved to substitute water for a rigid skeleton. Hydrostatic skeletons can be used for support, but also as water vascular systems that provide pressure for vascular transport and respiration. A recent review by William H. Kier sheds light on the interactions of different fibers and tissues in water based skeletons. Yet some plants can withstand a loss of 60% of their water, when just 15% dehydration is lethal to humans.... Read more »
Although research stories stating a link (an association if you will) between condition A and factor X make for interesting reading, not all science is so blessed with such news-worthy findings. That's not to say that 'negative findings' are any less important than the 'hey, we found this...' studies, just that they don't perhaps tend to grab the headlines as much as those finding something.In saying all that I'm standing up for negative findings today and some rather interesting science reported by Jennifer Duringer and colleagues  (open-access available here) on the lack of any significant relationship between current urinary mycotoxin content and their cohort of 25 young people diagnosed with an autism spectrum disorder (ASD).Just in case you didn't already know, mycotoxin refers to "“natural” environmental contaminants, defined as secondary metabolites produced by fungi that reside in our food supply and on every surface in our environment." There are various types of mycotoxins (lots!) that occur as a consequence of various exposure patterns including fungi/moulds growing on foods or being present in our environment. Generally speaking, mycotoxins are something to be avoided (being careful with any sweeping generalisations there).Duringer et al started their research journey on the basis that weather conditions pertinent to mycotoxin production have been linked to autism (see here) and some small-scale study that "suggested that individual exposure to mold increased the severity of neurophysiological abnormalities seen in autistic children" . I know that furrowed brows will ensue when one talks about precipitation correlating with autism as per 'other correlations' but that was the basis for their study and should so be respected.The technology used to test participants' urine sample for any presence of mycotoxin is not to be sniffed at as yet again (see here) tandem mass spectrometry steps up to the analytical plate. Some 87 mycotoxins were assayed for based on some previously published work and some important details such as the fact that urine samples were run in triplicate (even six times if you count the fact that each replicate was run in positive and negative ion modes) are included as part of the study protocol.Results: given the fact that the cohort consisted of 25 young people with autism and 29 age-matched controls, one has to be a little cautious about making too many sweeping generalisations. What we can say is this: 20% of the participants with autism (5/25) came up with a 'positive' sample defined as 'any mycotoxin' being present. This contrasted with 14% of controls (4/29). The amounts detected were low; in some cases very close to or below the limit of quantitation where suitable standards could be obtained and used as comparators. When pooled together, those 9 participants with a positive sample were compared with the participants with a negative result to see if any potential correlates might show statistical significance. They didn't.There are caveats to this work outside of the small participant group included for study. The authors highlight a particularly important one insofar as their focus on young adults "well after the in utero or infant-toddler exposure window when ASD develops and is diagnosed." In other words, the burden of current exposure to mycotoxins with autism in mind is probably low but that does not mean that "exposure windows" at other times might not exert an important effect. Indeed, other authors have speculated on other correlates  linked to the science of epigenetics for example, as perhaps being another area ripe for further study. This should be added to the list.For now however, we can only base conclusions on the available (peer-reviewed) evidence...---------- Duringer J. et al. No Association between Mycotoxin Exposure and Autism: A Pilot Case-Control Study in School-Aged Children. Toxins (Basel). 2016 Jul 20;8(7). pii: E224. Mezzelani A. et al. Ochratoxin A as possible factor trigging autism and its male prevalence via epigenetic mechanism. Nutr Neurosci. 2016;19(1):43-6.----------Duringer J, Fombonne E, & Craig M (2016). No Association between Mycotoxin Exposure and Autism: A Pilot Case-Control Study in School-Aged Children. Toxins, 8 (7) PMID: 27447670... Read more »
Duringer J, Fombonne E, & Craig M. (2016) No Association between Mycotoxin Exposure and Autism: A Pilot Case-Control Study in School-Aged Children. Toxins, 8(7). PMID: 27447670
It's not a fad diet, it is an actual diet -- as in the way a person eats normally -- and it may do more than just help your waistline. The Mediterranean diet can improve your mind, as well your heart.
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Hardman, R., Kennedy, G., Macpherson, H., Scholey, A., & Pipingas, A. (2016) Adherence to a Mediterranean-Style Diet and Effects on Cognition in Adults: A Qualitative Evaluation and Systematic Review of Longitudinal and Prospective Trials. Frontiers in Nutrition. DOI: 10.3389/fnut.2016.00022
"Comorbid anxiety symptoms are ubiquitous among psychiatric patients with mood or schizophrenia spectrum disorders, and in almost half of them, reportedly severe."So said the findings reported by Karpov and colleagues  who sought to put some further research flesh on to the bones of the idea that clinically relevant anxiety symptoms might not be unstrange bedfellows with a variety of other psychiatric labels.Based on the analysis of various patient groups included in the "Helsinki University Psychiatric Consortium Study" for the presence of anxiety symptoms (as measured by the Overall Anxiety Severity and Impairment Scale (OASIS)) researchers reported that approaching half of their cohort variously diagnosed with "schizophrenia or schizoaffective disorder (SSA, n=113), bipolar disorder (BD, n=99), or depressive disorder (DD, n=188)" reported as 'severe or extreme' their anxiety. Drilling down further into their data, authors concluded that said anxiety symptoms correlated with "high neuroticism, symptoms of depression and borderline personality disorder and low self-efficacy in all patients, and with early trauma in patients with mood disorders."Accepting that it is not necessarily new news that clinically relevant psychiatric signs and symptoms might extend beyond the handy diagnostic boxes that we currently use as part of our labelling system, I'd like to think there is another important feature of this 'interconnectedness'. The idea for example, that 'tackling' seemingly secondary issues such as anxiety might impact on more primary diagnosis is something that I'm keen to see extended in the research literature. There are various example of this being suggested/done with regards to other labels (see here for example) and indeed, how from a quality of life aspect, dealing with the very obvious disruption that chronic anxiety would bring, might be a target over and above intervention for other, more primary diagnoses...---------- Karpov B. et al. Anxiety symptoms in a major mood and schizophrenia spectrum disorders. Eur Psychiatry. 2016 Jul 19;37:1-7.----------Karpov, B., Joffe, G., Aaltonen, K., Suvisaari, J., Baryshnikov, I., Näätänen, P., Koivisto, M., Melartin, T., Oksanen, J., Suominen, K., Heikkinen, M., Paunio, T., & Isometsä, E. (2016). Anxiety symptoms in a major mood and schizophrenia spectrum disorders European Psychiatry, 37, 1-7 DOI: 10.1016/j.eurpsy.2016.04.007... Read more »
Karpov, B., Joffe, G., Aaltonen, K., Suvisaari, J., Baryshnikov, I., Näätänen, P., Koivisto, M., Melartin, T., Oksanen, J., Suominen, K.... (2016) Anxiety symptoms in a major mood and schizophrenia spectrum disorders. European Psychiatry, 1-7. DOI: 10.1016/j.eurpsy.2016.04.007
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