Triclosan is the active ingredient in many anti-bacterial products, but does it make our environment too clean? The hygiene hypothesis states that early childhood exposure to certain antigens can help to balance and control the immune system, and therefore result in lower levels of food and seasonal allergies. One particularly important antigen seems to be arabinogalactan, a fiber/sugar molecule found on farms – maybe that’s why farmers’ kids have lower levels of food and other allergies. If our environment doesn’t contain enough antigens, then the immune system seems to over-react and hypersensitivities develop. So – is it any wonder that triclosan use has been linked to higher rates of allergy?... Read more »
Gennady Cherednichenkoa, Rui Zhanga, Roger A. Bannisterb,Valeriy Timofeyevc, Ning Lic, Erika B. Fritscha, Wei Fenga, Genaro C. Barrientosa, Nils H. Schebbd, Bruce D. Hammockd, Kurt G. Beame, Nipavan Chiamvimonvatc, and Isaac N. Pessaha. (2012) Triclosan impairs excitation–contraction coupling and Ca2 dynamics in striated muscle. PNAS. DOI: 10.1073/pnas.1211314109
Sudden cardiac death among athletes most often occurred in African-American/Minorities and male athletes. Hypertrophic cardiomyopathy was the most common cause of sudden cardiac death.... Read more »
Maron BJ, Haas TS, Ahluwalia A, Murphy CJ, & Garberich RF. (2016) Demographics and Epidemiology of Sudden Deaths in Young Competitive Athletes: From the U.S. National Registry. The American Journal of Medicine. PMID: 27039955
Interview with Takashi Tsuji, team leader of the Laboratory for Organ Regeneration at the RIKEN Center for Developmental Biology... Read more »
Takagi, R., Ishimaru, J., Sugawara, A., Toyoshima, K., Ishida, K., Ogawa, M., Sakakibara, K., Asakawa, K., Kashiwakura, A., Oshima, M.... (2016) Bioengineering a 3D integumentary organ system from iPS cells using an in vivo transplantation model. Science Advances, 2(4). DOI: 10.1126/sciadv.1500887
I read with great interest the paper by Courtenay Frazier Norbury and colleagues  concluding that: "At school entry, approximately two children in every class of 30 pupils will experience language disorder severe enough to hinder academic progress."With the aim of characterising "the impact of varying NVIQ [nonverbal IQ] criteria on prevalence, clinical presentation and functional impact of language disorder in the first UK population study of language impairment at school entry", the authors have generated quite a bit of food for thought as a consequence of their findings (see here) based on data derived from The Surrey Communication and Language in Education Study (SCALES).Readers can peruse the hows and whys of the study design themselves, but some of the primary details were that based on an initial sample of some 7000 "who began a reception class (similar to kindergarten or school entry) in 2011" some 529 children were "selected for in-depth assessment in Year 1 (first grade, ages 5;1 – 6;10)" pertinent to issues such as language, NVIQ and other signs of emotional or behavioural problems.After assessment(s) and some number-crunching, authors reported on a prevalence estimate of 7.5% when it came to "a clinically significant language disorder of currently unknown cause that adversely impacts learning." With class sizes of approximately 30 children in mind, we arrive at that opening sentence of 2 children in every class at Year 1 (5-6 year olds) potentially being affected. Further: "estimates are based on a population of children in mainstream classrooms and do not include children in special schools for children with complex learning needs or children with English as an additional language." Other details are also mentioned including the fact that the geographical area under study (Surrey) is a relatively affluent area (apparently having 'the highest proportion of millionaires in the UK') and so differing factors such as socio-economic status (SES) in other regions of the UK might actually mean the results are an 'under-estimate' of the true position.There are a number of important implications from these findings, not least in terms of appropriate identification and support to be offered and "the need to raise awareness among education and health services regarding language disorder and its functional impact on children's daily lives." I note the authors have also zoomed in on the fact that language disorder had implications for "curriculum targets in the first year of school" (only 11% of those with a language disorder achieved those targets) and what that might mean in the wider context of schools being charged with 'raising standards, improving lives'. That also a greater number of children with a language disorder already had additional school support in place (39% vs. 6%) suggests that more needs to be done examining the impact of that support and whether it is actually helping children to achieve those 'curriculum targets' and more.I appreciate that there are still various conversations on the nature of language disorder and what it actually means in the context of both available diagnostic criteria and in relation to its presence alongside other developmental/behavioural labels. No doubt debates will continue in these areas. For now however, the realisation that at least two children in every infant class will present with such issues is a wake-up call for quite a bit more research on both the hows and whys but also the best strategies to manage such issues and enable a child to achieve to their full academic potential...---------- Norbury CF. et al. The impact of nonverbal ability on prevalence and clinical presentation of language disorder: evidence from a population study. Journal of Child Psychology and Psychiatry. 2016. May 16.----------Norbury, C., Gooch, D., Wray, C., Baird, G., Charman, T., Simonoff, E., Vamvakas, G., & Pickles, A. (2016). The impact of nonverbal ability on prevalence and clinical presentation of language disorder: evidence from a population study Journal of Child Psychology and Psychiatry DOI: 10.1111/jcpp.12573... Read more »
Norbury, C., Gooch, D., Wray, C., Baird, G., Charman, T., Simonoff, E., Vamvakas, G., & Pickles, A. (2016) The impact of nonverbal ability on prevalence and clinical presentation of language disorder: evidence from a population study. Journal of Child Psychology and Psychiatry. DOI: 10.1111/jcpp.12573
"Cow's milk protein intolerance is a common problem in young people with chronic fatigue syndrome, and is a treatable contributor to their symptoms."So said the paper by Peter Rowe and colleagues  who looked prospectively for signs of cow's milk protein intolerance (CMPI) in "55 adolescents and young adults with chronic fatigue syndrome" over the course of 2 years. Defining CMPI using 4 factors: "(1) no evidence of immediate or anaphylactic reactions to milk, (2) at least 2 of the following 3 chronic symptoms: gastroesophageal reflux, early satiety, and epigastric/abdominal pain, (3) improvement in upper gastrointestinal symptoms on a milk protein elimination diet, and (4) at least 2 recurrences of upper gastrointestinal symptoms > 2 hours following open re-exposure to milk protein" researchers set about on this fairly unusual study course to ascertain some preliminary prevalence data and to see what impact such food issues might have on self-reported quality of life.Nearly a third of their quite small participant group (17/55) hit their thresholds for CMPI and we are told that in comparison to non-CMPI participants, those with milk issues "had significantly worse health-related quality of life at baseline but not at 6 months (after institution of the milk-free diet)." As per that opening quote, prevalence of CMPI might be common in cases of CFS and might play some not insignificant role on quality of life.Wearing my 'diet and behaviour' hat (see here for example) the Rowe results make for interesting reading. The fact that some of the authors have quite a lot of research standing when it comes to chronic fatigue syndrome (CFS) adds to my interest in these results; specifically with another of their papers in mind on orthostatic intolerance and gastrointestinal (GI) symptoms  for example (orthostatic intolerance = development of symptoms when standing upright, and is thought to be linked to quite a few cases of CFS).Quality of life (health-related) when applied to CFS is something else that has already been covered on this blog (see here) and the observation that its presentation can be about as bad as it gets for some people in comparison to various other diagnostic labels. Anything therefore that can improve [elements of] such an important measure has to be taken seriously, particularly when it is something as 'treatable' as potentially eliminating milk from ones diet (I say this with no medical or clinical advice given or intended).But just before anyone decides to embark of a milk-free diet solely on the basis of Rowe results, a bit of a research 'to-do' list to think about in this area: (a) The sample size was quite small and we need to know more with larger sample sizes and perhaps more strenuous research methodologies. (b) The measures used to assess CMPI didn't appear to include anything 'biological'. I know this is still a bit of a grey area in terms of 'intolerance vs' allergy' but I'd like to think that more could be attempted during future study including that related to those bowel symptoms  given previous discussions in this area (see here). (c) Given that this was a study of CFS I think most people would like to know whether CFS symptoms were impacted by a milk-free diet as well as quality of life measures. Again, measuring CFS is not the easiest of tasks given the number of definitions (see here) but it's not impossible. (d) Acknowledging that not all milk is the same (see here and see here) and that protein is but one element of milk, I have to wonder whether it might be worthwhile doing some further study on this too. Given also that institution of a milk-free diet is not without potential complications, the question is once again: is there more science to be done?But that doesn't mean that the Rowe results are not interesting...---------- Rowe PC. et al. Cow's Milk Protein Intolerance in Adolescents and Young Adults with Chronic Fatigue Syndrome. Acta Paediatr. 2016 May 13. Sullivan SD. et al. Gastrointestinal symptoms associated with orthostatic intolerance. J Pediatr Gastroenterol Nutr. 2005 Apr;40(4):425-8. Frissora CL. & Koch KL. Symptom overlap and comorbidity of irritable bowel syndrome with other conditions. Curr Gastroenterol Rep. 2005 Aug;7(4):264-71.----------Rowe, P., Marden, C., Jasion, S., Cranston, E., Flaherty, M., & Kelly, K. (2016). Cow's Milk Protein Intolerance in Adolescents and Young Adults with Chronic Fatigue Syndrome Acta Paediatrica DOI: 10.1111/apa.13476... Read more »
Rowe, P., Marden, C., Jasion, S., Cranston, E., Flaherty, M., & Kelly, K. (2016) Cow's Milk Protein Intolerance in Adolescents and Young Adults with Chronic Fatigue Syndrome. Acta Paediatrica. DOI: 10.1111/apa.13476
Bacteria tend to smell. A classic example is the geosmin-producing Streptomyces species responsible for the nice earthy scent of freshly dug up soil. In general, though, bacteria have unpleasant odours. Just think of cheese, armpits, and poop. Lots of bacteria in or on all of those things. Some of the stinkiest bacteria are ones capable of infecting us. The distinctiveness of their disgusting bouquets may provide a means of identifying them. Hippocrates apparently diagnosed tuberculosis (caused by the bacterium Mycobacterium tuberculosis) based on the particularly nasty odour produced by pouring gunk coughed up by a patient onto hot coals. Yuck.Various strains of smelly Clostridium difficile (Source)Clostridium difficile is the bane of hospitals all over the world. This bacterium tends to infect the intestines of people who have been on certain antibiotics. The antibiotics clear out a large chunk of the bacteria normally inhabiting a person's intestines, allowing C. diff (as it's called) to establish a foothold. The bacterium pumps out toxins which cause damage and disrupt the proper movement of food through the intestines (read: lots of diarrhea). In some cases, the large intestine can become super inflamed, a potentially life-threatening situation. If your guts become filled with C. diff, your poop tends to become watery (snot-like) and smell really bad in a distinctive way. It's commonly described in the scientific literature as an odour similar to horse manure, although a quick search through nursing forum threads such as this one mention, among other things, mouldy bread with a dash of skunk, a hot outhouse, rotting chicken, and a fart mixed with hot decaying roadkill.Although the specific stench of a C. diff poop is reportedly difficult to miss, the one blinded study I found reported a group of 18 nurses were unable to identify poops from patients with C. diff infections based on their odour. That's not a particularly large sample group though, so it might be useful to do another study with more nurses to confirm these results.ReferencesBartlett JG, Gerding DN. 2008. Clinical recognition and diagnosis of Clostridium difficile infection. Clinical Infectious Diseases 46(Supplement 1):S12-S18. [Full text]Rao K, Berland D, Young C, Walk ST, Newton DW. 2013. The nose knows not: Poor predictive value of stool sample odor for detection of Clostridium difficile. Clinical Infectious Diseases 56(4):615-616. [Full text]Sethi S, Nanda R, Chakraborty T. 2013. Clinical application of volatile organic compound analysis for detecting infectious diseases. Clinical Microbiology Reviews 26(3):462-475. [Full text]http://www.phac-aspc.gc.ca/id-mi/cdiff-eng.php... Read more »
Rao K, Berland D, Young C, Walk ST, & Newton DW. (2013) The nose knows not: Poor predictive value of stool sample odor for detection of Clostridium difficile. Clinical Infectious Diseases, 56(4), 615-616. PMID: 23166192
You may have seen headlines such as: Florida Man Woke Up In A Motel Room Speaking Only Swedish. Or: Englishman wakes up speaking Welsh after stroke (“Rare brain disorder left English-speaking Alun Morgan only able to communicate in Welsh”). The first case was likely due to a fugue state, a type of dissociative disorder involving loss of personal identity and aimless wandering (Stengel, 1941). The second seems like an unusual example of bilingual aphasia involving loss of the ability to speak one's native language (rather than the more commonly affected second language). Perhaps you've even seen paranormal claims like:Under Hypnosis or Past Life Regression, A Physician's Wife Starts Speaking Swedish. . . In sessions conducted from 1955 to 1956, when Tania was under hypnosis, a personality emerged who spoke Swedish, a language that neither Tania nor Ken knew. As such, this represents a case of xenoglossy, where an individual can speak a language that has not been learned through normal means. Tania was born in Philadelphia and as such, English was her native language. Her parents, who were Jewish, were born in Odessa, Russia. No one in the family had ever been to Scandinavia and they knew no one who could speak Swedish. Xenoglossy is “the putative paranormal phenomenon in which a person is able to speak or write a language he or she could not have acquired by natural means.” Of course, there's always a logical explanation for such cases, but magical thinking leads people to believe that such phenomena are proof of past lives and reincarnation. A New Case of False XenoglossyAn amusingly written clinical report describes a 50 year old Italian man who stopped speaking his native Italian and insisted on speaking broken and somewhat fake French after a neurological event (Beschin et al., 2016). An abnormality in his basilar artery blocked the normal flow of cerebrospinal fluid, with hydrocephalus and brainstem vascular encephalopathy as a result. A typical example of the condition (known as megadolicho basilar artery) in another patient is shown below.Fig. 1 (Thiex & Mull, 2006). (A) CSF flow obstruction (arrow). (B) megadolicho basilar artery.The man had no previous psychiatric history and retained the ability to speak perfect Italian. The clinical report includes the only instance of the word “fling” that I recall seeing in a scientific journal, so I'll quote at length:He had superficially learned French at school, used it in his 20's due to a fling with a French girl but he has not spoken it for about 30 years. In his professional life he used English as his second language. Before brain damage he never manifested a particular attachment to French culture or French cuisine. His accent is not due to dysarthria and he speaks polished and correct Italian, his mother tongue. However, he now states that French is his preferred language refusing to speak in Italian spontaneously.. . .JC's French is maladroit and full of inaccuracies, yet he speaks it in a fast pace with exaggerated intonation using a movie-like prosody and posing as a typical caricature of a French man. His French vocabulary is reduced and he commits several grammatical errors but he does not speak grammelot or gibberish and never inserts Italian terms in his French sentences. He uses French to communicate with everybody who is prepared to listen; he speaks French with his bewildered Italian relatives, with his hospital inmates, with the consultants; he spoke French even in front of the befuddled Committee deciding on his pension scheme. He claims that he cannot but speak in French, he believes that he is thinking in French and he longs to watch French movies (which he never watched before), buys French food, reads French magazines and seldom French books, but he writes only in Italian. He shows no irritation if people do not understand him when he speaks in French.He performed well on picture naming and verbal fluency tests in Italian, although he first tried to name the item in French (substituting category names like ‘vegetable’ for the low frequency word ‘asparagus’). His episodic memory was poor and he could not recall autobiographical incidents from the previous few years (but could recall earlier memories). He performed well on most other cognitive tests. But he did show some psychiatric symptoms that were secondary to the brain injury.However, he presents with some delusions of grandeur, sleep disturbances and has some compulsive behaviours: he buys unnecessarily large quantities of objects (e.g., needing two hangers he bought 70) and he makes tons of bread to his wife's chagrin. He also shows unjustified euphoria (which he labels joie de vivre): for example in the morning he opens the windows and shouts bonjour stating that it is a wonderful day. He manifests signs of social disinhibition, for example proposing to organise a singing tour for his daughter's teenage friend or offering French lessons to his neighbours. These symptoms are indicative of secondary mania (Santos, Caeiro, Ferro, & Figueira, 2011) and were drug-resistant.This is certainly a highly usual consequence of megadolicho basilar artery, but note that the subtitle of Beschin et al.'s article is “A clinical observation not a mystery.” There is no true xenoglossy here (or anywhere else, for that matter).Further ReadingMan Wakes Up From Coma Speaking New Language: The media’s love of xenoglossyForeign Language Syndrome – “There actually isn’t a legitimate foreign language syndrome...”ReferencesBeschin, N., de Bruin, A., & Della Sala, S. (2016). Compulsive foreign language syndrome: A clinical observation not a mystery. Cortex DOI: 10.1016/j.cortex.2016.04.020Stengel, E. (1941). On the Aetiology of the Fugue States. British Journal of Psychiatry 87 (369): 572-599.Thiex R, Mull M. (2006). Basilar megadolicho trunk causing obstructive hydrocephalus at the foramina of Monro. Surg Neurol. 65(2):199-201. ... Read more »
Beschin, N., de Bruin, A., & Della Sala, S. (2016) Compulsive foreign language syndrome: A clinical observation not a mystery. Cortex. DOI: 10.1016/j.cortex.2016.04.020
"This study supports the hypothesis that environmental exposure to organic pollutants may play a significant role in the behavioral presentation of autism."Accepting that correlation is not the same as causation, the results published by Andrew Boggess and colleagues  (open-access here) make for some blogging fodder today and the idea that serum levels of various compounds headed under the description of organic pollutants (persistent or otherwise) might show some important connections to at least some autism.To get a few things straight first, this and other related research does not say that every diagnosis of autism is somehow the product of a 'toxic' exposure. Nor does it belittle the substantial contribution that genetics (whether structural or non-structural issues) confer when it comes to diagnosis. To my mind, it adds another level of complexity to the [various] hows and whys relating to how autism might come about . That, and offering some important biologically-led guidance on what might be done to decrease any body load of such pollutants as and when they are detected and there's quite a bit we can learn from such studies.Anyhow, Boggess et al started from the position of wanting to "evaluate the relationship between organic pollutants and behavioral severity in children with ASD [autism spectrum disorder] and matched controls." Thirty children diagnosed with autism were matched (age and sex) with 30 children without autism. Quite a panel of diagnostic and screening instruments were included as part of the study protocol, including ADOS (Autism Diagnostic Observation Schedule) and interestingly, the ATEC (see here). Each participant provided a blood sample, and the serum portion of the sample was subject to analysis by GC-MS (Gas Chromatography-Mass Spectrometry) for various compounds. Compounds included: "Three volatile organic compounds (VOC), benzene, toluene, and o-xylene; one alkane, hexane; five polychlorinated biphenyls (PCB), IUPAC congeners 28, 52, 101, 138, and 153; two polybrominated diphenylethers (PBDE), IUPAC congeners 47 and 99; two organochlorine pesticides, metolachlor and acetochlor; one dinitroanaline pesticide, pendimethalin; one organophosphate pesticide, chlorpyrifos; one phthalate, bis (2-ethylhexyl) phthalate (DEHP); and the chlorocarbon perchloroethylene."Results: well, looking directly at the metabolites under inspection and comparing the group results (autism group vs control group) in terms of individual quantified levels, there seemed very little see. The only compound that was statistically significant in terms of amounts between the groups was something called metolachlor, a herbicide, which was actually found in higher mean concentrations in the control group than the autism group. When also researchers compared "the pooled mean of all compounds from the ASD cohort to the pooled mean for all compounds in the control cohort" they similarly noted no significant difference. At this point you're probably thinking that this isn't particularly interesting data. Well, just hold it there...Researchers further examined whether there was something to see when comparing the mean xenobiotic body-burden (MXB) and those ADOS scores. Xenobiotic by the way, is another way of saying (foreign) compounds that were being assayed for, and combined with ADOS scores was a way of looking at whether behavioural severity might show some link to the concentrations of those compounds being reported on. In this respect: "Pooled serum-concentration correlated significantly with increasing behavioral severity on the ADOS in the ASD cohort... but not controls." The authors go on to say that such findings and others are "a fundamental expectation from the hypothesis of genetic predisposition for susceptibility to environmental triggers."Some other points are raised in the Boggess paper not least those connected to the various biological mechanisms designed to metabolise such compounds and where they may fit with regards to some autism. Personally, I think this is where the money is eventually going to be; with further work required on processes linked to glutathione (see here) and more specific genetic-biological issues (e.g. PON1 ) potentially showing how genetic fragility and non-genetic factors might combine specifically when it comes to getting rid of various pollutants from the body.There are methodological issues with the Boggess paper that do need to be mentioned not least the small participant group and the reliance on one blood sample showing a snapshot of current biology (combined with a snapshot of current behaviour). This last point in particular tells us little about any historical issues and whether there are important time-frames where environmental exposures might exert a more significant effect and the impact of any genetic issues. But, in the context of other research talking about environmental factors potentially being linked to autism (see here for example) it would be unwise to rule anything out just yet...---------- Boggess A. et al. Mean serum-level of common organic pollutants is predictive of behavioral severity in children with autism spectrum disorders. Sci Rep. 2016 May 13;6:26185. Vijayakumar NT. & Judy MV. Autism spectrum disorders: Integration of the genome, transcriptome and the environment. Journal of the Neurological Sciences. 2016; 364: 167-176. Gaita L. et al. Decreased serum arylesterase activity in autism spectrum disorders. Psychiatry Res. 2010 Dec 30;180(2-3):105-13.----------Boggess A, Faber S, Kern J, & Kingston HM (2016). Mean serum-level of common organic pollutants is predictive of behavioral severity in children with autism spectrum disorders. Scientific reports, 6 PMID: 27174041... Read more »
Boggess A, Faber S, Kern J, & Kingston HM. (2016) Mean serum-level of common organic pollutants is predictive of behavioral severity in children with autism spectrum disorders. Scientific reports, 26185. PMID: 27174041
New research explains why healthcare costs are running out of control, while costs to unemployment protection are kept in line. The answer is found deep in our psychology, where powerful intuitions lead us to view illness as the result of bad luck and worthy of help.
... Read more »
Jensen, C., & Petersen, M. (2016) The Deservingness Heuristic and the Politics of Health Care. American Journal of Political Science. DOI: 10.1111/ajps.12251
A team of scientists have shown that the brains of patients with schizophrenia have the capacity to reorganize and fight the illness. This is the first time that imaging data has been used to show that our brains may have the ability to reverse the effects of schizophrenia.
... Read more »
Guo, S., Palaniyappan, L., Liddle, P., & Feng, J. (2016) Dynamic cerebral reorganization in the pathophysiology of schizophrenia: a MRI-derived cortical thickness study. Psychological Medicine, 1-14. DOI: 10.1017/S0033291716000994
It's another research mash-up today as I bring to your attention two papers talking about potential correlates associated with psychosis and/or psychotic symptoms.First up are the findings reported by Joanne Newbury and colleagues  (open-access here) who observed that urban residency and certain factors associated with urban residency might link into a higher risk of childhood psychotic symptoms. A second paper by Tomasz Pawełczyk and colleagues  provides some further food for thought and the suggestion that "dietary patterns of PUFA [polyunsaturated fatty acids] consumption may play a role in the conversion to psychosis of HR [ultra high-risk] individuals."Newbury et al report findings from the Environmental Risk (E-Risk) Longitudinal Twin Study and specifically the idea of "whether specific features of urban neighborhoods increase children's risk for psychotic symptoms." Aside from finding a potential association between urban residency at aged 5 and aged 12 and psychotic symptoms at aged 12, researchers also suggested that: "Low social cohesion, together with crime victimization in the neighborhood explained nearly a quarter of the association between urbanicity and childhood psychotic symptoms after considering family-level confounders."Pawełczyk et al continued a research theme suggesting that what we do or do not eat might have implications for some with regards to transition to psychosis (see here). Focusing specifically on a group of HR individuals, they looked at the diet of those who did and did not transition into psychosis. They reported: "C-HR [converted into psychosis] individuals reported significantly higher consumption of n-6 fatty acids (linoleic acid, LA and arachidonic acid, AA) in comparison with individuals who did not develop psychosis (NC-HR)."Although not seemingly covering the same factors when it comes to psychosis/psychotic symptoms, one of the things that I thought might also unite both these findings is food. Yes, Pawełczyk et al already talk about food (albeit based on the warts and all use of "a validated Food-Frequency Questionnaire") but the Newbury paper might also include a food element insofar as what types of food might be more readily available and eaten in urban vs. not-so-urban environments.Bearing in mind that sweeping generalisations about food availability and importantly, what types of food are available depending on where one lives, are not required, I would like to suggest that spatial patterning of say, supermarkets vs. fast food outlets might be something that could potentially unite results. The paper by Lamichhane and colleagues  for example found that: "the availability of supermarkets and fast food outlets differed significantly by neighborhood characteristics; neighborhoods with supermarkets and with fast food outlets were significantly higher in socio-economic status." Research looking at the causes and/or drivers of obesity have tended to predominate in the area of how neighbourhood might influence eating patterns  but similar modelling could be done with more psychiatric outcomes in mind. Indeed to quote Newbury et al: "Neighborhood-level physical exposures such as noise, light, and air pollution, as well as exposure to viral infections warrant research in relation to early psychotic symptoms." Who says that food should not also be included?I don't want to gloss over just how complicated the factors might be bringing someone to clinically relevant psychotic symptoms nor to say that food is somehow the 'missing' element for all cases. But it's not outside of the realms of possibility that in these days of nutritional psychiatry, food might exert an important effect for some people and food availability (certain food availability) could be one factor contributing to the idea that where you live might affect your risk of psychosis...And if that wasn't enough speculating, how about sweeping generalisations about maternal smoking habits and prenatal nicotine exposure as a risk factor for psychosis+  as something else potentially linked to urban living?---------- Newbury J. et al. Why are Children in Urban Neighborhoods at Increased Risk for Psychotic Symptoms? Findings From a UK Longitudinal Cohort Study. Schizophr Bull. 2016 May 6. pii: sbw052. Pawełczyk T. et al. The association between polyunsaturated fatty acid consumption and the transition to psychosis in ultra-high risk individuals. Prostaglandins Leukot Essent Fatty Acids. 2016 May;108:30-7. Lamichhane AP. et al. Spatial patterning of supermarkets and fast food outlets with respect to neighborhood characteristics. Health & place. 2013;23:10.1016/j.healthplace.2013.07.002. Macdonald L. et al. Neighbourhood fast food environment and area deprivation—substitution or concentration? Appetite. 2007; 49: 251-254. Niemelä S. et al. Prenatal Nicotine Exposure and Risk of Schizophrenia Among Offspring in a National Birth Cohort. American Journal of Psychiatry. 2016. May 24.----------Pawełczyk, T., Trafalska, E., Kotlicka-Antczak, M., & Pawełczyk, A. (2016). The association between polyunsaturated fatty acid consumption and the transition to psychosis in ultra-high risk individuals Prostaglandins, Leukotrienes and Essential Fatty Acids (PLEFA), 108, 30-37 DOI: 10.1016/j.plefa.2016.03.010Newbury J, Arseneault L, Caspi A, Moffitt TE, Odgers CL, &am... Read more »
Pawełczyk, T., Trafalska, E., Kotlicka-Antczak, M., & Pawełczyk, A. (2016) The association between polyunsaturated fatty acid consumption and the transition to psychosis in ultra-high risk individuals. Prostaglandins, Leukotrienes and Essential Fatty Acids (PLEFA), 30-37. DOI: 10.1016/j.plefa.2016.03.010
Newbury J, Arseneault L, Caspi A, Moffitt TE, Odgers CL, & Fisher HL. (2016) Why are Children in Urban Neighborhoods at Increased Risk for Psychotic Symptoms? Findings From a UK Longitudinal Cohort Study. Schizophrenia bulletin. PMID: 27153864
Dynamic positioning of lysosomes in the cytoplasm plays an important role in their function and is, in part, regulated by cellular nutrient status. The FLCN/FNIP complex is known to be active on the lysosome surface, where it interacts with Rag GTPases, supports the nutrient‐dependent recruitment and activation of mTORC1, and regulates the localisation of lysosome associated transcription factors (Petit et al., 2013; Tsun et al., 2013). New research from Starling et al. (2016) now shows that folliculin (FLCN) also controls the dynamic cytoplasmic position of the lysosome itself.... Read more »
Starling GP, Yip YY, Sanger A, Morton PE, Eden ER, & Dodding MP. (2016) Folliculin directs the formation of a Rab34-RILP complex to control the nutrient-dependent dynamic distribution of lysosomes. EMBO reports. PMID: 27113757
The topic prevention of brain disorders is commonly neglected. This is despite increasing evidence for evidence-based support for prevention opportunities.This issue is highlighted in a recent study out of Finland that examined prenatal nicotine metabolite levels and offspring diagnosis of schizophrenia.In this study, Solja Niemela and the Finnish research team examined all live births in Finland between 1983 and 1998.What makes this study powerful is the measurement of maternal serum cotinine levels in maternal serum during the early and mid stages of prenancy. Cotinine is a metabolite and the levels of cotinine reflect the level of nicotine consumption.The key findings from this study include the following points:Measuring cotinine levels as a continuous variable yielded an increased odds ratio for schizophrenia of 3.41 (95% CI 1.86-6.24)Mothers in the highest cotinine level group had a 38% increase in offspring schizophrenia ratesThese findings included controlling for potential confounding variables including maternal age and parental history of psychiatric disordersInterestingly a PubMed search found a second study linking maternal smoking with increased risk of offspring diagnosis of bipolar disorder (odds ratio 2.01, 95% CI 1.48-2.53).These two studies in combination support a potential non-specific effect of prenatal nicotine exposure on risk for two of the most impairing psychiatric disorders. These two studies also support aggressive smoking cessation efforts in young women before pregnancy or at the latest very early after conception.You can find more information about these two studies by clicking on the citation links below.Follow the author on Twitter WRY999Photo of pair of pin-tail ducks is from my files.Niemelä, S., Sourander, A., Surcel, H., Hinkka-Yli-Salomäki, S., McKeague, I., Cheslack-Postava, K., & Brown, A. (2016). Prenatal Nicotine Exposure and Risk of Schizophrenia Among Offspring in a National Birth Cohort American Journal of Psychiatry DOI: 10.1176/appi.ajp.2016.15060800 Talati A, Bao Y, Kaufman J, Shen L, Schaefer CA, & Brown AS (2013). Maternal smoking during pregnancy and bipolar disorder in offspring. The American journal of psychiatry, 170 (10), 1178-85 PMID: 24084820... Read more »
Niemelä, S., Sourander, A., Surcel, H., Hinkka-Yli-Salomäki, S., McKeague, I., Cheslack-Postava, K., & Brown, A. (2016) Prenatal Nicotine Exposure and Risk of Schizophrenia Among Offspring in a National Birth Cohort. American Journal of Psychiatry. DOI: 10.1176/appi.ajp.2016.15060800
Talati A, Bao Y, Kaufman J, Shen L, Schaefer CA, & Brown AS. (2013) Maternal smoking during pregnancy and bipolar disorder in offspring. The American journal of psychiatry, 170(10), 1178-85. PMID: 24084820
I know that I'm probably starting to sound like a broken record on the topic of wandering (elopement) and autism on this blog (see here and see here and see here) but I am yet again going to briefly talk about peer-reviewed research in this area simply because it's just too damned important not to.This time around the results from Catherine Rice and colleagues  are the source of my musings and the conclusion that: "wandering among children with ASD [autism spectrum disorder], regardless of intellectual disability status, is relatively common." Based on the analysis of data from The Survey of Pathways to Diagnosis and Services (SPDS) initiative, where specific questions about 'wandering and wandering prevention' are asked (see page 29) researchers reported that: "For children with special healthcare needs diagnosed with either ASD, intellectual disability, or both, wandering or becoming lost during the previous year was reported for more than 1 in 4 children." A diagnosis of ASD seemed to be a key factor in the frequency of wandering, where those with additional learning disability were the most likely to wander (37% of the sample) and figures for those without intellectual disability came in at about 32%.As per previous occasions when I've blogged about this topic, the differences (kingdoms) that might divide various groups/people when it comes to autism tend to take second place when it comes to tackling this issue and preventing (yes, preventing) wandering from turning into something rather more ominous. After all, there are a range of measures that can be employed to reduce the frequency of wandering/elopement and, if and when it does happen, reduce the probability of 'adverse outcomes' for the wanderer. First and foremost I would say, is for more people to take note of actual accounts about wandering as per those discussed by Solomon and Lawlor  for example. One can learn a lot about the circumstances around why wandering occurs and the different types of wandering (including the issue of bolting) from listening to parent and caregiver accounts. They are the experts on their own children and no doubt some of those accounts might generalise to more than just one child.Next up are the various instruments that could be used to help find wanderers in a timely fashion. I'm thinking specifically about technology such as GPS trackers and the need for science to provide some further insight into the effectiveness of such items and what needs to be done to improve their effectiveness. I appreciate that 'tracking people' might have implications for things like civil liberties but just remember that the mobile (cell) phone you're carrying might not also be bad at telling others where you are. Improving autism awareness among first responders such as police and related agencies may also help them in their efforts if and when wandering becomes an issue.Finally and bearing in mind that 'if you've met one person with autism, you've met one autistic person' (or words to that effect) is the importance of teaching things like road and water safety to those on the autism spectrum. I appreciate that the concept of 'danger' might not be something easily taught to some children and communication issues can be barriers to effective teaching. But, one should not assume that it is impossible to do , alongside the strategies for making lessons like swimming classes for example 'fun' as well as potentially lifesaving. And yes, swimming lessons can be particularly fun for many children on the autism spectrum .---------- Rice CE. et al. Reported Wandering Behavior among Children with Autism Spectrum Disorder and/or Intellectual Disability. J Pediatr. 2016 May 2. pii: S0022-3476(16)00428-5. Call NA. et al. Clinical outcomes of behavioral treatments for elopement in individuals with autism spectrum disorder and other developmental disabilities. Autism. 2016 May 12. pii: 1362361316644732. Eversole M. et al. Leisure Activity Enjoyment of Children with Autism Spectrum Disorders. J Autism Dev Disord. 2016 Jan;46(1):10-20.----------Rice, C., Zablotsky, B., Avila, R., Colpe, L., Schieve, L., Pringle, B., & Blumberg, S. (2016). Reported Wandering Behavior among Children with Autism Spectrum Disorder and/or Intellectual Disability The Journal of Pediatrics DOI: 10.1016/j.jpeds.2016.03.047... Read more »
Rice, C., Zablotsky, B., Avila, R., Colpe, L., Schieve, L., Pringle, B., & Blumberg, S. (2016) Reported Wandering Behavior among Children with Autism Spectrum Disorder and/or Intellectual Disability. The Journal of Pediatrics. DOI: 10.1016/j.jpeds.2016.03.047
An investigational app and online program to reduce alcohol intake is now available free to the public.This tool is an application of cognitive bias modification. A link to a study supporting cognitive bias modification is noted in the citation below. Click on the PMID link to get to the abstract.The program uses a 15 minutes per day tool for four days.The program was developed at the London School of Economics by Professor Paul Dolan.Users who sign up to use the tool will be providing data to further determine the effectiveness of the app.Read more about this tool at Science Daily HERE.A link to the program and app can be found HERE.Follow me on Twitter @WRY999 HERE.Photo of painting titled "Peasants Enjoying a Beer at Pub in Fribourg" is from Wikipedia Creative Common file. Citation: By François Louis Jaques (1877–1937) (Beurret & Bailly) [Public domain], via Wikimedia CommonsGladwin TE, Rinck M, Eberl C, Becker ES, Lindenmeyer J, & Wiers RW (2015). Mediation of cognitive bias modification for alcohol addiction via stimulus-specific alcohol avoidance association. Alcoholism, clinical and experimental research, 39 (1), 101-7 PMID: 25623410... Read more »
Gladwin TE, Rinck M, Eberl C, Becker ES, Lindenmeyer J, & Wiers RW. (2015) Mediation of cognitive bias modification for alcohol addiction via stimulus-specific alcohol avoidance association. Alcoholism, clinical and experimental research, 39(1), 101-7. PMID: 25623410
If you feel brave enough, today I will direct your reading attention to the paper by Michael Williams and colleagues  detailing the application of a particularly important genome editing technique called CRISPR-Cas9  to autism-related science.Titled: "A Retroviral CRISPR-Cas9 System for Cellular Autism-Associated Phenotype Discovery in Developing Neurons" the Williams paper probably won't win any awards for plain English but don't be fooled about just how important this paper might be in the grand era of 'we can edit genomes' and how this might translate into modelling particular types of autism or genetic issues linked to autism in mice or other animals for example.I really wish that I could say I was an expert on CRISPR-Cas9 and understood every detail included in the Williams paper but alas, I'm not and I didn't. Bearing in mind my non-expertise ('a cobbler should stick to his last') I did want to include it on this blog given the excitement in this area. Take my observations however, with a large pinch of salt...So a definition of CRISPR [clustered regularly interspaced short palindromic repeats] -Cas9 - well, I don't want to reinvent the wheel so I'll use that offered in reference  with full credit given to the writer (Steph Yin): "Here’s how CRISPR/Cas works in bacteria: When bacteria encounter an invading source of DNA, such as from a virus, they can copy and incorporate segments of the foreign DNA into their genome as “spacers” between the short DNA repeats in CRISPR. These spacers enhance the bacteria’s immune response by providing a template for RNA molecules to quickly identify and target the same DNA sequence in the event of future viral infections. If the RNA molecules recognize an incoming sequence of foreign DNA, they guide the CRISPR complex to that sequence. There, the bacteria’s Cas proteins, which are specialized for cutting DNA, splice and disable the invading gene." The application of this process outside of just bacteria was subsequently recognised and a 'gene editing tool' was eventually born whereby a CRISPR-Cas9 system could replace any gene sequence.Clear as mud right?Well, Williams et al add to a small but emerging peer-reviewed research base at the time of writing suggesting that CRISPR-Cas9 might provide some important insights into at least 'some' autism. Their particular idea was to "mimic nonsense PTEN mutations from autism patients in developing mouse neurons" on the back of some previous research suggesting that various genetic issues with PTEN might be present in some autism . Nonsense mutation by the way, normally ends in 'nonfunctional proteins' based on the knowledge that [some] genes provide the template to make proteins.To achieve such mutations in PTEN authors used "retroviral implementation of the CRISPR-Cas9 system" where engineered retroviruses were purposed to deliver something mimicking a genetic mutation previously noted in cases of autism that were then injected into "the hippocampus of postnatal day 7 (P7) mice." Researchers then monitored the retrovirus infected cells to see what they looked like in terms of carrying the mutation and hence showing loss of PTEN function or not. They noted that there was a degree of 'hit-and-miss' based on their approach but were "able to clearly discern the established hypertrophic phenotype due to loss of Pten function across the cell population on average."Not content with such molecular engineering, authors also turned their attention to designing viruses "to target a gene that has recently been associated with autism, KATNAL2." KATNAL2 has been described by other authors as a 'genuine' autism risk factor  (er, right...) and on that basis researchers designed a retrovirus carrying a mutation designed to disrupt expression of the gene. After some preliminary work to test out how successful their retrovirus delivered mutation was in the test tube, they injected it and/or a control retrovirus into the brain of another set of mice. They found some interesting changes in the experimental retrovirus-infected brains pertinent to "decreased dendritic arborization of developing neurons." In layman's terms this equates as evidence of "disruption of normal neuronal development" that "may lead to synaptic circuit dysfunction underlying the autism phenotype."As per my earlier 'pinch of salt' sentiments I am not offering any authoritative opinion about the Williams paper and the techniques included. My interpretation is just that; interested readers are advised to do a little more reading around this subject before quoting my text as 'truth'. What I do hope that I've got across is the message that CRISPR-Cas9 and the delivery of engineered genetic mutations via something like a retrovirus is already here and will no doubt be impacting on autism research in times to come. In an era where 'the autism gene' has been replaced by a more general model of many different genes potentially producing many different autisms (see here), one can perhaps see how focusing in on specific genes linked to 'some' autism might be ripe for this kind of analysis (see here). I say all that recognising that whilst many would love to be able to say that autism is solely a genetic condition, the role of non-genetic factors variably affecting risk is not to be forgotten (see here).We will see what else emerges in the peer-reviewed domain in this brave new world...---------- Williams MR. et al. A Retroviral CRISPR-Cas9 System for Cellular Autism-Associated Phenotype Discovery in Developing Neurons. Sci Rep. 2016 May 10;6:25611. Yin S. What Is CRISPR/Cas9 and Why Is It Suddenly Everywhere? Motherboard. 2015. April 30. Neale BM. et al. Patterns and rates of exonic de novo mutations in autism spectrum disorders. Nature. 2012 Apr 4;485(7397):242-5.----------Williams MR, Fricano-Kugler CJ, Getz SA, Skelton PD, Lee J, Rizzuto CP, Geller JS, Li M, & Luikart BW (2016). A Retroviral CRISPR-Cas9 System for Cellular Autism-Associated Phenotype Discovery in Developing Neurons. Scientific reports, 6 PMID: 27161796... Read more »
Williams MR, Fricano-Kugler CJ, Getz SA, Skelton PD, Lee J, Rizzuto CP, Geller JS, Li M, & Luikart BW. (2016) A Retroviral CRISPR-Cas9 System for Cellular Autism-Associated Phenotype Discovery in Developing Neurons. Scientific reports, 25611. PMID: 27161796
There are many risk factors for Alzheimer's Disease (AD) including history of head trauma and family history of AD.The strongest risk factor is advanced age. Yearly risk for AD is about 1% per year in 70 year old populations jumping to around 7% in 90 year old groups.Now a recent study is shedding some light on a new risk for AD in men. This risk appears to be related to a chromosome Y phenomenon known to be associated with aging.Elderly men show a tendency to lose the Y chromosome from a small percentage of cells over time. This phenomenon is known as loss of Y or LOY.The percentage of blood cells with LOY can be determined. A study recently published in Journal of Human Genetics (see citation below) found significant support for higher percentage of LOY being linked to AD risk.Here are the key findings:In a sample of 3218 elderly men 17% showed evidence of LOY chromosome mosaicismLOY percentage rates were strongly positively correlated with older ageMen with AD had higher rates of LOY than age-matched men without AD (adjusted odds ratio=2.80)Two prospective studies found higher rates of incident AD in men with LOY (adjusted odds ratio=6.80)These findings are not simply minor as the effect of LOY on risk appears similar in magnitude to the strongest genetic risk factor for AD, APOE gene status.LOY has also been linked to a higher risk of cancer, so it appears to be a non-specific risk factor.The authors of this study note;"Regardless of the underlying mechanism(s) for the increased risk of AD and cancer in men with LOY in blood, our and other's published results reinforce a role of factors on chromosome Y in various, still poorly explored biological processes, other than sex determination and sperm production."LOY is not yet a common test in clinical practice. However, I think we will be hearing much more on this association with potential for screening and intervention studies.Access the free full-text manuscript by clicking on the DOI link in the citation below.Follow me on Twitter WRY999Photo of eastern screech owl is from my photo files.d sperm production.Dumanski JP et al (2016). Mosiac loss of chromosome Y in blood is associated with Alzheimer's disease American Journal of Human Genetics : 10.1016/j.ajhg.2016.05.014... Read more »
Dumanski JP et al. (2016) Mosiac loss of chromosome Y in blood is associated with Alzheimer's disease. American Journal of Human Genetics. info:/10.1016/j.ajhg.2016.05.014
The fight against aging Ever since the ancient Sumerians, men has sought eternal life. We still do. Anti-aging science has become quite an industry. As we dive deeper and deeper into our biological foundations, we’re learning more and more about how and why we age. A lot of mysteries remain, but there’s still talk about […]... Read more »
Just like some people have a tendency to go overboard, so do some immune systems. Here’s all the ways that your immune system can get it wrong and leave you with allergies – and how some allergies can save your life.... Read more »
Calboli FC, Cox DG, Buring JE, Gaziano JM, Ma J, Stampfer M, Willett WC, Tworoger SS, Hunter DJ, Camargo CA Jr, Michaud DS. (2011) Prediagnostic plasma IgE levels and risk of adult glioma in four prospective cohort studies. J Natl Cancer Inst. . DOI: 10.1093/jnci/djr361
Joseph A Jackson, Ida M Friberg, Luke Bolch, Ann Lowe, Catriona Ralli, Philip D Harris, Jerzy M Behnke, Janette E Bradley. (2009) Immunomodulatory parasites and toll-like receptor-mediated tumour necrosis factor alpha responsiveness in wild mammals. BMC Biology. DOI: 10.1186/1741-7007-7-16
Knee flexion to 90 degrees limits ankle laxity with the talar tilt test in comparison to a fully extended knee. However, knee position has no effect on anterior drawer laxity. Muscle guarding will limit our ability to accurately assess ankle laxity with a talar tilt or anterior drawer test. ... Read more »
Hanlon S, Caccese J, Knight CA, Swanik CB, & Kaminski TW. (2016) Examining Ankle-Joint Laxity Using 2 Knee Positions and With Simulated Muscle Guarding. Journal of Athletic Training, 51(2), 111-7. PMID: 26881870
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