"The prevalence of ID [intellectual disability] in WA [Western Australia] has increased over the past 10 years compared with previous estimates... This increase is associated in a large part with an increased prevalence of ASDs [autism spectrum disorder] for whom 70% had comorbid ID or an unknown level of ID."Those were some of the findings reported by Jenny Bourke and colleagues  (open-access available here). Drawing on data derived from the Intellectual Disability Exploring Answers (IDEA) database, a resource designed to 'provide high-quality complete and population-based information on Western Australians with an intellectual disability', authors set about looking at cases of ID for those born between 1983 and 2010. Intellectual disability (ID) - sometimes called learning disability here in Blighty - is typically diagnosed when IQ is assessed as being below 70 where a score of between 55-69 denotes mild ID, a score of between 40-54 denotes moderate ID and a score below 40 denotes severe ID. Authors were also able to cross-reference cases with information in other databases in terms of race, gender and location of birth.Results: covering a total of nearly 750,000 live births during the period of inspection, some 10,000 infants "were identified with an ID by 2010." This equated to a total prevalence of ID of 17 per 1,000 live births. Most cases of ID were defined as being mild or moderate in terms of IQ scores (where available) and when compared to previous data from this authorship group  authors reported "an overall increase in prevalence of ID of 19% from 1999 to 2010."Insofar as the possible causes of ID, various factors are reported to be potentially contributory including ID accompanying Down's syndrome, ID linked to various other genetic/chromosomal issues, birth defects and infection(s). Increasing preterm birth and survival rates are also suggested to be another contributory factor. The authors also add: "It is also possible that a proportion of the observed increase in mild or moderate ID may be attributable to un-diagnosed Fetal Alcohol Syndrome."The link between autism and ID is also discussed by Bourke et al. On the basis of other research (see here) suggesting that approximately 30-40% of cases of autism will also include a degree of ID, I was pretty interested to see the authors of this latest research suggesting something a little bit different. To quote: "Of the 2307 [diagnosed with an ASD], 675 (29.3%) definitely did not have an ID." I've underlined the word 'not' because the implication is that up to 70% of those with autism did have some level of ID. I say this bearing in mind that Bourke did include children diagnosed with an ASD where "children with an autism diagnosis but an unknown level of ID were classified within the comorbid ASD and ID group." But how far will the true figure of autism and ID combined fall by excluding such unknowns?There is just one more detail of the results that I want to draw your attention to with regards to ID: "The prevalence for Aboriginal children was 39.0/1000 compared with 15.7/1000 for non-Aboriginal children." The idea of disparities in rates of ID among Indigenous Australians and other groups is not necessarily a new one as per other research  and strengthen calls for a lot more research focus on this and other groups  from a variety of different clinical perspectives.In terms of what to make of these combined findings, I'd like to think there are some important issues requiring further study. The idea that autism and ID can and do frequently co-exist is paramount to discussions. We can talk and discuss about the hows and whys until the cows come home but the link remains strong and indeed, among different populations, might be more variable  than previously suggested. Also, for many years in autism research circles, there have been discussions upon discussions about how the quite spectacular rise in autism cases (including that in Australia) might have been at the expense of diagnostic switching from categories such as ID. The Bourke data seem to suggest that not everywhere in the world is necessarily experiencing a corresponding 'drop' in cases of ID supportive of this diagnostic switching argument. Indeed, I'm minded to suggest that one has to be quite careful about explaining away any 'real increase' in autism cases solely using the ID switching argument (see here)...---------- Bourke J. et al. Population-Based Prevalence of Intellectual Disability and Autism Spectrum Disorders in Western Australia: A Comparison With Previous Estimates. Medicine (Baltimore). 2016 May;95(21):e3737. Leonard H. et al. Prevalence of intellectual disability in Western Australia. Paediatr Perinat Epidemiol. 2003 Jan;17(1):58-67. Leonard H. et al. Autism and intellectual disability are differentially related to sociodemographic background at birth. PLoS One. 2011 Mar 30;6(3):e17875. Bennett M. & Hodgson V. The missing voices of Indigenous Australians with autism in research. Autism. 2016 May 25. pii: 1362361316643696. Postorino V. et al. Intellectual disability in Autism Spectrum Disorder: Investigation of prevalence in an Italian sample of children and adolescents. Research in Developmental Disabilities. 2016; 48: 193-201.----------Bourke J, de Klerk N, Smith T, & Leonard H (2016). Population-Based Prevalence of Intellectual Disability and Autism Spectrum Disorders in Western Australia: A Comparison With Previous Estimates. Medicine, 95 (21) PMID: 27227936... Read more »
Bourke J, de Klerk N, Smith T, & Leonard H. (2016) Population-Based Prevalence of Intellectual Disability and Autism Spectrum Disorders in Western Australia: A Comparison With Previous Estimates. Medicine, 95(21). PMID: 27227936
As Breaking Bad has taught us, the clandestine manufacture of methamphetamine is a very dangerous undertaking. It involves the use of many harmful substances, which depending on the synthesis method include highly corrosive acids and bases, cancer-causing benzene, brain-damaging mercury and lead, jaw-wrecking phosphorus, and blood-breaking sodium cyanide. Blending these various substances together can produce noxious fumes, making gas masks and chemical suits a necessity if you want to avoid getting seriously hurt.Meth cooks, at least those involved in small scale operations, tend not to be trained chemists. If they don't follow the correct recipe, either because they lack the necessary knowledge or skill, or they just don't care, the aforementioned harmful substances can end up in the final product. Lead is a particularly dangerous meth contaminant. A batch of meth responsible for an outbreak of acute lead poisoning in Oregon in 1988 was found to contain >60 percent lead by weight, which is insane! If meth is synthesized using crushed tablets of pseudoephedrine, granules from the tablets can make their way into the veins of intravenous users, causing skin irritation and the increased likelihood of nasty bacterial infections. Meth can also be contaminated with organic compounds closely related to something called alpha-benzyl-N-methylphenethylamine, which when tested in mice proved to be more potent inducers of seizures compared to meth.In addition to the nasty stuff inadvertently introduced into a batch of meth during its manufacture, an interesting collection of substances are used to dilute meth prior to selling it (got to maximize those profits). These cutting agents are known to include sugars such as lactose and mannitol (cheap way to add bulk), methylsulfonylmethane (physically resembles meth, improving the perceived quality of the drug), mild stimulants such as caffeine and ephedrine (mimic the effects of meth), and sidewalk chalk (used to provide a splash of colour). ReferencesBurton BT. 1991. Heavy metal and organic contaminants associated with illicit methamphetamine production. NIDA Research Monograph 115:47-59. [Full text]Cole C, Jones L, McVeigh J, Kicman A, Syed Q, Bellis M. 2011. Adulterants in illicit drugs: A review of empirical evidence. Drug Testing and Analysis 3(2):89-96. [First page]Poulsen EJ, Mannis MJ, Chang SD. 1996. Keratitis in methamphetamine abusers. Cornea 15(5):477-482.Strathdee SA et al. 2008. The color of meth: Is it related to adverse health outcomes? An exploratory study in Tijuana, Mexico. American Journal on Addictions 17(2):111-115. [Full text]... Read more »
Cole C, Jones L, McVeigh J, Kicman A, Syed Q, & Bellis M. (2011) Adulterants in illicit drugs: A review of empirical evidence. Drug Testing and Analysis, 3(2), 89-96. PMID: 21322119
Evolution brings wisdom with age – and bacteria are ancient. Bacteria have evolved defenses ranging from evasion or inhibition of immune systems to protecting crucial functions from environmental injury. New studies have identified spring-loaded spikes that can be assembled and disassembled for puncturing other bacteria and delivering toxins, while other work is focused on using those same toxins to kill antibiotic resistant organisms, with E. coli have been engineered to produce toxins against MRSA organisms. More amazing, the engineered bacteria only produce the toxin when enough S. aureus is present, and then lyse themselves to allow the toxin to reach the target organisms. ... Read more »
Basler, M., Pilhofer, M., Henderson, G., Jensen, G., & Mekalanos, J. (2012) Type VI secretion requires a dynamic contractile phage tail-like structure. Nature, 483(7388), 182-186. DOI: 10.1038/nature10846
Saeidi, N., Wong, C., Lo, T., Nguyen, H., Ling, H., Leong, S., Poh, C., & Chang, M. (2011) Engineering microbes to sense and eradicate Pseudomonas aeruginosa, a human pathogen. Molecular Systems Biology. DOI: 10.1038/msb.2011.55
Lower overall quality of life after an anterior cruciate ligament (ACL) reconstruction was associated with higher body mass index (BMI) and not returning to sport.... Read more »
Filbay, S., Ackerman, I., Russell, T., & Crossley, K. (2016) Return to sport matters-longer-term quality of life after ACL reconstruction in people with knee difficulties. Scandinavian Journal of Medicine . DOI: 10.1111/sms.12698
"The subsample that no longer fulfilled an autism spectrum disorder had full-time jobs or studies (10/11), independent living (100%), and reported having two or more friends (100%)."So said the paper by Adam Helles and colleagues  continuing a research theme from this authorship group on what happens to autism, or rather Asperger syndrome, in the longer-term (see here). Indeed, if you have the time, the thesis from Helles covering this area of study is well worth a read (see here).This time around the focus was on the often fuzzy concept called 'quality of life' (see here) in terms of "work, academic success, living situation, relationships, support system" for 50 males "with Asperger syndrome diagnosed in childhood and followed prospectively over two decades." Alongside those 'objective' measures of quality of life (QoL), Helles et al also sought some information about more 'subjective' reports of QoL with the use of the "Sense of Coherence and Short-Form Health Survey-36" schedules.As per the opening sentence to this post, I've initially focused in on those participants where diagnosis was not stable (i.e. the sub-group who did not continue to fulfil criteria for Asperger syndrome) as providing yet more evidence  on how objective outcomes were seemingly improved compared to those who still reached diagnostic thresholds. Allied to other work by other independent research groups (see here), these findings continue to demonstrate just how heterogeneous the autism spectrum is and that dogma about autism being a 'lifelong condition' might not necessarily be applicable to everyone who at one time or another met diagnostic thresholds. I know such a line of thought is not always received well by all, but I am of the opinion that remitting autism is at least as likely and important as remitting schizophrenia or remitting depression for example. As to the mechanisms, well, I don't want to speculate too much at this time but 'autisms' (plural) is a word that springs to mind as a first thought when it comes to such experiences (see here).When compared to this subgroup of those no longer meeting diagnostic criteria, those who remained within the diagnostic boundaries of Asperger syndrome did not appear to fare so well on those objective measures of QoL: "41% had full-time job or studies, 51% lived independently, and 33% reported two or more friends, and a significant minority had specialized employments, lived with support from the government, or had no friends." I say that bearing in mind the difference in participant numbers falling into one or other grouping.In terms of those subjective measures of QoL, we are also told that: "Stability of autism spectrum disorder diagnosis was associated with objective but not subjective quality of life" and that "psychiatric comorbidity was associated with subjective but not objective quality of life." This is perhaps not unexpected as per the growing body of research suggesting that various psychiatric comorbidity might be over-represented when a diagnosis of autism is received (see here) and how some of it can be truly disabling (see here). It's not then beyond the realms of possibility that one could have (and hold down) a job for example (objective QoL), but feel that one's subjective QoL is still poor as a result of said comorbidity and its impact on areas of life like employment. Indeed, I'd perhaps forward a research case for how what we term 'comorbidity' might actual be more central to the presentation of various types of autism (see here) outside of being just another add-on diagnosis.I don't want to come across as being too focused on outcomes around diagnostic instability when it comes to the autism spectrum because for the majority of people the diagnosis, whilst liable to fluctuation with regards to certain facets and skills, is very much a lifelong thing. That also definitions of long-term outcome and QoL say little about important concepts such as happiness and life satisfaction is another important point to make (see here). But the accumulating longitudinal work from Helles and others is providing something of an important window into autism in the long-term and how, wearing the cold, objective spectacles of science, the remittance of core symptoms might not be an unfavourable outcome for some...---------- Helles A. et al. Asperger syndrome in males over two decades: Quality of life in relation to diagnostic stability and psychiatric comorbidity. Autism. 2016 May 26. pii: 1362361316650090. Gillberg IC. et al. Boys with Asperger Syndrome Grow Up: Psychiatric and Neurodevelopmental Disorders 20 Years After Initial Diagnosis. J Autism Dev Disord. 2016 Jan;46(1):74-82.----------Helles A, Gillberg IC, Gillberg C, & Billstedt E (2016). Asperger syndrome in males over two decades: Quality of life in relation to diagnostic stability and psychiatric comorbidity. Autism : the international journal of research and practice PMID: 27233289... Read more »
Helles A, Gillberg IC, Gillberg C, & Billstedt E. (2016) Asperger syndrome in males over two decades: Quality of life in relation to diagnostic stability and psychiatric comorbidity. Autism : the international journal of research and practice. PMID: 27233289
Stigma is a major barrier preventing people with mental health issues from getting the help they need. Even in a private and anonymous setting online, someone with greater self-stigma is less likely to take that first step to get information about mental health concerns and counseling.
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Lannin, D., Vogel, D., Brenner, R., Abraham, W., & Heath, P. (2016) Does self-stigma reduce the probability of seeking mental health information?. Journal of Counseling Psychology, 63(3), 351-358. DOI: 10.1037/cou0000108
My photo of Mozart No one denies the importance of public education. Raising graduation rates and academic ability in the general population are highly accepted education system goals. Additionally, identification of learning disorders and the barriers to academic progress are the focus of many.However, the study of the gifted is perhaps no less important but this topic receives less attention and research.Matthew Makel and colleagues at Duke University and Vanderbilt University recently published an important study of gifted populations.Using the Duke University Talent Identification Program they identified 259 U.S. adolescents designated as "profoundly gift" (top 0.01% or top score of 10,000 tested) using the following criteria:U.S. adolescents completing SAT before age 13 Achieving a score of 700 or better on the SAT-math Achieving a score of 630 or better on the SAT-verbal The research team then followed this profoundly gifted group using a validated web-based search strategy. The found the following results confirming the validity of early gifted status as a predictor of academic and occupational success:1. Thirty seven percent had gone on to receive a doctorate degree2. Academic tenure was achieved by 7.5%3. U.S. patents were held by 9%4. A significant number of the group held high level positions in major organizationsThe manuscript provides fascinating graphic showing the diverse disciplines of the graduate degrees from this cohort. STEM degrees predominate but many also achieved doctorates in arts and humanities as well as law.This current study confirmed a previous outcome analysis using the Study of Mathematically Precocious Youth cohort (see Kell et al citation below).The authors note "Profound intellectual talent, and its patterning, has cross-disciplinary and policy implications."Individual interest appears to play a key role in outcome. School systems need to provide a wide ranges of exposures to various academic disciplines. Early identification of profoundly gifted individuals is important. This group benefits by guidance and academic opportunity.This is an important study and highlights the need to develop gifted identification and nurturing the gifted programs.Follow the author on Twitter WRY999Photo of Mozart is a graphic design modification of a painting on the wall outside of the birthplace of Amadeus Mozart.Makel MC, Kell HJ, Lubinski D, Putallaz M, & Benbow CP (2016). When Lightning Strikes Twice: Profoundly Gifted, Profoundly Accomplished. Psychological science PMID: 27225220 Ke... Read more »
Makel MC, Kell HJ, Lubinski D, Putallaz M, & Benbow CP. (2016) When Lightning Strikes Twice: Profoundly Gifted, Profoundly Accomplished. Psychological science. PMID: 27225220
Kell HJ, Lubinski D, Benbow CP, & Steiger JH. (2013) Creativity and technical innovation: spatial ability's unique role. Psychological science, 24(9), 1831-6. PMID: 23846718
A small magnetic device might transform breast cancer surgeries... Read more »
Rahusen, F., Bremers, A., Fabry, H., Taets van Amerongen, A., Boom, R., & Meijer, S. (2002) Ultrasound-guided lumpectomy of nonpalpable breast cancer versus wire-guided resection: A randomized clinical trial. Annals of Surgical Oncology, 9(10), 994-998. DOI: 10.1007/BF02574518
Anderson, R., Kimmick, G., McCoy, T., Hopkins, J., Levine, E., Miller, G., Ribisl, P., & Mihalko, S. (2011) A randomized trial of exercise on well-being and function following breast cancer surgery: the RESTORE trial. Journal of Cancer Survivorship, 6(2), 172-181. DOI: 10.1007/s11764-011-0208-4
Medina-Franco, H., Abarca-Pérez, L., García-Alvarez, M., Ulloa-Gómez, J., Romero-Trejo, C., & Sepúlveda-Méndez, J. (2008) Radioguided occult lesion localization (ROLL) versus wire-guided lumpectomy for non-palpable breast lesions: A randomized prospective evaluation. Journal of Surgical Oncology, 97(2), 108-111. DOI: 10.1002/jso.20880
Lovrics, P., Cornacchi, S., Vora, R., Goldsmith, C., & Kahnamoui, K. (2011) Systematic review of radioguided surgery for non-palpable breast cancer. European Journal of Surgical Oncology (EJSO), 37(5), 388-397. DOI: 10.1016/j.ejso.2011.01.018
Postma, E., Koffijberg, H., Verkooijen, H., Witkamp, A., van den Bosch, M., & van Hillegersberg, R. (2013) Cost-Effectiveness of Radioguided Occult Lesion Localization (ROLL) Versus Wire-Guided Localization (WGL) in Breast Conserving Surgery for Nonpalpable Breast Cancer: Results from a Randomized Controlled Multicenter Trial. Annals of Surgical Oncology, 20(7), 2219-2226. DOI: 10.1245/s10434-013-2888-7
Ahmed, M., & Douek, M. (2013) A systematic review and meta-analysis of intra-operative ultrasound versus wire-guided localization in the surgical management of non-palpable breast cancers. European Journal of Surgical Oncology (EJSO), 39(11). DOI: 10.1016/j.ejso.2013.07.212
"Children with ADHD [attention-deficit hyperactivity disorder] and ASD [autism spectrum disorder] had low levels of EPA [eicosapentaenoic acid], DHA [docosahexaenoic acid] and AA [arachidonic acid] and high ratio of n-6/n-3 PUFAs [polyunsaturated fatty acid] and these correlated significantly with symptoms. Future research should further investigate abnormal fatty acid metabolism in these disorders."So said the research publication by Natalie Parletta and colleagues  (open-access available here) who completed assessments on erythrocytes in blood samples from "565 children aged 3-17 years with ADHD (n = 401), ASD (n = 85) or controls (n = 79)." Alongside fatty acid analyses (undertaken at "a commercial Pathology Laboratory") researchers also included various behavioural measures with their participant group looking at aspects such as attention and impulsivity and also autistic symptoms (via the CARS). Importantly we are told that: "Participants who had taken any nutritional supplement during the previous year were excluded" from the study.Results: well as I've mentioned, compared to the asymptomatic (not autism nor ADHD) controls, group values for those with autism or ADHD were lower in terms of EPA and DHA among other things. In fact we are told that: "Children with ASD had lower DHA, EPA and AA and higher n-3/n-6 ratio than children with ADHD" suggesting that fatty acid metabolism might be even more irregular in this group compared to the others. EPA and DHA specifically fall under the banner of omega-3 fatty acids and are generally thought to be the 'good guys' when it comes to all-manner of health effects. I might particularly mention the word 'inflammation' when it comes to this class of fatty acids  which could be relevant to quite a bit of the autism spectrum as well (see here). When it however came to the overall ratio between omega 3 and omega 6 fatty acids (sometimes thought of the not-so-good guys), it was ADHD that beat autism that beat controls. The authors make a case for some interesting correlations between fatty acids levels and the various behavioural scores obtained but to be honest, I'm not all that impressed with the figures as they stand.I've used the word 'again' in the title of this post to denote how this is not the first time that unusual fatty acid metabolism has been described with both autism and ADHD in mind (see here and see here respectively). Minus any sweeping generalisations, the body of peer-reviewed evidence looking at fatty acids and autism or ADHD is pretty consistent in the the findings being reported that one for reason or another, there seems to be 'issues' with fatty acids and screening services should perhaps be preferentially offered as and when a diagnosis (or both) is received."This cross-sectional study is the largest of its kind, supporting previous work that showed low n-3 PUFA levels, particularly DHA, in children with neurodevelopmental disorders." Indeed.Then comes the question of whether supplementation as and when an atypical fatty acid profile is detected might be useful or not. The jury is still out on this side of things particularly when it comes to autism and the possible effects of supplementation (see here). For ADHD the evidence is a little stronger (see here) and continues to garner research attention  as a potentially cost-effective intervention option for some. I was also intrigued to read the authors' reasoning on a possible role for the trillions of wee beasties that call us home (the gut microbiota) and how: "Another explanation could involve the influence of gut microbiota on PUFA uptake and metabolism." In an unrelated post, I've talked about research suggesting a possible role for fatty acids in terms of gut bacteria and something like obesity (see here). One therefore wonders how deep the rabbit hole might go?For now however, we have more scientific evidence for a potential role for fatty acid metabolism and at least some autism and ADHD...---------- Parletta N. et al. Omega-3 and Omega-6 Polyunsaturated Fatty Acid Levels and Correlations with Symptoms in Children with Attention Deficit Hyperactivity Disorder, Autistic Spectrum Disorder and Typically Developing Controls. PLoS One. 2016 May 27;11(5):e0156432. Simopoulos AP. Omega-3 fatty acids in inflammation and autoimmune diseases. J Am Coll Nutr. 2002 Dec;21(6):495-505. Gow RV. et al. Current evidence and future directions for research with omega-3 fatty acids and attention deficit hyperactivity disorder. Curr Opin Clin Nutr Metab Care. 2015 Mar;18(2):133-8.----------Parletta N, Niyonsenga T, & Duff J (2016). Omega-3 and Omega-6 Polyunsaturated Fatty Acid Levels and Correlations with Symptoms in Children with Attention Deficit Hyperactivity Disorder, Autistic Spectrum Disorder and Typically Developing Controls. PloS one, 11 (5) PMID: 27232999... Read more »
Parletta N, Niyonsenga T, & Duff J. (2016) Omega-3 and Omega-6 Polyunsaturated Fatty Acid Levels and Correlations with Symptoms in Children with Attention Deficit Hyperactivity Disorder, Autistic Spectrum Disorder and Typically Developing Controls. PloS one, 11(5). PMID: 27232999
The May entry of "This Month in Blastocystis Research" focusses especially on the increasing interest in Blastocystis in a gut microbiota context. ... Read more »
Audebert C, Even G, Cian A, Blastocystis Investigation Group, Loywick A, Merlin S, Viscogliosi E, & Chabé M. (2016) Colonization with the enteric protozoa Blastocystis is associated with increased diversity of human gut bacterial microbiota. Scientific reports, 25255. PMID: 27147260
Andersen LO, Bonde I, Nielsen HB, & Stensvold CR. (2015) A retrospective metagenomics approach to studying Blastocystis. FEMS microbiology ecology, 91(7). PMID: 26130823
O'Brien Andersen L, Karim AB, Roager HM, Vigsnæs LK, Krogfelt KA, Licht TR, & Stensvold CR. (2016) Associations between common intestinal parasites and bacteria in humans as revealed by qPCR. European journal of clinical microbiology . PMID: 27230509
Ramírez JD, Sánchez A, Hernández C, Flórez C, Bernal MC, Giraldo JC, Reyes P, López MC, García L, Cooper PJ.... (2016) Geographic distribution of human Blastocystis subtypes in South America. Infection, genetics and evolution : journal of molecular epidemiology and evolutionary genetics in infectious diseases, 32-5. PMID: 27034056
The antibiotic arms race is on, while we are rushing to find new antibiotics, bacteria are working on finding ways around them. With that in mind, a new experimental antibiotic developed by a team of scientists successfully treats the deadly MRSA infection and restores the efficacy of a commonly prescribed antibiotic that has become ineffective against MRSA.
... Read more »
Kaul M, Mark L, Zhang Y, Parhi AK, Lyu YL, Pawlak J, Saravolatz S, Saravolatz LD, Weinstein MP, LaVoie EJ.... (2015) TXA709, an FtsZ-Targeting Benzamide Prodrug with Improved Pharmacokinetics and Enhanced In Vivo Efficacy against Methicillin-Resistant Staphylococcus aureus. Antimicrobial agents and chemotherapy, 59(8), 4845-55. PMID: 26033735
Given my own research interest in the use of specific dietary modifications as possible intervention tools for some aspects of some autism (see here) I was more than interested to read the results published by Faezeh Ghalichi and colleagues  following their randomised-controlled trial of a gluten-free diet (GFD) including some 80 children diagnosed with an autism spectrum disorder (ASD).As part of an area of much discussion, debate and also heated argument down the years, the authors' conclusion that a "GFD may be effective in controlling gastrointestinal symptoms and ASD behaviors" once again swings the research pendulum towards the idea that for at least some on the autism spectrum - perhaps those with a specific 'diet-related autism phenotype'  - there may be some merit in looking at dietary changes.Ghalichi et al assigned 40 children to a GFD for a 6-week period and 40 to a regular diet for the same period. Said participants were assessed using the Autism Diagnostic Interview-Revised (ADI-R) as being autistic. Alongside examining behaviour over the experimental period (via the GARS-2), researchers also assessed participants for the presence of gastrointestinal (GI) issues using the ROME Ш questionnaire, the gold-standard for examining functional GI disorders. Both types of assessment were administered before and after intervention.Results: well, first and foremost we are told that the presence of GI disorders was pretty high in the group as a whole (~60%). For those in the know when it comes to GI issues and autism, this is perhaps not an unexpected finding (see here). We are also told that following the use of a GFD "the prevalence of gastrointestinal symptoms decreased significantly" something not seen in those following the regular (non gluten-free) diet. Then also: "GFD intervention resulted in a significant decrease in behavioral disorders"; again, something not seen with those on a regular diet as a group. All-in-all, over the short period of experimental observation, the 'horror' that is a GFD (see here) might show some interesting 'effects' for at least some on the autism spectrum.As per other research in this area, there are words of caution with regards to the Ghalichi study insofar as the lack of blinding or use of a placebo element with the current work. As a screening instrument for autism, GARS-2 is also not without methodological 'issues' . Alongside there being some holes in the way intervention 'success or failure' is measured more generally when it comes to autism (see here), I can also think of a few additional instruments that could have been used in studies like this one (see here). In short, the Ghalichi study is open to some methodological criticism (which I'm quite sure it will encounter!)But the idea that corresponding changes to functional bowel issues might go hand-in-hand with behavioural changes when a GFD is adopted for at least some on the autism spectrum is an interesting one. Indeed, in my blogging appraisal of the Susan Hyman study results  eventually published last year (2015) (see here) I did mention that divorcing GI issues from autism when looking at such dietary intervention might not be an optimal course of research action. I will also reiterate that the Harland Winter study results are very much needed to help clarify this situation...Should it be so surprising that the presence of GI issues or more severe bowel pathology (see here) might in some way be linked to [some] behaviour with autism in mind? No, it shouldn't given the increasingly interesting links between aspects such as anxiety and sensory issues and bowel finding with autism in mind for example (see here). Real gut-brain axis stuff. The idea also that biological gluten-related 'issues' might also be over-represented when it comes to the diagnosis of autism is something else to bear in mind (see here); also is the not-so-long-lost-idea that certain foods might actually have pharmacological activity (see here) pertinent to some autism. Oh, and I'll also draw your attention to the concept of 'leaky gut' with autism in mind (see here)...So yes, there is quite a bit more research indicated in this area of investigation and no, any dietary effect is not likely to be universally applicable to 'all autism' (autisms people, autisms). But once again, use of a gluten-free diet rears it's head in the peer-reviewed autism research literature...---------- Ghalichi F. et al. Effect of gluten free diet on gastrointestinal and behavioral indices for children with autism spectrum disorders: a randomized clinical trial. World J Pediatr. 2016 Jun 10. Whiteley P. Nutritional management of (some) autism: a case for gluten- and casein-free diets? Proc Nutr Soc. 2015 Aug;74(3):202-7. Volker MA. et al. Factor Structure, Internal Consistency, and Screening Sensitivity of the GARS-2 in a Developmental Disabilities Sample. Autism Res Treat. 2016;2016:8243079. Hyman SL. et al. The Gluten-Free/Casein-Free Diet: A Double-Blind Challenge Trial in Children with Autism. J Autism Dev Disord. 2016 Jan;46(1):205-20.----------Ghalichi F, Ghaemmaghami J, Malek A, & Ostadrahimi A (2016). Effect of gluten free diet on gastrointestinal and behavioral indices for children with autism spectrum disorders: a randomized clinical trial. World journal of pediatrics : WJP PMID: 27286693... Read more »
Ghalichi F, Ghaemmaghami J, Malek A, & Ostadrahimi A. (2016) Effect of gluten free diet on gastrointestinal and behavioral indices for children with autism spectrum disorders: a randomized clinical trial. World journal of pediatrics : WJP. PMID: 27286693
Human skin emits light (albeit the glow is extremely weak) and a wide variety of small molecules that may be sometimes "sniffed" by dogs or even other humans. These chemicals tell a story about our health and wellness, things we eat and drink, touch and breathe. Mosquitoes use such emissions to assess our "attractiveness" from indicators such as Indoles (unpleasantly smelling but healthy "inner soil" biomarker) or carbon dioxide (amount of which correlates with the size of the person producing it) in the air. Sampling air for health indicators is much less invasive than drawing blood and could be an invaluable diagnostic tool. Many applications of gas sensors have been proposed over decades ranging from sweat patches to sensorized garments. Where are we now? What is the 2016 state of the art? Last month, BACtrack won 1st Prize in “Wearable Alcohol Sensor Challenge” Issued by National Institutes of Health. Milo Sensors, employing a different approach to identify ethanol molecules diffusing through the skin, won 2nd prize. BACtrack Skyn will be available in limited quantities later this year, marking an important step from bulky alcohol-monitoring ankle bracelets remotely monitoring offenders to inconspicuous devices. Perhaps, one day, drug patches, too, won't require sending them to a lab for analysis.Human skin is a super-highway of many small molecules reflecting our health and wellbeing. Various devices capable of "seeing" through our skin were announced in the past several years. Some of them - like AIRO watch claiming to detect metabolites in your bloodstream as they are released during and after meals - turned out to be vaporware. The jury is still out on many others like HealbeGobe. And the remaining ones are still in prototyping stages. EU-funded Biotex textiles and Perspiration Detective patch development at the University of Cincinnati started from detecting sodium ions in sweat as indicators of hydration levels. A tattoo-like electronic sweat sensor built by a team in UCSD demonstrated that measuring a change in lactate might be sufficient to find when an athlete is about to “hit the wall.” Startup Electrozyme, later renamed to Biolinq, was formed to commercialize this technology. The picture shows their prototype of a skin-applied electrochemical sensor that analyses body fluids to provide actionable health information. The goal is to develop temporary tattoo biosensors providing blood level info without accessing blood.Halo Wearables will launch their non-invasive hydration monitoring wearable in early 2016. It is tailored specifically for elite athletes. Halo's optical sensors track sodium and potassium levels in the user's blood.Researchers from the University of California, Berkeley, Stanford and Lawrence Berkeley National Laboratory have also developed a wearable sensor that can monitor sodium, potassium and lactate levels in sweat. A paper with their findings was published in Nature earlier this year.Startup Xsensio, accepted this year in Mass Challenge accelerator, works on “intelligent stamps” the size of a credit card (Lab-on-Skin wearables) including a unique low-power sensor for sweat analysis.ECHO smart patch from Kenzen aims to "silently follow your health, and notify you only when it's most important". It analyzes sodium and potassium in sweat to monitor hydration, lactic acid and glucose analysis energy expenditure. ... Read more »
Andreoni G, Standoli CE, & Perego P. (2016) Defining Requirements and Related Methods for Designing Sensorized Garments. Sensors (Basel, Switzerland), 16(6). PMID: 27240361
Gao W, Emaminejad S, Nyein HY, Challa S, Chen K, Peck A, Fahad HM, Ota H, Shiraki H, Kiriya D.... (2016) Fully integrated wearable sensor arrays for multiplexed in situ perspiration analysis. Nature, 529(7587), 509-14. PMID: 26819044
Imani S, Bandodkar AJ, Mohan AM, Kumar R, Yu S, Wang J, & Mercier PP. (2016) A wearable chemical-electrophysiological hybrid biosensing system for real-time health and fitness monitoring. Nature communications, 11650. PMID: 27212140
Lee H, Choi TK, Lee YB, Cho HR, Ghaffari R, Wang L, Choi HJ, Chung TD, Lu N, Hyeon T.... (2016) A graphene-based electrochemical device with thermoresponsive microneedles for diabetes monitoring and therapy. Nature nanotechnology, 11(6), 566-72. PMID: 26999482
Panneer Selvam A, Muthukumar S, Kamakoti V, & Prasad S. (2016) A wearable biochemical sensor for monitoring alcohol consumption lifestyle through Ethyl glucuronide (EtG) detection in human sweat. Scientific reports, 23111. PMID: 26996103
Is copper deficiency contributing to the obesity epidemic? Though small amounts of copper are essential to health - oysters, liver, beans and nuts are good sources - copper's role in metabolism has been unclear: Some studies found that it boosted fat burning, others that it depressed it.
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I don't want to keep you today. Just long enough to draw your attention to the paper by Jones and colleagues  regarding "ongoing efforts toward identification of early biological markers specific to subphenotypes of ASD [autism spectrum disorder]."The potential biomarkers in question this time around were the cytokines/chemokines - those various signalling molecules that seem to have more than a few connections to important processes like inflammation - and how their profile ("mid-gestational serum profiles") might show some interesting links to different phenotypes of autism. Similar sentiments are already present in the peer-reviewed literature (see here) I might add.Comparing 22 different cytokines and chemokines from mothers' samples across various groupings (ASD, developmental delay, 'not-autism' controls) and importantly including a distinction between autism diagnosed with intellectual (learning) disability (ASD+ID) and autism on its own (ASD-noID), researchers reported some interesting trends. Not least was the suggestion of an "immunologic distinction between mothers of children with ASD+ID from mothers of children with ASD-noID" including elevations in something called interleukin-6 (IL-6) (see here).Bearing in mind a continued focus on immune function in relation to [some] autism (see here) taking into account the very wide heterogeneity present across the spectrum (autisms people, autisms), the requirement for yet further study in this area is immense. With all that's starting to be known about the various presentations of immune function in autism (see here and see here for example) and beyond (see here), I find it surprising that so little research has so far been translated from 'bench-to-bedside' in terms of screening and intervention when immune-related issues are found. Yes, dogma about what autism(s) is and isn't still pervades the scientific literature and beyond (in many areas!), but surely routine immune panel screening could be looked at being rolled out for example?Just one more thing to add about the Jones paper. The eagle-eyed among you might already have noted the involvement of the MIND Institute in the authorship group bearing in mind their long (long) history in autism research (see here). But did you also pick up a certain Robert Yolken from the 'Stanley Division of Developmental Neurovirology' as also being present? Yes, one and the same researcher, who along with various other members of the this facility, are making some real research waves when it comes to the interplay between behaviour, immune function and infection (see here and see here for examples).Methinks this could be the start of a beautiful (and hopefully rewarding) research relationship ...---------- Jones KL. et al. Autism with intellectual disability is associated with increased levels of maternal cytokines and chemokines during gestation. Molecular Psychiatry. 2016. May 24. Grether JK. et al. Prenatal and Newborn Immunoglobulin Levels from Mother-Child Pairs and Risk of Autism Spectrum Disorders. Front Neurosci. 2016 May 18;10:218.----------Jones KL, Croen LA, Yoshida CK, Heuer L, Hansen R, Zerbo O, DeLorenze GN, Kharrazi M, Yolken R, Ashwood P, & Van de Water J (2016). Autism with intellectual disability is associated with increased levels of maternal cytokines and chemokines during gestation. Molecular psychiatry PMID: 27217154... Read more »
Jones KL, Croen LA, Yoshida CK, Heuer L, Hansen R, Zerbo O, DeLorenze GN, Kharrazi M, Yolken R, Ashwood P.... (2016) Autism with intellectual disability is associated with increased levels of maternal cytokines and chemokines during gestation. Molecular psychiatry. PMID: 27217154
Scientists have developed a powerful tool for exploring and determining the inherent biological differences between individuals, which overcomes a major hurdle for personalized medicine.
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Dong et al., (2016) have recently reported two BHD syndrome patients also affected with papillary thyroid cancer. Lesions were bilateral and multifocal and small lymph node metastases occurred. Due to the small number of patients in the study the authors are unsure whether thyroid cancer in BHD patients is susceptible to exhibiting bilaterally and lymph node metastasis. However, they suggest considering thyroidectomy and prophylactic lymph node dissection for thyroid cancer patients with BHD. They also strongly recommend neck ultrasound for BHD patients and their families and suggest a large-scale investigation be conducted to evaluate the prevalence of thyroid cancer or nodules in patients with BHD.... Read more »
Dong L, Gao M, Hao WJ, Zheng XQ, Li YG, Li XL, & Yu Y. (2016) Case Report of Birt-Hogg-Dubé Syndrome: Germline Mutations of FLCN Detected in Patients With Renal Cancer and Thyroid Cancer. Medicine, 95(22). PMID: 27258496
Anti-NMDA-receptor encephalitis is not something that I ever envisaged talking about so much on this blog primarily concerned with autism research. Describing an often severe form of encephalitis where the body mounts an immune response against self ("the NR1 subunit of the NMDA receptor"), this condition is more readily associated with the symptoms of psychosis than anything specifically autism-related.But yet again (see here and see here) I'm talking about peer-reviewed research suggesting that when one talks about the appearance of 'autistic regression' one might consider testing for anti-NMDA-receptor encephalitis just to rule it out as a possible cause. This time around the findings are those reported by Yael Hacohen and colleagues  and their description of "two toddlers who presented with developmental regression, particularly of their social communication skills, mimicking an autistic regression, who were found to have NMDAR-Ab [N-methyl-d-aspartate receptor antibodies] in the serum and cerebrospinal fluid." Aside from various "other neurological features" hampering timely diagnosis of anti-NMDA-receptor encephalitis, the authors report that subsequent "immunotherapy was beneficial in both patients, with significant improvement of their language skills and behaviour."A few more details are worthy of discussion: Case 1 talks about a 2-year old girl who following a typical developmental profile experienced an "acute onset of behavioural change, disrupted sleep, and loss of motor, language and social communication skills." Even after some investigation for "an organic brain syndrome" everything came out as within typical ranges despite her continuing to regress after initial discharge. Following a second admission, during which time "she was mute and had orofacial and right hand sterotypies" she was found to have positive NMDAR-Ab and treatment was initiated in the form of methylprednisolone. We are told: "At follow-up, aged 4 years, 2 years from symptom onset, she is well, has age-appropriate language acquisition, no behaviour and psychiatric concerns, and remains relapse-free."Case 2 was another young girl also aged 2 years who following a similar pattern to case 1 followed a typical pattern of development that was quite suddenly replaced with "abnormal behaviour" including a loss of speech, biting, pinching and "banging her head." Again, most parameters were in the typical zone when it came to assessments, although her sleep EEG "revealed occasional focal and generalized epileptiform discharges." Those NMDAR-Ab were detected and treatment initiated. Interestingly, authors reported that methlyprednisolone only provided short-term improvements for this child and so more aggressive treatment (rituximab and then mycophenolate mofetil) was put in place. The longer-term prospect for this child also did not seem to mirror case 1 as we are told that despite improvements in speech for example, "she continues to suffer from ongoing behavioural concerns and sleep disruption."Combined with those other reports that dot the autism research literature, anti-NMDA-receptor encephalitis does seem to be at least one probable 'cause' of autistic regression. The important idea that one can screen for the presence of those antibodies (although looking in cerebrospinal fluid is quite invasive) also opens up a role for medicine and investigation when such a clinical outcome presents. And then there is the idea that when detected alongside certain autistic or autistic-like symptoms this type of encephalitis might be 'treatable'. No matter what your views are on autism or which 'kingdom' you subscribe to, I don't think anyone would truly suggest that a medical diagnosis of encephalitis should not be treated in an appropriate and timely manner. Indeed, various interventions could be indicated for such encephalitic cases  including the use of IVIg and methylprednisolone, all under appropriate medical supervision (I say this without any medical or clinical advice given or intended). Corticosteroid 'therapy' for regressive autism for example, has been previously discussed in the peer-reviewed literature (see here) so there may be quite a bit more research to do in this area. I might also add that none of the treatments discussed in the Hacohen paper are without potential side-effects so caution and medical input is a must.Regression occurring in cases of autism is, at last, moving out of the shadows and becoming more readily accepted these days. I would hope that reports such as the one from Hacohen and colleagues are finally moving the conversation on in terms of what might cause instances of regression (see here for another example) and what interventions might be possible, all set within the context of the very plural and very heterogeneous autisms.I will leave you with a few final sentences from Hacohen et al: "NMDRAR-Ab should be tested in cases of regression of social and communication skills with additional neurological symptoms such as movement disorder or seizures. Unlike autism, early diagnosis and treatement of NMDAR-Ab encephalitis is associated with much improved outcome." Make of that what you will...---------- Hacohen Y. et al. N-methyl-d-aspartate (NMDA) receptor antibodies encephalitis mimicking an autistic regression. Developmental Medicine & Child Neurology. 2016. June 3. Luca N. et al. Anti-N-Methyl-D-Aspartate Receptor Encephalitis: A Newly Recognized Inflammatory Brain Disease in Children. Arthritis and rheumatism. 2011;63(8):2516-2522. ----------Hacohen Y, Wright S, Gadian J, Vincent A, Lim M, Wassmer E, & Lin JP (2016). N-methyl-d-aspartate (NMDA) receptor antibodies encephalitis mimicking an autistic regression. Developmental medicine and child neurology PMID: 27255282... Read more »
Hacohen Y, Wright S, Gadian J, Vincent A, Lim M, Wassmer E, & Lin JP. (2016) N-methyl-d-aspartate (NMDA) receptor antibodies encephalitis mimicking an autistic regression. Developmental medicine and child neurology. PMID: 27255282
New research is giving a whole new meaning to feeling your skin crawl. Skin cells typically spend their entire existence in one place on your body. But researchers have seen how the cells will alter the proteins holding them in place and move to repair a wound.
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Hiroyasu, S., Colburn, Z., & Jones, J. (2016) A hemidesmosomal protein regulates actin dynamics and traction forces in motile keratinocytes. The FASEB Journal, 30(6), 2298-2310. DOI: 10.1096/fj.201500160R
"Another reason why pregnant women shouldn’t smoke: schizophrenia" went one media headline reporting on the findings by Solja Niemelä and colleagues  who concluded that their results were the "most definitive evidence to date that smoking during pregnancy is associated with schizophrenia."Analysing data from nearly 1000 people identified with schizophrenia whose information, and that of their mothers, were held in one of two databases - the Finnish Prenatal Study of Schizophrenia and the Finnish Maternity Cohort - researchers embarked on a case-control study. Maternal cotinine levels - a metabolite of nicotine - were analysed from archive serum samples taken during pregnancy ("early- to mid-gestation") and compared across groups based on offspring who did or did not go on to receive a diagnosis of schizophrenia. Authors concluded that: "A higher maternal cotinine level, measured as a continuous variable, was associated with an increased odds of schizophrenia." The increased 'risk' of offspring schizophrenia to those mothers with the highest cotinine levels (highest nicotine exposure) was somewhere in the region of 38% and "were not accounted for by maternal age, maternal or parental psychiatric disorders, socioeconomic status, and other covariates."Accepting that correlation is not the same as causation and that one has to be slightly careful when analysing just one biomarker, I was intrigued by these latest findings. A quick trawl of the research literature in this area suggests that this is not the first time that maternal smoking behaviour might have implications for offspring risk of schizophrenia . I don't doubt however, that any relationship is likely to be complicated and potentially influenced by various other factors as we are reminded that elevated levels of maternal cotinine indicative of heavy smoking were also reported in nearly 15% of mothers of control (not schizophrenia) participants in the Niemelä study. I might also add that when it comes to other labels not necessarily a million miles away from schizophrenia, the suggestion of a link with smoking during pregnancy is not strong at all (see here).Where perhaps the latest findings are so interesting is the idea of a possible relationship between a proxy measure for foetal nicotine exposure and risk of schizophrenia. The emphasis is on 'nicotine exposure' and not necessarily the myriad of other toxins that are present when tobacco combusts (although I'm sure they might exert some kind of effect) thus potentially suggesting that quite a bit more research is indicated on other sources of nicotine exposure during pregnancy such as the use of nicotine replacement skin patches or even e-cigarettes. Indeed, having recently watched the ever-intrepid Dr Michael Mosley discuss the question: 'Are e-cigarettes really a menace?', with the Niemelä findings in mind, one might have to conclude, very possibly if used during pregnancy depending on what level of nicotine they might deliver. Just however, to confuse you further, the use of nicotine - "targeting nicotinic and nicotinic receptor subtypes"  - as a potential intervention for [some] schizophrenia has to be mentioned although perhaps not necessarily in the long-term.Irrespective of the plausibility or generalisability of the Niemelä findings, giving up smoking when pregnant to protect the developing foetus from potential schizophrenia or lots of other things, really is a no-brainer...---------- 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. Stathopoulou A. et al. Prenatal tobacco smoke exposure, risk of schizophrenia, and severity of positive/negative symptoms. Schizophrenia Research. 2013; 148: 105-110. Featherstone RE. & Siegel SJ. The Role of Nicotine in Schizophrenia. Int Rev Neurobiol. 2015;124:23-78.----------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... 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
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