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  • February 12, 2017
  • 11:10 AM

More than Meets the Eye

by Aurametrix team in Aurametrix Blog

Eyeglasses are almost as old as the civilization itself. They have not changed much since Benjamin Franklin's bifocals in the 18th century. Nor were they made obsolete by laser surgery and contacts. Still, eyeglass technology leaves much to be desired. But new technologies are unfolding before our eyes. ... Read more »

Gudlavalleti VS, Allagh KP, & Gudlavalleti AS. (2014) Self-adjustable glasses in the developing world. Clinical ophthalmology (Auckland, N.Z.), 405-13. PMID: 24570581  

Hasan N, Banerjee A, Kim H, & Mastrangelo CH. (2017) Tunable-focus lens for adaptive eyeglasses. Optics express, 25(2), 1221-1233. PMID: 28158006  

  • February 11, 2017
  • 04:43 AM

Pregnancy exposure to SSRIs and offspring autism risk: debate continues

by Paul Whiteley in Questioning Answers

"It remains unclear whether the association between first trimester SSRI [selective serotonin reuptake inhibitor] exposure and child autism that was present in the case-control studies even after adjustment for MMI [maternal mental illness] is a true association or a product of residual confounding."So said the results of the systematic review and meta-analysis undertaken by Hilary Brown and colleagues [1] looking at a potentially important association between pregnancy use of a class of medicines typically used as antidepressants (albeit with some caveats [2]) and risk of offspring autism. This topic has previously received some airtime on this blog (see here and see here) and specifically, how maternal mental health - as per the question 'why were mothers taking SSRIs during pregancy?' - might be a rather large confounding variable affecting any possible correlation.Unfortunately even with the Brown paper, the debates will continue as to whether the SSRI-offspring autism correlation is a 'true' correlation or not. Based on the results of 6 studies - "4 case-control studies and 2 cohort studies" - where MMI was adjusted for/restricted to, authors reported some interesting trends. So in their meta-analysis of the data where results from case-control studies were adjusted for a potential impact from MMI, researchers observed that "first trimester exposure remained statistically significant." In "MMI-restricted analyses" covering the same study type, the collected studies did not show any connection between pregnancy SSRI use and offspring autism during either the first trimester or 'any time during pregnancy'. Similar results were found in the cohort studies included in the Brown paper (although both first trimester and 'any point during pregnancy' SSRI use both showed significant correlations to offspring autism in adjusted studies). I might also add that the Brown meta-analysis on this topic is not the only recent addition to the peer-reviewed literature [3]; indeed, there are several [4] others."Future studies require robust measurement of MMI prior to and during pregnancy" said Brown et al. I would agree with this sentiment added to the caveat that we may never truly know whether there is a definitive connection between pregnancy SSRI use and offspring autism risk on the basis of observational studies alone. Yes, I know it is unethical to withhold treatment such as SSRIs when clinically indicated even during pregnancy and so investigations utilising this kind of 'interventionist' study design are not likely to be undertaken anytime soon. But it does strike me that we could do quite a bit more modelling any potential effects (or not) in animal studies for example, as per some investigations with fish a while back (see here) as a start.And finally, although it is not my place to give clinical or medical advice on this blog, I should point out that much like investigations on another medicine prescribed during pregnancy potentially linked to offspring outcomes (see here), SSRIs are not generally given willy-nilly to pregnant women; there are very valid reasons for managing mum's psychiatric health particularly during pregnancy. If anyone is in doubt, please consult your doctor (and not just Dr Google).To close, before 'fake news' there was The Day Today (and they did it oh so well)...----------[1] Brown HK. et al. The Association Between Antenatal Exposure to Selective Serotonin Reuptake Inhibitors and Autism: A Systematic Review and Meta-Analysis. J Clin Psychiatry. 2017 Jan;78(1):e48-e58.[2] Jakobsen JC. et al. Selective serotonin reuptake inhibitors versus placebo in patients with major depressive disorder. A systematic review with meta-analysis and Trial Sequential Analysis. BMC Psychiatry. 2017; 17: 58.[3] Kaplan YC. et al. Prenatal selective serotonin reuptake inhibitor use and the risk of autism spectrum disorder in children: A systematic review and meta-analysis. Reprod Toxicol. 2016 Dec;66:31-43.[4] Kobayashi T. et al. Autism spectrum disorder and prenatal exposure to selective serotonin reuptake inhibitors: A systematic review and meta-analysis. Reprod Toxicol. 2016 Oct;65:170-178.----------Brown HK, Hussain-Shamsy N, Lunsky Y, Dennis CE, & Vigod SN (2017). The Association Between Antenatal Exposure to Selective Serotonin Reuptake Inhibitors and Autism: A Systematic Review and Meta-Analysis. The Journal of clinical psychiatry, 78 (1) PMID: 28129495... Read more »

  • February 10, 2017
  • 12:15 PM

Scientific reliability and the role of theory

by Multiple Authors in EPPI-Centre blog

The replication crisis, publication bias, p-hacking, harking, bad incentives, undesirable pressures and probably other factors all contribute to diminish the trustworthiness of published research, with obvious implications for research synthesis. Sergio Graziosi asks whether demanding simple theoretical clarity might be part of the solution.
... Read more »

Kerr NL. (1998) HARKing: hypothesizing after the results are known. Personality and social psychology review : an official journal of the Society for Personality and Social Psychology, Inc, 2(3), 196-217. PMID: 15647155  

Head ML, Holman L, Lanfear R, Kahn AT, & Jennions MD. (2015) The extent and consequences of p-hacking in science. PLoS biology, 13(3). PMID: 25768323  

Munafò, M., Nosek, B., Bishop, D., Button, K., Chambers, C., Percie du Sert, N., Simonsohn, U., Wagenmakers, E., Ware, J., & Ioannidis, J. (2017) A manifesto for reproducible science. Nature Human Behaviour, 1(1), 21. DOI: 10.1038/s41562-016-0021  

  • February 10, 2017
  • 07:19 AM

BHD in patients undergoing chest CT and characteristics of BHD in Korea.

by Joana Guedes in BHD Research Blog

To date, there have been no prospective studies attempting to diagnose BHD syndrome or literature reviews on BHD in Korea. Park et al. (2017) address this in their new study that aims to detect BHD prospectively in patients undergoing chest computed tomography (CT) scans and to classify the characteristics of BHD in Korea.... Read more »

  • February 10, 2017
  • 03:27 AM

A few-foods diet for ADHD: a systematic review of meta-analyses of double-blind, placebo-controlled trials

by Paul Whiteley in Questioning Answers

"... the effect sizes of a few-foods diet are medium to large, justifying implementation of a diagnostic FFD [few-foods diet] in subgroups of children with ADHD [attention-deficit hyperactivity disorder], thus offering innovative treatment opportunities for ADHD."So said the "Systematic Review of Meta-Analyses of Double-Blind Placebo-Controlled Trials" published by Lidy Pelsser and colleagues [1] (open-access available here) looking at various dietary interventions that have been studied with ADHD in mind. Pelsser, I might add, is a name not completely unfamiliar to this area of investigation as per other research on elimination diets and ADHD (see here).The few-foods diet mentioned in the opening sentence of this post, could include a few things but Pelsser et al make specific reference to it consisting of "lamb, chicken, potatoes, rice, banana, apple and brassica: foods chosen as they were unlikely to produce an adverse response." You'll perhaps note that there are a few food groups missing from that list of foods, not least the grains (including the gluten protein), dairy products (containing the casein protein) and those processed foods that we all like to enjoy.The Pelsser paper is an interesting one insofar as their systematically reviewing meta-analyses that were already conducted on dietary intervention(s) for ADHD. Said meta-analyses included in their paper were only allowed in if they meta-analysed double-blind placebo-controlled trials (the gold-standard of clinical trial design). If one assumes that a meta-analysis - where data from different trials is analysed and condensed into a sort of position statement - sits at the top of the evidence-based science hierarchy, the Pelsser study design perhaps sits on top of the top!Although the FFD receives some welcome scientific backing in the review paper, it was not the only dietary intervention looked at the Pelsser and colleagues. To quote: "six supplement meta-analyses—all investigating the effects of poly-unsaturated fatty acids (PUFA)... —and eight elimination meta-analyses, examining respectively the effects of sugar..., AFC [artificial food colour elimination]..., the Feingold diet..., and the FFD... on ADHD" were reported on. The other interventions did not - for various possible reasons - match up to the research success reported with regards to the current standing of the few-foods diet for ADHD. This included the story on fatty acids for ADHD which has been mentioned previously on this blog (see here for example).I do not make recommendations on this blog when it comes to intervention and the like for anything. I will however, once again quote Pelsser et al based on their very thorough analysis of the peer-reviewed science in the area of dietary intervention for ADHD: "the effect sizes of a few-foods diet are medium to large, justifying implementation of a diagnostic FFD in subgroups of children with ADHD, thus offering innovative treatment opportunities for ADHD". Also: "FFD research should focus on the mechanism of food in children with ADHD." Their words not mine, and based on some rather credible evidence. I might also add that appropriate dietetic input is a must before anyone heads into the FFD willy-nilly and no, this is not about 'clean eating' or any related fad...And just before you go, how about casting your eye over the observations made by Alejandra Ríos-Hernández and colleagues [2] and their raising the question of "whether low adherence to a Mediterranean diet might play a role in ADHD development"? Food for thought in the context of the Pelsser data, although perhaps minus the [pregnancy] licorice?----------[1] Pelsser LM. et al. Diet and ADHD, Reviewing the Evidence: A Systematic Review of Meta-Analyses of Double-Blind Placebo-Controlled Trials Evaluating the Efficacy of Diet Interventions on the Behavior of Children with ADHD. PLoS One. 2017 Jan 25;12(1):e0169277.[2] Ríos-Hernández A. et al. The Mediterranean Diet and ADHD in Children and Adolescents. Pediatrics. 2017. Jan 30.----------Pelsser LM, Frankena K, Toorman J, & Rodrigues Pereira R (2017). Diet and ADHD, Reviewing the Evidence: A Systematic Review of Meta-Analyses of Double-Blind Placebo-Controlled Trials Evaluating the Efficacy of Diet Interventions on the Behavior of Children with ADHD. PloS one, 12 (1) PMID: 28121994... Read more »

  • February 9, 2017
  • 03:01 AM

On dietary and nutritional therapies for ME/CFS

by Paul Whiteley in Questioning Answers

ME/CFS in case you don't already know refers to Myalgic Encephalomyelitis / Chronic Fatigue Syndrome and, according to the findings reported by Nadia Campagnolo and colleagues [1], is in need of quite a bit more scientific investigation when it comes to the application of dietary changes and nutritional supplements to potentially alter the course of the condition(s).Surveying the peer-reviewed literature "from 1994 to May 2016" the authors looked for peer-reviewed studies where "CFS/ME patients modified their diet or supplemented their habitual diet on patient-centred outcomes (fatigue, quality of life, physical activity and/or psychological wellbeing)." They found 17 studies that included 14 different interventions. Unfortunately they concluded that: "Many studies did not show therapeutic benefit on CFS/ME" alongside the observation that the methodological quality of the research in this areas 'could do better'.But it was not all research doom-and-gloom as some approaches seemed to show promise: "Improvements in fatigue were observed for nicotinamide adenine dinucleotide hydride (NADH), probiotics, high cocoa polyphenol rich chocolate, and a combination of NADH and coenzyme Q10." Without wishing to toot my blogging trumpet, some of these approaches have been discussed before on this blog (Coenzyme Q10 and NADH supplementation for Chronic Fatigue Syndrome? and Coenzyme Q10 and NADH supplementation for Chronic Fatigue Syndrome continued) and beyond that, the target organ of something like the use of probiotics for CFS has made an appearance more than once too (see here for example). I might also add that just outside of the search dates used by Campagnolo et al was the suggestion that issues with a staple foodstuff - cows milk - might be over-represented in cases of CFS (see here) and that a milk-free diet could be useful [2] for some at least. By saying all that, I'm not giving any medical or clinical advice...As science starts to move further away from the the biopsychosocial (BPS) model of CFS/ME (see here) and starts looking at genetics, biology and somatic disease processes with regards to the various presentations included under the banner of ME/CFS (see here) I foresee some interesting developments further down the line. Granted, dietary and nutritional approaches to CFS/ME are probably not considered 'mainstream' in terms of management strategies but that does not mean they aren't important or at least important in the context of a diagnosis of ME/CFS seemingly being protective of nothing. Central to any future studies in this or any related area is the idea that there may be lots going on under the 'plural' diagnostic umbrella of ME/CFS (see here). Indeed, something that even the PACE trial is starting to take on board [3].----------[1] Campagnolo N. et al. Dietary and nutrition interventions for the therapeutic treatment of chronic fatigue syndrome/myalgic encephalomyelitis: a systematic review. J Hum Nutr Diet. 2017 Jan 22.[2] Rowe PC. et al. Cow's milk protein intolerance in adolescents and young adults with chronic fatigue syndrome. Acta Paediatr. 2016 Sep;105(9):e412-8.[3] Williams TE. et al. Heterogeneity in chronic fatigue syndrome - empirically defined subgroups from the PACE trial. Psychol Med. 2017 Jan 23:1-12.----------Campagnolo N, Johnston S, Collatz A, Staines D, & Marshall-Gradisnik S (2017). Dietary and nutrition interventions for the therapeutic treatment of chronic fatigue syndrome/myalgic encephalomyelitis: a systematic review. Journal of human nutrition and dietetics : the official journal of the British Dietetic Association PMID: 28111818... Read more »

Campagnolo N, Johnston S, Collatz A, Staines D, & Marshall-Gradisnik S. (2017) Dietary and nutrition interventions for the therapeutic treatment of chronic fatigue syndrome/myalgic encephalomyelitis: a systematic review. Journal of human nutrition and dietetics : the official journal of the British Dietetic Association. PMID: 28111818  

  • February 8, 2017
  • 04:33 AM

On atopic disease and ADHD: 'strong evidence' for an association

by Paul Whiteley in Questioning Answers

"This current systematic review provides strong evidence that ADHD [attention-deficit hyperactivity disorder] is associated with atopic diseases and that individuals have a 30% to 50% greater chance of developing ADHD compared to controls."So said the results of the systematic review and meta-analysis published by Jurjen van der Schans and colleagues [1] looking at the collected peer-reviewed science literature on how conditions such as asthma, eczema and rhinitis might increase the risk of a subsequent diagnosis of ADHD.New news? Not to this blog it isn't (see here for example) as the Schans data really just adds the 'cherry on top' to the idea that such somatic conditions might *connect to* behavioural and/or developmental diagnoses. Preferential screening is of course implied but then also comes the million dollar question: what are the biological mechanisms linking atopy to something like ADHD? The answer is likely to be complex - immune system complex for example - but I might suggest that some starting clues may be found in some of the [limited] peer-reviewed literature talking about what happens to ADHD signs and symptoms for some when treatment for atopic disease is initiated (see here).----------[1] van der Schans J. et al. Association of atopic diseases and attention-deficit/hyperactivity disorder: A systematic review and meta-analyses. Neurosci Biobehav Rev. 2017 Jan 19. pii: S0149-7634(16)30359-1.----------Schans JV, Çiçek R, de Vries TW, Hak E, & Hoekstra PJ (2017). Association of atopic diseases and attention-deficit/hyperactivity disorder: A systematic review and meta-analyses. Neuroscience and biobehavioral reviews PMID: 28111269... Read more »

  • February 8, 2017
  • 04:30 AM

Physical Activity Within 7 Days May Lead to Better Long-Term Outcomes After a Concussion

by Jane McDevitt in Sports Medicine Research (SMR): In the Lab & In the Field

Among children and adolescents with acute concussion, participation in physical activity within 7 days of acute injury compared with no physical activity was associated with lower risk of persistent postconcussion symptoms at 28 days post injury.... Read more »

  • February 7, 2017
  • 04:35 AM

Psychiatric disorders among male juvenile detainees in South Korea

by Paul Whiteley in Questioning Answers

"Juvenile detainees evidence high rates of psychiatric disorders and comorbidities. Assessment of and intervention in psychiatric disorders, especially alcohol use disorder and comorbid alcohol use disorder with disruptive behavior disorders, may help prevent further offenses."So concluded Johanna Inhyang Kim and colleagues [1] (open-access) following their investigation into the prevalence of DSM-IV psychiatric criteria in a sample of 173 male juvenile detainees aged between 15-19 years old held at a "male juvenile detention center in Seoul, South Korea, during the period of December 2015 to January 2016." Most of the detainees were held in relation to crimes against property (49%) but violent crimes (39%), traffic offences (24%) and sexual offences (19%) also featured in offending patterns.The presence of a psychiatric diagnosis was made using the Mini International Neuropsychiatric Interview (MINI) screening for various groups of disorders: disruptive behavioural disorders (DBDs), substance use disorder (SUD) and "any anxiety disorder." Researchers also looked for the presence of psychotic disorder and major depression too, alongside collecting various demographic data and information about recidivism (repeat offending).Results: "In total, 157 (90.8%) participants had at least one psychiatric diagnosis" is the standout figure from the paper compared with other independent data from this part of the world "of 15–38% among the general adolescent population." Alcohol use disorder was the most frequently mentioned label mentioned in the study, but 'comorbidity seems to be the rule' as we are told that: "Alcohol use disorder with DBDs was the most common combination, accounting for 46.2% of the detainees, followed by DBDs with anxiety disorders (22.5%)."When it came to the important issue of repeat offending, researchers also report some interesting patterns. Dropping out of school, present in about a quarter of the total cohort, was reported to be a factor in relation to recidivism (present in about 90% of detainees). The presence of two psychiatric disorders also showed a notable connection to repeat offending particularly where an alcohol use disorder was one of them. The message seems to be that keeping kids/young adults in school and away from alcohol might be an important combination in relation to affecting repeat offending rates.There is quite a lot of other data included in the Kim study and I would encourage interested parties to take a more detailed look. One thing that struck me about the Kim data was the apparent lack of results when it came to attention-deficit hyperactivity disorder (ADHD) in relation to offending and repeat offending outcomes. Minus any sweeping generalisations, I've talked before on this blog about how a diagnosis of ADHD might elevate the risk of contact with law enforcement agencies (see here) for whatever reason(s) and how a combination of ADHD and conduct disorder in particular, might be tied into a range of long-term adverse outcomes including 'risk of criminality' (see here). Kim and colleagues paint a slightly different clinical picture whereby a different combination of psychiatric factors might be specifically related to this group of people in this part of the world.More investigations are implied including reference to what potential nutritional changes might do to [some] behaviour in this population (see here).----------[1] Kim JI. et al. Prevalence of psychiatric disorders, comorbidity patterns, and repeat offending among male juvenile detainees in South Korea: a cross-sectional study. Child Adolesc Psychiatry Ment Health. 2017 Jan 18;11:6.----------Kim JI, Kim B, Kim BN, Hong SB, Lee DW, Chung JY, Choi JY, Choi BS, Oh YR, & Youn M (2017). Prevalence of psychiatric disorders, comorbidity patterns, and repeat offending among male juvenile detainees in South Korea: a cross-sectional study. Child and adolescent psychiatry and mental health, 11 PMID: 28115987... Read more »

  • February 6, 2017
  • 04:41 AM

Natural course of "chronic disabling fatigue" in adolescents

by Paul Whiteley in Questioning Answers

"We use the term 'chronic disabling fatigue' (CDF) because CFS/ME [chronic fatigue syndrome / myalgic encephalomyelitis] was not verified by clinical diagnosis."That was one of the important details included in the findings reported by Tom Norris and colleagues [1] (open-access) who "aimed to describe the epidemiology and natural course of CFS/ME in adolescents aged 13–18 years." Relying on data derived from The Avon Longitudinal Study of Parents and Children (ALSPAC) (something this research group have previously used in their peer-reviewed research), information on some 6700 adolescents at 13 years old, 5700 at 16 years old and 4200 at 18 years old were available to researchers.At those ages (13, 16 and 18 years old) the estimated prevalence rates of CDF - chronic disabling fatigue - ascertained slightly differently at different ages were: "1.47% (95% CI 1.05% to 1.89%) at age 13, 2.22% (1.67% to 2.78%) at age 16 and 2.99% (2.24% to 3.75%) at age 18." I say that CDF was ascertained slightly differently at each age point because mothers of participants reported on "fatigue lasting >6 months that was associated with absence from full-time school or that had prevented them from taking part in activities ‘quite a lot’ or ‘a great deal’" at aged 13 years which then moved to mothers and participants reporting at aged 16 and finally at aged 17-18 years a computer-based interview being used. The key point of all of this is that CDF is assumed to be a proxy for CFS/ME but is not an actual diagnosis of CFS/ME bearing in mind how complicated that side of things already is (see here for example).Insofar as the 'natural course' of CDF, the authors paint a picture where "the prevalence of CDF increased with advancing age" but also that around 8% of those diagnosed with CDF at aged 13, held on to the 'diagnosis' at 16 and 18 years old. The authors note: "These adolescents may represent a group who were experiencing a more severe form of the disease, characterised by increased persistence or recurrence of the disease." Personally, I would be careful with the word 'disease' in that context because it seems to me that CDF is describing a symptom not necessarily a condition and a symptom that could be present for all manner of different reasons.This is interesting data but I have to say I did feel a little 'misled' by the title of the Norris paper - "Natural course of chronic fatigue syndrome/myalgic encephalomyelitis in adolescents" - because of the use of the CDF definition as a proxy for the real thing. I refer you to other instances where ALSPAC has used/formulated measures as a proxy for diagnosis (with autism in mind) but even in that other case, authors used the term 'behavioural traits of autism spectrum disorder' [2] over and above calling it 'autism'. Surely it would have been better for Norris et al to say something like 'a trait of CFS/ME' rather than insinuating that they were examining defined cases of ME/CFS? Peer reviewers, please take note...To close, The Golden Girls and chronic fatigue syndrome. Ground-breaking.----------[1] Norris T. et al. Natural course of chronic fatigue syndrome/myalgic encephalomyelitis in adolescents. Arch Dis Child. 2017 Jan 19. pii: archdischild-2016-311198.----------Norris T, Collin SM, Tilling K, Nuevo R, Stansfeld SA, Sterne JA, Heron J, & Crawley E (2017). Natural course of chronic fatigue syndrome/myalgic encephalomyelitis in adolescents. Archives of disease in childhood PMID: 28104625... Read more »

Norris T, Collin SM, Tilling K, Nuevo R, Stansfeld SA, Sterne JA, Heron J, & Crawley E. (2017) Natural course of chronic fatigue syndrome/myalgic encephalomyelitis in adolescents. Archives of disease in childhood. PMID: 28104625  

  • February 4, 2017
  • 04:27 AM

ADHD, obesity and bariatric surgery?

by Paul Whiteley in Questioning Answers

"The findings suggest that a considerable number of patients before and after bariatric surgery screened positive for ADHD [attention-deficit hyperactivity disorder]. It can be hypothesized that some core ADHD symptoms improve after surgery."Bariatric surgery, where several surgical options are available to aid weight loss in those who present with 'dangerous' obesity, was the topic of the paper by Nielsen and colleagues [1] (open-access available here) who set out to compare "pre- and post-bariatric surgery patients using the internationally used Conners' Adult ADHD Rating Scale (CAARS™) to screen for ADHD" among other measures. The authors came up with some interesting details. They reported that the rate of 'probably ADHD' (defined using the CAARS and also the Wender Utah Rating Scale Short Version (WURS-k) cut-off scores) were 8.3% in their pre-surgery sample (n=120) and 6.3% in their post-surgery sample (n=128).When looking at the behavioural profiles of those pre- and post-surgery, there were some not entirely unexpected differences when it came to items related to depression and eating-related psychopathology - both scoring lower in the post-surgery participants. But also those post-surgery reported some potentially important information in relation to generally better attention and memory compared to pre-surgery participants. I was intrigued by the authors explanation of this: "The finding of a better attention and memory function in the post-surgery sample is in line with the results of longitudinal studies demonstrating improvements in cognitive functioning following bariatric surgery." Further: "It is reasonable to assume that postoperative cognitive improvement in attention and memory might have impacted the self-report on the respective CAARS subscale." Does this imply that bariatric surgery might act as some kind of nootropic for [some of] those with obesity?In these days of ADHD being 'linked' to obesity (see here), the Nielsen results fit nicely. Alongside the idea that weight loss surgery might link into improved cognitive functioning and onwards, impacting on facets of ADHD I'd have to question what the biological mechanism(s) might be. Does the restriction of food intake as a consequence of surgery indicate a role for food in some cognitive processes? Does such surgery potentially impact on the trillions of wee beasties that populate our gut and then onwards exert an effect of cognitive processes? There are several questions that still need answering...----------[1] Nielsen F. et al. Attention Deficit Hyperactivity Disorder Prevalence and Correlates Pre- and Post-Bariatric Surgery: A Comparative Cross-Sectional Study. Obes Facts. 2017 Jan 20;10(1):1-11.----------Nielsen F, Georgiadou E, Bartsch M, Langenberg S, Müller A, & de Zwaan M (2017). Attention Deficit Hyperactivity Disorder Prevalence and Correlates Pre- and Post-Bariatric Surgery: A Comparative Cross-Sectional Study. Obesity facts, 10 (1), 1-11 PMID: 28103594... Read more »

  • February 3, 2017
  • 11:22 AM

Brain Shape and Personality Type

by William Yates, M.D. in Brain Posts

Personality has often been conceptualized a a human feature shaped largely by nurture and environment.Unlike major neuroscience medicine disorders, personality features have been considered less influenced by brain structure and genetic influences.A recent brain structure (morphology) study puts these assumptions at risk.Roberta Riccelli along with colleagues in Italy and Florida State University studied brain structural features across 507 participants in the Human Connectome Project.All subjects completed a personality assessment using the five-factor model (FFM), a widely validated measure of five personality features.Here were the key findings from the study for each personality feature:High neuroticism: increased cortical thickness in supramarginal gyrus, superior parietal cortex, superior temporal cortex, superior prefrontal cortex and frontal pole. Also decreased surface area of superior parietal cortex, middle temporal gyrus, cuneus, superior prefrontal cortex and frontal pole.High extraversion: increased cortical thickness in precuneus and lower surface area and volume of superior temporal gyrus. Also lower cortical volume of entorhinal cortex and greater folding in the fusiform gyrus.High openness: lower cortical thickness in the postcentral gyrus, rostral anterior cingulate cortex, superior prefrontal cortex and lateral occipital gyrus. Increased surface area, cortical volume and folding in a series of parietal, temporal and frontal regions.High Agreeableness: Decreased cortical thickness, surface area, cortical volume and local gyrus formation in frontotemporal regions. Increased local gyrus formation in inferior temporal gyrus.High concientiousness: increased cortical thickness in prefrontal cortex along with lower surface area and cortical volume in middle/inferior temporal gyrus and lateral occipital gyrus regions. Decreased cortical folding in prefrontal gyrus and several other regions.These findings are of note for the diffuse number and types of structural correlates of personality features in man. The authors note the importance of the prefrontal cortex in personality:  "significantly evolved in human beings and great apes relative to other species. This could reflect that several FFM personality traits are linked to high-level socio-congnitive skills as well as the ability to modulate "core" affective responses."Look for more structural, functional and genetic study of the five factor model of personality features in human to come.Readers with more interest in this research can access the free full-text manuscript by clicking on the PMID link in the citation below.Follow the author on Twitter WRY999Photo of bald eagle head in profile is from the author's bird photography file. Riccelli R, Toschi N, Nigro S, Terracciano A, & Passamonti L (2017). Surface-based morphometry reveals the neuroanatomical basis of the five-factor model of personality. Social cognitive and affective neuroscience PMID: 28122961... Read more »

  • February 3, 2017
  • 03:03 AM

"Schizophrenia confers a high endogenous risk for diabetes"

by Paul Whiteley in Questioning Answers

"Schizophrenia confers a high endogenous risk for diabetes, and the risk is further increased by both first-generation and second-generation antipsychotics."So concluded Anto Rajkumar and colleagues [1] who relied on participant data in the thousands derived from several of those very helpful Scandinavian population registries (this time in Denmark) to add some further science to the idea that psychiatric diagnoses like schizophrenia seem to carry an elevated risk for all-manner of somatic conditions.From a total population of 2.7 millions people born in Denmark between 1977 and 2013, researchers reported that: "14,118 (0.52%) developed diabetes, and 8,945 (0.33%) developed schizophrenia during follow-up (49,582,279 person-years)." When looking at the risk of developing diabetes (bearing in mind there is more than one type of diabetes) in those with schizophrenia not following any antipsychotic medication regime, researchers reported that: "The adjusted hazard ratio for diabetes was 3.07 (95% confidence interval [CI], 1.71–5.41) in antipsychotic-naive schizophrenia compared with the general population." In other words, compared with those without a diagnosis of schizophrenia, there was something of an increased risk of developing diabetes in those diagnosed with schizophrenia.Then to the potential effect of antipsychotic medication, and as the authors note: "The risk for diabetes after starting antipsychotic treatment was significantly higher (adjusted hazard ratio, 3.64; 95% CI, 1.95–6.82) than the risk in antipsychotic-naive schizophrenia." The use of an adjusted hazard ratio means that researchers took into account potentially confounding variables such as a family history of diabetes known to potentially elevate the risk of the condition. The focus on medication is also perhaps the side of the whole schizophrenia-diabetes story that people might more readily recognise.If all that wasn't enough to convince you that schizophrenia - medicated and unmedicated - might show a rather important relationship with diabetes, perhaps the results reported by Pillinger and colleagues [2] might ease your scepticism and the suggestion (from the authors) that "higher levels of insulin, and increased levels of insulin resistance" are a facet of quite a few cases of schizophrenia alongside demonstrating that "people with schizophrenia had higher levels of glucose in the blood." On the basis of these and various other studies, the onus is on regular screening for diabetes and its symptoms alongside other related measures (see here for example) when it comes to schizophrenia under multiple 'medicated or not' conditions.Music to close, and having bumped into the excellent film 'Stand By Me' again recently, the song of the same name...----------[1] Rajkumar AP. et al. Endogenous and Antipsychotic-Related Risks for Diabetes Mellitus in Young People With Schizophrenia: A Danish Population-Based Cohort Study. Am J Psychiatry. 2017 Jan 20:appiajp201616040442.[2] Pillinger T. et al. Impaired Glucose Homeostasis in First-Episode Schizophrenia: A Systematic Review and Meta-analysis. JAMA Psychiatry. 2017 Jan 11.----------Rajkumar AP, Horsdal HT, Wimberley T, Cohen D, Mors O, Børglum AD, & Gasse C (2017). Endogenous and Antipsychotic-Related Risks for Diabetes Mellitus in Young People With Schizophrenia: A Danish Population-Based Cohort Study. The American journal of psychiatry PMID: 28103712... Read more »

  • February 2, 2017
  • 03:25 AM

Hyperuricemia present in both medicated and unmedicated kids with autism

by Paul Whiteley in Questioning Answers

I was intrigued to read the findings reported by Natchaya Vanwong and colleagues [1] talking about the presence of hyperuricemia - an excess of uric acid in the blood - in their cohort of children and young adults diagnosed with an autism spectrum disorder (ASD). Intrigued not only because the authors discuss how the use of the atypical antipsychotic risperidone might *correlate* with elevations of uric acid but also how: "Hyperuricemia was present in 44.70% of risperidone-naïve patients with ASD."Uric acid, more readily associated with the condition gout, has been mentioned before on this blog in the context of autism (see here) and other conditions/states (see here) not totally unfamiliar to autism. It's therefore not necessarily new news that elevations of the stuff might have been found again. The Vanwong study looked at uric acid levels in "127 children and adolescents with ASD treated with risperidone and 76 age-matched risperidone-naïve patients with ASD" alongside a few other biological parameters. They concluded that yes, quite a few participants in their cohort presented with hyperuricemia "defined as the level of uric acid concentration in the blood >5.5 mg/dL" bearing in mind no 'not-autism' control group was included for direct study (including those not diagnosed with autism but in receipt of risperidone).Implications following the Vanwong study? Well, bearing in mind that gout is traditionally seen as a disease of middle-to-older age, the first thing would be to screen for gout in those with high uric acid levels and keep monitoring just in case gout develops. Next up would be to perhaps also look at some of the "rare inherited genetic disorders that cause hyperuricemia" and whether they might 'overlap' with the presentation of autism; y'know in the context that 'autism genes are probably not just genes for autism' and all that. At this point, I'm also minded to remind readers of the important (but often forgotten work) by Mary Coleman and Ted Page [2] on the topic of autism and uric acid, bringing in purine metabolism 'issues' as something potentially important to some autism (uric acid comes about as a consequence of the metabolism of purines). This, in the context of the autisms (plural)...Insofar as the potential correlation posed between uric acid and risperidone usage, a word of caution is perhaps warranted but big words about 'risperidone causing hyperuricemia' are not required at this point in time without further study. Remember: "Hyperuricemia was present in 44.70% of risperidone-naïve patients with ASD and 57.50% of ASD patients treated with risperidone." I say this mindful that there are biological parameters that do need careful inspection when such antipsychotic therapy is put in place (see here) but the data is not yet so convincing when it comes to uric acid elevations and risperidone use.----------[1] Vanwong N. et al. Hyperuricemia in Children and Adolescents with Autism Spectrum Disorder Treated with Risperidone: The Risk Factors for Metabolic Adverse Effects. Front. Pharmacol. 2017. 5 Jan.[2] Page T. & Coleman M. Purine metabolism abnormalities in a hyperuricosuric subclass of autism. Biochim Biophys Acta. 2000 Mar 17;1500(3):291-6.----------Vanwong N, Srisawasdi P, Ngamsamut N, Nuntamool N, Puangpetch A, Chamkrachangpada B, Hongkaew Y, Limsila P, Kittitharaphan W, & Sukasem C (2017). Hyperuricemia in Children and Adolescents with Autism Spectrum Disorder Treated with Risperidone: The Risk Factors for Metabolic Adverse Effects. Frontiers in pharmacology, 7 PMID: 28105014... Read more »

  • February 1, 2017
  • 04:30 AM

Overtrained Athletes Have Abnormal Biochemical Response to Exercise

by Nicole Cattano in Sports Medicine Research (SMR): In the Lab & In the Field

Overtrained athletes have abnormal inflammatory and anabolic responses to exercise, indicating that their body is not responding to exercise the way that it should.... Read more »

  • February 1, 2017
  • 03:21 AM

Autism and a 'clear' reduction of behavioural severity in cases diagnosed

by Paul Whiteley in Questioning Answers

"This study provides the first clear evidence of a reduction over time in the behavioral severity of individuals diagnosed with Autistic Disorder during a period of stability in diagnostic criteria."So said the study findings reported by Andrew Whitehouse and colleagues [1] (a man not afraid to make waves when it comes to thinking about autism or about approaches to intervention) looking at "whether there were changes over time in the qualitative and quantitative phenotype of individuals who received the diagnosis of Autistic Disorder."Based on prospective registry data of new autism / autism spectrum disorder (ASD) cases (N=1252) in Western Australia (a research favourite) between 2000 and 2006, researchers reported that the severity of the presentation of autism seemed to 'change' between the years. They concluded: "A shift toward diagnosing individuals with less severe behavioral symptoms may have contributed to the increasing prevalence of Autistic Disorder diagnoses." At least in Australia that is...This is an interesting study. It kinda reiterates that when one talks about the quite phenomenal increase in diagnoses of autism being received, at least one factor contributory to that increase is the inclusion of a wider presentation of the condition. It also feeds into the discussions that have already happened, and will continue to happen, following the introduction of DSM-5 to autism diagnosis and in particular, the future role of the catch-all category that is social (pragmatic) communication disorder (SCD) (see here) when it comes to stiffer ASD diagnostic criteria not being met.But just before anyone breaks out with the sweeping generalisation that the increasing prevalence of autism over the past two decades is somehow all 'manufactured' (exhibit one) according to the diagnostic procedures used, the available data points to something far more multi-faceted and complex (see here for example)...----------[1] Whitehouse AJ. et al. Evidence of a reduction over time in the behavioral severity of autistic disorder diagnoses. Autism Res. 2017 Jan 19.----------Whitehouse AJ, Cooper MN, Bebbington K, Alvares G, Lin A, Wray J, & Glasson EJ (2017). Evidence of a reduction over time in the behavioral severity of autistic disorder diagnoses. Autism research : official journal of the International Society for Autism Research PMID: 28102641... Read more »

Whitehouse AJ, Cooper MN, Bebbington K, Alvares G, Lin A, Wray J, & Glasson EJ. (2017) Evidence of a reduction over time in the behavioral severity of autistic disorder diagnoses. Autism research : official journal of the International Society for Autism Research. PMID: 28102641  

  • January 31, 2017
  • 03:18 AM

S100B protein and autism continued

by Paul Whiteley in Questioning Answers

"Our findings showing an increase in peripheral concentrations of S100B and TNF-α provide limited support to the hypothesis about the roles of altered immune function and S100B in autism spectrum disorder (ASD)."So said the findings reported by Selin Aktan Guloksuz and colleagues [1] (open-access available here) continuing some discussions a few years back on a possible role for S100B in relation to at least some autism (see here).S100B - S100 calcium-binding protein B - is a compound involved in quite a few biological reactions not least "as a biomarker of global glial activity." Elevations of the S100B have been reported in relation to several states including that of [traumatic] brain injury. Outside of some research suggesting that elevations of S100B might also be a feature of diagnoses such as schizophrenia (see here), it has also been the topic of investigations with [some] autism in mind [2] too. The name of the game is elevations in S100B in relation to autism and more.Based on analyses of fasting blood samples from "40 unmedicated children with autism" (where autism diagnoses were confirmed by study researchers) and 35 asymptomatic control children, researchers measured levels of plasma S100B alongside various markers of immune function (cytokines). Among the suite of cytokines examined, levels of "tumor necrosis factor alpha (TNF-α), interferon gamma, interleukin (IL)-1β, IL-4, IL-6, IL-10, and IL-17A" were included. The idea of using unmedicated children with autism stems from the suggestion that at least one medication used for some autism might have the ability to elevate S100B [3].Results: as per the opening sentence to this post, levels of S100B and TNF-α were 'different' between the groups (both elevated) and this finding remained "after controlling for age, sex, and BMI [body mass index]." Researchers also reported some results looking at whether ASD symptom presentation might show any 'association' with S100B levels. On this topic they reported that: "Plasma S100B concentrations in children with severe ASD symptoms were higher than in children with mild-moderate ASD symptoms" but when again controlling for age, sex and BMI this association did not hold (significantly). As for the other cytokines outside of TNF-α... nothing came up as significant between the groups. This is interesting in light of recent work (see here) and even Guloksuz et al talk about future "prospective longitudinal studies investigating a broad set of immune markers, both in serum and CSF [cerebrospinal fluid], in large samples" and the pros- and cons of looking in CFS.Where next for this area of investigation? Well, taking into account the link between S100B and brain injury and what that could mean for cognitive processes for example, I'd be minded to suggest that more study is needed looking at the effect of S100B levels in relation to cognition and autism. Take for example the study results from Chen and colleagues [4] who reported that "serum S100B level was an independent contributor to the global cognitive dysfunctions, particularly for the speed of processing, attention/vigilance, visual learning and reasoning/problem solving subscores" in their cohort of participants with schizophrenia. Might similar correlations be present alongside S100B elevations in relation to autism? I'd also be minded to suggest looking at a possible role for comorbidities potentially accompanying a diagnosis of autism as being important for S100B elevations in light of other research on depression for example [5]. Depression (various types) and autism is very much an important area of overlap (see here for example) and might actually offer at least one way to target elevations in S100B.There is more to do on this topic.----------[1] Guloksuz SA. et al. Elevated plasma concentrations of S100 calcium-binding protein B and tumor necrosis factor alpha in children with autism spectrum disorders. Rev Bras Psiquiatr. 2017 Jan 12:0.[2] Al-Ayadhi LY. & Mostafa GA. A lack of association between elevated serum levels of S100B protein and autoimmunity in autistic children. J Neuroinflammation. 2012 Mar 16;9:54.[3] Quincozes-Santos A. et al. Effect of the atypical neuroleptic risperidone on morphology and S100B secretion in C6 astroglial lineage cells. Mol Cell Biochem. 2008 Jul;314(1-2):59-63.[4] Chen S. et al. Cognitive dysfunction correlates with elevated serum S100B concentration in drug-free acutely relapsed patients with schizophrenia. Psychiatry Res. 2017 Jan;247:6-11.[5] Rajewska-Rager A. & Pawlaczyk M. The role of S100B protein as a potential marker in affective disorders. Psychiatr Pol. 2016;50(4):849-857.----------Guloksuz SA, Abali O, Aktas Cetin E, Bilgic Gazioglu S, Deniz G, Yildirim A, Kawikova I, Guloksuz S, & Leckman JF (2017). Elevated plasma concentrations of S100 calcium-binding protein B and tumor necrosis factor alpha in children with autism spectrum disorders. Revista brasileira de psiquiatria (Sao Paulo, Brazil : 1999) PMID: 28099628... Read more »

Guloksuz SA, Abali O, Aktas Cetin E, Bilgic Gazioglu S, Deniz G, Yildirim A, Kawikova I, Guloksuz S, & Leckman JF. (2017) Elevated plasma concentrations of S100 calcium-binding protein B and tumor necrosis factor alpha in children with autism spectrum disorders. Revista brasileira de psiquiatria (Sao Paulo, Brazil : 1999). PMID: 28099628  

  • January 30, 2017
  • 03:08 AM

High frequency of (self-reported) ADHD symptoms in eating disorders

by Paul Whiteley in Questioning Answers

"There is a high frequency of ADHD [attention-deficit hyperactivity disorder] symptoms in patients with binge eating/purging eating disorders that motivates further studies."That was the conclusion reached in the study by Nils Erik Svedlund and colleagues [1] (open-access) who, among other things, set out to "explore the prevalence and types of self-reported ADHD symptoms in a large, unselected group of ED [eating disorder] patients assessed in a specialized ED clinic." Participants (over 1100 of them) were "seeking help at the Stockholm Centre for Eating Disorders (SCED) from 4 February 2013 through 18 September 2015" and as well as being confirmed to have an eating disorder were also screened for ADHD-type behaviours using the WHO ADHD Self-Rating Scale for Adults (ASRS-screener). Notice the 'self-rated' part of that last sentence...Based on a ASRS screener score of 14 or above, researchers reported that some 30% of females (N=1094) self-reported 'issues' associated with a diagnosis of ADHD. Some 34% of men included for study (N=47) reported similar ADHD traits (31.3% of the total group including those diagnosed with 'Eating Disorder Not Otherwise Specified (EDNOS) type 5' were on or above the ASRS screener score of 14).Bearing in mind the presence of various types of different eating disorders in their cohort, researchers also looked at how those self-reported ADHD traits might correlate with sub-groupings. They report that: "The highest frequency of possible ADHD was found in BN [Bulimia Nervosa] and in AN-BP [Anorexia Nervosa bingeing/purging subtype], respectively." They also noted that specific symptoms of ED correlated with the ASRS-screener scores: binge eating, purging, loss of control over the eating and BMI [body mass index] > 17.5. I might add that based on responses to another schedule - the Comprehensive Psychiatric [Psychopathological] Rating Scale (CPRS) - included as part of the study, authors noted something of a link between the ASRS trait scores and "the CPRS scales for depression..., anxiety... and obsession-compulsion." But: "Psychiatric comorbidity correlated to ADHD symptoms without explaining the differences between eating disorder diagnoses."Keeping in mind that answering 6 questions on a screener questionnaire does not an ADHD diagnosis make, I am rather interested in these and other findings. I am by no means an expert on eating disorder but I have previously been interested in the suggestion that autistic traits may be 'over-represented' when it comes to ED (see here). Combined with the idea that autism and [diagnosed] ADHD might not also be unstrange diagnostic bedfellows (see here) and you can perhaps see that there is potentially more research to do in this area in these times of overlap and ESSENCE. And speaking of ESSENCE [2]...With a word or two of caution, I note the authors also talked about potential 'treatment' options given the overlap between ADHD traits (self-reported) and ED. So: "This motivates further randomized trials with stimulant treatment for bingeing/purging ED-patients with and without a concomitant ADHD diagnosis." Certain stimulants have quite a good track record when it comes to ADHD (see here) but the authors rightly note that 'appetite suppression' is a potential side-effect of such pharmacotherapy and something perhaps not ideal if someone is already underweight. More studies are indicated to disentangle what is linked to what.And while I'm on the topic, the link between autism traits and anorexia nervosa might actually be a little more tenuous that you perhaps think [3]...----------[1] Svedlund NE. et al. Symptoms of Attention Deficit Hyperactivity Disorder (ADHD) among adult eating disorder patients. BMC Psychiatry. 2017; 17: 19.[2] Karjalainen L. et al. Eating disorders and eating pathology in young adult and adult patients with ESSENCE. Compr Psychiatry. 2016 Apr;66:79-86.[3] Postorino V. et al. Investigation of Autism Spectrum Disorder and Autistic Traits in an Adolescent Sample with Anorexia Nervosa. J Autism Dev Disord. 2017. Jan 24.----------Svedlund, N., Norring, C., Ginsberg, Y., & von Hausswolff-Juhlin, Y. (2017). Symptoms of Attention Deficit Hyperactivity Disorder (ADHD) among adult eating disorder patients BMC Psychiatry, 17 (1) DOI: 10.1186/s12888-016-1093-1... Read more »

  • January 28, 2017
  • 04:26 PM

RCT of traditional running shoes vs minimalist running shoes

by Craig Payne in Running Research Junkie

RCT of traditional running shoes vs minimalist running shoes... Read more »

  • January 28, 2017
  • 04:15 AM

"Should gluten-free foods be available on prescription?"

by Paul Whiteley in Questioning Answers

Continuing the theme of blogging outside of the core material typically included on this site, I couldn't resist a mention of the 'head-to-head' debate talked about in the article by Matthew Kurien and colleagues [1] published in the British Medical Journal (BMJ).As per the title of this post, the name of the game was gluten-free products being available on prescription here in Blighty, and in particular, the prescribing of gluten-free products to patients diagnosed with coeliac disease. The head-to-headers were Matthew Kurien, Sarah Sleet & David Sanders* (*a name not unfamiliar to this blog) all in favour of keeping the status quo and James Cave presenting the opposing view and why prescriptions of gluten-free products to those with coeliac disease might not be the only way.OK, first things first. A gluten-free diet is not some dietary 'fad' for people living with coeliac disease (CD); it is a clinically-indicated treatment tool for this autoimmune condition. As I've said a few times on this blog, not only are there are physiological effects linked to CD mostly 'solved' by use of a gluten-free diet, but there may be psychological effects too (see here). Gluten is most definitely the 'baddie' when it comes to CD and should not be in the diet of those with CD.The head-to-head piece makes for interesting reading in terms of how in these days of focus on the finances of the National Health Service (NHS), the idea that removing food prescriptions as one way to "reduce costs in the short term" might have some important repercussions in the longer-term. Indeed I was taken by one quote in the 'keep gluten-free food prescriptions' camp: "Would clinical commissioning groups consider this if the treatment for coeliac disease was an immunosuppressive drug and not food?" Food as medicine? I like that sentiment (see here).I have to say however that I did find the viewpoint from James Cave rather appealing in some aspects. Within his various facts and figures he shows how perverse it is that one can go into a supermarket and buy a gluten-free loaf of bread for one price and yet the same loaf is bought by the NHS for prescription for quite a bit more. Sorry to focus on cost and finances but this is salient point in these days of continued austerity and financial/political uncertainty. Cave also adds that gluten-free food prescriptions tend to be restricted to set items, come in bulk and generally need to be collected from a pharmacy. There are additional costs added to the supply of such goods.The two viewpoints do however agree that slight changes could be made to the system to make it both run more efficiently and provide those with coeliac disease a little more 'opportunity' in what they select. As Cave notes: "A national voucher scheme or a personalised health budget could be provided to ensure that patients receive recompense for the extra expense of gluten-free products." As Kurien and colleagues note: "Alternative strategies to prescriptions, such as direct supply schemes from community pharmacies, or voucher allowances, may be a more efficient way of delivering NHS support." A voucher scheme for gluten-free products? Interesting.In these days where areas of England are already seeing changes to gluten-free prescriptions (see here for example) I'm wondering if a voucher scheme might be the [inevitable] way forward, at least for the majority of patients. Not only does this offer more choice to the consumer in terms of what products they buy (and indeed, what they might prefer) but the whole process of the NHS ordering, buying and dispensing such products is also reduced. For those who perhaps do not have access to a full-range of gluten-free products as their local supermarket for example or have mobility issues, exceptions could be made but for the most part, patients are handed choice and a lot more buying power and freedom. A voucher scheme might also 'normalise' the idea of gluten-free products when it comes to CD. By 'normalise' I mean that a young adult diagnosed with CD for example, no longer has to go to their local pharmacy for their 'months supply' but rather can shop - pick and choose - from the growing range of gluten-free products that adorn supermarket shelves these days. Compliance to the gluten-free diet will no doubt benefit when there is more choice and a voucher scheme will bring choice.Change is often difficult when it comes to the NHS and it's been over 50 years since gluten-free products were put on prescription for those with CD so this would be a big change. But gluten-free is everywhere these days and there is seemingly little to hold the NHS back from further empowering those diagnosed with CD in terms of their dietary choices...----------[1] Kurien M. et al. Should gluten-free foods be available on prescription? BMJ 2017: 356.----------Kurien M, Sleet S, Sanders DS, & Cave J (2017). Should gluten-free foods be available on prescription? BMJ (Clinical research ed.), 356 PMID: 28073799... Read more »

Kurien M, Sleet S, Sanders DS, & Cave J. (2017) Should gluten-free foods be available on prescription?. BMJ (Clinical research ed.). PMID: 28073799  

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