So there has been a lot of noise about whether giving women 'safety tips' to avoid being raped is a form of 'victim blaming'.Don't get Raped (source)This culminated in a great hashtag (as many things do). Follow #safetytipsforladies to see some lovely tips for avoiding rape.For example:Don't be anywhere. 100% of rapes happen in places and locations. #safetytipsforladies— Conna Stevenson (@1000DaysOfRain) March 25, 2013Others suggest simply not being a woman, not ever drinking anything, not ever wearing anything (but not being naked either), not ever leaving the house (or since many rapes happen inside the house, not ever being home). And so forth.The main point is that it's absurd to tell women to not get raped. Rape by definition is NOT under the victim's control.Yet people still tend to blame the victim in rape cases. An interesting study was published in 2011 showing that people were more likely to blame the victim in a rape case than in a robbery case. The authors gave people short vignettes describing either a rape or a robbery, and had these participants fill out a perpetrator blame scale and a victim blame scale.Bienek and Krahe 2011 Figure 4 Interestingly, but maybe not surprisingly, rape always had more victim blame and less perpetrator blame than robbery and this difference increased with how close the victim and perpetrator were to each other (stranger, acquaintance, ex-partner). Now some people say 'hey, I'm just trying to keep women safe by telling them to avoid dark places, and not take drinks from strangers.' But here's the thing, maybe the mere suggestion that women can do something to avoid being raped is enough to subtly nudge one's opinion toward thinking that if a woman got raped, she should have done something to avoid it and is therefore somewhat to blame.So I propose the following study:Have one group of people read a short article on tips for women to avoid being raped (a serious and well meaning one), and one group of people read some unrelated article. Then have both groups read rape vignettes similar to the ones described in the Bienek and Krahe study and fill out the victim and perpetrator blame scales. They would also fill out a scale for how much punishment the perpetrator should get in a court of law. I hypothesize that simply reading a list of well meant tips for how women can avoid being raped would increase victim blame and would make people more lenient in their prescribed punishment for the perpetrator.Somebody please do this experiment!© TheCellularScale Bieneck S, & Krahé B (2011). Blaming the victim and exonerating the perpetrator in cases of rape and robbery: is there a double standard? Journal of interpersonal violence, 26 (9), 1785-97 PMID: 20587449... Read more »
Bieneck S, & Krahé B. (2011) Blaming the victim and exonerating the perpetrator in cases of rape and robbery: is there a double standard?. Journal of interpersonal violence, 26(9), 1785-97. PMID: 20587449
The paper does address some interesting aspects of resuscitation.
ROSC (Return Of Spontaneous Circulation) is the goal for many people.
ROSC is a red herring.
Those of us who think ROSC is important do not seem to understand how much long-term damage we can do in our attempts to get ROSC, or to get ROSC quickly.
This study helps to point out some of the inconsistencies with our ROSC fetish.... Read more »
Koscik, C., Pinawin, A., McGovern, H., Allen, D., Media, D., Ferguson, T., Hopkins, W., Sawyer, K., Boura, J., & Swor, R. (2013) Rapid Epinephrine Administration Improves Early Outcomes in Out-of-Hospital Cardiac Arrest. Resuscitation. DOI: 10.1016/j.resuscitation.2013.03.023
Over the course of hundreds of millions of years, the combustible, black rock we call coal was formed from the vast peat bogs of flooded forests. For centuries, people have burned lumps of coal for smoky fuel, such that opposition to its pollution had been voiced as early as the fourteenth century. Today, as anti-coal movements emphasize a role in climate change and miners cope with unemployment, a novel, microporous material may challenge objections to coal by cleaning up its carbon emissions.... Read more »
Lyndon R, Konstas K, Ladewig BP, Southon PD, Kepert PC, & Hill MR. (2013) Dynamic photo-switching in metal-organic frameworks as a route to low-energy carbon dioxide capture and release. Angewandte Chemie (International ed. in English). PMID: 23401101
Baxter PJ, Kapila M, & Mfonfu D. (1989) Lake Nyos disaster, Cameroon, 1986: the medical effects of large scale emission of carbon dioxide?. BMJ (Clinical research ed.), 1437-1441. PMID: 2502283
Ahern MM, Hendryx M, Conley J, Fedorko E, Ducatman A, & Zullig KJ. (2011) The association between mountaintop mining and birth defects among live births in central Appalachia, 1996-2003. Environmental research, 838-46. PMID: 21689813
Hendryx M, Wolfe L, Luo J, & Webb B. (2012) Self-reported cancer rates in two rural areas of West Virginia with and without mountaintop coal mining. Journal of community health, 320-327. PMID: 21786205
I've hinted before on this blog and its sister blog about how one of the most unappealing of interventions - fecal bacteriotherapy - is starting to make some waves in managing various conditions. I know its not everyone's cup of tea but the concept of transplanting whole stools or specific types of enteric bacteria from one person to another is actually providing some well needed relief for quite a few people.Insert here.... @ Wikipedia If it sounds like an undesirable treatment option, put yourself in the shoes of someone who for example is suffering as result of infection due to C. difficile and the potential consequences that this can entail after other treatment options have been exhausted and then wonder again. Better still, have a look at that probiotic yoghurt drink that is sitting in your fridge and ponder the question: where did the 'special' bacteria included in this drink originally come from? (hint: 'donor zero' is probably smiling at all of us).Whilst fecal bacteriotherapy is moving into more mainstream medicine circles for conditions linked to things like C.diff, various other states and diseases are also starting to be discussed with the s--t transplant in mind. One person in particular is leading these discussions, Dr Thomas Borody, following his groundbreaking work on triple therapy for H.pylori infection (see here), and some discussions on 'emerging' applications* (no pun intended). Indeed Dr Borody is quite the leading light when it comes to fecal bacteriotherapy.I was particularly interested to read the paper by Borody and colleagues** looking at the potential application of bacteriotherapy to cases of chronic fatigue syndrome (CFS). Regular readers might already know of my tendency to stray into the research domain of CFS (and ME) on this blog and beyond not least because quite a bit of the research there seems to overlap with what I talk about with autism in mind (e.g. immune function, mitochondrial issues, even HERVs..).Anyhow, with many thanks to Sarah Finlayson, one of Dr Borody's co-authors, for sending me a copy of their paper, a few points are worth noting:This is a paper which kills two birds with one stone. On the one hand, there is quite a nice summary of CFS and the gut microbiome (hopefully this link still works for non-members). On the other hand, the paper describes the experiences of 60 patients with CFS attending Dr Borody's clinic some time in the mid-1990s and in receipt of transcolonoscopic (TC) and rectal infusions of "anaerobic bacterial culture". Distinct from the 'full works' of of a stool transplant or 'fecal microbiota transplantation (FMT)', bacteriotherapy involves the 'fusion of a mixture of 13 non-pathogenic enteric bacteria" which include those of the Bacteroidetes, Clostridia and E.coli families/phyla/species.Every participant received at least one TC infusion; most also received a second rectal infusion (n=52); a small number received two days of additional rectal infusion (n=3). Actually, as you'll see in a minute, there was a bit more to this than what is mentioned in the methods section of the paper.Results: it is slightly difficult to gauge what specific results were achieved from this trial given that participants were judged to be responders or non-responders at 4 weeks based on some fairly nebulous criteria. So for example, responders signified "a resolution of CFS symptoms (sleep deprivation, lethary/fatigue)" but without the paper actually saying how these outcomes were measured or what tools were used. I'd hazard a guess that it was a case of participant interview or questionnaire but I can't confirm this. On the basis of this responder / non-responder coding, 35 (58%) were judged responders to bacteriotherapy. This figure improved when initial non-responders (n=15) were given a second TC infusion "followed by rectal infusion (n=4) or an oral course of cultured bacteria (n=6)"; up to 42 / 60 (70%) responders.Gastrointestinal (GI) symptoms were reported to be resolved in 37 of the 42 final responders.Follow-up of participants some 15-20 years later (12 of the original cohort) suggested that over half of them remained free of their CFS symptoms; although importantly, some relapsed (5/12) between 18-36 months post-bacteriotherapy.I probably don't need to highlight the fact that this was very much an observational case-series study over anything like a clinical trial. My initial excitement at reading this paper was very slightly dampened by the way results were reported and those all-important missing details regarding how the authors measured change over the period of baseline vs. bacteriotherapy. Even the reported resolution of GI symptoms leaves me asking questions like: what GI symptoms, how were they measured and who did the measuring? There are gaps in this work, make no mistake of that. Bear however in mind issues such as when this study was initially carried out and how the diagnostic criteria of CFS might not necessarily have been as well-defined as they are today. Just sayin.I can also imagine some people are reading this post and thinking what the .... ! How can a condition like CFS be sensitive to a bacterial transplant, and what about those methods used to introduce such a therapy... yeah right. Bear in mind however that our nether regions are actually quite good routes of drug administration bypassing for example, hostile environments like the stomach and onward the first-pass effect. Indeed the question should be: would you prefer this to the insertion of a naso-gastric tube as is the other option when delivering bacteria to where it is needed? Your choice...Having said all that I am still interested in this line of inquiry. The authors for example, suggest a possible link between "the resolution of gastrointestinal and CFS symptoms" and how this "supports the theory of a possible gastrointestinal-associated etiology, potentially arising from alterations to the bowel flora". I kinda speculated about the many faces (Man-E-Faces?) of CFS in a previous post on HERVs and ME (see here) and how the spectrum of CFS/ME might be just that, a spectrum. It strikes me that one could very easily investigate this possible sub-types issue within a well-defined population.There is obviously more to do in this area of endeavour. As per ... Read more »
Thomas Borody, Anna Nowak, & Sarah Finlayson. (2012) The GI microbiome and its role in Chronic Fatigue Syndrome: A summary of bacteriotherapy. Journal of the Australasian College of Nutritional and Environmental Medicine, 31(3). info:/
WARNING: Wall of text on the yummy neuroprotective effect of ketosis from a molecular neuroscience point of view. Proceed with caution. Remember when your high school biology teacher said that the brain absolutely NEEDS glucose to function? Well, that’s not entirely true. Under severe carbohydrate restriction, the brain can adapt and start burning ketones as [...]... Read more »
Hallböök T, Ji S, Maudsley S, & Martin B. (2012) The effects of the ketogenic diet on behavior and cognition. Epilepsy research, 100(3), 304-9. PMID: 21872440
Ruskin DN, Ross JL, Kawamura M Jr, Ruiz TL, Geiger JD, & Masino SA. (2011) A ketogenic diet delays weight loss and does not impair working memory or motor function in the R6/2 1J mouse model of Huntington's disease. Physiology , 103(5), 501-7. PMID: 21501628
Krikorian R, Shidler MD, Dangelo K, Couch SC, Benoit SC, & Clegg DJ. (2012) Dietary ketosis enhances memory in mild cognitive impairment. Neurobiology of aging, 33(2), 2147483647-27. PMID: 21130529
Denke, M. (2001) Metabolic effects of high-protein, low-carbohydrate diets. The American Journal of Cardiology, 88(1), 59-61. DOI: 10.1016/S0002-9149(01)01586-7
Researchers at UPENN have provided evidence for muscle regulation of sleep in a simple model organism; the roundworm. Whether this has any replicational potential in mammalian species remains unknown, but I definitely think it will be a hott topic in research (and the media)... Read more »
Driver, R., Lamb, A., Wyner, A., & Raizen, D. (2013) DAF-16/FOXO Regulates Homeostasis of Essential Sleep-like Behavior during Larval Transitions in C. elegans. Current Biology, 23(6), 501-506. DOI: 10.1016/j.cub.2013.02.009
The Pain of CrossFit WODs The agony of a CrossFit WOD may be worse than the agony of any other sport. There are many little voices to that big voiceThe post CrossFit WOD 13.4: Vitamin C may help reduce WOD pain. appeared first on WODMasters Stiff Competition.... Read more »
Huck CJ, Johnston CS, Beezhold BL, & Swan PD. (2013) Vitamin C status and perception of effort during exercise in obese adults adhering to a calorie-reduced diet. Nutrition (Burbank, Los Angeles County, Calif.), 29(1), 42-5. PMID: 22677357
A new study, done by scientists at The University of Nottingham, however, has found no link between the ‘measured’ level of noise from small and micro wind turbines and reports of ill health.... Read more »
Taylor, J., Eastwick, C., Lawrence, C., & Wilson, R. (2013) Noise levels and noise perception from small and micro wind turbines. Renewable Energy, 120-127. DOI: 10.1016/j.renene.2012.11.031
Taylor, J., Eastwick, C., Wilson, R., & Lawrence, C. (2013) The influence of negative oriented personality traits on the effects of wind turbine noise. Personality and Individual Differences, 54(3), 338-343. DOI: 10.1016/j.paid.2012.09.018
In the comments to what I wrote yesterday about seizures and a study comparing lorazepam (Ativan), diazepam (Valium), and placebo, Brooks Walsh had the following comment –
"Although I’ve read the study before, I am only wondering now how the IRB for Alldredge 2001 thought there was 'equipoise' between placebo and benzos."... Read more »
Alldredge BK, Gelb AM, Isaacs SM, Corry MD, Allen F, Ulrich S, Gottwald MD, O’Neil N, Neuhaus JM, Segal MR, Lowenstein DH. (2001) A Comparison of Lorazepam, Diazepam, and Placebo for the Treatment of Out-of-Hospital Status Epilepticus. New England Journal of Medicine, 345(25), 1860-1860. DOI: 10.1056/NEJM200112203452521
Callaway, C. (2012) Questioning the Use of Epinephrine to Treat Cardiac Arrest. JAMA: The Journal of the American Medical Association, 307(11), 1198. DOI: 10.1001/jama.2012.313
Hagihara A, Hasegawa M, Abe T, Nagata T, Wakata Y, Miyazaki S. (2012) Prehospital Epinephrine Use and Survival Among Patients With Out-of-Hospital Cardiac Arrest. JAMA: The Journal of the American Medical Association, 307(11), 1161. DOI: 10.1001/jama.2012.294
It can be hard job for truck drivers to stay alert while working, so, as you can imagine, they like to consume coffee and energy drinks. But do these really help? A new study took the first step in proving they can.... Read more »
Sharwood LN, Elkington J, Meuleners L, Ivers R, Boufous S, & Stevenson M. (2013) Use of caffeinated substances and risk of crashes in long distance drivers of commercial vehicles: case-control study. BMJ (Clinical research ed.). PMID: 23511947
The paper by Emma Frans and colleagues* looking at autism risk across the generations is the focus of this post. Published in the journal JAMA Psychiatry alongside a provocative article by Andrea Roberts and colleagues** on maternal exposure to child abuse being "associated" with elevated risk for offspring autism (see here and here), the theme is transgenerational effects and quote: "that your father's and grandfather's lifestyle choices can affect you" as per some of media on this paper.Ο Κακός Εγγονός @ Wikipedia I'm not going to head too heavily into the Frans study because others have already discussed it far better than I ever could (see here and here). Indeed NHS Choices carries a particularly good run-down of the study which is well worth a read (see here).The main details were that based on an analysis of nearly 6000 cases of autism spectrum disorder (ASD) in Sweden, grandfathers who had fathered their daughter when aged 50 or above were 1.79 times more likely to have a grandchild diagnosed with autism than younger fathering grandfathers.If grandfathers fathered a son when aged 50 or above, they were 1.67 times more likely to have a grandchild diagnosed with autism (again compared to grandfathers having children when they were younger).The magic word 'epigenetics' is also mentioned to potentially account for results alongside the mutation side of things. I should also point out that Frans has published on similar things before with schizophrenia in mind***.I'm interested in studies like the current Frans one despite their reliance on association and relatively limited increased risk of autism. Interested because alongside the 'older dads and autism risk' research (see here), I have actually talked about grandparents and risk of autism and schizophrenia previously on this blog (see here) based partly on some interesting data derived from ALSPAC published by Jean Golding and colleagues**** (open-access) and also that 2011 Frans study. In particular was the emphasis on the Golding 3M - meiotic mismatch methylation - hypothesis used to account for their results on grandmother's age as potentially being relevant to grandchild autism risk (please read the Golding article for more information on 3M complete with nice diagram).I know it might sound a little far-fetched that the lives of our grandparents might so profoundly be able to affect the lives of subsequent generations but before we put this down to mere coincidence, let me draw your attention to some work that was done on a dark period of quite recent history: the Hongerwinter. The basics: the Dutch famine of 1944, where a Nazi blockade led to the deaths of thousands. As per the often cruel twists of fate, science actually learned something from the suffering of the Dutch people in these dark days. Not only the confirmation that wheat was tied into coeliac (celiac) disease but also the suggestion that famine exposure during a critical period of gestation *might* potentially affect offspring physical and mental health. I've kinda talked about something similar before with 'thin-fat bodies' and David Barker in mind (see here).Granted in the current Frans study we are heading back even further through the germline as potentially hosting some effect, but to all intents and purposes, the theory is the same as per the intergenerational effects noted in other conditions like depression*****. I suppose one could ask whether specific types of autism might be more related to this grandparental age hypothesis over others. So for example, older grandparents at time of fathering or mothering impacting on the genome of their offspring - themselves then expressing certain traits associated with autism or the broader phenotype (not necessarily hitting the diagnostic threshold) - which are then transmitted (amplified?) to the next generation. Perhaps even some link to things like assortative mating theory too? I'm not saying that this is the only scenario and such 'transmission' works on its own to elevate risk of an autism diagnosis but the theory is an interesting one; even more so if we assume for example, that the autism and schizophrenia spectrums might not necessarily be poles apart (see here).By the same token one might also extend such a hypothesis to include other variables other than just parental age at offspring conception. The availability of and exposure to certain food in these 'olden days', exposure events to pollutants, pharmaceuticals (yes, we did have them then) or lifestyle factors such as smoking and drinking habits, various psychological and somatic stressors; the list is seemingly endless. In at least some of these factors, there are subtle clues to potential future directions for autism research and beyond already being examined (see here and here). Assuming also that epigenetics might be tied into all of this, we also open up the concept of epigenetic reprogramming of the germline as per the very interesting article by Petra Hajkova****** (open-access); something which I think might be/have been discussed at the recent Environmental Epigenetics symposium hosted by the MIND Institute.But let's not get too carried away with this area of inquiry or where it potentially leads in terms of the autism 'blame game'. Although I've not been able to find specific figures, I assume the actual numbers of grandfathers who fathered their children aged 50+ years is probably not going to be all that frequent if more current rates, at least here in the UK, are anything to go by (see this paper by Bray and colleagues*******). And then we have to wonder whether other variables might come into play such as the effect of paternal age at conception on birth factors such as birth weight or time of gestation even fecundity itself and how that might relate to autism risk.Such transgenerational effects whilst interesting, should also not detract research attention away from other more here-and-now possibilities which might affect autism risk as per the recent ... Read more »
Frans, E. (2013) Autism Risk Across GenerationsA Population-Based Study of Advancing Grandpaternal and Paternal AgeAutism Risk. JAMA Psychiatry, 1. DOI: 10.1001/jamapsychiatry.2013.1180
by Shelly Fan in Science of Eating Disorders
In my previous post, I looked at two hormones released during the cephalic phase (gastric secretion that occurs before food is eaten), ghrelin and obestatin, and how they may contribute to runaway eating behavior. Today I’m going to be looking at insulin release during chew and spit (CHSP), a fairly common symptom in eating disorders where the food is tasted, chewed and spit out. Insulin is a small peptide hormone that acts as a key regulator of metabolism; deregulation of insulin signalling plays a role in illnesses such as diabetes and metabolic syndrome. Some people have theorized that CHSP behavior may influence insulin regulation. In fact, there are a number of individuals stating on internet forums that chronic CHSP could lead to insulin resistance, potentially promoting diabetes. As interesting as these theories are, recent data have shown that they are probably not true.
INSULIN RELEASE DURING THE CEPHALIC RESPONSE
The taste of food activates the vagus nerve, a part of the peripheral nervous system that sends signals to the pancreas. In response, the pancreas releases insulin (as well as other …
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Teff KL, & Engelman K. (1996) Palatability and dietary restraint: effect on cephalic phase insulin release in women. Physiology , 60(2), 567-73. PMID: 8840920
Teff KL. (2011) How neural mediation of anticipatory and compensatory insulin release helps us tolerate food. Physiology , 103(1), 44-50. PMID: 21256146
Researchers at Moffitt Cancer Center just announced the results of a phase II clinical trial on patients with with higher-risk myelodysplastic syndrome (MDS), chronic myelomonocytic leukaemia, or acute myeloid leukaemia arising from MDS, who had previously failed to respond to conventional treatment (azanucleosides). Purpose of the trial was to assess the safety and efficacy of dasatinib in treating these conditions. The researchers say that although the drug won't help all patients, it does help the ones with the trisomy 8 chromosomal disorder.Full Story... Read more »
Duong, V., Jaglal, M., Zhang, L., Kale, V., Lancet, J., Komrokji, R., & List, A. (2013) Phase II pilot study of oral dasatinib in patients with higher-risk myelodysplastic syndrome (MDS) who failed conventional therapy. Leukemia Research, 37(3), 300-304. DOI: 10.1016/j.leukres.2012.11.001
CrossFit Games Competition and New Research. There have been several new papers out on recovery from repeated sets of resistance exercise. These may be important for people headed to theThe post CrossFit Games Competition: Recovery between WODs appeared first on WODMasters Stiff Competition.... Read more »
Bacon NT, Wingo JE, Richardson MT, Ryan GA, Pangallo TC, & Bishop PA. (2012) Effect of two recovery methods on repeated closed-handed and open-handed weight-assisted pull-ups. Journal of strength and conditioning research / National Strength , 26(5), 1348-52. PMID: 22516908
If you ever find yourself working in an infectious disease laboratory, whether it’s of the diagnostic or research variety, the overarching goal is not to put any microbes in your eye, an open wound or your mouth. Easy enough, right? Wear gloves, maybe goggles, work in fume hoods and don’t mouth pipette. When working with pathogenic bacteria and viruses, priority number one is Do Not Self-Inoculate.
Today our manual pipettes are rather sophisticated, plastic-y devices perfectly calibrated for moving precisely exact milliliters, microliters and picoliters of valuable solution from one vessel to another, whether it's of a urine sample, some spare radioactive material you have lying about or toxic solvents. But before the development of cheap mechanical pipettes in the '70s, using your mouth to pipette solutions was more than a common sight, it was a way of the lab.... Read more »
HILL, N. (1999) Laboratory-acquired Infections: History, Incidence, Causes and Preventions, 4th edition. Eds. C. H. Collins and D. A. Kennedy. Butterworth Heinemann, Oxford 1999. Pp. 324. ISBN 0 7506 4023 5. Epidemiology and Infection, 123(1), 181-181. DOI: 10.1017/S0950268899002514
by amikulak in Daily Observations
Prevailing wisdom suggests that our genes remain largely fixed over time. But, an emerging field of research is beginning to prove this intuition wrong. Scientists are uncovering increasing evidence that ... Read more »
An estimated 1 in 50 US children aged between 6 - 17 years old present with an autism spectrum disorder (ASD). Attention-grabbing isn't it?Today's post is based on the source of that soundbite, the publication by Stephen Blumberg and colleagues* (open-access) describing results from data mining of the 2007 and 2011-2012 US National Survey of Children's Health (NSCH) relevant to the numbers of cases of ASD.Testing 1, 2, 3 @ Wikipedia The autism-numbers game is something that has been discussed previously on this blog; most recently with the CDC 1 in 88 estimate in mind (see here) and the even more recent data from New Jersey (see here). The direction of the figures seems only one way - up - but the reason(s) for the increase still remain the source of discussion.The Blumberg report is open-access, but a few pointers might be useful:Based on 91,642 telephone interviews in 2007 and 95,677 interviews between 2011-2012, parental reports of receipt of an ASD diagnosis (autism, Asperger syndrome, PDD) in offspring were noted, alongside other variables such as age of the child, severity of presentation (mild, moderate, severe) and aged when first diagnosed.Actually in the age range 6-17 years old, data were collected from 63,967 interviews (2007) and 65,556 (2011-2012).Results: "based on parental reports, the prevalence of diagnosed ASD in 2011-2012 was estimated to be 2.00% for children aged 6-17". This compared with 1.16% or 1 in 86 for 6-17 year olds in 2007.The increase in prevalence was noted across the age ranges when they were sub-categorised and perhaps not surprisingly, there was a greater increase in prevalence in boys (2007: 1.8% vs. 2011-2012: 3.23%) than girls (2007: 0.49% vs. 2011-2012: 0.70%). Reported severity also shifted between the various data points (and age ranges) indicating that there was a trend towards less severe presentation (milder ASD) post 2008 diagnosis.The authors were able to some degree, rule out "survey-based measurement error" as being a major contributor to the prevalence increase and there is some discussion about the data not necessarily reflecting "factors that exist prior to or occur just after birth". Indeed the authors very firmly suggest that the changes are a consequence of either "recognition of ASD by health professionals or survey-based measurement changes over time". They also conclude that increases in the prevalence of parent-reported ASD especially for children aged 6-13 "was the result of diagnoses of children with previously unrecognized ASD".As per the report on this story in USA Today "15% to 20% of children who were once diagnosed with autism no longer have the condition". Which raises similar questions as to that of the Fein study on 'outgrowing autism' and 'optimal outcomes' which created so many column inches recently (see here and here).Bearing in mind that this was a prevalence study not an incidence study (see here for the difference) and issues with regards to response rates (2007: 46.7% vs. 2011-2012: 23.0%), and the sole reliance on parental judgement of variables like severity, the data being presented are indeed stark.That the rates of autism have seen an inordinate shift from what was once considered a rare condition to something which theoretically should appear in every school classroom at least once is an eye-opener. As mentioned, the debates rumble on about factors such as better awareness of autism, better case ascertainment, diagnostic switching and broadening, etc. as being the source of the increase. A real increase in cases? Hardly a mention in this latest data. The implication that for example our screening methods and skilled professionals have been able to miss or mis-diagnoses a staggering number of children presenting with an ASD is truly mind-boggling and worthy of an inquiry or two in the US and beyond. Indeed better be quick with that investigation with the DSM-V revision deadline fast approaching and the potential impact that might have on the autism numbers game (including adult numbers**).So 1 in 50 children with an ASD. What happens next? Sure, many children were described as falling into the mild and moderate ability ranges but as I've said before, terms like 'high-functioning' don't necessarily mean 'can function' with regards to daily living skills, quality of life and onwards translating into positive outcomes in adulthood. Certainly society has to play its role in helping people with autism reach their potential (I have a post scheduled on job interviews and autism coming up soon) and changes are indeed on-going (e.g. the implementation of the Autism Act here in the UK). But let's not be too proud of the achievements done in this area, as still many people on the autism spectrum, their families and concerned others have to fight daily for appropriate recognition, provisions and services.Another important issue also springs to my mind on the basis of the new prevalence figure. Comorbidity, of which autism is by no means immune from, are not mentioned. The realisation that autism is often very much more than the sum of its triad - soon to be dyad - in terms of comorbidity must surely factor into the potential impact of the latest figures. Not least because of the quite startling health inequalities which seem to be present when an ASD is diagnosed and how as was very recently detailed in the CIPOLD report, such inequality can in some cases, have the most profound and far-reaching effects. I'm not trying to scare anyone; just sayin' that we need to be mindful of the whole person not just their autism.----------* Blumberg SJ. et al. Changes in prevalence of parent-reported autism spectrum disorder in school-aged U.S. children: 2007 to 2011–2012. National Health Statistics Reports. 2013: 65.** Wilson CE. et al. Comparison of ICD-10R, DSM-IV-TR and DSM-5 in an adult autism spectrum disorder diagnostic clinic. J Autism Dev Disord. March 2013.----------... Read more »
Wilson, C., Gillan, N., Spain, D., Robertson, D., Roberts, G., Murphy, C., Maltezos, S., Zinkstok, J., Johnston, K., Dardani, C.... (2013) Comparison of ICD-10R, DSM-IV-TR and DSM-5 in an Adult Autism Spectrum Disorder Diagnostic Clinic. Journal of Autism and Developmental Disorders. DOI: 10.1007/s10803-013-1799-6
Tumours develop a chaotic system of blood vessels to raid the body’s normal blood supply. Some of the latest anti-cancer drugs (Vascular Disrupting Agents) work by damaging these vessels: the tumour is then denied access to nutrients essential for its growth. However, to reveal the extent to which such therapies actually conquer the tumour we need to measure blood flow in the tumour vessels.... Read more »
Brunker J, & Beard P. (2012) Pulsed photoacoustic Doppler flowmetry using time-domain cross-correlation: accuracy, resolution and scalability. The Journal of the Acoustical Society of America, 132(3), 1780-91. PMID: 22978905
Religions tend to evolve and adapt to benefit a society the most. The first religion can be uncovered from ancient anthropomorphic sculptures 42,000 years ago.... Read more »
WU Fei-fei,JIN Li-ji,LI Xiao-yu,LI Hua-qiang,CAO Zhen-hui,YOU Jian-song,XU Yong-ping(Ministry of Education Center for Food Safety of Animal Origin,College of Life Science and Technology, Dalian University of Technology,Dalian 116024,China). (2012) Research progress in active ingredients and pharmacological effects of deer antler. Chinese Journal. info:/
Q: Why don’t I write much about nutrition? A: I barely believe anything I read about it. After spending the last decade with my head in the ‘health and fitness’ industry, I’ve developed a healthy skepticism – literally. It’s probably because I’ve seen so many fads come and go, myths busted, and contradictory research. Now, I take most of what I read with a grain of salt – and I’m probably healthier because of it.
Here’s why:... Read more »
Bjelakovic G, Nikolova D, Gluud LL, Simonetti RG, & Gluud C. (2012) Antioxidant supplements for prevention of mortality in healthy participants and patients with various diseases. Cochrane database of systematic reviews (Online). PMID: 22419320
Smith-Spangler C, Brandeau ML, Hunter GE, Bavinger JC, Pearson M, Eschbach PJ, Sundaram V, Liu H, Schirmer P, Stave C.... (2012) Are organic foods safer or healthier than conventional alternatives?: a systematic review. Annals of internal medicine, 157(5), 348-66. PMID: 22944875
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