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  • May 17, 2017
  • 01:00 PM

Epigenetic Marks Associated to Severe Obesity

by Delphine Fradin in EpiBeat

There is growing evidence that DNA methylation might contribute to obesity. Candidate gene methylation studies in animal models and humans have demonstrated methylation changes in promoters of various genes that are implicated in obesity, appetite control and/or metabolism, insulin signaling, immunity, growth and circadian clock regulation.

Severe obesity in children is defined as greater than or equal to 99th percentile of body mass index (BMI) for age and gender or a BMI z-score ≥3.5. Population surveys demonstrate a significant increase in obesity prevalence among children, where severe obesity is the most rapidly growing paediatric obesity subgroup. Compared to youth with BMI in the obese range, those with severe obesity have higher rates of immediate and long-term diseases. It stands to reason that youth with obesity and severe obesity may also differ in aetiological factors and consequences, including epigenetic.... Read more »

Fradin, D., Boëlle, P., Belot, M., Lachaux, F., Tost, J., Besse, C., Deleuze, J., De Filippo, G., & Bougnères, P. (2017) Genome-Wide Methylation Analysis Identifies Specific Epigenetic Marks In Severely Obese Children. Scientific Reports, 46311. DOI: 10.1038/srep46311  

  • May 17, 2017
  • 03:48 AM

EEG abnormalities and "high functioning" autism

by Paul Whiteley in Questioning Answers

I'm not a great fan of the term 'functioning' when it comes to autism (see here) hence the quote marks around high-functioning in the title of this post. Yes, I understand the message that it's trying to convey and that we don't have viable alternatives at the moment. It just however seems a little sweeping in terms of 'generalised' describing and labelling of people...No mind. Today I'd like to bring the paper by Özdem Ertürk Çetin and colleagues [1] to your attention and the observation that their results "support the fact that EEG abnormalities are observed at a higher rate also in ASD [autism spectrum disorder] with a better functionality." EEG - electroencephalographic or electroencephalogram - refers to the recording of electrical activity in the brain. Although in small amounts, our cells use electrical signals to message each other; said activity in the brain can be picked up and recorded using some rather sensitive equipment. EEGs are the method of choice when it comes to investigating epilepsy or related seizure disorders (such conditions are epitomised by abnormal electrical activity between cells).The connection between autism and epilepsy / seizure disorder is one that has persisted for many years (see here); even now to the point where research is starting to talk about autism / autistic traits being a feature of some cases of epilepsy (see here). Quite a bit of the research looking at autism and epilepsy has tended to suggest that epilepsy may be a little more over-represented for those towards the more severe end of the autism spectrum (i.e. in relation to presentation of symptoms and the presence of some degree of learning / intellectual disability). The Ertürk Çetin findings report that even in those with described 'better functionality' there may be disturbances in relation to the measurement of EEGs.Looking for "the presence of EEG abnormalities in sixteen children diagnosed with high-functioning ASD" researchers reported that whilst none of the participants had clinical seizures (the overt expression of epilepsy) "5 patients (31.3%) were detected to have EEG abnormalities." Bearing in mind the quite small participant numbers and the fact that no control groups (asymptomatic or otherwise) were included for comparisons, this is quite an important finding. I agree with the authors when they say that: "The potential impact of EEG abnormalities on cognition and behavior, and the risk of epilepsy should be considered during long-term follow-up of these patients." In other words, whenever a diagnosis of autism or ASD is received, one should always consider the possibility that a heightened risk of epilepsy / seizure / abnormal EEG patterns might also be a feature of presentation irrespective of "functioning" status.----------[1] Ertürk Çetin Ö. et al. EEG abnormalities and long term seizure outcome in high functioning autism. Acta Neurol Belg. 2017 Apr 26.----------Ertürk Çetin Ö, Korkmaz B, Alev G, & Demirbilek V (2017). EEG abnormalities and long term seizure outcome in high functioning autism. Acta neurologica Belgica PMID: 28447214... Read more »

  • May 16, 2017
  • 11:15 AM

Fatal Attraction: Praying Mantises (A Guest Post)

by Miss Behavior in The Scorpion and the Frog

By Britta Bibbo We all know the character: an incredibly beautiful woman that seduces the rough-and-tumble action hero, only for him to later find himself chained up over a lava pit with sharks in it! …Or something like that. A “femme fatal” is the idea of a beautiful woman who leads men to their demise. None are more perfect for this role than the female praying mantis. Praying mantis females practice the art of deception through sexual cannibalism. It’s exactly how it sounds: the male is attracted to the female and tries to make some babies, but instead ends up being devoured. Sexual cannibalism hardly seems like a good strategy for keeping the mantis population up, but some argue it’s merely females taking advantage of every scrap of food they can find… even if it’s a loving male. False garden mantis (Pseudomantis albofimbriata). Image by Donald Hobern from Wikimedia Commons.When male mantises encounter a female in the wild they only have one thing on the brain, while a female may be more interested in self-preservation. If she hasn’t encountered food for a few days she will be VERY hungry and not all that interested in mating; in many species of mantises it is known that female mantises will eat males, even while having sex! So how do female mantises attract males? For most insects, females are able to attract males with pheromones, chemicals released from an individual that affect other individuals of the same species. For instance, females can emit pheromones that will be telling of their age, reproductive status, and body condition. Males are able to detect pheromones from great distances and these pheromones play a role in allowing a male to determine how attractive a female could be. Before any sexy time can begin, females have to show that they are open to male advances. Showing a male you’ve never met before that you’re interested can be a difficult task- so females typically emit pheromones that are known as honest signals. These signals accurately convey female interest in mating, as well as her reproductive status, age, and body condition. Because the majority of females are being honest, males don’t have to think twice about their mate’s intentions. This is where female deception comes into play. If a female takes advantage of the lack of male wariness, she could end up with an easy meal. This deception by the females is what scientists know as the Femme Fatale hypothesis. This hypothesis explains that female mantises are naturally selected to deceive male mantises, and exploit them as food. This idea hasn’t had much backing evidence until Dr. Kate Barry of Macquarie University in Sydney, Australia sought to test this hypothesis with the false garden mantis (Pseudomantis albofimbriata). After considering the test subjects and how the mantises communicate, Kate expected one of three possible outcomes: 1. There will be no pattern between female hunger and male attraction (if female false garden mantises are not femme fatales and false garden mantis pheromones do not communicate feeding-related information). 2. The well-fed females will attract the most males, while hungry females will attract the fewest males (if female false garden mantises are not femme fatales and females are always honest about their quality and willingness to mate). 3. The hungriest females will attract the most males, while well-fed females will still attract some males (if female false garden mantises are femme fatales and females are dishonest about their quality and willingness to mate when they are hungry). To test her expectations, Kate gathered juvenile mantises that were close to their adult forms to have many male and female mantises that have no previous mating experience. Once the mantises were adults, females were given different feeding regimens to have a range of hunger. Categories included Good (well-fed), Medium (slightly less fed), Poor (hungry), and Very Poor (very, very hungry). Adult mantises were housed in a circular cage that separated each female individually around the edge, while the males were kept in the center. Diagram of cage experiment was conducted in. Image by Britta Bibbo.To allow the males to smell the female pheromones, researchers separated males by special walls that the males could not see through, but could still detect the pheromones given off by a female. The number of males on a female’s side of the cage was used to measure how attractive her pheromones were to the males. The results of this study concluded that pheromones produced by the females that were very hungry were the most attractive to males. Through deception, the hungriest females are seen as sexier than well-fed, healthy females that are willing to mate! This result is surprising; normally females that are well-fed are seen as “sexier” because they have more nutrients available to them, making them more fertile. Hungry females have fewer nutrients available to them, making them less fertile, and therefore not as “sexy”. These hungry female mantises are advertising themselves as well-fed, fertile, and ready to rock when really, they’re not. Simply put, these results show that males are being catfished, and then consumed. Whether hungry females are actively trying to deceive males or if it’s just coincidental still needs to be looked into, but for now, be thankful for a partner who will see you as more than just a piece of meat! Literature Cited:Barry, K. (2014). Sexual deception in a cannibalistic mating system? Testing the Femme Fatale hypothesis Proceedings of the Royal Society B: Biological Sciences, 282 (1800), 20141428-20141428 DOI: 10.1098/rspb.2014.1428 ... Read more »

  • May 16, 2017
  • 06:02 AM

IMFAR, the autism numbers game and 12% showing 'optimal outcome'

by Paul Whiteley in Questioning Answers

A post recently published on the Spectrum website led to my blogging entry today, and the observation that: 'Alternative screen finds high autism prevalence in U.S. state'.Discussing results delivered at IMFAR 2017 the research in question was that presented by Laura Carpenter and colleagues [1] (someone with quite a track record in autism research). This was a conference presentation and seemingly not yet peer-reviewed publication, so one needs to be a little cautious about making big claims just yet. That being said, there have been research hints that these results would be forthcoming [2] around this time.The headline finding was that the prevalence of autism spectrum disorder (ASD) in one particular part of the United States for the birth year 2004 was probably quite a bit higher than that previously reported/estimated based on initial screening for possible ASD and then actual assessment. Details of the initiative used in this research - the South Carolina Children’s Educational Surveillance Study (SUCCESS) - can be found here.Some 4100 children were "screened for ASD using the Social Communication Questionnaire." Those who were deemed 'at risk' for autism and a small proportion of those not hitting those *might be autism* thresholds were asked back for a more detailed interview. Although the number of children actually followed-up and interviewed who were eligible for further assessment was not particularly great, the authors were able to draw up an estimated prevalence of autism based on those who did complete the study. The figure: "ASD prevalence in this sample is 3.62%" roughly equivalent to 1 in 28 children. I say this in the context that in the United States and elsewhere, autism rates and/or numbers of cases are still high (see here and see here) and acknowledgement of the implications of such increases when it comes to services such as education, healthcare and the like.The Spectrum article focuses quite a bit on the participation rate noted in the Carpenter study but another snippet of information is also included in the conference abstract that is worthy of discussion. A detail that reads: "Six children (6/52; 12%) had a clear developmental history of ASD but did not display clinically significant symptoms at the time of participation in this study." Further: "12% with a history of ASD no longer had significant ASD-related symptoms, providing further support for the potential for optimal outcomes in some individuals."I'm rather interested in that 12% figure with 'optimal outcome'. Optimal outcome describes cases where a clear indication/diagnosis of autism has been seen/received, but for whatever reason(s) diagnostic thresholds are not longer met at a future assessment point. I've covered this group quite a few times on this blog, most notably in relation to a previous estimate of 9% of those diagnosed with autism potentially falling into this category (see here). Appreciating that such data challenges the assumption that *all* autism is a lifelong condition (indeed, stretching across the entire autism spectrum - see here), I'd reiterate that those described as being 'optimal outcomers' represent an important subgroup on the autism spectrum in these days of plural autisms (see here). Not least is the question: Why? Why do these children not maintain their diagnosis and what lessons (if any) can be learned for the wider autism spectrum, particularly also in the context that various quite disabling comorbidities might also be 'reduced' alongside core autism symptoms in this group.We await formal peer-reviewed publication of the Carpenter findings and perhaps some further details.To close, upon introducing my brood to the music of Kate Bush, I am yet again reminded just how good a singer/performer she really is...----------[1] Carpenter LA. et al. The Prevalence of Autism Spectrum Disorder in School Aged Children: Population Based Screening and Direct Assessment. IMFAR 2017.[2] Carpenter LA. et al. Screening and direct assessment methodology to determine the prevalence of autism spectrum disorders. Ann Epidemiol. 2016 Jun;26(6):395-400.----------Carpenter LA, Boan AD, Wahlquist AE, Cohen A, Charles J, Jenner W, & Bradley CC (2016). Screening and direct assessment methodology to determine the prevalence of autism spectrum disorders. Annals of epidemiology, 26 (6), 395-400 PMID: 27230493... Read more »

Carpenter LA, Boan AD, Wahlquist AE, Cohen A, Charles J, Jenner W, & Bradley CC. (2016) Screening and direct assessment methodology to determine the prevalence of autism spectrum disorders. Annals of epidemiology, 26(6), 395-400. PMID: 27230493  

  • May 15, 2017
  • 05:33 AM

Intestinal dysbiosis, irritable bowel syndrome and ME/CFS

by Paul Whiteley in Questioning Answers

I don't want to spend too much time talking about yet another paper from the research tag-team that is Hornig & Lipkin [1] (open-access) on the topic of myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS). But this latest addition to their research repertoire (see here) is deserving of several comments.Not least are the observations made by the authors - including one Brent Williams who some might remember from autism research history (see here) and Jose Montoya who has also made a mark in CFS/ME research circles (see here) - on how the collected wee beasties that inhabit our gastrointestinal (GI) tract might have some role to play when it comes to at least some cases of CFS/ME. Yes it's gut microbiome research time again.The press release accompanying the paper by Dorottya Nagy-Szakal and colleagues can be seen here. The long-and-short of it was that: "Independent of IBS [irritable bowel syndrome], ME/CFS is associated with dysbiosis and distinct bacterial metabolic disturbances that may influence disease severity." Further: "Plasma cytokines did not define ME/CFS disease groups in our cohort." There could be some good reasons for that last sentence looking at immune-related molecules on the basis of other study results (see here) but further investigations are required.I have to say that outside of the observations that particular types of bacteria seem to be more or less prevalent in cases of CFS/ME (yet again) I was rather more interested in the finding that over 40% of the cohort also met criteria for IBS. I say that on the basis that I've already talked about 'abdominal discomfort syndrome' as a feature of some CFS/ME (see here) alongside findings that certain foods *might* also play a role in the bowel symptoms accompanying CFS/ME (see here).In these days of increasing pluralisation of spectrums (the autisms, the schizophrenias, etc) it is probably also quite useful to think about pluralising the diagnostic label CFS/ME too. Assuming we can get the diagnostic criteria right (see here) we could have a phenotype of CFS/ME that, for example, has a stronger bowel-related clinical signature than other forms. The further implications that the GI tract might play a role in CFS/ME in relation to either primary or secondary symptoms might also inform intervention. So, we kinda know that use of probiotics might be something to think about for some cases of IBS (see here). There is also some preliminary evidence that certain probiotics might also impact on some of the 'psychological' features (careful with that term) which can accompany CFS/ME [2]. The possibility of connections exist and therefore require further scientific exploration.----------[1] Nagy-Szakal D. et al. Fecal metagenomic profiles in subgroups of patients with myalgic encephalomyelitis/chronic fatigue syndrome. Microbiome. 2017; 5: 44.[2] Rao AV. et al. A randomized, double-blind, placebo-controlled pilot study of a probiotic in emotional symptoms of chronic fatigue syndrome. Gut Pathog. 2009 Mar 19;1(1):6.----------Nagy-Szakal D, Williams BL, Mishra N, Che X, Lee B, Bateman L, Klimas NG, Komaroff AL, Levine S, Montoya JG, Peterson DL, Ramanan D, Jain K, Eddy ML, Hornig M, & Lipkin WI (2017). Fecal metagenomic profiles in subgroups of patients with myalgic encephalomyelitis/chronic fatigue syndrome. Microbiome, 5 (1) PMID: 28441964... Read more »

Nagy-Szakal D, Williams BL, Mishra N, Che X, Lee B, Bateman L, Klimas NG, Komaroff AL, Levine S, Montoya JG.... (2017) Fecal metagenomic profiles in subgroups of patients with myalgic encephalomyelitis/chronic fatigue syndrome. Microbiome, 5(1), 44. PMID: 28441964  

  • May 13, 2017
  • 05:42 AM

Welcoming zonulin into autism research

by Paul Whiteley in Questioning Answers

I was VERY happy to read the paper published by Erman Esnafoglu and colleagues [1] suggesting that: "zonulin, which regulates intestinal permeability, plays a role in the development of symptoms of ASD [autism spectrum disorder]."Zonulin - something that "can be used as a biomarker of impaired gut barrier function for several autoimmune, neurodegenerative, and tumoral diseases" [2] - is a compound that I've been interested in for a while on this and other blogs (see here). The primary reason for the interest is that connection to intestinal permeability and how 'leaky gut' may well show some relevance to some autism (see here and see here). The thing that was up-to-now missing from the research chatter about intestinal hyperpermeability and autism was the measurement of zonulin on the basis that elevated levels of zonulin show a connection to dietary elements such as gliadin (a facet of gluten) [3]. This is particularly relevant because previous data has observed a possible link between use of a gluten-free diet and a reduction in intestinal permeability in relation to autism [4]. All this is [peer-reviewed] research music to my ears (see here)...Esnafoglu et al set about measuring serum levels of zonulin in 32 participants diagnosed with an autism spectrum disorder (ASD) compared with 33 not-autism controls. Yet again, the words 'healthy controls' are used by the authors to define the control group and yet again, the assumption is that those participants with autism are somehow 'unhealthy'. Researchers, please just call it what it is: not-autism controls (the term 'neurotypical' also tells us nothing about control groups either). Measurement of zonulin was via ELISA (enzyme-linked immunosorbent assay) and researchers also threw in a measure of autism severity based on use of the Childhood Autism Rating Scale (CARS).Results: well, the results seemed to be in the expected direction: "Serum zonulin levels were significantly higher in the patients with ASD (122.3 ± 98.46 ng/mL) compared with the healthy controls (41.89 ± 45.83 ng/mL)." Authors also identified a fairly healthy correlation between the CARS score and zonulin levels. These results imply that issues with intestinal permeability - leaky gut - seem to be present in relation to at least some autism. A shocker, I know.Obviously there is more research to do in this area; not least to increase the sample size, look at dietary intake/status as a function of zonulin measurement and explore the possibility that the genetics of zonulin production might also be *involved* in some autism [5]. I might add that other research on zonulin in relation to diagnoses not necessarily uncommon to autism might also be revealing (see here).Insofar as what to do about elevations in zonulin as and when detected in cases of autism, well the dietary link to zonulin production implies that the horror that is a gluten-free (GF) diet might be something to consider. The suggestion of a 'bacterial link' to zonulin production also suggests another possible intervention target in these days of gut microbiomes and autism (see here) although I think we have to be slightly careful about the use of some preparations. There is also another avenue for research speculation based on the development of zonulin (receptor) inhibitors such as Larazotide acetate [6] (otherwise known as AT-1001). With no medical or clinical advice given or intended, the evidence base for this zonulin-affecting compound is looking promising [7] with much more to come...In conclusion, zonulin has arrived on the autism research scene, and I'm expecting to see more peer-reviewed science on this topic in future times. Intestinal hyperpermeability, diet and [some] autism looks to be squarely back on the research agenda.----------[1] Esnafoglu E. et al. Increased Serum Zonulin Levels as an Intestinal Permeability Marker in Autistic Subjects. J Pediatrics. 2017. May 11.[2] Fasano A. Zonulin, regulation of tight junctions, and autoimmune diseases. Annals of the New York Academy of Sciences. 2012; 1258(1) :25-33.[3] Lammers KM. et al. Gliadin induces an increase in intestinal permeability and zonulin release by binding to the chemokine receptor CXCR3. Gastroenterology. 2008 Jul;135(1):194-204.e3.[4] de Magistris L. et al. Alterations of the intestinal barrier in patients with autism spectrum disorders and in their first-degree relatives. J Pediatr Gastroenterol Nutr. 2010 Oct;51(4):418-24.[5] Tripathi A. et al. Identification of human zonulin, a physiological modulator of tight junctions, as prehaptoglobin-2. Proc Natl Acad Sci U S A. 2009 Sep 29;106(39):16799-804.[6] Fasano A. Intestinal Permeability and its Regulation by Zonulin: Diagnostic and Therapeutic Implications. Clinical gastroenterology and hepatology : the official clinical practice journal of the American Gastroenterological Association. 2012;10(10):1096-1100.[7] Leffler DA. et al. Larazotide Acetate for Persistent Symptoms of Celiac Disease Despite a Gluten-Free Diet: A Randomized Controlled Trial. Gastroenterology. 2015; 148: 1311-1319.----------Esnafoglu, E., Cırrık, S., Ayyıldız, S., Erdil, A., Ertürk, E., Daglı, A., & Noyan, T. (2017). Increased Serum Zonulin Levels as an Intestinal Permeability Marker in Autistic Subjects The Journal of Pediatrics DOI: 10.1016/j.jpeds.2017.04.004... Read more »

Esnafoglu, E., Cırrık, S., Ayyıldız, S., Erdil, A., Ertürk, E., Daglı, A., & Noyan, T. (2017) Increased Serum Zonulin Levels as an Intestinal Permeability Marker in Autistic Subjects. The Journal of Pediatrics. DOI: 10.1016/j.jpeds.2017.04.004  

  • May 12, 2017
  • 11:43 AM

A Cuttlefish Clash: The Strongest, Stripeyist Guy Gets the Girl

by Melissa Chernick in Science Storiented

I know what you’re thinking: “Why hasn’t she written about cuttlefish mating systems?” I understand, cuttlefish are ridiculously cool and you just need to know more about them. You are in luck as a brand new study has been published online about just that topic!Cuttlefish are cephalopods, which are all predatory marine animals that have at least eight arms, a siphon for jet-propulsion, and highly developed nervous and sensory systems (specifically the most sophisticated eye of all invertebrates). Those last characteristics make them highly intelligent, with complex learning behavior, to the point that many consider them to be “conscious.” Unlike other cephalopods, all of their hard parts (if any) are internal. That means all of their outside parts are soft, squishy and covered in color-changing skin. Their ability to change color is absolutely amazing, particularly in cuttlefish (just google ‘Flamboyant Cuttlefish’!). Located in their skin are tons of chromatophores (pigment filled bags) that expand or contract to reveal/hide their color. And it’s crazy-fast too. They can alter their appearance in as little as half a second! They use this color change for camouflage, courtship rituals, or just to show you how they feel about you interrupting them with your dive camera (a little personal experience with a mama octopus thrown in there).Cuttlefish are in the clade Coloidea that also includes squid and octopuses, and a sister group to the Nautilus. They look like squid but have stouter bodies and a fin fringe that runs around their body that they undulate to move. They have separate sexes and an often elaborate courtship ritual. Should a female find a male worthy, she accepts his spermatophore (sperm packet), which he transfers to her with a specially modified arm (hectocotylus). Then the females will use the contents of this packet to fertilize their eggs and lay them in clusters. Cuttlefish can be seasonal in their mating habits, with some species gathering in the hundreds to find their special someone. Where animals gather to mate, they also gather to strut their stuff. One of the ways they do this is through shear brawn. Basically, the strongest guy gets the girl. A study currently in press in The American Naturalist describes competition between male cuttlefish. Males compete vigorously for female mates. The researchers took a close look at the Common Cuttlefish (Sepia officinalis), a species “renowned for its visual capabilities, rapid adaptive camouflage, learning, and memory.” All those amazing qualities and yet oddly lacking in its ability to identify individual mates or rivals. Seriously, telling boy from girl is a challenge. This means that they must use a signal-response system to recognize each other. This system employs the use of intense zebra-stripe displays. Respond to a zebra with a zebra and you are male. If you don’t want to fight, darken your whole body (sign of alarm), ink and jet away. But extend your fourth arm, darken the skin around your eyes, and dilate your pupils and you know that shit is about to get real: inking, swiping, grappling, lunging, rolling, and biting. An all-out cuttlefish brawl.A lot of this information is known from lab studies of cuttlefish, but how do they act in their natural environment. To test this, the researchers went to the Aegean Sea near Çeşmealtı, Turkey and filmed a bunch of cuttlefish. They brought the footage back to the lab to analyze mate guarding and fighting behaviors, frequencies of a series of agnoistic behaviors in individual males, and aggressive behaviors (e.g., bar room brawl scenario). Since it all starts with the zebra stripes, they also compared the intensity between males. They found a generalized sequence of events that correlated to the amount of aggression. For example, just a dark ring around the eye is low-level aggression, adding a dilated pupil ramps it up to medium-level aggression, intensifying the zebra pattern and arching and tilting the body ramps it up even more. The more medium- to high-level aggressive behaviors the more likely the male was to win. The researchers summarize it this way: “weak zebra banding, fourth arm extension, dark eye ring > dark eye ring with dilated pupil, dark face, strong zebra banding, inking > intense zebra display > swiping, grappling > biting, rolling.” This makes sense if you think about it. Fighting may result in injury and injury is costly, sometimes fatal. So you need to make sure you can win. The series of stages allow each male to assess both themselves and their opponent to see if an actual brawl is worth it.Now, take what you’ve just learned and apply it to this video. It shows exactly the type of bout the authors describe. You may need to watch it twice, once to read the descriptions of what is going on and another to watch for the subtle differences described above. Can you see the color and eye changes? Just imagine what we will find out as camera systems get faster. Considering the extremely fast rate at which cuttlefish are able to change their colors, it is very likely that we are missing a lot of the more subtle details in communications between males (and probably with females too). We’ll have to revisit this subject in the future.Allen, J., Akkaynak, D., Schnell, A., & Hanlon, R. (2017). Dramatic Fighting by Male Cuttlefish for a Female Mate The American Naturalist DOI: 10.1086/692009Learn more about Cephalopods at the University of California Berkeley’s Museum of Palentology and the Monterey Bay AquariumImage from the Monterey Bay Aquarium... Read more »

Allen, J., Akkaynak, D., Schnell, A., & Hanlon, R. (2017) Dramatic Fighting by Male Cuttlefish for a Female Mate. The American Naturalist. DOI: 10.1086/692009  

  • May 12, 2017
  • 09:30 AM

Could Parasites Be Causing Prostate Cancer?

by Bill Sullivan in The 'Scope

New study shows that a common parasite called Toxoplasma gondii forms tissue cysts and causes inflammation in mouse prostates. ... Read more »

  • May 12, 2017
  • 08:00 AM

Friday Fellow: Spreading Earthmoss

by Piter Boll in Earthling Nature

by Piter Kehoma Boll If you still think mosses are uninteresting lifeforms, perhaps you will change your mind after knowing the spreading earthmoss, Physcomitrella patens. Found in temperate regions of the world, except for South America, but more commonly recorded in … Continue reading →... Read more »

Cove, D. (2005) The Moss Physcomitrella patens. Annual Review of Genetics, 39(1), 339-358. DOI: 10.1146/annurev.genet.39.073003.110214  

  • May 12, 2017
  • 04:02 AM

Physical exercise as a nootropic of choice

by Paul Whiteley in Questioning Answers

Nootropic, defined as a 'smart drug' or cognitive enhancer, is generally taken to mean a substance/compound/medicine that has some positive effect(s) on aspects of cognition. I've talked about the possibility that various compounds might fit this bill on this blog (see here for example) but today I'm discussing another quite important potential nootropic: exercise.It was the paper by Joseph Michael Northery and colleagues [1] (open-access) that added exercise to the nootropic categorisation on the premise of their meta-analysis results suggesting that "physical exercise interventions are effective in improving cognitive function in adults aged >50 years, regardless of cognitive status." As you can imagine, findings such as that tend to generate news headlines as per this one.Including the results of some 39 studies where exercise and cognition were included as watchwords and trials were of the randomised-controlled design, researchers set about analysing the collected data covering various types of exercise and various cognitive outcomes. Aside from some issues with various forms of bias, most prominently with regards to blinding(!), they concluded that various types of exercise seemed to positively impact on cognitive functions. Particularly notable were the positive effects on executive functions: "a set of cognitive processes responsible for the initiation and monitoring of goal-orientated behaviours" and aspects of memory via the use of resistance training (i.e. using weights). Other more aerobic exercise regimes also seemed to have positive effects on other aspects of cognition too. It seems some combination of aerobic and resistance exercise regimes might provide the best generalised advice according to the authors "of at least moderate intensity and at least 45 min per session, on as many days of the week as possible." Just going back to that resistance training - executive functioning link being proposed, I wonder whether there may be other investigations to be carried out here with specific labels in mind [2].Added to other research talking about 'exercise as medicine' (see here) and more particularly that exercise *might* have some important effects for aspects of psychological health and wellbeing (see here and see here for examples) there is a peer-reviewed, evidence-based picture emerging. It suggests that messages about moving more (see here) as being important for weight and BMI might be only the tip of iceberg.And although not for everyone, I'm minded to yet again extol the virtues of the martial arts which also might have some "positive effect on some aspects of cognition" [3] (even for those under 50 years old with middle-aged hips like mine)...----------[1] Northey JM. et al. Exercise interventions for cognitive function in adults older than 50: a systematic review with meta-analysis. Br J Sports Med. 2017. April 24.[2] Demetriou EA. et al. Autism spectrum disorders: a meta-analysis of executive function. Molecular Psychiatry. 2017. April 25.[3] Fabio RA. & Towey GE. Cognitive and personality factors in the regular practice of martial arts. J Sports Med Phys Fitness. 2017 May 5.----------Northey, J., Cherbuin, N., Pumpa, K., Smee, D., & Rattray, B. (2017). Exercise interventions for cognitive function in adults older than 50: a systematic review with meta-analysis British Journal of Sports Medicine DOI: 10.1136/bjsports-2016-096587... Read more »

  • May 11, 2017
  • 10:26 AM

Land snails on islands: fascinating diversity, worrying vulnerability

by Piter Boll in Earthling Nature

by Piter Kehoma Boll The class Gastropoda, which includes snails and slugs, is only beaten by the insects in number of species worldwide, having currently about 80 thousand described species. Among those, about 24 thousand live on land, where they are … Continue reading →... Read more »

  • May 11, 2017
  • 04:08 AM

Could an "ill-state" associated with anorexia nervosa mimic the symptoms of autism?

by Paul Whiteley in Questioning Answers

The question posed in the title of this post 'Could an "ill-state" associated with anorexia nervosa mimic the symptoms of autism?' stems from the findings reported by Heather Westwood and colleagues [1] (open-access).They continued a research theme looking at the potential 'overlap' when it comes to autism and eating disorders such as anorexia nervosa (AN) (see here). Notably, researchers questioned whether the finding that some 50% of their cohort "scored above the clinical cut-off on the ADOS-2" but "when developmental history was obtained, only 10% met diagnostic criteria for ASD [autism spectrum disorder]" could be due to "the ill-state associated with AN."The Westwood paper is open-access so doesn't need any further grand explanations from me. The research caveats alongside relying on quite a small cohort - "40 females aged between 12 and 18" - were that this was a snapshot study not a longitudinal one and whilst relying on data other than that just linked to the presence of autism traits, they did not control for things like social anxiety "which could lead to high scores on the ADOS-2." Interesting.On the question of whether 'active AN' (please pardon my lack of knowledge on this topic) might have the ability to 'provoke' autistic traits, I have to say that I'm quite intrigued. This might have a few, quite important, implications not least that (a) autistic traits can be 'acquired' as per what has been noted under other different circumstances (see here and see here for examples) and (b) the potential stability of said traits might not be particularly stable for everyone at every time (see here). On that last point, we do need a lot more data as to what happens/happened when AN is treated/managed or goes into remission for example and any subsequent impact on autistic traits.It's too early to start talking mechanisms when it comes to AN and autistic traits in light of this data alone. I might also venture into the idea that other comorbidities than can appear alongside AN might also have some impact on clinical presentation (see here) and are also in need to further investigation in the context of any eating disorders - autism correlation. Indeed, there are potentially lots of variables that need to be kept in mind (see here and see here) before any sweeping generalisation are made...----------[1] Westwood H. et al. Assessing ASD in Adolescent Females with Anorexia Nervosa using Clinical and Developmental Measures: a Preliminary Investigation. J Abnorm Child Psychol. 2017 Apr 17.----------Westwood, H., Mandy, W., Simic, M., & Tchanturia, K. (2017). Assessing ASD in Adolescent Females with Anorexia Nervosa using Clinical and Developmental Measures: a Preliminary Investigation Journal of Abnormal Child Psychology DOI: 10.1007/s10802-017-0301-x... Read more »

  • May 10, 2017
  • 05:56 AM

Sustainable hunting regulations take the speed of trophy growth into account

by sschindler in sschindlerblog

Hunting regulations aim to keep trophy hunting sustainable. Yet most regulations fall short of this aim and trophy size is becoming shorter over time in most hunted populations, such as Bighorn sheep, Impala, Mouflon, and Sable antelope. This might be due to ignoring the speed of trophy growth when deciding on hunting regulations. more Schindler, […]... Read more »

Schindler, S., Festa-Bianchet, M., Hogg, J., & Pelletier, F. (2017) Hunting, age structure, and horn size distribution in bighorn sheep. The Journal of Wildlife Management. DOI: 10.1002/jwmg.21259  

  • May 10, 2017
  • 03:35 AM

Conviction for violence and autism: comorbidity counts

by Paul Whiteley in Questioning Answers

I tread carefully when discussing the results published by Ragini Heeramun and colleagues [1] on the topic of "whether autism is associated with convictions for violent crimes" and "the associated risk and protective factors." Carefully because, as I've indicated on other occasions (see here), people commit crimes not labels, and sweeping generalisations about labels, specific types of crime and/or the concept of 'dangerousness' tend to do very little to help anyone in the long term.Still, I do think it is important that issues such as offending in the context of autism spectrum disorder (ASD) are not brushed under the carpet. I say this bearing in mind that a few high profile cases where autism has been mentioned alongside have been highlighted in the media recently here in Blighty (see here and see here). Indeed, in these days of cyber-terrorism linked to extremism for example, I'd like to see quite a bit more scientific investigation into the ways of protecting those on the autism spectrum from being lured into such activities alongside studies on the possible hows-and-whys of people entering into such behaviours.Heeramun et al relied on data from the Stockholm Youth Cohort where some 5,700 participants had a recorded ASD diagnosis. Data was cross-referenced with that from the Swedish National Crime Register to ascertain how many people were charged with offences where violence was a factor. Comparing those with autism with those with not-autism, researchers concluded that: "Individuals with autism, particularly those without intellectual disability, initially appeared to have a higher risk of violent offending." They do temper that finding with the observation that "these associations markedly attenuated after co-occurring attention-deficit/hyperactivity disorder (ADHD) or conduct disorder were taken into account" suggesting that comorbidity might count. Indeed, this data tallies with other independent findings suggesting that a range of 'adverse' life events can be a significant feature of ADHD and conduct disorder in the long-term (see here) and for example, that autism and ADHD in the prison population should considered (see here).Alongside, authors talked about how various other factors might also influence risk of violent offending ("parental criminal and psychiatric history and socioeconomic characteristics") and importantly, how: "Better school performance and intellectual disability appeared to be protective." That intellectual (learning) disability accompanying autism seems to be protective against conviction for a violent crime with autism in mind is probably due in part to the increased supervision given to such individuals. This is a point that has been raised in previous peer-reviewed research too (see here).The take-away messages are once again, sweeping generalisations about all autism being *linked to* violent crime are not needed and that comorbidity might count (as it seems to on many occasions) when it comes to variables being linked to autism (see here for another example). As with such crime in the general population, there are a myriad of often quite individual factors contributing to such behaviours, but alongside: "Better understanding and management of comorbid psychopathology in autism may potentially help preventive action against offending behaviors in people with autism."----------[1] Heeramun R. et al. Autism and Convictions for Violent Crimes: Population-Based Cohort Study in Sweden. JAACAP. 2017. April 3.----------Heeramun, R., Magnusson, C., Gumpert, C., Granath, S., Lundberg, M., Dalman, C., & Rai, D. (2017). Autism and Convictions for Violent Crimes: Population-Based Cohort Study in Sweden Journal of the American Academy of Child & Adolescent Psychiatry DOI: 10.1016/j.jaac.2017.03.011... Read more »

Heeramun, R., Magnusson, C., Gumpert, C., Granath, S., Lundberg, M., Dalman, C., & Rai, D. (2017) Autism and Convictions for Violent Crimes: Population-Based Cohort Study in Sweden. Journal of the American Academy of Child . DOI: 10.1016/j.jaac.2017.03.011  

  • May 9, 2017
  • 05:24 AM

"Medical Conditions in the First Years of Life Associated with Future Diagnosis of ASD"

by Paul Whiteley in Questioning Answers

I rank the paper by Stacey Alexeeff and colleagues [1] (open-access available here) as being in the 'pretty important' category when it comes to hierarchy in autism research. Not only because of their use of data derived from Kaiser Permanente (KP) (quite a large US healthcare provider that has some autism research history) including some "3911 ASD [autism spectrum disorder] cases and 38,609 controls" but also because some of the findings reiterate what is already 'known' about in relation to autism and how various medical conditions might be quite important to at least some 'types' of autism. These results are also being presented at IMFAR 2017 (see here) which will be opening its doors very soon...The Alexeeff paper is open-access but a few choice details are worthwhile pulling out:As per those participant numbers, the authors confirmed that "ASD cases were defined as children with either (a) an ASD diagnosis from an ASD specialist or (b) two or more ASD diagnoses from non-specialists, separated in time." This contrasted with controls who "were required to never have had an ASD diagnosis as of June 2012" (the period of study covered those born between 2000 and 2009).The medical conditions screened for in participant records were quite wide-ranging: "Over 1000 ICD-9 codes were grouped into 79 medical conditions (e.g., constipation) within 19 domains (e.g., gastrointestinal)" and importantly, relied on physician/clinician input. Researchers ascertained how frequently said medical conditions occurred in each of the groups: "whether certain medical conditions occurring in early childhood were associated with a higher risk of future ASD diagnosis."Results: "38 of the 79 medical conditions had statistically significant associations with ASD risk after multiple testing adjustment." These conditions ranged from various types/forms of developmental delay (language, learning, motor) to more somatic conditions: "nutrition, genetic, ear nose and throat, and sleep conditions." It's also worth noting that some types of diagnosis/conditions displayed only a weak association with subsequent risk of ASD including that related to asthma (previously discussed quite a bit on this blog).Researchers also looked at what clusters of medical conditions might be associated with lower or higher likelihood of an ASD diagnosis being given. They concluded that: "Developmental delay and mental health condition clusters were associated with the highest relative risks of ASD." They further suggest that "combinations of medical comorbidities could aid in risk stratification for ASD prior to ASD diagnosis using a supervised clustering analysis based on machine-learning methods." Machine learning yet again, applied to autism research eh?There's little more for me to discuss about this work other than to say that much more targeted research is needed to build on these latest findings from Alexeeff and colleagues. Coinciding with the ideas that (i) autism rarely exists in some sort of diagnostic vacuum (see here) and that (ii) autism genes are not necessarily just genes for autism (see here) (indeed a topic rising in research importance [2]) the lessons to be learned are becoming a little clearer. I might also focus a little more on those somatic diagnoses discussed in the Alexeeff paper as being quite important to the clinical picture when it comes to autism. Y'know how various medical comorbidities are indeed over-represented when it comes to autism and how appropriate screening and management/treatment [3] should be offered when and where they are identified (see here) save any further healthcare inequalities arising...To close, I appreciate that there are quite a lot of opinions out there about a certain US autism organisation, but a recent document of theirs talking about the various conditions/comorbidities that can follow a diagnosis of autism (see here) deserves an airing. Not that they were however the first group to talk about this important part of the autism spectrum (see here) but better late than never...----------[1] Alexeeff SE. et al. Medical Conditions in the First Years of Life Associated with Future Diagnosis of ASD in Children. J Autism Dev Disord. 2017 Apr 22.[2] Diaz-Beltran L. et al. Cross-disorder comparative analysis of comorbid conditions reveals novel autism candidate genes. BMC Genomics 2017. 18: 315.[3] Flor J. et al. Developmental functioning and medical Co-morbidity profile of children with complex and essential autism. Autism Res. 2017 May 5.----------Alexeeff SE, Yau V, Qian Y, Davignon M, Lynch F, Crawford P, Davis R, & Croen LA (2017). Medical Conditions in the First Years of Life Associated with Future Diagnosis of ASD in Children. Journal of autism and developmental disorders PMID: 28434058... Read more »

Alexeeff SE, Yau V, Qian Y, Davignon M, Lynch F, Crawford P, Davis R, & Croen LA. (2017) Medical Conditions in the First Years of Life Associated with Future Diagnosis of ASD in Children. Journal of autism and developmental disorders. PMID: 28434058  

  • May 8, 2017
  • 02:08 PM

Neuropeptides and Peer Review Failure

by Neuroskeptic in Neuroskeptic_Discover

A new paper in the prestigious journal PNAS contains a rather glaring blooper.

The paper, from Oxford University researchers Eiluned Pearce et al., is about the relationship between genes and social behaviour. The blooper is right there in the abstract, which states that "three neuropeptides (β-endorphin, oxytocin, and dopamine) play particularly important roles" in human sociality. But dopamine is not a neuropeptide.

Neither are serotonin or testosterone, but throughout the paper, Pea... Read more »

  • May 8, 2017
  • 04:04 AM

Vitamin D genes and autism

by Paul Whiteley in Questioning Answers

"Vitamin D deficiency is a putative environmental risk factor for autism spectrum disorder (ASD)."And..."We provide straightforward genetic evidences for the first time that VDRGs [vitamin D-related genes] with a strong degree of DNM [de novo mutations] burden in ASD and DNMs of VDRGs could be involved in the mechanism underlying in ASD pathogenesis."That was the research bottom line reported on by Jinchen Li and colleagues [1] examining an important part of the whole 'vitamin D - autism' link (see here). Specifically, how outside of just looking at functional levels of vitamin D in relation to autism (see here) and implying that groups on the autism spectrum may not be getting enough vitamin D through sunlight exposure or diet, there may be other underlying issues to consider. As other authors have hinted, the genetics of vitamin D metabolism may also be part and parcel of the autism - vitamin D story (see here).This time around, researchers "analyzed publicly-available DNMs from 4,327 ASD probands and 3,191 controls." Among those DNMs - alterations to the genetic code present in probands but not extended family members - "18 of the VDRGs were found to harbor recurrent functional DNMs in the probands, compared with only one in the controls." In other words, small 'glitches' in the genes thought to be involved in vitamin D metabolism were more frequently present in the autism group than the not-autism group. Said glitches *may* have the ability to affect the working of those vitamin D metabolising genes with onward effects.This is interesting work. It kinda reiterates that (i) vitamin D and the metabolism of vitamin D might be important for at least some parts of the autism spectrum and, (ii) issues with deficiency or insufficiency of vitamin D metabolites in relation to autism may be the product of both genetic and environmental issues. We obviously need to see more investigations done in this area; not least to define how widespread said genetic issues affecting vitamin D metabolism might be in relation to the very wide and very heterogeneous autism spectrum. I'd put a bet on such issues perhaps affecting only part of the autism spectrum and perhaps related to one or more phenotypes. Other authors seem to think so too [2].  I'd also wager that something quite important might emerge when it comes to the specificity of any findings too (see here).The other question that needs to be answered is what can be done as and when issues with vitamin D metabolising genes are detected. Does this mean that additional supplementation of vitamin D (in it's typically supplemented form(s)) is unlikely to be of use (bearing in mind the recent data in this area) as a result of those DNMs? As with everything related to autism, simple answers to seemingly simple questions are very, very unlikely...----------[1] Li J. et al. Vitamin D-related genes are subjected to significant de novo mutation burdens in autism spectrum disorder. Am J Med Genet B Neuropsychiatr Genet. 2017 Apr 13.[2] Gillberg C. et al. The role of cholesterol metabolism and various steroid abnormalities in autism spectrum disorders: A hypothesis paper. Autism Res. 2017 Apr 12.----------Li J, Wang L, Yu P, Shi L, Zhang K, Sun ZS, & Xia K (2017). Vitamin D-related genes are subjected to significant de novo mutation burdens in autism spectrum disorder. American journal of medical genetics. Part B, Neuropsychiatric genetics : the official publication of the International Society of Psychiatric Genetics PMID: 28407358... Read more »

Li J, Wang L, Yu P, Shi L, Zhang K, Sun ZS, & Xia K. (2017) Vitamin D-related genes are subjected to significant de novo mutation burdens in autism spectrum disorder. American journal of medical genetics. Part B, Neuropsychiatric genetics : the official publication of the International Society of Psychiatric Genetics. PMID: 28407358  

  • May 8, 2017
  • 01:56 AM

Finding real rewards in a virtual world

by adam phillips in It Ain't Magic

A new study shows that mice who learn to find goals in virtual reality use their hippocampus the same was as in the real world.... Read more »

  • May 6, 2017
  • 06:03 AM

Congenital heart disease and autism and ADHD: Taiwan wades in

by Paul Whiteley in Questioning Answers

"The incidence rates of perinatal comorbidities, EDD [early developmental disorders], ADHD [attention-deficit hyperactivity disorder], and ASD [autism spectrum disorder] were higher in the CHD [congenital heart disease] group than in the control group."So said the findings reported by Pei-Chen Tsao and colleagues [1] investigating an issue that has cropped up more than once on this blog in relation to the developmental/behavioural correlates possibly associated with a diagnosis of congenital heart disease (CHD) (see here and see here). As per the title of this post, the scientific weight of the Taiwanese National Health Insurance Research Database (NHIRD) was brought into this research area, examining the developmental records of some 3500 under 18-year olds diagnosed with CHD compared with over 14,000 age- and sex-matched controls. Researchers looked for both diagnoses of ADHD and ASD in participant records as well as: "Comorbid perinatal conditions and early developmental disorders (EDD) that were diagnosed before ADHD and ASD diagnosis."Results: well, just about everything looked for in the groups was found more frequently in the CHD grouping even after adjustment for various potentially confounding variables. Authors also reported that: "the risk for ADHD... and ASD... was greatly increased in CHD subjects with EDD than in non-CHD subjects without EDD" and onwards something of a cumulative effect when EDD and CHD were found comorbid.The implications of such results? Well, yet again I'll refer you back to the first time I talked about CHD and autism on this blog (see here) in terms of possible hows-and-whys and future research directions. The added issue of preferential screening for developmental issues/diagnoses when a diagnosis of CHD is received also comes to the forefront (yet again). Said screening might also include other elements too [2]...----------[1] Tsao PC. et al. Additive effect of congenital heart disease and early developmental disorders on attention-deficit/hyperactivity disorder and autism spectrum disorder: a nationwide population-based longitudinal study. Eur Child Adolesc Psychiatry. 2017 Apr 17.[2] Wu XL. et al. Chromosome microarray analysis in the investigation of children with congenital heart disease. BMC Pediatrics. 2017; 17: 117.----------Tsao PC, Lee YS, Jeng MJ, Hsu JW, Huang KL, Tsai SJ, Chen MH, Soong WJ, & Kou YR (2017). Additive effect of congenital heart disease and early developmental disorders on attention-deficit/hyperactivity disorder and autism spectrum disorder: a nationwide population-based longitudinal study. European child & adolescent psychiatry PMID: 28417257... Read more »

  • May 5, 2017
  • 08:00 AM

Friday Fellow: Toxo

by Piter Boll in Earthling Nature

by Piter Kehoma Boll If I had to bet on a parasite that you who are reading this probably have in your body, I’d go for today’s fellow, the protist Toxoplasma gondii, sometimes simply called toxo. Found worldwide, the toxo is … Continue reading →... Read more »

Tenter, A., Heckeroth, A., & Weiss, L. (2000) Toxoplasma gondii: from animals to humans. International Journal for Parasitology, 30(12-13), 1217-1258. DOI: 10.1016/S0020-7519(00)00124-7  

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