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  • March 3, 2017
  • 03:48 PM
  • 281 views

Brain Activity At The Moment of Death

by Neuroskeptic in Neuroskeptic_Discover

What happens in the brain when we die?



Canadian researchers Loretta Norton and colleagues of the University of Western Ontario examine this grave question in a new paper: Electroencephalographic Recordings During Withdrawal of Life-Sustaining Therapy Until 30 Minutes After Declaration of Death

Norton et al. examined frontal EEG recordings from four critically ill patients at the point where their life support was withdrawn. Here are some details on the four:



Here's the EEG recor... Read more »

Norton L, Gibson RM, Gofton T, Benson C, Dhanani S, Shemie SD, Hornby L, Ward R, & Young GB. (2017) Electroencephalographic Recordings During Withdrawal of Life-Sustaining Therapy Until 30 Minutes After Declaration of Death. The Canadian Journal of Neurological Sciences, 44(2), 139-145. PMID: 28231862  

  • March 3, 2017
  • 05:14 AM
  • 186 views

Rare Disease Day – Findacure Scientific Conference: Drug Repurposing for Rare Diseases

by Joana Guedes in BHD Research Blog

This year’s Findacure Scientific Conference took place in London on Rare Disease Day and was again focused on Drug Repurposing for Rare Diseases. The conference brought together over 100 representatives from patient groups, researchers and members of the healthcare industry to discuss the importance and the latest developments in drug repurposing for rare diseases.... Read more »

  • March 3, 2017
  • 02:56 AM
  • 258 views

Poverty status and autism, ADHD and asthma

by Paul Whiteley in Questioning Answers

The paper by Christian Pulcini and colleagues [1] talking about poverty status potentially influencing "parent-reported lifetime prevalence and comorbidities" when it comes to three target conditions (autism, attention-deficit hyperactivity disorder [ADHD] and asthma) should have been a call to action. Concluding that "poor and near poor children had a higher lifetime prevalence of asthma and ADHD, but not ASD [autism spectrum disorder]" [2], some of the findings have instead attracted criticism based on the content of the abstract (see here); specifically the line: "the lifetime prevalence of ASD rose almost 400%."Poverty and diagnosis is a topic that I've covered before on this blog (see here for example) and how not every research study has linked poverty (measures of poverty) to something like autism and/or ADHD. At least that is, when taking into account "elevated emotional problems among children with ASD + ADHD" [3].On this most recent occasion, Pulcini et al drew on data derived from the "National Survey of Children's Health [NSCH] for years 2003, 2007, and 2011-2012" and specifically "trends in parent reported lifetime prevalence and comorbidity among children with asthma, ADHD, and ASD" taking into account variables like poverty status. The NSCH initiative has again, been talked about previously on this blog (see here and see here) in terms of parent-reported prevalence of autism and parent-reported epilepsy appearing alongside autism. It's a good rough-and-ready measure of what estimated prevalence rates might look like (with the need for further, more detailed study).This time around the authors illustrated that - yet again - the only way is up when it comes to estimated prevalence rates for all the 'target' conditions examined. I don't think anyone should be too surprised at such findings given data from other studies in other geographic areas (see here) specifically with the autism spectrum in mind. I'm not going to head into the debate about whether the 400% increase figure is right or wrong but will note previous findings [4] that suggested that: "differential survey measurement error over time was not a major contributor to observed changes in the prevalence of parent-reported ASD. Rather, much of the prevalence increase from 2007 to 2011–2012 for school-aged children was the result of diagnoses of children with previously unrecognized ASD." This for when data from the 2007 and 2011-2012 surveys were contrasted (not the 2003 survey).The contribution of poverty or near poverty was not to be sniffed at when it comes to those ADHD and asthma diagnoses. This is perhaps even more important when one considers that these two labels might be rather more 'entangled' than many people might have previously realised (see here). That a poverty and ADHD link might also generalise to somewhere like here in the UK is also worth noting (see here) and implies that quite a bit more research is needed to answer the question: why? With regards to autism (ASD), the observation that the "rise in ASD was associated with being nonpoor"adds to an on-going debate, with some studies saying yes, we agree, and other studies saying no, we don't (see here). In short, it is slightly more complicated when it comes to how social factors might affect autism rates.Music: Three steps to heaven.----------[1] Pulcini CD. et al. Poverty and Trends in Three Common Chronic Disorders. Pediatrics. 2017 Feb 13. pii: e20162539.[2] Dreyer BP. Congress Should Adopt a “Do No Harm to Children” Standard in Changes to Public Health Insurance. Pediatrics. 2017. Feb 2017.[3] Flouri E. et al. Poverty and the Growth of Emotional and Conduct Problems in Children with Autism With and Without Comorbid ADHD. J Autism Dev Disord. 2015 Sep;45(9):2928-38.[4] Blumberg SJ. et al. Changes in Prevalence of Parent-reported Autism Spectrum Disorder in School-aged U.S. Children: 2007 to 2011–2012. Natl Health Stat Report. 2013 Mar 20;(65):1-11.----------Pulcini CD, Zima BT, Kelleher KJ, & Houtrow AJ (2017). Poverty and Trends in Three Common Chronic Disorders. Pediatrics PMID: 28193790... Read more »

Pulcini CD, Zima BT, Kelleher KJ, & Houtrow AJ. (2017) Poverty and Trends in Three Common Chronic Disorders. Pediatrics. PMID: 28193790  

  • March 2, 2017
  • 03:11 AM
  • 267 views

Subgroups in autism (without intellectual disability)

by Paul Whiteley in Questioning Answers

"Children with ASD [autism spectrum disorder] without ID [intellectual disability] could be differentiated into Moderate and Severe Social Impairment subgroups when core ASD symptoms were more closely examined."So said the findings reported by Felicity Klopper and colleagues [1] looking at an important part of the autism research scene related to the 'plurality' of the term autism and the seemingly vast range of presentations included under the label. Reliant on data obtained from "the ‘gold standard’ ASD diagnostic instruments" (including the ADOS and ADI), researchers looked at the "presence of phenotypic subgroups" in their cohort.As per the opening sentence to this post, there were some differences to be seen in the cohort, and in particular, how social interaction issues might be a key part of any differentiation. The authors talk about how social interaction issue differences seemed to tie into other core behavioural features such as communication and the presence of restricted/repetitive behaviours. They concluded: "both categorical and dimensional approaches may be useful in classifying ASD, with neither alone being adequate."It is not necessarily new news that the label of autism is good for diagnosis but seemingly says little about the range of presentation included under the heading (see here for example). Indeed, in these days of ESSENCE I might forward the view that even the label autism might be part of a wider heterogeneous presentation (see here) and one should further expand those subgroup notions at the label as well as symptom level. The focus on overt behaviour (as assessed by those gold-standard instruments) in the Klopper study is but one part of looking at such 'heterogeneity' (see here for example) as the authors argue that: "The dissociated profiles of ASD features could represent different underlying neurobiological mechanisms for each subgroup." At least one of the authors on the Klopper paper probably, more than most, realises that fact (see here).There are other key areas to this focus on the presentation of autism that also need to be factored in: sex differences and comorbidity profiles. Specifically, the growing realisation that girls and boys on the autism spectrum probably show subtle differences in presentation (see here) and, minus any sweeping generalisations, should be considered in future studies in this area. Oh, and keep in mind that those diagnosed with autism with an intellectual disability (ID) could also be 'sub-grouped' according to symptom presentation too with similar caveats. The question is: how many sub-groups of autism will we eventually end up with?Music, and because Spring has Sprung... In Bloom.----------[1] Klopper F. et al. A cluster analysis exploration of autism spectrum disorder subgroups in children without intellectual disability. Research in Autism Spectrum Disorders. 2017; 36: 66-78.----------Felicity Klopper, Renee Testa, Christos Pantelis, & Efstratios Skafidas (2017). A cluster analysis exploration of autism spectrum disorder subgroups in children without intellectual disability Research in Autism Spectrum Disorders : 10.1016/j.rasd.2017.01.006... Read more »

Felicity Klopper, Renee Testa, Christos Pantelis, & Efstratios Skafidas. (2017) A cluster analysis exploration of autism spectrum disorder subgroups in children without intellectual disability. Research in Autism Spectrum Disorders. info:/10.1016/j.rasd.2017.01.006

  • March 1, 2017
  • 08:00 AM
  • 216 views

Transient Imprinting of Genes in the Human Placenta

by Marta Sanchez Delgado in EpiBeat

When the fertilization occurs, the maternal and paternal pronuclei have thousands of opposite methylated regions. Most of this germline methylation are resolved during the postfertilization epigenetic reprogramming by active mechanism for the sperm-derived methylated regions and depending on DNA replication for the oocyte-derived ones. There is a subset of regions that are known to avoid this demethylation: the imprinted differentially methylated regions (DMRs). The imprinted DMRs are in general located in promoter regions ,where the cytosine methylation marks one of the parental alleles influencing in the allelic expression of surrounding genes. The majority of known germline-derived imprinted DMRs are maternally methylated and this differentially methylated pattern are maintained throughout development– and latter in the adult tissue – except for the primordial germ cells, where imprinted are erased and the new methylation pattern will be established depending on the embryos gender.1

Recently, it have been identified in mouse preimplantational embryos a subset of transient differentially methylated regions. This tDMRs inherits their methylation mainly from the oocyte and subsequently gain methylation on their paternal alleles at implantation.2 In 2014 it was published the “DNA methylation dynamics of the human preimplantation embryo” but it is currently unknown how many germline methylation differences survive embryonic reprogramming as a tDMRs in humans.3... Read more »

Sanchez-Delgado M, Court F, Vidal E, Medrano J, Monteagudo-Sánchez A, Martin-Trujillo A, Tayama C, Iglesias-Platas I, Kondova I, Bontrop R.... (2016) Human Oocyte-Derived Methylation Differences Persist in the Placenta Revealing Widespread Transient Imprinting. PLoS genetics, 12(11). PMID: 27835649  

Smallwood SA, & Kelsey G. (2012) De novo DNA methylation: a germ cell perspective. Trends in genetics : TIG, 28(1), 33-42. PMID: 22019337  

Smith ZD, Chan MM, Humm KC, Karnik R, Mekhoubad S, Regev A, Eggan K, & Meissner A. (2014) DNA methylation dynamics of the human preimplantation embryo. Nature, 511(7511), 611-5. PMID: 25079558  

Barbaux S, Gascoin-Lachambre G, Buffat C, Monnier P, Mondon F, Tonanny MB, Pinard A, Auer J, Bessières B, Barlier A.... (2012) A genome-wide approach reveals novel imprinted genes expressed in the human placenta. Epigenetics, 7(9), 1079-90. PMID: 22894909  

Hanna CW, Peñaherrera MS, Saadeh H, Andrews S, McFadden DE, Kelsey G, & Robinson WP. (2016) Pervasive polymorphic imprinted methylation in the human placenta. Genome research, 26(6), 756-67. PMID: 26769960  

  • March 1, 2017
  • 03:13 AM
  • 255 views

Sex and age might affect comorbidity profiles in autism

by Paul Whiteley in Questioning Answers

The paper by Supekar and colleagues [1] provides some food for thought today specifically with the idea that comorbidity profiles accompanying autism might be influenced by age and gender in mind.To quote: "These results highlight crucial differences between cross-sectional comorbidity patterns and their interactions with sex and age, which may aid in the development of effective sex- and age-specific diagnostic/treatment strategies for ASD [autism spectrum disorder] and comorbid conditions."From a starting point assuming that the diagnosis of autism rarely exists in some sort of diagnostic vacuum (see here), researchers set about looking at comorbidity patterns for quite a few conditions/labels "using cross-sectional data from 4790 individuals with ASD and 1,842,575 individuals without ASD." The sorts of things that looked for were not uncommon to discussions about comorbidity accompanying autism on this blog (epilepsy, attention-deficit hyperactivity disorder (ADHD) and "bowel disorders" for example). The variables of sex (gender) and age were also included in the research mix.Bearing in mind that sweeping generalisations about autism comorbidity profiles are not required, the authors highlighted a couple of important points. First: "Epilepsy, ADHD, and CNS/cranial anomalies showed exceptionally large proportions in both male (>19%) and female (>15%), children/adolescents with ASD. Notably, these prevalence rates decreased drastically with age in both males and females." This is interesting. With a rather large research gap quite visible when it comes to the concept of ageing and autism (see here), the author's data seems to be suggesting that the burden of comorbidity (some comorbidity) might decline as people diagnosed on the autism spectrum get older. Yes, the words "cross-sectional comorbidity" are important (more longitudinal study is required where people are 'followed' as they age) and there is no doubt that intervention to manage diagnoses such as epilepsy (and/or seizure disorder) probably plays a hand in presentation, but more investigation is certainly required.Next: "the prevalence of schizophrenia increased with age affecting a disproportionately large number of older (≥35 year) adult males (25%), compared to females (7.7%), with ASD." Two points are made here: (a) rates of schizophrenia might be affected by sex, and (b) age might play a role in the presentation of schizophrenia in the context of autism. This follows a theme re-emerging over these past few years suggesting that the autism and schizophrenia spectrums might not be as separate and independent as many might believe (see here and see here). Quite a lot of [research] focus has been directed at some of the signs and symptoms of schizophrenia with [some] autism in mind (see here for example) and perhaps queries whether history was 'too quick' to try and distance the two labels from each other (were Mildred Creak and colleagues correct?). Given the significant issues potentially linked to a diagnosis of schizophrenia (see here) in terms of health inequality and the like (something also sadly not unfamiliar to autism too), the onus should surely be to screen (and keep screening) for schizophrenia when autism is present into adulthood? Said screening could be preferentially driven by the Supekar findings taking into account that caveat about not over-generalising findings.I'm gonna stop there with discussing these results so as not to over-analyse the findings. The important take-away point is that autism is generally not a 'stand-alone' condition and that age and gender might have some important roles to play when it comes to at least some comorbidity.Music: something lively I think so increase the volume please...----------[1] Supekar K. et al. The influence of sex and age on prevalence rates of comorbid conditions in autism. Autism Res. 2017 Feb 11.----------Supekar K, Iyer T, & Menon V (2017). The influence of sex and age on prevalence rates of comorbid conditions in autism. Autism research : official journal of the International Society for Autism Research PMID: 28188687... Read more »

Supekar K, Iyer T, & Menon V. (2017) The influence of sex and age on prevalence rates of comorbid conditions in autism. Autism research : official journal of the International Society for Autism Research. PMID: 28188687  

  • February 28, 2017
  • 06:00 PM
  • 195 views

Cataloging a year of blogging: complexity in evolution, general models, and philosophy

by Artem Kaznatcheev in Evolutionary Games Group

Last month, with just hours to spare in January, I shared a linkdex of the 14 cancer-related posts from TheEGG in 2016. Now, as February runs out, it’s time to reflect on the 15 non cancer-specific posts from last year. Although, as we’ll see, some of them are still related to mathematical oncology. With a […]... Read more »

  • February 28, 2017
  • 02:00 PM
  • 203 views

A Weekend Camping Trip Is Enough to Reset Your Internal Clock

by Elizabeth Preston in Inkfish



Humans have been fighting our internal clocks ever since we invented sitting around a campfire. We have powerful natural rhythms that keep us on a 24-hour cycle; if you've ever been steamrollered by jet lag after an intercontinental flight, you know how powerful those rhythms are. But we muffle them with caffeine, alarm clocks, and electric lights. It's easy to undo the damage, though. One weekend of camping can do the trick—and it'll even cure your case of the Mondays.



In 2013, resea... Read more »

Stothard ER, McHill AW, Depner CM, Birks BR, Moehlman TM, Ritchie HK, Guzzetti JR, Chinoy ED, LeBourgeois MK, Axelsson J.... (2017) Circadian Entrainment to the Natural Light-Dark Cycle across Seasons and the Weekend. Current biology : CB, 27(4), 508-513. PMID: 28162893  

  • February 28, 2017
  • 02:42 AM
  • 244 views

Premature mortality in intellectual disability in Australia (and England)

by Paul Whiteley in Questioning Answers

"Adults with ID [intellectual disability] experience premature mortality and over-representation of potentially avoidable deaths."The paper by Julian Trollor and colleagues [1] (open-access available here) provides some sombre reading today, as once again the topic of early mortality is raised on this blog. Looking at several measures - the "Age Standardised Mortality Rate (ASMR), Comparative Mortality Figure (CMF), years of productive life lost (YPLL) and proportion of deaths with potentially avoidable causes" - authors paint a depressing picture of a 'mortality gap' between those diagnosed with a learning (intellectual) disability and the wider, general population.I don't want to trawl through the Trollor paper in great detail given that it is open-access for all to see, but a few points are worthwhile raising. So, based on data from some 20,000 adults (aged 20 or over) registered with an intellectual disability (ID) in New South Wales (NSW) in Oz, there were 732 deaths reported (4%) "equivalent to a crude death rate of 5.9 deaths per 1000 people per year." The median age at death was 54 years and about 60% of deaths were in men. A control cohort consisting of adults from NSW was used as a comparator where "a crude death rate of 9.1 deaths per 1000 person years" was calculated. The median age at death however, for the control group, was 81 years. When looking at death rates between the groups according to age banding (20-44 years, 45-64 years, 65+ years) authors noted that: "People with ID in the 20–44 years age category had four times the death rate of the comparison group."Looking at the causes of death between the ID and control groups, authors noted some potentially important trends. So: "Cause of death in [the] ID cohort was dominated by respiratory, circulatory, neoplasm and nervous system." This bearing in mind that cause of death was not available for everyone diagnosed with an ID (only 87%). Such causes were not wildly different from those noted in the control population but when it came to 'potentially avoidable deaths' the ID group were placed at some quite notable disadvantage, with 31% of deaths falling into this category (revised up to 38% depending on the 'death classification' used) compared with 17% in the general population. Readers should also note that: "Potentially avoidable deaths are deaths from conditions that are preventable through individualised care and/or treatable through existing primary or hospital care for persons aged under 75 years and which are avoidable in the context of the present health system."As you can see, there are some quite shocking details noted in the Trollor paper. The emerging picture that some of the most vulnerable people in society (certainly in Australia) are (a) at risk of dying earlier than the general population and (b) at greater risk of suffering a 'potentially avoidable death' is one that no-one should be proud of. And just in case you though the results might not be generalisable to other parts of the world... you're wrong [2] (open-access here) as data from England reveals that: "Mortality rates for people with ID were significantly higher than for those without. Their all-cause standardised mortality ratio was 3.18. Their life expectancy at birth was 19.7 years lower than for people without ID." Truly shocking.What can society do about such a state of affairs? Well, potentially lots (and it doesn't take monumental shifts to achieve better outcomes either). "Particularly stark is the large proportion ofpotentially avoidable deaths due to infections. Such deaths suggest that people with ID experience delays, difficulties or differences in accessing specific and effective interventions for infections. Medical assistance must be sought assertively in individuals who manifest symptoms, but this is made difficult as patients with ID may not readily report symptoms, and some providing direct carelack skills in early identification of relevant physical signs. Primary care providers should consider careful assessment, proactive treatment and close monitoring of progress if there are infections in this population." Sorry for the large chunk of replication text there but several important themes are laid out by Trollor, some of which overlap with other work in relation to autism for example (see here). Not least is the need for 'proactivity' on the part of clinicians and other professionals, potentially dealing with a group who may not be able to readily communicate their physical state for example and so shifting the responsibility on medical care being inspective and proactive. This means regular health screening and, at the basic level, understanding that a diagnosis of ID (or autism or schizophrenia [3]) does not seemingly provide any protection against the development of life-threatening illness or other conditions becoming evident.I close with an article discussing another part of the reason why people with ID are being placed at an unacceptably high risk of early death: when those who are supposed to provide care, fail.----------[1] Trollor J. et al. Cause of death and potentially avoidable deaths in Australian adults with intellectual disability using retrospective linked data. BMJ Open. 2017. Feb 7.[2] Glover G. et al. Mortality in people with intellectual disabilities in England. J Intellect Disabil Res. 2017 Jan;61(1):62-74.[3] Hjorthøj C. et al. Years of potential life lost and life expectancy in schizophrenia: a systematic review and meta-analysis. Lancet Psychiatry. 2017 Feb 22. pii: S2215-0366(17)30078-0.----------Trollor J, Srasuebkul P, Xu H, & Howlett S (2017). Cause of death and potentially avoidable deaths in Australian adults with intellectual disability using retrospective linked data. BMJ open, 7 (2) PMID: 28179413... Read more »

  • February 27, 2017
  • 05:29 AM
  • 285 views

Know your brain: Mammillary bodies

by neurosci in Neuroscientifically Challenged

Where are the mammillary bodies?























The mammillary bodies are part of the diencephalon, which is a collection of structures found between the brainstem and cerebrum. The diencephalon includes the hypothalamus, and the mammillary bodies are found on the inferior surface of the hypothalamus (the side of the hypothalamus that is closer to the brainstem). The mammillary bodies are a paired structure, meaning there are two mammillary bodies---one on either side of the midline of the brain. They get their name because they were thought by early anatomists to have a breast-like shape. The mammillary bodies themselves are sometimes each divided into two nuclei, the lateral and medial mammillary nuclei. The medial mammillary nucleus is the much larger of the two, and is often subdivided into several subregions.  What are the mammillary bodies and what do they do?The mammillary bodies are best known for their role in memory, although in the last couple of decades the mammillary bodies have started to be recognized as being involved in other functions like maintaining a sense of direction. The role of the mammillary bodies in memory has been acknowledged since the late 1800s, when mammillary body atrophy was observed in Korsakov's syndrome---a disorder characterized by amnesia and usually linked to a thiamine deficiency. Since then a number of findings---anatomical, clinical, and experimental---have supported and expanded upon a mnemonic role for the mammillary bodies.The mammillary bodies are directly connected to three other brain regions: the hippocampus via the fornix, thalamus (primarily the anterior thalamic nuclei) via the mammillothalamic tract, and the tegmental nuclei of the midbrain via the mammillary peduncle and mammillotegmental tract. Two of the three connections are thought to primarily carry information in one direction: the hippocampal connections carry information from the hippocampus to the mammillary bodies and the thalamic connections carry information from the mammillary bodies to the thalamus (the tegmental connections are reciprocal). These connections earned the mammillary bodies the reputation of being relay nuclei that pass information from the hippocampus on to the anterior thalamic nuclei to aid in memory consolidation. This hypothesis is supported by the fact that damage to pathways that connect the mammillary bodies to the hippocampus or thalamus is associated with deficits in consolidating new memories. Others argue, however, that the mammillary bodies act as more than a simple relay, making independent contributions to memory consolidation. Both perspectives emphasize a role for the mammillary bodies in memory but differ as to the specifics of that role.Further supporting a role for the mammillary bodies in memory, there is evidence from humans that suggests damage to the mammillary bodies is associated with memory deficits. Several cases of brain damage involving the mammillary bodies as well as cases of tumor-related damage to the area of the mammillary bodies suggests that damage to the mammillary bodies is linked to anterograde amnesia. Indeed, mammillary body dysfunction has been identified as a major factor in diencephalic amnesia, a type of amnesia that originates in the diencephalon (Korsakoff's syndrome, an amnesia that is seen primarily in long-term alcoholics, is one type of diencephalic amnesia).Experimental evidence from animal studies also underscores the importance of the mammillary bodies in memory. Studies with rodents and monkeys have found deficits in spatial memory to occur after damage to the mammillary bodies or the mammillothalamic tract. In addition to involvement in memory functions, there are cells in the mammillary bodies that are activated only when an animal's head is facing in a particular direction. These cells are thought to be involved in navigation and may act somewhat like a compass in creating a sense of direction.Vann SD, & Aggleton JP (2004). The mammillary bodies: two memory systems in one? Nature reviews. Neuroscience, 5 (1), 35-44 PMID: 14708002... Read more »

Vann SD, & Aggleton JP. (2004) The mammillary bodies: two memory systems in one?. Nature reviews. Neuroscience, 5(1), 35-44. PMID: 14708002  

  • February 27, 2017
  • 03:16 AM
  • 267 views

Low muscle tone and autistic traits

by Paul Whiteley in Questioning Answers

"This large study showed a prospective association of infant muscle tone with autistic traits in childhood."So said the findings reported by Fadila Serdarevic and colleagues [1] who, looking at nearly 3000 children, were able to assess early motor development and muscle tone "between ages 2 and 5 months" and later parental ratings of autistic traits in children at 6 years of age. Said autistic traits were surveyed using the "the Social Responsiveness Scale (SRS) and the Pervasive Developmental Problems (PDP) subscale of the Child Behavior Checklist." Authors concluded that there was something of a connection between low muscle tone and autistic traits: "Low muscle tone in infancy predicted autistic traits measured by SRS... and PDP" and further: "early detection of low muscle tone might be a gateway to improve early diagnosis of ASD [autism spectrum disorder]."Just before anyone gets ahead of themselves with this data, it is worth pointing out that despite the large participant group included for study and the prospective nature of the study design, this was a study only really looking at two sets of variables across quite a long time-frame. It's not beyond the realms of possibility that other factors might influence the presentation of [parent-reported] autistic traits outside of just early measures of muscle tone or anything related...But let's set this research in some context. Muscle tone in a broader sense had been noted to be potentially 'linked' to autism in some of the earliest texts on the topic (see here). More recent discussions on how motor skill in the context of gait for example, might be something important to at least some autism (see here) add to the relevance. One might also look to the some of the typical reasons why low muscle tone (hypotonia) may present to see whether there are areas that could inform autism research too. I note for example, mention of Ehlers-Danlos syndrome (EDS) in some of the texts and this would perhaps appeal to further investigation on any overlap between EDS (or other connective tissues disorders) and autism (see here). Serious infections such as encephalitis and meningitis have also been mentioned in the context of hypotonia, and again, might be indicated in relation to hypotonia and some autism (see here). There is also a possibility that hypotonia could (in some cases) be tied into mitochondrial disease; something else that could be relevant to at least some 'types' of autism (see here). All of these areas are worthy of further research inspection added to the idea that muscle tone might be rather more core to autism than many people might appreciate.'And the best picture goes to'...----------[1] Serdarevic F. et al. Infant muscle tone and childhood autistic traits: A longitudinal study in the general population. Autism Res. 2017 Feb 9.----------Serdarevic F, Ghassabian A, van Batenburg-Eddes T, White T, Blanken LM, Jaddoe VW, Verhulst FC, & Tiemeier H (2017). Infant muscle tone and childhood autistic traits: A longitudinal study in the general population. Autism research : official journal of the International Society for Autism Research PMID: 28181411... Read more »

Serdarevic F, Ghassabian A, van Batenburg-Eddes T, White T, Blanken LM, Jaddoe VW, Verhulst FC, & Tiemeier H. (2017) Infant muscle tone and childhood autistic traits: A longitudinal study in the general population. Autism research : official journal of the International Society for Autism Research. PMID: 28181411  

  • February 25, 2017
  • 04:07 AM
  • 299 views

1 in 5 children "met criteria for low language at 7 years"

by Paul Whiteley in Questioning Answers

Although primarily looking at the potential predictors of language outcome, the study results published by Cristina McKean and colleagues [1] revealed the rather important title heading this blog entry: "Almost 19% of children (22/1204;18.9%) met criteria for low language at 7 years."The source of the finding was a cohort of some 1900 infants "recruited at age 8 to 10 months" who were followed until aged 7 years old and subject to quite a bit of research inspection looking at "early life factors", maternal factors and "child language ability" at various points through the childhood years. I believe this was part of the The Early Language in Victoria Study (ELVS) initiative; something that has previously created a bit of stir in speech and language circles. The authors reported that alongside the quite high percentage of children who met 'low language' criteria (based on standardized receptive or expressive language scores "≥1.25 SD below the mean"): "Child language ability at 4 years more accurately predicted low language at 7 than a range of early child, family, and environmental factors." Said low language abilities at 7 years old were also "associated with a higher prevalence of co-occurring difficulties."Aside from pointing out that language ability at 4 years old might be quite important to language ability at 7 years old, the question that should be in most people's minds is 'why?' Why are nearly 1 in 5 children presenting with low language ability at 7 years old (and presumably at 4 years old too)? Yes, there are variables such as adverse early life factors (prematurity, birth weight, coming from a non-English speaking background, etc) that will no doubt influence various aspects of language ability, but the authors note that such factors only account for roughly 15% at most of the variation in language scores seen in their cohort (not including "child language scores at ages 2 and 4"). Ergo, there are other factors involved with regards to these findings.In light of the McKean findings, I'm also going to draw your attention back to another occasion when language ability has been discussed on this blog (see here) and specifically: "At school entry, approximately two children in every class of 30 pupils will experience language disorder severe enough to hinder academic progress." [2] Low language (ability) is not necessarily the same as a diagnosed language disorder, and probably accounts for the variation between the studies (1 in 5 vs. 1 in 15). But in amongst a spectrum of language ability (disorder?) the questions about 'why?' still very much remain (and please, no sweeping generalisations about us 'just being better at diagnosing').----------[1] McKean C. et al. Language Outcomes at 7 Years: Early Predictors and Co-Occurring Difficulties. Pediatrics. 2017 Feb 8. pii: e20161684.[2] Norbury CF. et al. The impact of nonverbal ability on prevalence and clinical presentation of language disorder: evidence from a population study. Journal of Child Psychology and Psychiatry. 2016. May 16.----------McKean C, Reilly S, Bavin EL, Bretherton L, Cini E, Conway L, Cook F, Eadie P, Prior M, Wake M, & Mensah F (2017). Language Outcomes at 7 Years: Early Predictors and Co-Occurring Difficulties. Pediatrics PMID: 28179482... Read more »

McKean C, Reilly S, Bavin EL, Bretherton L, Cini E, Conway L, Cook F, Eadie P, Prior M, Wake M.... (2017) Language Outcomes at 7 Years: Early Predictors and Co-Occurring Difficulties. Pediatrics. PMID: 28179482  

  • February 24, 2017
  • 06:18 PM
  • 296 views

Symbiote Separation: Coral Bleaching and Climate Change

by Melissa Chernick in Science Storiented

It’s been a while since I’ve broken down some studies for you, so I took on a big one.I’m sure you’ve heard of coral bleaching. What is it? Why does it happen? Why does it matter? To start off, you need to know a little bit more about the individuals that make up a head (fan, whip, etc.): the polyp. Coral polyps look like tiny plants but are actually tiny animals (less than ½ an inch in diameter). They produce calcium carbonate to create a protective shell or skeleton that, when thousands are living together, make up what you see as a single coral head. Really, only the outer-most layer of a coral head is actually alive (yes, they build their houses on top of the skeletons of their ancestors). Lots of individual corals make up a reef. Polyps have stinging cells (nematocysts) on their tentacles that capture any prey that swims a little too close. But a polyp does not live alone inside of its skeleton-house; it is actually in a symbiotic relationship with dinoflagellates (a.k.a. marine algae) called zooxanthellae (zo-o-zan-THELL-ee). Zooxanthellae live inside the tissues of the coral and photosynthesize, passing some of the energy they make to the polyp. They get a place to live and the polyp gets some energy, it’s a win-win. And, it is the zooxanthellae that give the corals much of their color.When the coral gets stressed, it expels the zooxanthellae, causing them to turn completely white. Not dead, but very stressed and more likely to die. This is coral bleaching.All sorts of things can stress a coral and cause them to eject their zooxanthellae: temperature, light, tides, salinity, or nutrients. A polyp as cemented itself in its skeleton-house so it isn’t able to relocate when conditions change. Coral reefs are one of the most diverse ecosystmes on the planet, definitely in the oceans. Coral is serves as both food and/or shelter for many other species, up to ¼ of all ocean species. And their location means they protect shorelines too. That is a lot of responsibility.Now let’s look at those stressors. Remember middle school chemistry? Yeah, me neither. Here’s a little refresher: water reacts with carbon dioxide to make carbonic acid (H2O + CO2 = H2CO3). Rising atmospheric carbon dioxide (yes, we’re talking climate change here) both increases surface water temperature and water more acidic. That’s two stressors, y’all. And more than 30 percent of human emitted CO2 gets taken up by the oceans. A paper published by Anthony et al. (2008) in PNAS did a nice experiment looking at what happens to coral when the ocean acidifies and/or warms. They collected three of the most important “framework builders” in Heron Reef in the Indo-Pacific and transferred them to lab aquaria: Porolithon onkodes (common crustose coralline algae [CCA] species), Acropora intermedia (a fast growing, branching species), and Porites lobata (a massive species). Next, they used a custom-built CO2 dosing (bubbling) and temperature control system to test different acidification and temperature regimes that simulate doubling and 3- to 4-fold CO2 level increases as projected by the Intergovernmental Panel on Climate Change (IPCC). Then, they waited, they watched, and they took pictures for 8 weeks. From these digital images, they measured the amount of color and reduction in luminance of the corals. They also measured net rates of photosynthesis, respiration, and rates of calcification. They found that increased CO2 (i.e., acidification) led to 40-50 percent bleaching in the Porolithon and A. intermedia. For both of these species, the effect of increased CO2 on bleaching was stronger than the effect of temperature. Porites was less sensitive to increased CO2 alone, but was most sensitive in both stressors. High temperature amplified the bleaching by 10-20 percent in Porolithon and Acropora and 50 percent in Porites. In Porolithon, increased CO2 lead to a severe decline in productivity and calcification that was exacerbated by warming. Acropora’s productivity actually maximized with intermediate increases in CO2, but dropped at higher levels. Porites's productivity dropped with high CO2 but not like that of the Acropora. These species had similar calcification responses to each other, each much less than Porolithon. Overall, the authors proposed that CO2 induces bleaching through its impact on photoprotective mechanisms. Porolithon was the most sensitive to acidification, which is concerning because it is a primary reef-builder and serves as a settlement cue for invertebrate larvae (including other corals).A very recent study by Perry and Morgan (2017) in Scientific Reports zoomed out to look at corals at a large scale. They looked at magnitude of changes that followed the El Niño/Southern Oscillation (ENSO)-induced Sea Surface Temperature (SST) warming anomaly that affected the central Indian Ocean region in mid-2016, sort of a natural experiment. The ENOS-induced SST warming was above the NOAA “bleaching threshold,” defined as the point where SST is 1°C warmer than the highest monthly mean temperature. To do this they went to reefs in the southern Maldivian atoll of Gaafu Dhaalu, ran transects (basically, a line along which you measure stuff), and collected data on coral mortality, substrate composition, reef rugosity (a measure of complexity), and gross carbonate production and erosion. Then they determined carbonate budgets for the 3-dimensional surface of the reefs (there are equations…I won’t go into it…you’re welcome). They found extensive coral mortality over 70 percent. This was mostly driven by branching and tabular Acropora species (remember them from the last study?), which declined by an average of 91 percent! All of this coral death resulted in a decline in the net carbonate budgets. This decline reflected both reduced coral carbonate production and increased erosion by parrotfish as they graze on the algal film that grows on coral rock. Pre-coral bleaching, carbonate production was dominated by branching, corymbose and tabular species of Acropora; post-bleaching production by non-Acropora increased, with massive and sub-massive taxa (e.g., Porites species) more than doubling. Together, carbonate budgets were reduced by an average of 157 percent! All of this equates to a rapid loss in coral cover, growth potential, and structural complexity. The overall impact of the carbonate budget was profound and has major ecological implications. These habitats have gone from a state of strong growth potential to one of net framework erosion and breakdown; basically, the reefs are eroding faster than they are growing. And it may take 10-15 years for a full recovery, depending on the frequency of similar anomalies.So what’s the take-away from all of this? Corals are sensitive to their environment, but not all species of corals respond equally. Climate change is a huge factor in health and recovery of coral reefs, and steps need to be taken soon if we want to keep these little guys and the phenomenal habitats that they create. Here are the studies:... Read more »

  • February 24, 2017
  • 06:00 AM
  • 263 views

Friday Fellow: B. coli

by Piter Boll in Earthling Nature

by Piter Kehoma Boll It’s time to give more space for parasites, including human parasites! So today our fellow comes right from the stool of many mammals, including humans. Its name is Balantidium coli, or B. coli for short. B. coli is … Continue reading →... Read more »

Schuster, F., & Ramirez-Avila, L. (2008) Current World Status of Balantidium coli. Clinical Microbiology Reviews, 21(4), 626-638. DOI: 10.1128/CMR.00021-08  

  • February 24, 2017
  • 03:07 AM
  • 291 views

Say my name

by Paul Whiteley in Questioning Answers

"At 9 months of age, infants developing ASD [autism spectrum disorder] were more likely to fail to orient to their names, persisting through 24 months."So said the findings reported by Meghan Miller and colleagues [1] investigating an often over-looked but typically informative question relevant to childhood autism screening and assessment: the response to name. Anyone who knows a little about instruments such as the ADOS (Autism Diagnostic Observation Schedule) will already know about the importance of response to name ("a full response is defined as orientating to and making eye contact with the examiner who calls his name") as part of assessment.Based on the inclusion of some 150 infants, siblings of children with or without a diagnosis of autism, a response to name task was carried out at various intervals in infancy in this prospective study ("6, 9, 12, 15, 18, and 24 months of age"). At 3 years of age, child participants were "classified into 1 of 3 outcome groups: group with ASD (n = 20), high-risk group without ASD (n = 76), or low-risk group without ASD (n = 60)." As per the opening sentence, consistently not responding to their name was a feature of quite a few of those children who subsequently went on to develop autism. Some but not all. Alongside other findings reported in relation to receptive language for example, the authors concluded: "Infants who consistently fail to respond to their names in the second year of life may be at risk not only for ASD but also for greater impairment by age 3 years."Such work continues a theme from some of the authors on the Miller paper [2] and how relatively simple observations during play interaction [3], could be valuable variables when it comes to ascertaining potential risk of developing autism. Of course one needs to be careful that a lack of response to name does not automatically mean that an autism diagnosis is imminent or indicated as per the typical requirement to check a child's hearing for example and to consider the possibility of other diagnoses being applicable. I might also remind readers of the potential effects of regression when it comes to autism (see here) and how not every child presents with autistic features in early infancy (something that needs to be taken into account when it comes to other recent research too).To close, say my name...----------[1] Miller M. et al. Response to Name in Infants Developing Autism Spectrum Disorder: A Prospective Study. J Pediatr. 2017 Feb 2. pii: S0022-3476(16)31566-9.[2] Nadig AS. et al. A prospective study of response to name in infants at risk for autism. Arch Pediatr Adolesc Med. 2007 Apr;161(4):378-83.[3] Trillingsgaard A. et al. What distinguishes autism spectrum disorders from other developmental disorders before the age of four years? Eur Child Adolesc Psychiatry. 2005 Mar;14(2):65-72.----------Miller M, Iosif AM, Hill M, Young GS, Schwichtenberg AJ, & Ozonoff S (2017). Response to Name in Infants Developing Autism Spectrum Disorder: A Prospective Study. The Journal of pediatrics PMID: 28162768... Read more »

Miller M, Iosif AM, Hill M, Young GS, Schwichtenberg AJ, & Ozonoff S. (2017) Response to Name in Infants Developing Autism Spectrum Disorder: A Prospective Study. The Journal of pediatrics. PMID: 28162768  

  • February 23, 2017
  • 02:59 AM
  • 314 views

"Autoimmune epilepsy is an underrecognized condition..."

by Paul Whiteley in Questioning Answers

"Among adult patients with epilepsy of unknown etiology, a significant minority had detectable serum Abs [autoantibodies] suggesting an autoimmune etiology."So said the findings reported by Divyanshu Dubey and colleagues [1] continuing a research theme previously discussed on this blog (see here) on how epilepsy / seizure-type disorder(s) for some might have more to do with immune function than many people might think.OK, a brief bit of background: epilepsy is a blanket term covering a wide variety of different presentations that affect the brain and specifically, 'the electrics' of the brain. Seizures are the most common symptom. Treatment typically comes in the form of anti-epileptic medicines (although other options are being considered for some). It's been known for a while that outside of the 'brain' focus of epilepsy, other biological systems might also play a role in the development/maintenance of the condition(s); specifically the immune system and quite often in cases where traditional anti-epileptic medicines don't seem to be able to control seizures effectively. The details are still a little sketchy but studies like the one from Dubey et al are trying to put some scientific flesh on to the bones of what facets of the immune system are potentially involved, specifically under 'autoimmune' conditions where the body fails to recognise 'self' as self and mounts an immune response against the body's own tissue(s).Dubey and colleagues looked at a group of participants "presenting to neurology services with new-onset epilepsy or established epilepsy of unknown etiology" and tested donated serum samples "for Abs reported to be associated with autoimmune epilepsy (NMDAR-Ab, VGKCc-Ab, leucine-rich glioma-inactivated protein 1 [LGI1] Ab, GAD65-Ab, γ-aminobutyric acid type B receptor [GABAB] Ab, α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic receptor [AMPAR] Ab, antineuronal nuclear antibody type 1 [ANNA-1 or anti-Hu] Ab, Purkinje cell cytoplasmic antibody type 2 [PCA-2] Ab, amphiphysin Ab, collapsin-response mediator protein 5 [CRMP-5] Ab, and thyroperoxidase [TPO] Ab)." Quite a lot of those autoantibodies probably sound like gibberish to the lay reader but some of them have been discussed in other contexts on this blog (see here and see here for examples).Results: some (15) of the 127 participants initially enrolled in the study were "subsequently excluded after identification of an alternative diagnosis." This in itself is interesting, as diagnoses such as "hypoxic or anoxic injury following cardiac arrest" and "ischemic stroke" are mentioned, illustrating how several different roads can lead to epilepsy and/or the presentation of seizures.Then: "Serum Abs suggesting a potential autoimmune etiology were detected in 39 (34.8%) cases." Over a third of the cohort showed serological evidence of autoantibodies and some presented with more than one type of autoantibody as being present. Breaking down those serologically positive participants, we are told that: "19 patients (48.7%) had new-onset epilepsy and 20 patients (51.3%) had established epilepsy." The authors did also subsequently limit their findings to those cases excluding TPO-Ab and low-titer GAD65-Ab (autoantibodies where a specific role to epilepsy is unclear or not specific) but even then reported that: "23 patients (20.5%) with unexplained epilepsy had positive serologic findings strongly suggestive of an autoimmune cause of epilepsy." There is also a final part to the Dubey paper which also merits mention: "Among the 23 patients who were seropositive, 15 (65.2%) received some sort of immunotherapy. Better seizure outcome was associated with use of immunomodulatory therapy... especially with use of intravenous methylprednisolone... or plasmapheresis."Alongside other (independent) studies in this area, the peer-reviewed evidence does seem to growing to suggest that within the wide (and heterogeneous) 'spectrum' that is epilepsy, at least some of that epilepsy might have an important immune component to it. To quote again from Dubey: "The data presented here suggest that autoimmune encephalitis may explain at least 20% of adult-onset epilepsies of unknown etiology." Aside from the importance of screening for said autoantibodies when certain cases of epilepsy appear at clinic, there are a few other potentially important points that could be raised about such data. Autism is area that I would be interested to see some further investigations carried out on with the Dubey findings in mind. Epilepsy is an important comorbidity 'over-represented' when it comes to autism (see here) and given the suggestions down the years that immune function (specifically autoimmunity) might be a facet of 'some' autism (see here for example) it's not beyond the realms of possibility that comorbid epilepsy might be a further facet of any autoimmune processes. Birds of an autoimmune feather tend to stick together and all that (see here). Add in the findings specifically talking about 'anti-NMDA-receptor encephalitis "mimicking an autistic regression"' (see here) and how methlyprednisolone might not be an uncommon medicine for some types of (autoimmune-related autistic presentation) and the hypotheses to be tested are laid out in front of you. By saying that, I don't want to take anything away from the more typical forms of epilepsy that can present (either alone or alongside autism) but rather point to the expanding knowledge base suggesting that immune functions may extend much further than just protecting the host from infection et al...To close, slightly related to some of the content included in this post, the trailer for the film Brain on Fire (from the book of the same name) is out and looking like required viewing.----------[1] Dubey D. et al. Neurological Autoantibody Prevalence in Epilepsy of Unknown Etiology. JAMA Neurol. 2017 Feb 6.----------Dubey D, Alqallaf A, Hays R, Freeman M, Chen K, Ding K, Agostini M, & Vernino S (2017). Neurological Autoantibody Prevalence in Epilepsy of Unknown Etiology. JAMA neurology PMID: 28166327... Read more »

Dubey D, Alqallaf A, Hays R, Freeman M, Chen K, Ding K, Agostini M, & Vernino S. (2017) Neurological Autoantibody Prevalence in Epilepsy of Unknown Etiology. JAMA neurology. PMID: 28166327  

  • February 22, 2017
  • 07:18 AM
  • 272 views

Hydrolagus erithacus: New Species of Ghost Shark Discovered

by beredim in Strange Animals



Kristin Walovich holds the newly described species of ghost shark
Photo Credit: Kristin Walovich




Researchers recently announced the discovery of a new species of ghost shark, Hydrolagus erithacus. Ghost sharks - which aren’t actually sharks but instead their closest living relatives - are an extraordinarily rare sighting. Actually, it was just a few months ago, when a ghost shark was filmed... Read more »

  • February 22, 2017
  • 04:20 AM
  • 338 views

History of bipolar disorder = elevated risk of dementia: is vitamin D important?

by Paul Whiteley in Questioning Answers

"History of BD [bipolar disorder] is associated with significantly higher risk of dementia in older adults."So said the systematic review and meta-analysis published by Breno Diniz and colleagues [1] taking in the accumulated peer-reviewed literature on this topic. Including data for some 3000 individuals diagnosed with bipolar disorder and nearly 200,000 controls (without bipolar disorder), authors calculated something of a significantly higher risk of dementia in those with a documented history of bipolar disorder. They note that there is more research to do in this area, specifically on mechanisms and "to evaluate interventions that may reduce the risk of dementia in this population."Outside of the literature included in the Diniz study, similar findings have been reported in the science literature. The paper by Almeida and colleagues [2] noted that: "Bipolar disorder in later life is associated with increased risk of dementia" based on their analysis of ~38,000 older men (65-85 years old) and their "13-year risk of dementia." Perhaps more worryingly were their findings that: "Bipolar disorder was also associated with increased mortality" in relation to "death by suicide, accidents, pneumonia or influenza, and diseases of the liver and digestive system." Other data looking more generally at clinical depression paints a similar picture [3] suggesting something of a connection between various types of depression and risk of various types of dementia: "depressive symptomatology is associated with pathological mechanisms associated with neurodegeneration."I've tackled the topic of dementia a couple of times on this blog; most recently in relation to how incidental vitamin D deficiency *could be* something important when it comes to at least some cases of dementia (see here). Minus any sweeping generalisations and accepting that there may be many different roads leading to dementia and/or bipolar disorder, I am intrigued at the possibility that the sunshine vitamin might be something to consider as a 'connector' between elements of the depression and dementia spectrums as per other findings (see here for example). At the very least, it invites lots more targeted investigation, including whether vitamin D might indeed be a nootropic of choice for some (see here)...----------[1] Diniz BS. et al. History of Bipolar Disorder and the Risk of Dementia: A Systematic Review and Meta-Analysis. The American Journal of Geriatric Psychiatry. 2017. Jan 4.[2] Almeida OP. et al. Risk of dementia and death in community-dwelling older men with bipolar disorder. Br J Psychiatry. 2016 Aug;209(2):121-6.[3] Cherbuin N. et al. Dementia risk estimates associated with measures of depression: a systematic review and meta-analysis. BMJ Open. 2015 Dec 21;5(12):e008853.----------Diniz BS, Teixeira AL, Cao F, Gildengers A, Soares JC, Butters MA, & Reynolds CF 3rd (2017). History of Bipolar Disorder and the Risk of Dementia: A Systematic Review and Meta-Analysis. The American journal of geriatric psychiatry : official journal of the American Association for Geriatric Psychiatry PMID: 28161155... Read more »

Diniz BS, Teixeira AL, Cao F, Gildengers A, Soares JC, Butters MA, & Reynolds CF 3rd. (2017) History of Bipolar Disorder and the Risk of Dementia: A Systematic Review and Meta-Analysis. The American journal of geriatric psychiatry : official journal of the American Association for Geriatric Psychiatry. PMID: 28161155  

  • February 21, 2017
  • 09:00 PM
  • 245 views

Redrawing Ratite Relationships

by Jente Ottenburghs in Evolutionary Stories

Scientists have sequenced the DNA of two extinct birds: the moa and the elephantbird. Comparison with their living relatives led to some surprising findings.... Read more »

Maderspacher F. (2017) Evolution: Flight of the Ratites. Current biology : CB, 27(3). PMID: 28171755  

Yonezawa T, Segawa T, Mori H, Campos PF, Hongoh Y, Endo H, Akiyoshi A, Kohno N, Nishida S, Wu J.... (2017) Phylogenomics and Morphology of Extinct Paleognaths Reveal the Origin and Evolution of the Ratites. Current biology : CB, 27(1), 68-77. PMID: 27989673  

  • February 21, 2017
  • 09:02 AM
  • 341 views

Who Can Swim Further: A Race to the Depths and Back (A Guest Post)

by Miss Behavior in The Scorpion and the Frog

By Jefferson LeThe blue whale (Balaenoptera musculus) is the largest mammal on the planet. Image byNMFS Northeast Fisheries Science Center (NOAA) available at Wikimedia Commons.Helloooooo! My name is Bailey and I am a 25 meter long blue whale, the largest living mammal on Earth! My friend Finley, a 21 meter long fin whale comes in second for largest in size. We had an interesting adventure recently where we were followed by humans. While Finley and I were foraging for food, I overheard the humans talking about investigating our diving behavior when we hunt and not hunt. With that, I will tell you what these foreigners did to investigate our behavior and also what happens when we dive. A chart of whales of different sizes. Image by Smithsonian Institute.To record our dives, the humans travelled to Mexican waters to attach recorders onto our mid-backs using a crossbow. Now, it didn’t hurt much due to my thick blubber. These devices recorded depth of how far we dived, time of dives, and our location. These recorders eventually came off between 5 to 13 hours later. Finley and I were not the only test subjects. Other members of our species were also tagged. After all the data on the devices were collected, the humans finally left our waters and did statistical analyses on our diving behavior. The fin whale (Balaenoptera physalus) rarely exposes its fluke when it prepares to diveto the abyss. Image by Aqqa Rosing-Asvid at Wikimedia Commons.Now, before we talk about what the humans found, I want to share with you the whale secret to a great dive. In case that you ever find yourself in the ocean or your local pool, you can try it! The nose for Finley and I are called blowholes, which are found on top of our heads. This tract is separated from our digestive tract so we do not have to worry about having food go down our blowhole. When I am about to dive, instead of gulping in lots of oxygen, I exhale out as much as I can. This causes my lungs to collapse and flexible walls in my chest allow even more compression. Also, tiny structures in my lungs called alveoli collapse which halts any gas exchange. All of the decrease in lung space decreases buoyancy so I can descend down to the depths. As I descend, my heart rate lessens to reduce energy used during the dive. The oxygen that I had obtained before the dive is stored in my blood and muscle tissue. Since the deep depths are really cold, blood flow is temporarily halted at the thinner areas of my body, like flippers, and some organs to keep the main body going. When I ascend back up, I gradually increase space in my lungs and my alveoli regain full function to allow gas exchange. If you were to ascend too quickly, you could get shallow water blackout or even worse, the “bends” (where nitrogen bubbles in your blood) and I heard it is painful. After ascending is complete, I can release my blowhole open and take in fresh oxygen again. I was secretly told what the results to the humans’ experiments were. They found out that fin and blue whales dove deeper when hunting on shallow dives when not hunting. It makes sense! Why spend so much energy diving when not hunting? Also, they noted that our lunge feeding frequency was different. Lunge feeding is where we propel ourselves towards our prey with our mouth open and grab as much food as we can into our mouth. Blue whales lunged about 2.5 times more than fin whales! That’s a point for the blue! However, the record dive depth came from a fin whale. Hmm… I wonder if Finley broke that record. Did you find my secret and what the humans found interesting? I surely did. I never thought about how I dive and how I behave as it is practically in my blood! Well, the next time you are at a deep pool, try those secrets I spilled to you. It might be fun! Then again, you might be thinking, how does a whale communicate with a human and understand scientific data? That is a secret you may never know… Literature Cited:Croll DA, Acevedo-Gutiérrez A, Tershy BR, & Urbán-Ramírez J (2001). The diving behavior of blue and fin whales: is dive duration shorter than expected based on oxygen stores? Comparative biochemistry and physiology. Part A, Molecular & integrative physiology, 129 (4), 797-809 PMID: 11440866Hill, R. W., G. A., Wyse, M. Anderson. (2008). Animal Physiology. 2:641-660 ... Read more »

Croll DA, Acevedo-Gutiérrez A, Tershy BR, & Urbán-Ramírez J. (2001) The diving behavior of blue and fin whales: is dive duration shorter than expected based on oxygen stores?. Comparative biochemistry and physiology. Part A, Molecular , 129(4), 797-809. PMID: 11440866  

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