New research looks at the factors that influence how we feel after euthanizing a pet.The loss of a pet is a difficult process. People’s feelings of grief may be the same as for losing a human family member. New research investigates some of the factors that may affect people’s grief and sorrow after euthanizing a dog or cat.The study, by Sandra Barnard-Nguyen (University of Sydney) et al, is one of the first to use a survey designed specifically to measure people’s responses to loss of a pet, rather than a human. This takes account of differences in the experience, including the decision to euthanize a pet.A reaction of grief and sorrow on the loss of a pet can be seen as part of a normal psychological process. However in some people there may be feelings of guilt and anger that are more problematic. This type of grief is seen as ‘complicated’ and may sometimes develop into depression or other mental health issues.The study looked at these three types of grief in people who had euthanized a pet in the previous year. Sorrow and grief was measured by questions like “I miss my pet enormously.” Anger might be directed at the person themselves, or at veterinary staff (e.g. “I feel anger at the veterinarian for not being able to save my pet.” Guilt included feeling that “I feel bad that I didn’t do more to save my pet.”One way of understanding our relationship with pets is through attachment theory, the idea being that we become attached to our pets in much the same way as we do to people. From this perspective, you would expect people with a stronger attachment to their pet to feel more grief when the pet dies.And this is one of the findings of the study. People who were more attached to their pet reported more grief and sorrow, and also more feelings of anger (but not guilt).The scientists write,“While guilt can certainly be related to the decision to euthanize a companion animal, it may be the case that pet owners are effectively rationalizing this decision as being in the best interest of the pet. Additionally, veterinary staff may be helpful in explaining the need for euthanasia in end-of-life situations and in supporting and validating the decisions made by pet owners.”The researchers expected to find that people who were younger or lived alone would be more like to experience complicated grief, perhaps because they might have less social support. However, this was not the case, even though it has been found in earlier work. It shows that more research is needed into possible links between owner characteristics and experiences of grief.Finally, they found that the circumstances of euthanasia made a difference to people’s grief. A sudden death for the animal was linked to greater feelings of anger. In contrast, if the pet had had cancer, people had lower feelings of both anger and guilt.The scientists have recommendations for veterinarians:“Identifying pet owners who may be at greatest risk for problematic grief reactions has substantial clinical value for veterinary staff. While veterinary staff should be prepared to support all clients in their grief, recognizing that an owner is highly attached to their pet or that a pet has died a sudden or traumatic death, for example, should trigger additional support responses.”The survey was completed by 409 people who had euthanized a dog (78.5%) or cat in the previous year. The average age of the pet was 10 years old; 52% had died suddenly and 43% had been diagnosed with cancer.Earlier research by Tzivian et al (2015) found that losing a pet is a stressful life event, and social support is important to help people cope. This new research by Barnard-Nguyen et al is an important addition to the literature and helps us to better understand people’s experiences of grief when losing a pet.Although social support is important to everyone who loses a pet, this study suggests some pet owners may need that support even more than others. It also suggests that the way veterinarians support their clients to make decisions about euthanasia and to understand what is in the best interests of the pet may make a difference to people's subsequent grief response.What helped you to cope with losing a pet?Reference Barnard-Nguyen, S., Breit, M., Anderson, K., & Nielsen, J. (2016). Pet Loss and Grief: Identifying At-risk Pet Owners during the Euthanasia Process Anthrozoös, 29 (3), 421-430 DOI: 10.1080/08927936.2016.1181362Photos: mannpuku and Grigorita Ko (both Shutterstock.com)... Read more »
Barnard-Nguyen, S., Breit, M., Anderson, K., & Nielsen, J. (2016) Pet Loss and Grief: Identifying At-risk Pet Owners during the Euthanasia Process. Anthrozoös, 29(3), 421-430. DOI: 10.1080/08927936.2016.1181362
A Blanket high dose vitamin D supplement plan results in elevated levels of vitamin D metabolites after the supplementation is completed. This could result in lower than normal levels of vitamin D, which is the opposite effect of the intended supplementation.... Read more »
Owens DJ, Tang JC, Bradley WJ, Sparks SA, Fraser WD, Morton JP, & Close GL. (2016) Efficacy of High Dose Vitamin D Supplements for Elite Athletes. Medicine and science in sports and exercise. PMID: 27741217
It would be great if, before starting a therapy, it was possible to test small doses of several drugs, at the same time, in a patient and compare their effects on the tumor, so to identify the one that works best.
The study of Yaari and colleagues from the Israel Institute of Technology in Haifa, published in Nature Communication, opens a way to this achievement.... Read more »
Yaari, Z., da Silva, D., Zinger, A., Goldman, E., Kajal, A., Tshuva, R., Barak, E., Dahan, N., Hershkovitz, D., Goldfeder, M.... (2016) Theranostic barcoded nanoparticles for personalized cancer medicine. Nature Communications, 13325. DOI: 10.1038/ncomms13325
Insomnia of sufficient severity to meet clinical significance is estimated to affect up to 20% of the general population.This makes insomnia an important public health challenge.Effective, inexpensive and accessible programs to treat insomnia are needed.One recent controlled clinical trial supports the promise of an online intervention that incorporates key elements of cognitive behavioral therapy (CBT).Lee Ritterband and colleagues at the University of Virginia recently published a controlled clinical trial of online CBT in 303 adults with chronic insomnia. The key elements of design in their study included the following elements:Subjects: Adults with chronic insomnia defined as 30 minutes of insomnia (at onset or during night) 3 nights per week for the last 6 months. Subjects were also required to have total sleep times of 6.5 hours per night or less. Additionally, the insomnia was required to produce significant distress or impairment in function. Subjects had to have a reliable source of access to the internet.Intervention: The experimental intervention was a online automated program known as "Sleep Healthy Using the Internet (SHUTi). This intervention is a weekly internet-based program lasting 6 weeks. The program mimics elements of face-to-face CBT for insomnia. The control intervention consisted of a non-tailored internet-based informational program about insomnia.Outcome Measures: Self-report measure known as the Insomnia Severity Index (ISI) along with sleep diaries. The study demonstrated a statistically significant improvement in multiple sleep measures including the ISI score, duration of onset insomnia and duration of wake time after sleep onset with SHUTi compared to control.SHUTi subjects showed a reduction of sleep onset insomnia time from an average of around 45 minutes at baseline to about 20 minutes at one year follow up.Interestingly there was no difference between experimental treatment and control in total sleep time. However, both groups showed about a 50 minute increase in total sleep time at one year of follow-up.This study is important because it not only demonstrated a significant therapeutic effect for SHUTi but this effect was maintained for a full year. This supports the durability of the the therapeutic effect for this intervention.The authors note limitations to the study include a sample that tended to be highly educated with internet access. Additionally, it was impossible for complete blinding as some subjects likely could guess their assignment based on the content of their internet intervention.Readers with more interest in the SHUTi program can access the official site HERE. The site allows completing the online program for a fee of $135. Readers can access the free full-text manuscript by clicking on the link located in the citation below.Follow me on Twitter WRY999Photo of Christmas lights at Rhema in Tulsa Oklahoma is from my files.Ritterband LM, Thorndike FP, Ingersoll KS, Lord HR, Gonder-Frederick L, Frederick C, Quigg MS, Cohn WF, & Morin CM (2016). Effect of a Web-Based Cognitive Behavior Therapy for Insomnia Intervention With 1-Year Follow-up: A Randomized Clinical Trial. JAMA psychiatry PMID: 27902836... Read more »
Ritterband LM, Thorndike FP, Ingersoll KS, Lord HR, Gonder-Frederick L, Frederick C, Quigg MS, Cohn WF, & Morin CM. (2016) Effect of a Web-Based Cognitive Behavior Therapy for Insomnia Intervention With 1-Year Follow-up: A Randomized Clinical Trial. JAMA psychiatry. PMID: 27902836
The vast majority of professors will gladly meet a prospective graduate student and discuss research opportunities as well as long-term career options, especially if the student requesting the meeting clarifies the goal of the meeting. However, there are cases when students wait in vain for a response. Is it because their email never reached the professor because it got lost in the internet ether or a spam folder? Was the professor simply too busy to respond? A research study headed by Katherine Milkman from the University of Pennsylvania suggests that the lack of response from the professor may in part be influenced by the perceived race or gender of the student.... Read more »
Milkman KL, Akinola M, & Chugh D. (2015) What happens before? A field experiment exploring how pay and representation differentially shape bias on the pathway into organizations. The Journal of applied psychology, 100(6), 1678-712. PMID: 25867167
Occasionally the Sun ejects a pair of magnetized plasma clouds, called coronal mass ejections (CMEs), roughly into the same propagation direction in closely timed sequence. If the second CME is faster than the first one, the CMEs could either just slip through each other or they could collide and interact, [...]... Read more »
Mäkelä, P., Gopalswamy, N., Reiner, M., Akiyama, S., & Krupar, V. (2016) SOURCE REGIONS OF THE TYPE II RADIO BURST OBSERVED DURING A CME–CME INTERACTION ON 2013 MAY 22. The Astrophysical Journal, 827(2), 141. DOI: 10.3847/0004-637X/827/2/141
Increased body fat and physical inactivity may be modifiable risk factors for osteoporosis and sarcopenia. ... Read more »
Lee I, Cho J, Jin Y, Ha C, Kim T, & Kang H. (2016) Body Fat and Physical Activity Modulate the Association Between Sarcopenia and Osteoporosis in Elderly Korean Women. Journal of sports science , 15(3), 477-482. PMID: 27803626
Identify everyone born in Denmark between 1985-2002. Identify those treated "in the primary care setting" for an infection. Identify those diagnosed with schizophrenia and affective disorders. Look-see whether there is an overlap between infection or treated infection and schizophrenia / affective disorders. Report results.That's basically the study published by Köhler and colleagues  (a name that has appeared on this blog before) who concluded that: "Infections treated with anti-infective agents and particularly infections requiring hospitalizations were associated with increased risks of schizophrenia and affective disorders, which may be mediated by effects of infections/inflammation on the brain, alterations of the microbiome, genetics, or other environmental factors."Mention of Denmark as being the source material for such a discovery means, yet again, that those various Scandinavian population registries are proving their 'big data' scientific worth. Indeed, such resources really do put countries such as Blighty to shame insofar as tracking the health of the Nation and at the same, providing science with lots and lots of research nuggets.Taking into account various "confounders", authors report that alongside a possible connection between infection or treatment for infection being 'associated' with schizophrenia / affective disorders there was "a dose-response and temporal relationship" further substantiating their findings. Indeed, those who had to be hospitalised for infection (a serious infection then) were at much greater risk of subsequently being diagnosed with schizophrenia or affective disorders. This tallies with other research on this topic (see here).One more thing: "The excess risk was primarily driven by infections treated with antibiotics, whereas infections treated with antivirals, antimycotics, and antiparasitic agents were not significant after mutual adjustment." Interesting. This suggests that bacterial infections or their treatments, e.g. antibiotics seem to be important factors in relation to the subsequent risk of schizophrenia and/or affective disorders. Again, this is not the first time that this point has been raised (see here and see here) and provides some corroborative evidence as to why the microbiome was mentioned by authors in relation to possible mechanisms to account for their findings.I could start talking about how this research is further evidence for a role for the immune system and/or inflammatory processes in relation to psychiatric labels (see here for example) but you've probably heard it all before I'm sure. What we are also starting to understand with some confidence, is that infection and the effects of it's treatment might go way beyond just the somatic...---------- Köhler O. et al. Infections and exposure to anti-infective agents and the risk of severe mental disorders: a nationwide study. Acta Psychiatr Scand. 2016 Nov 21.----------Köhler O, Petersen L, Mors O, Mortensen PB, Yolken RH, Gasse C, & Benros ME (2016). Infections and exposure to anti-infective agents and the risk of severe mental disorders: a nationwide study. Acta psychiatrica Scandinavica PMID: 27870529... Read more »
Köhler O, Petersen L, Mors O, Mortensen PB, Yolken RH, Gasse C, & Benros ME. (2016) Infections and exposure to anti-infective agents and the risk of severe mental disorders: a nationwide study. Acta psychiatrica Scandinavica. PMID: 27870529
Individual differences may be seen in baseline SCAT3 data between sex, history of concussion, and history of comorbidities. Therefore, using the patient’s personal medical history may add value to the SCAT3 sideline screening.... Read more »
Snedden TR, Brooks MA, Hetzel S, & McGuine T. (2016) Normative Values of the Sport Concussion Assessment Tool 3 (SCAT3) in High School Athletes. Clinical journal of sport medicine. PMID: 27606952
It was inevitable ("it is your destiny") that I would formulate a post about the paper published by Khaled Saad and colleagues  reporting results based on "a double-blinded, randomized clinical trial (RCT)" looking at the potential usefulness of a vitamin D supplement on "the core symptoms of autism in children." Inevitable because the peer-reviewed research literature looking at the sunshine vitamin/hormone in relation to autism is getting rather voluminous (see here and see here for examples) with the promise of lots more to come (see here). The fact that the name Saad in relation to this area of autism research has appeared before on this blog (see here) indicates that this researcher/research group are no strangers to this area of autism science.First, thanks to Alex for the Saad paper. And so... utilising the premier research design, where 109 children* (aged 3-10 years old) diagnosed with an autism spectrum disorder (ASD) were randomly allocated to receive vitamin D drops - "300 IU [international units] vitamin D3/kg/day, not to exceed 5,000 IU/day" - or a placebo drops over 4 months and then tested blind "by the Childhood Autism Rating Scale (CARS), Aberrant Behavior Checklist (ABC), Social Responsiveness Scale (SRS), and the Autism Treatment Evaluation Checklist (ATEC)" before and after their vitamin D or placebo, some interesting results emerged. Their trial and protocol, by the way, was also registered. [*Actually, 120 children were initially allocated to vitamin D or placebo but 11 were lost to follow-up or discontinued participation in the study.]Results: well first and foremost the tenet 'do no harm' seemed to be adhered to as we are told that "vitamin D was well tolerated by the ASD children" at least for the study duration. This is particularly important in light of that case report a few weeks back talking about vitamin D toxicity in the context of autism (see here). Indeed: "The serum levels of 25-hydroxycholecalciferol (25 (OH)D) were measured at the beginning and at the end of the study" kinda shows that authors were probably mindful of possible toxicity issues  alongside wanting to get a little more information about baseline vs. endpoint levels of the stuff. Having said all that the use of vitamin D was not completely side-effect free as 5 children taking the vitamin D drops reported symptoms such as "skin rashes, itching, and diarrhea."Further: "The autism symptoms of the children improved significantly, following 4-month vitamin D3 supplementation, but not in the placebo group." Scores on the CARS (Total scores) showed a "significant decrease" in the vitamin D group compared with the group taking the placebo drops. This was in the direction of vitamin D supplementation positively impacting on the presentation of autistic symptoms. Scores on the ATEC also showed something akin to improvement for those taking the vitamin D drops. As one might expect, measured levels of vitamin D - "serum levels of 25 (OH)D" - rose in the vitamin D supplemented group compared to those in the placebo group.These are interesting results providing some of the first double-blind RCT findings in relation to vitamin D supplementation and autism. I particularly like the fact that alongside well-validated instruments such as the CARS for 'measuring autism', the authors also included the ATEC, an instrument that I have growing fondness for (see here). They also measured functional vitamin D levels (albeit via an ELISA assay - I'd prefer via mass spec!) so it's not difficult to see that minus any unknown variables, the behavioural changes seem to match the biological changes to vitamin D status.There is more to do and indeed, more research in this area is already underway. Larger groups of participants still following that gold standard research methodology will give a more accurate picture and perhaps provide some details about potential best responders to such an intervention (something already hinted at in the Saad data). And then there is the question of 'how' vitamin D might be affecting the presentation of [some] autism. Well, far be it from me to speculate too much, and also taking into account what Saad et al have to say on this matter, I suggest that we might learn a thing or two from looking at vitamin D use in other areas of medicine (see here) and taking things from there...For now, here is what the UK Government says about vitamin D and the population at large although not everyone is convinced...Music: Kate Bush and This Woman's Work....---------- Saad K. et al. Randomized controlled trial of vitamin D supplementation in children with autism spectrum disorder. J Child Psychol Psychiatry. 2016 Nov 21. Vogiatzi MG. et al. Vitamin D supplementation and risk of toxicity in pediatrics: a review of current literature. J Clin Endocrinol Metab. 2014 Apr;99(4):1132-41.----------Saad K, Abdel-Rahman AA, Elserogy YM, Al-Atram AA, El-Houfey AA, Othman HA, Bjørklund G, Jia F, Urbina MA, Abo-Elela MG, Ahmad FA, Abd El-Baseer KA, Ahmed AE, & Abdel-Salam AM (2016). Randomized controlled trial of vitamin D supplementation in children with autism spectrum disorder. Journal of child psychology and psychiatry, and allied disciplines PMID: 27868194... Read more »
Saad K, Abdel-Rahman AA, Elserogy YM, Al-Atram AA, El-Houfey AA, Othman HA, Bjørklund G, Jia F, Urbina MA, Abo-Elela MG.... (2016) Randomized controlled trial of vitamin D supplementation in children with autism spectrum disorder. Journal of child psychology and psychiatry, and allied disciplines. PMID: 27868194
Most neuroscientists will tell you that long-term memories are stored in the brain in the form of synapses, the connections between neurons. On this view, memory formation occurs when synaptic connections are strengthened, or entirely new synapses are formed.
However, in a new piece in Frontiers in Systems Neuroscience, Austrian researcher Patrick C. Trettenbrein critiques the synapse-memory theory: The Demise of the Synapse As the Locus of Memory.
Trettenbrein acknowledges that "t... Read more »
Trettenbrein, P. (2016) The Demise of the Synapse As the Locus of Memory: A Looming Paradigm Shift?. Frontiers in Systems Neuroscience. DOI: 10.3389/fnsys.2016.00088
Fig. 4 (Wexler, 2016). Lindstrom's Electro-Medical Apparatus (ca. 1895), courtesy of the Bakken.
Think the do-it-yourself transcranial direct current stimulation movement (DIY tDCS) is a technologically savvy and hip creation of 21st century neural engineering? MIT graduate student Anna Wexler has an excellent and fun review of late 19th and early 20th century electrical stimulation
... Read more »
Do not mess with Lois.Today I'm posting on the topic of the paper by Rose Nevill and colleagues  concluding: "that while most outcome domains of parent-delivered intervention are associated with small effects, the quality of research is improving."Parent-mediated interventions in relation to autism have been covered on this blog quite recently (see here) accompanied by that 'super-parenting' headline fail. Such approaches work on the idea that helping parents to "develop strategies for interaction and management of behaviour"  might be one route of early intervention when it comes to autism. The research road has however not been smooth when it comes to this class of intervention (see here) and despite some positives (see here) has perhaps not been the overwhelming success that many had hoped for.Nevill and colleagues reviewed 19 trials of parent-mediated interventions for autism ("randomized clinical trials") looking at various outcomes in relation to core symptoms of autism and aspects such as communication and cognitive functions. The results kinda reiterate what we already know that so far, parent-mediated interventions aren't really cutting the statistical mustard when it comes to outcomes and important statistics related to effect sizes. Indeed, the [weighted] Hedge's g statistics produced by the authors on the cumulative data in this area can, at best, be described as 'modest' (and I mean at best). As a comparison, have a look at the Hedge's g stats produced by a meta-analysis of the placebo response when it came to autism : "a moderate effect size for overall placebo response (Hedges' g=0.45, 95% confidence interval (0.34-0.56), P<0.001)" (based on "25 data sets (1315 participants)"). This bearing in mind that the parent-mediated intervention trials don't usually include a placebo condition (and indeed, typically don't even blind - how could you?)I don't want to poo-poo all of this area of autism science because it may still be pretty important. A few things do however worry me about the attention here based on the ideas that parent-child interactions are somehow the be-all-and-end-all of autism (also harking back to the bad 'ole days) and that in these times of continued cost-savings and austerity, parents are being expected to carry out the same services as other professionals. On that first point focused on parent-child interactions, I've always been a little cautious about what this means. Certainly in light of the primary focus on this blog, looking at genetics, epigenetics and biochemistry when it comes to autism, parent-mediated interventions are to be seen as a reactive strategy attempting to deal with 'symptoms' not necessarily causes. Yes, I know 'symptoms' are what parents and other family members see and deal with day in day out, but I'm wondering how successful parent-mediated intervention would be if used in the context of autism secondary to an inborn error of metabolism for example? Surely it makes more sense to spend a little more time ruling out some of the potential reasons why autism or particular autistic features might come about (i.e. screening - see here and see here for some other examples) rather than universally providing a parent-mediated intervention manual and hoping for the best? I might also add that a greater recognition that among 'the autisms' (see here) there may be some important waxing and waning of presentation(s) (see here) potentially influenced by things like the presence of comorbidity too reiterates that every person is an individual and set manuals on parent-child interactions don't necessarily cover all that heterogeneity. And there's also the suggestion that some parent-mediated intervention options are also seemingly failing when it comes to important comorbidities such as anxiety (knowing how disabling these can be) as being something else that needs to be kept in mind.We'll have to see how this area develops further but for now, I don't think anyone can seriously say the existing research on this topic has shown anything like the successes that everyone hoped for. And whilst we should celebrate the fact that "the quality of research is improving" I'm not sure one can blame the limited success of such an approach on previous poor quality research.To close, today is a really, really big day for some of my brood who have their 1st Dan black belt grading. After several years of training, hard work and effort pertinent to their voyages through Shotokan karate it all comes down to examination this evening. Thanks and credit need to go to their Sensei for all their efforts in getting them this far, as well as a certain practitioner who is Shotokan YouTube royalty. Whoever you are, thank you.---------- Nevill RE. et al. Meta-analysis of parent-mediated interventions for young children with autism spectrum disorder. Autism. 2016. Nov 14. Oono IP. et al. Parent-mediated early intervention for young children with autism spectrum disorders (ASD). Cochrane Database Syst Rev. 2013 Apr 30;(4):CD009774. Masi A. et al. Predictors of placebo response in pharmacological and dietary supplement treatment trials in pediatric autism spectrum disorder: a meta-analysis. Transl Psychiatry. 2015 Sep 22;5:e640.----------Nevill, R., Lecavalier, L., & Stratis, E. (2016). Meta-analysis of parent-mediated interventions for young children with autism spectrum disorder Autism DOI: 10.1177/1362361316677838... Read more »
Nevill, R., Lecavalier, L., & Stratis, E. (2016) Meta-analysis of parent-mediated interventions for young children with autism spectrum disorder. Autism. DOI: 10.1177/1362361316677838
Lab protocols on Blastocystis culture, cryopreservation, and subtyping are now available in Wiley Online Library.... Read more »
Stensvold CR, & Clark CG. (2016) Molecular Identification and Subtype Analysis of Blastocystis. Current Protocols in Microbiology. PMID: 27858971
Clark CG, & Stensvold CR. (2016) Blastocystis: Isolation, Xenic Cultivation, and Cryopreservation. Current protocols in microbiology. PMID: 27858970
"I was at a conference, and a colleague was talking about the locomotion of great apes in the trees," says Lewis Halsey, a physiologist at the University of Roehampton in London. The colleague mentioned that it's tough to measure how these animals use energy. That's when Halsey had an epiphany. "I was working with parkour athletes on another project," he says, studying how much energy the athletes used while jumping and climbing around a city. Why not use these human athletes to stand in for... Read more »
Halsey LG, Coward SR, & Thorpe SK. (2016) Bridging the gap: parkour athletes provide new insights into locomotion energetics of arboreal apes. Biology letters, 12(11). PMID: 27881766
Matsutani et al. (2016) reported for the first time BHD syndrome accompanied by pulmonary arteriovenous malformation. The patient, a young male with no significant medical history, presented with chest pain. Chest X-ray and CT revealed emphysematous changes in both lungs and a tumour with pleural fluid. A thoracoscopy revealed dark red pleural fluid and multiple cysts in the lung. The tumour lesion was resected and identified as a non-malignant intrapulmonary hematoma caused by a significant haemorrhage in the pulmonary parenchyma, which was diagnosed as intrapulmonary hematoma. ... Read more »
Matsutani, N., Dejima, H., Takahashi, Y., Uehara, H., Iinuma, H., Tanaka, F., & Kawamura, M. (2016) Birt-Hogg-Dube syndrome accompanied by pulmonary arteriovenous malformation. Journal of Thoracic Disease, 8(10). DOI: 10.21037/jtd.2016.09.68
Gunji-Niitsu, Y., Kumasaka, T., Kitamura, S., Hoshika, Y., Hayashi, T., Tokuda, H., Morita, R., Kobayashi, E., Mitani, K., Kikkawa, M.... (2016) Benign clear cell “sugar” tumor of the lung in a patient with Birt-Hogg-Dubé syndrome: a case report. BMC Medical Genetics, 17(1). DOI: 10.1186/s12881-016-0350-y
by Piter Kehoma Boll Today’s Friday Fellow may not seem to be such an astonishing plant, but it has its peculiarities, some of them quite interesting. Commonly known as Indian shot, African arrowroot, purple arrowroot, and many other names, it … Continue reading →... Read more »
Cui, L., Ouyang, Y., Lou, Q., Yang, F., Chen, Y., Zhu, W., & Luo, S. (2010) Removal of nutrients from wastewater with Canna indica L. under different vertical-flow constructed wetland conditions. Ecological Engineering, 36(8), 1083-1088. DOI: 10.1016/j.ecoleng.2010.04.026
Woradulayapinij, W., Soonthornchareonnon, N., & Wiwat, C. (2005) In vitro HIV type 1 reverse transcriptase inhibitory activities of Thai medicinal plants and Canna indica L. rhizomes. Journal of Ethnopharmacology, 101(1-3), 84-89. DOI: 10.1016/j.jep.2005.03.030
Yes, it is childish but...With all the continued chatter on a possible role for the collected gut microbiota - those wee beasties that inhabit our deepest, darkest recesses - in relation to some autism (see here for example), the paper by Roberta Grimaldi and colleagues  (open-access available here) provides yet more potentially important information.So, poo(p) samples were the starring material in the paper - "obtained from three non-autistic children and three autistic child donors"- and specifically what happened when something called B-GOS "a prebiotic galactooligosaccharide" was added to samples following their journey through a "Three stage continuous culture gut model system" otherwise known as an artificial gut. Said gut model based at Reading University has already been the topic of other news (see here).As well as looking at the initial bacterial profile of those stool samples, researchers plotted the changes to the stool's inhabitants (or what was left of the stool) over the course of B-GOS addition, as well as looking at things like the "production of SCFAs [short-chain fatty acids] in the fermentations" and other metabolites via the gold-standard chemical analytical technique called 1H-NMR (see here for more details).Results: "Consistent with previous studies, the microbiota of ASD [autism spectrum disorder] children contained a higher number of Clostridium spp. and a lower number of bifidobacteria compared to non-autistic children." With the addition of B-GOS to the 'mixture', researchers reported on a significant increase in bifidobacterial populations at the different stages of their gut model and in samples from both those with autism and those without autism. Such "bifidogenic properties of B-GOS" are not unheard of.As to the metabolites of those bacteria present in the poo(p) samples, there were some interesting knock-on effects noted in both raw and B-GOS supplemented samples. "Our data show a lower concentration of butyrate and propionate in autistic models, compared to non-autistic models, but nodifferences in acetate before adding B-GOS into the system." Propionic acid (propionate) has some research history with autism in mind (see here). Butyric acid (butyrate) is something of a rising star in quite a few domains, having also been mentioned in the context of autism too (see here). Indeed it's interesting to note that B-GOS administration "mediated significant production of... butyrate... simulating the transverse and distal colon respectively. There was no effect on propionate." The findings of lower starting levels of butyrate in samples from children with autism were also substantiated by the NMR analyses undertaken. Increases in butyrate and changes to various other metabolites ("increasing ethanol, lactate, acetate and butyrate and decreasing propionate and trimethylamine") were also noted via this analytical method for this group.A long quote coming up: "This in vitro study showed promising and positive results in that supplementing the microbiota of ASD children with 65%B-GOS may manipulate the gut bacterial population and alter metabolic activity towards a configuration that might represent a health benefit to the host. However, further work will be required to assess such changes in an in vivo human intervention study."Just before anyone makes a run on B-GOS or any similar product however, I do need to stress a few important points. First, this was a study of poo(p) samples from 3 autistic children compared with samples from 3 non-autistic children. Aside from the small participant numbers, we don't know anything about participants' various comorbidities (although we know they were "free of any metabolic and gastrointestinal diseases") and only limited information on their dietary habits and medication history. Second, poo(p) was the target material included for analysis and what happened when B-GOS was supplemented during the journey through the artificial gut model. This study said nothing about what happens when real people with autism take B-GOS orally for example, and how it might affect gut bacterial populations and metabolites as it progresses down a real gastrointestinal (GI) tract. This also includes a lack of information on any potential side-effects in a real-world situation. We are also assuming that any supplement survives the stomach. There is quite a bit more to do in this area.But for now, I stick to the idea that the Grimaldi paper provides some potentially important information and certainly, some new routes/methods for further study of the link between prebiotics, probiotics and synbiotics in the context of the gut microbiota and autism...---------- Grimaldi R. et al. In vitro fermentation of B-GOS: Impact on faecal bacterial populations and metabolic activity in autistic and non-autistic children. FEMS Microbiol Ecol. 2016 Nov 16. pii: fiw233.----------Grimaldi R, Cela D, Swann JR, Vulevic J, Gibson GR, Tzortzis G, & Costabile A (2016). In vitro fermentation of B-GOS: Impact on faecal bacterial populations and metabolic activity in autistic and non-autistic children. FEMS microbiology ecology PMID: 27856622... Read more »
Grimaldi R, Cela D, Swann JR, Vulevic J, Gibson GR, Tzortzis G, & Costabile A. (2016) In vitro fermentation of B-GOS: Impact on faecal bacterial populations and metabolic activity in autistic and non-autistic children. FEMS microbiology ecology. PMID: 27856622
Foam rolling may lead to small improvements in dorsiflexion range of motion in the contralateral limb. ... Read more »
Kelly S, & Beardsley C. (2016) SPECIFIC AND CROSS-OVER EFFECTS OF FOAM ROLLING ON ANKLE DORSIFLEXION RANGE OF MOTION. International journal of sports physical therapy, 11(4), 544-51. PMID: 27525179
"Dietary fiber deprivation, together with a fiber-deprived, mucus-eroding microbiota, promotes greater epithelial access and lethal colitis by the mucosal pathogen, Citrobacter rodentium."So said the findings reported by Mahesh Desai and colleagues  meriting an editorial in the publishing journal  as the sentiments of 'eating your greens' applies to some rather interesting [mouse] findings.Fibre (UK spelling) comes in various different forms typically categorised as soluble and insoluble depending on their relationship with water. Using a "gnotobiotic mouse model" - where mice were "colonized with a synthetic human gut microbiota composed of fully sequenced commensal bacteria" - Desai et al reported on the effects of different diets with different fibre content. Their results make for important reading as a fibre-deprived gut was associated with the rise of some rather potent bacteria that seemed to enjoy dining out on the "colonic mucus barrier, which serves as a primary defense against enteric pathogens." Yes, mice gut barriers - or some of their components at least - were being eaten by the very bacteria they contain. Enjoy your lunch.I'm not dwelling too much on the Desai findings, bearing in mind their focus on mice not humans, but I do want to raise a couple of potentially relevant points. First is the focus on the intestinal barrier and how that so-called 'leaky gut' seems to show a connection to dietary fibre intake. Yet more research bringing this woo-like term in from the scientific cold (see here). Next is the idea that if the Desai results are transferable from mouse to humans, they could be relevant to quite a lot of people who perhaps don't enjoy as much dietary fibre as they should. Further, there may be particular groups of people who might be particularly prone to a poor diet  (see here too) where the already discussed term 'leaky gut' is also relevant (see here); also bringing in the idea of a role for those trillions of wee beasties (the gut microbiota) that call us home.I'll be watching for how this research area pans out...---------- Desai MS. et al. A Dietary Fiber-Deprived Gut Microbiota Degrades the Colonic Mucus Barrier and Enhances Pathogen Susceptibility. Cell. 2016 Nov 17;167(5):1339-1353.e21. Gazzaniga FS. & Kasper DL. Veggies and Intact Grains a Day Keep the Pathogens Away. Cell. 2016 Nov 17;167(5):1161-1162. Bandini LG. et al. Changes in Food Selectivity in Children with Autism Spectrum Disorder. J Autism Dev Disord. 2016 Nov 19.----------Desai MS, Seekatz AM, Koropatkin NM, Kamada N, Hickey CA, Wolter M, Pudlo NA, Kitamoto S, Terrapon N, Muller A, Young VB, Henrissat B, Wilmes P, Stappenbeck TS, Núñez G, & Martens EC (2016). A Dietary Fiber-Deprived Gut Microbiota Degrades the Colonic Mucus Barrier and Enhances Pathogen Susceptibility. Cell, 167 (5), 1339-2147483647 PMID: 27863247... Read more »
Desai MS, Seekatz AM, Koropatkin NM, Kamada N, Hickey CA, Wolter M, Pudlo NA, Kitamoto S, Terrapon N, Muller A.... (2016) A Dietary Fiber-Deprived Gut Microbiota Degrades the Colonic Mucus Barrier and Enhances Pathogen Susceptibility. Cell, 167(5), 1339-2147483647. PMID: 27863247
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