Masters athletes complain about aches and pain just as much as anyone else. Maybe more. They may complain more because they tend to hurt themselves fairly often. Masters athletesThe post Masters Athletes: life-long physical activity helps keep your brain from falling apart appeared first on WODMasters.... Read more »
Tseng BY, Gundapuneedi T, Khan MA, Diaz-Arrastia R, Levine BD, Lu H, Huang H, & Zhang R. (2013) White matter integrity in physically fit older adults. NeuroImage, 510-6. PMID: 23769914
Debette S, & Markus HS. (2010) The clinical importance of white matter hyperintensities on brain magnetic resonance imaging: systematic review and meta-analysis. BMJ (Clinical research ed.). PMID: 20660506
I spent last night rewatching the Steven Soderbergh classic “Contagion“. Halfway through I realized that a story of an unidentified, mind-bending infectious brain disease would make the perfect neuroscience halloween tale. This is not “based” on a true story. It IS a true story. The year is 1917. Dr. Constantin Economo sat deep in thought, staring […]... Read more »
Vilensky JA, Foley P, & Gilman S. (2007) Children and encephalitis lethargica: a historical review. Pediatric neurology, 37(2), 79-84. PMID: 17675021
Dourmashkin RR, Dunn G, Castano V, & McCall SA. (2012) Evidence for an enterovirus as the cause of encephalitis lethargica. BMC infectious diseases, 136. PMID: 22715890
Dale RC, Church AJ, Surtees RA, Lees AJ, Adcock JE, Harding B, Neville BG, & Giovannoni G. (2004) Encephalitis lethargica syndrome: 20 new cases and evidence of basal ganglia autoimmunity. Brain : a journal of neurology, 127(Pt 1), 21-33. PMID: 14570817
I ran across an interesting genetic study examining the potential genetic contributions to educational attainment. There have been quite a few genome-wide association studies (GWAS) of intelligence quotient (IQ).... Read more »
Rietveld CA, Medland SE, Derringer J, Yang J, Esko T, Martin NW, Westra HJ, Shakhbazov K, Abdellaoui A, Agrawal A.... (2013) GWAS of 126,559 individuals identifies genetic variants associated with educational attainment. Science (New York, N.Y.), 340(6139), 1467-71. PMID: 23722424
FVIII light chain expressed in Pichia. Antibody AND phospholipid both bind this light chain. Literature says either but not both can bind. ... Read more »
Sudheer Reddy AR, Padikara Kutty Satheeshkumar, & Mookambeswaran A. Vijayalakshmi. (2013) Expression, purification, and partial in vitro characterization of biologically active human coagulation Factor VIII chain (A3-C1-C2) in Pichia pastoris. Applied Biochemistry and Biotechnology. DOI: 10.1007/s12010-013-0338-4
In today’s economic environment, globalization of pharmaceutical products has turned into the key to success for drug manufacturers. Investors in new drug development are therefore required to do more at less cost and faster rate now. However, sponsors are facing a new challenge due to ethnic factors, as the pharmacodynamic or clinical data in the original population could vary with the population in the new region. ... Read more »
by Andrea in Science of Eating Disorders
Recently, I was browsing the Twittersphere and came across (yet another) tweet about so-called “drunkorexia,” or the phenomenon of drinking to excess coupled with restrictive behaviours around food. After firing off a mildly miffed tweet bemoaning our societal tendency to add the suffix “orexia” to all “new” potentially problematic behaviours around food, I took to Scholar’s Portal to see if academics, too, were using this term. I wondered if “drunkorexia” was piquing scholarly interest, or just circulating in media headlines.
Beyond its problematic moniker, coupling problem drinking and restrictive eating is a phenomenon that might be worth delving into in greater detail, particularly if, as the reports claim, its incidence is rising. Barry & Piazza-Gardner (2012) explored the co-occurrence of weight maintenance behaviours and alcohol consumption, and their article clarifies what people mean when they say “drunkorexia.” I’ll get more into my issues with this terminology following a brief overview of the authors’ study.
Alcohol and “Weight Management” Behaviours
Barry & Piazza-Gardner begin their article with reference to an interesting trend observed by those studying problem drinking in …
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Barry AE, & Piazza-Gardner AK. (2012) Drunkorexia: understanding the co-occurrence of alcohol consumption and eating/exercise weight management behaviors. Journal of American College Health, 60(3), 236-43. PMID: 22420701
The effects of IBS on quality of life may be more substantial than those of many other chronic diseases. It affects school, work and life, putting the sufferers at risk for social isolation. Numerous books, columns and blogs about this condition usually affirm that social problems arise because the sufferers are trying to hide the fact they have IBS from others. Keeping secrets is stressful, while being upfront and coming out of the closet is the best strategy. Is it really? Studies about emotional reactions towards people with chronic condition often lead to mixed results. For example, there was a slight increase in the readiness to feel pity to depressed people since the 90s, yet there was no increase in compassion.The most important consequence of TMAU - a metabolic disorder causing an offensive body odor - is social. This condition is not a subject of compassion, but rejection and ridicule resulting in low self-esteem, social ostracizing, anxiety and depression.Obese people (body mass index of 35 or higher - a condition that can't be hidden and kept in secret) are more likely to report day-to-day interpersonal discrimination and mistreatment. Recent study showed that weight discrimination makes people 2.5 times more obese after 4 years of discrimination instead of helping them to reduce their weight. People don't feel compassion as they consider obese individuals lazy, unsuccessful and weak-willed. Same can be applied to IBS."The hardest thing is that other people who don’t have IBS can never understand what it is like”, says a sufferer in comments to an online article. People with IBS are often discriminated and the blows to self-esteem make it harder for them to make meaningful changes to their lifestyle, and to ease the symptoms. Compassion is a very valuable process that motivates sufferers as well as people around them to cooperate in achieving better outcomes. Professional education - based on visual arts and other methods - is often recommended in developing compassionate physicians, dietitians and nurses. But shouldn't we teach society as a whole to be non-judgemental and treat sufferers of chronic conditions with respect and compassion? And what should those with chronic illness do in the current society? Don't view your condition as a weakness and - when you need to tell others about it - keep it unemotional. People don't like sob stories, no matter how true or heartbreaking they are. Don't look for pity, impress them with your strength. Be able to tell the difference between a joke and bullying. Have a laugh with them and try to find better job environments and people that care.REFERENCESSutin AR, & Terracciano A (2013). Perceived weight discrimination and obesity. PloS one, 8 (7) PMID: 23894586Angermeyer MC, & Matschinger H (2004). Public attitudes to people with depression: have there been any changes over the last decade? Journal of affective disorders, 83 (2-3), 177-82 PMID: 15555711Bray L, O'Brien MR, Kirton J, Zubairu K, & Christiansen A (2013). The role of professional education in developing compassionate practitioners: A mixed methods study exploring the perceptions of health professionals and pre-registration students. Nurse education today PMID: 23880325... Read more »
I’m guessing you’ve all heard of oral or genital thrush. It’s very common- one-third of women will have an incidence of vaginal thrush once in their lifetime. You may think thrush is a nasty infection, however the fungus that causes it (Candida albicans) can also enter the bloodstream and spread throughout the body to cause invasive candidiasis, which is much worse.
Symptoms for invasive candidiasis are non-specific, generally they include fever and chills and other symptoms that vary depending on the site of infection. If I haven’t convinced you that it’s bad yet, due to these non-specific symptoms detection and diagnosis generally occurs late in the disease, resulting in a death rate as high as 40%!
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Shapiro RS, Uppuluri P, Zaas AK, Collins C, Senn H, Perfect JR, Heitman J, & Cowen LE. (2009) Hsp90 orchestrates temperature-dependent Candida albicans morphogenesis via Ras1-PKA signaling. Current biology : CB, 19(8), 621-9. PMID: 19327993
The recent PBS Frontline series on concussion sequelae in the NFL is an important advance in the discussion on this important topic. Significant research is needed to better understand the risk of football-related brain injury.An additional important issue on this topic related to the interaction between sport-related brain trauma and developmental stage. Football training and full-contact games begin during elementary school in many parts of the U.S. So this is not just an NFL issue but one throughout the developmental period.I recently reviewed research related to the epidemiology of concussion and concussion sequelae. There is not much good data. I did find one Mayo Clinic study informative and helpful.This study used a historical prospective cohort design utilizing medical record linkage. Briefly, the key elements of the design of this study included:Subjects: Male students playing high school football in Rochester, Minnesota between 1946 and 1956. Controls included male high school students in band, glee club or choir during the same time periodOutcome: Medical record review to identify later diagnoses of dementia, Parkinson's disease or amyotrophic lateral sclerosis (ALS)Analysis: Hazard ratios for football players versus control using Cox proportional hazards analysis and rates of outcome diagnoses compared to expected for populationThe study identified 438 football players who were an average age of about 48 years by the time of study. Thirteen (3.0%) of football players had a medical record diagnosis of dementia, ten (2.3%) a diagnosis of Parkinson's disease and two (0.5%) a diagnosis of ALS.In a case-control analysis, none of the three outcomes were statistically increased in high school football players. Although, it should be noted the hazard ratio estimate for dementia was 1.58 with a 95% confidence interval of 0.36 to 7.01. Dementia rates in the football players were also lower than rates in the general population. There was a slight increase in Parkinson's disease rates in the football players (as well as band/choir) cohort compared to population rates.There are some weaknesses in the study design but this still represents one of the very few studies of long-term outcome among high-school footballers. Of note, this cohort played during a time before modern helmets and the style of play may have been significantly different without helmets. The authors note, skull fractures and deaths related to football have decreased since the development of modern helmets. The risk of concussion with helmets is unclear. Current helmets may have limited effect in reducing concussion risk.The current study and the PBS Frontline special highlight the need for better longitudinal studies of football, brain injury and brain injury sequelae risk. This Mayo Clinic study should provide some reassurance that playing high school football during the 1950s and 60s may not have been a severe environmental risk for later trauma-related dementia.Photo of two University of Nebraska football players preparing for game is from the authors files. Information about the PBS Frontline NFL Concussion project can be found here. Savica R, Parisi JE, Wold LE, Josephs KA, & Ahlskog JE (2012). High school football and risk of neurodegeneration: a community-based study. Mayo Clinic proceedings. Mayo Clinic, 87 (4), 335-40 PMID: 22469346... Read more »
Savica R, Parisi JE, Wold LE, Josephs KA, & Ahlskog JE. (2012) High school football and risk of neurodegeneration: a community-based study. Mayo Clinic proceedings. Mayo Clinic, 87(4), 335-40. PMID: 22469346
Ginger a sailor's best friend? An apple a day keeps the docter away? All kinds of health benefits of seawater, seaweed and silver? I decided to find out if actual peer-review concurs in any way to these claims. Turns out there is some agreement.... Read more »
Slapak I, Skoupá J, Strnad P, & Horník P. (2008) Efficacy of isotonic nasal wash (seawater) in the treatment and prevention of rhinitis in children. Archives of otolaryngology--head , 134(1), 67-74. PMID: 18209140
Nezamoddin Berjis, Seyyed Mehdi Sonbolastan, Seyyed Hanif Okhovat, Ali Asghar Narimani, & Jaleh Razmjui. (2011) Normal Saline Versus Hypertonic 3% Saline: It’s Efficacy in Non-Acute Rhinosinusitis . Iranian Journal of Otorhinolaryngology. info:/
Zava TT, & Zava DT. (2011) Assessment of Japanese iodine intake based on seaweed consumption in Japan: A literature-based analysis. Thyroid research, 14. PMID: 21975053
Jun Sung Kim, DVM, PhD,a Eunye Kuk, MS,b Kyeong Nam Yu, MS,a Jong-Ho Kim, MS,g, Sung Jin Park, BS,a Hu Jang Lee, DVM, PhD,c So Hyun Kim, DVM, PhD,d, Young Kyung Park, DVM, MS,d Yong Ho Park, DVM, PhD,d, Cheol-Yong Hwang, DVM, PhD,e Yong-Kwon Kim, PhD,f Yoon-Sik Lee, PhD,g, Dae Hong Jeong, PhD,b,, & Myung-Haing Cho, DVM, PhD. (2007) Antimicrobial effects of silver nanoparticles. Nanomedicine: Nanotechnology, Biology, and Medicine. DOI: 10.1016/j.nano.2006.12.001
Nanthakomon T, & Pongrojpaw D. (2006) The efficacy of ginger in prevention of postoperative nausea and vomiting after major gynecologic surgery. Journal of the Medical Association of Thailand . PMID: 17725149
Regular readers are probably quite tired of hearing me go on about autoimmunity and autism. It's a research topic which seems to come up pretty regularly these days for all manner of reasons and in all manner of places (see here). Indeed, now even being linked to the new kid on the block that is MAR autism (see here).As I've mentioned before, I don't think we can quite say that all autism (all of the autisms sorry) 'are autoimmunity' because immune function is a pretty varied thing when it comes to autism. But there is a growing evidence base to suggest that we should be looking into this issue with much greater assiduity for at least some on the autism spectrum and whether markers of autoimmunity might be related to presented symptoms or at the very least, affecting aspects of quality of life.A further addition to the area of autoimmunity and autism is that of the paper by Careaga and colleagues* who quite recently reported on the presence of increased anti-phospholipid antibodies** in a cohort of children diagnosed with an autism spectrum condition as part of the CHARGE study.As per the very informative description by Misita and Moll**, anti-phospholipid antibodies (APLAs) reflect activity by the immune system against a class of substances called phospholipids which are a vitally important part of cell membranes. Some of the main issues associated with the presence of APLAs relates to blood clots and pregnancy loss as per the description of anti-phospholipid syndrome (APS) or Hughes syndrome.Careaga et al (carrying quite an impressive authorship list it has to be said) looked at the presentation of various APLAs across three groups: children diagnosed with an autism spectrum disorder (ASD) (n=54), children diagnosed with a developmental delay (but not autism) (n=22) and typically developing controls (n=33). They looked at antibodies to anticardiolipin, antiphosphoserine, and anti-β2-glycoprotein 1 across each of the groups and further whether levels of these APLAs correlated with specific behaviours or impairments in behaviours.The results: well, comparing the autism group vs. the typically developing group, levels of each of the APLAs were higher in autism (and significantly so). Aside from the cardiolipin antibodies, the other APLAs were also significantly higher in the autism group compared with the developmental delay group too. Ergo, another study finding "increased presence of autoantibodies in children with ASD". When examined alongside various behavioural functions derived from schedules such as the VABS, there were also some significant correlations noted (see here) but "no significant differences found when analyzing within the individual groups based on diagnosis".It is worth pointing out that although these APLAs were detected in higher concentrations in the autism group (a) not every child with autism had significant elevations in these antibodies and (b) "the levels are below what is considered clinically significant levels for APS". Importantly too that even if levels of APLAs were getting into the APS diagnostic range, the study results in themselves probably wouldn't be able to diagnose APS given the need for two separate testing occasions (see here) and other criteria.Looking at some of the published research literature around APLAs, I stumbled across a few potentially important connections. Abisror and colleagues*** reported on some preliminary observations of offspring autism in children born to mums with APS. This following similar preliminary reporting (see here) bearing in mind that a chance association cannot at this point, be ruled out. That being said, all that recent chatter about MAR autism (see here) and maternal immune activation and behavioural issues (see here) must also be thrown into the research mix too. When looking also at a condition like attention-deficit hyperactivity disorder (ADHD) however, which has more than once been linked to cases of autism (see here), other investigations have not found any relationship between APLAs and behavioural presentation****. So one needs to remain a little guarded about how the Careaga results will eventually pan out.I do think there is more to do in the area of APLAs and autism. The link between APLAs during pregnancy and adverse birth outcomes such as preterm birth (see here) and low birth weight (see here) must be seen as important confounding variables given the complicated links made in these areas with offspring autism risk (see here). The findings that at least some people with APLAs will eventually go on to be diagnosed with autoimmune conditions such as systemic lupus erythematosus (SLE) or related mixed connective tissue disorder is also worthy of greater investigation; indeed whether conditions like SLE are likely to be more prevalent among mums and dads of children with autism (as per the recent suggestion) particularly those with elevated APLAs (oh, we're back to MAR autism again).I'm gonna stop there for now. On purpose I've not headed too far into the mechanism of how elevated levels of APLAs detected in cases of autism might work, simply because I'd rather see some independent replication of these results first before heading down the path of speculation. But still I remain very interested in the Careaga findings....Some music to close, and in memory of Lou Reed, a Velvet Underground special: I'm Waiting for the Man.----------* Careaga M. et al. Increased Anti-Phospholipid Antibodies in Autism Spectrum Disorders. Mediators of Inflammation. 2013: 935608.** Misita CP. & Moll S. Antiphospholipid Antibodies. Circulation. 2005; 112: e39-e44.*** Abisror N. et al. Autism spectrum disorders in babies born to mothers with antiphospholipid syndrome. Semin Arthritis Rheum. 2013 Jul 30. pii: S0049-0172(13)00149-2. doi: 10.1016/j.semarthrit.2013.07.001.**** Bujanover S. et al. Lack of association between anti-phospholipid antibodies (APLA) and Attention Deficit/Hyperactivity Disorder (ADHD) in children. Clin Dev Immunol. 2003 Jun-Dec;10(2-4):105-9.----------... Read more »
Milo Careaga,Robin L. Hansen,Irva Hertz-Piccotto,Judy Van de Water,Paul Ashwood. (2013) Increased Anti-Phospholipid Antibodies in Autism Spectrum Disorders. Mediators of Inflammation. DOI: 10.1155/2013/935608
Photo: Steven PamThere is an industry in Australia that relies on an integral piece of equipment, but the system behind product development process is flawed, and lives are at stake. From farm dogs to military explosive detection dogs, guide dogs to greyhounds, Australia’s working and sporting dog industry claims a 50-70% fail rate as normal. The welfare of these dogs is intimately linked to their working performance. It can be an emotive topic, so let’s take the emotion out of it and objectively consider current practice.A diverse industry, with four sectors operating in different domains, is dependent on one key piece of equipment. A tool that can vary in price from free to $40,000, can be purchased new or second hand, but is unequivocally required to get the job done. Hundreds of thousands of units are currently used daily throughout Australia in government, human health, sporting and private operations.SourcePractitioners invest resources in this equipment, only to find that the tool doesn't work. It’s unsuitable. It operates at the wrong speed. It breaks. It just doesn't do the work it was meant to - at least half of the time! In some industry sectors, the equipment fail rate is estimated as high as eighty percent. Waste units are disposed of and new ones sourced. Perhaps from a large scale manufacturer, perhaps from a private artisan, or some people go ahead and take a crack at making their own. Recycling within the industry is extremely low, at less than ten percent. The production of this equipment is currently inefficient; the industry has no validated minimum standards in place and the product lacks quality assurance. From an industry business and performance perspective, what should be done? A review of the purpose and production life-cycle analysis for this tool seems indicated? Absolutely. A review of how the equipment is being employed, handled, maintained and stored by practitioners? Yes. Perhaps a review of the training courses and educational materials available to the practitioners and the people who train them? For sure.SourceWithout objective review and subsequent improvement, this industry is leaving itself open to scrutiny by the media and risks losing public support. Review of this kind is common. In industrial design and quality management fields, validation of product integrity, ongoing review and updating of evidence-based best practice are standard. Re-purposing of surplus or malfunctioning stock into other areas rather than directly to landfill may require additional resources. However, this extra spend is important as tolerance for unnecessary waste in the 21st century is limited. Indeed, the sustainability and economic viability of this industry into the future relies on improved accountability, higher transparency and demonstrated responsibility.We owe this commitment to review and refine the production, management and education surrounding this device to the industry, the people involved and the tasks they achieve. It’s sound business practice. And we owe it to the dogs.Hi Julie,I wrote this because I wanted to consider if there was a good case to be made for improving the welfare of working dogs, without the emotion or emotive slant often inherent in animal welfare discussions. This came about after recent conversations with people who have suggested my work towards improved working dog welfare is based on me 'loving dogs' or having bleeding-heart, idealistic expectations about the way dogs should be cared for. I hope I have been able to demonstrate that this is a) not about me, and b) that a good argument for objective review and assessment of how working dogs are produced can be made, even before adding consideration for the fact these are sentient animals with capacity to thrive or suffer as a result of how we manage their lives.I'm looking forward to continuing these conversations at the Working Dog Conference 2013 next week.Wish you were here,... Read more »
Kruger Justin, & Dunning David. (1999) Unskilled and unaware of it: How difficulties in recognizing one's own incompetence lead to inflated self-assessments. Journal of Personality and Social Psychology, 77(6), 1121-1134. DOI: 10.1037//0022-3518.104.22.1681
Dunning David, Johnson Kerri, Ehrlinger Joyce, & Kruger Justin. (2003) Why people fail to recognize their own incompetence. Current Directions in Psychological Science, 12(3), 83-87. DOI: 10.1111/1467-8721.01235
Ehrlinger Joyce, Johnson Kerri, Banner Matthew, Dunning David, & Kruger Justin. (2008) Why the unskilled are unaware: Further explorations of (absent) self-insight among the incompetent. Organizational Behavior and Human Decision Processes, 105(1), 98-121. DOI: 10.1016/j.obhdp.2007.05.002
Dunning David. (2011) The Dunning-Kruger effect: On being ignorant of one's own ignorance. Advances in Experimental Social Psychology, 247-296. DOI: 10.1016/B978-0-12-385522-0.00005-6
There are lots of exciting new ideas for fighting cancer. One idea is to genetically engineer T cells against cancer – but how exactly do we go about programming this ‘search and destroy’ activity? ... Read more »
Does your workweek schedule dig you into an ever-deepening hole of sleep deprivation? Do you sleep in on the weekends to try to boost yourself back out? You're in good company. But even if you feel recovered by the following week, your brainpower might be suffering.
In a survey by the National Sleep Foundation, 40 percent of respondents said they try to "catch up" on sleep during the weekend. Pennsylvania State University professor and physician Alexandros Vgontzas, along with a group of colleagues, recruited 30 subjects to study how well this catching up really works. The subjects were healthy men and women between 18 and 34 (who didn't mind the prospect of sleeping with a catheter in their arm).
For two weeks before the study, researchers made sure subjects got 7.5 to 8 hours of sleep every night. Then the subjects came into the sleep lab. The experiment began with three "baseline" nights of 8 hours' sleep. For the next five nights, their sleep was restricted to just 6 hours, mimicking a full workweek of uncomfortably early rising. Then subjects had two "recovery" nights where they were left sleeping for 10 hours.
During most days of the experiment, subjects were allowed to go home and follow their normal routine—though monitors on their wrists made sure they followed strict no-napping instructions. At night, they returned to the lab. And after each phase of the experiment, subjects spent a full 24 hours undergoing tests: researchers tracked the levels of hormones circulating in their blood and gave them cognitive tests. They also asked subjects to rate how sleepy they felt. To measure their actual sleepiness, researchers had subjects lie down to nap, recorded how long it took them to conk out, and woke them up again—six times a day.
Predictably, subjects were sleepier during their week of sleep deprivation. It took them less time to fall asleep during the day, and the easiest time for them to nap was 9:00 in the morning (as opposed to 3:00 in the afternoon during the baseline period). After their two recovery days, subjects' sleepiness returned to normal.
One hormone the scientists monitored was IL-6, a marker of inflammation in the body. They found that IL-6 increased when subjects lost sleep. This fits with what earlier studies have found, and suggests one way sleep deprivation is bad for your health. IL-6 levels dropped back to normal after the two nights of recovery sleep.
The only measurement that didn't go back to normal was performance on a test called the psychomotor vigilance task (PVT). Subjects did this test every two hours during their lab days. In it, they watched a screen for ten minutes and pressed a button every time a certain number appeared. It's a test that measures a person's ability to sustain attention; astronauts on the International Space Station do a similar test on themselves to check for fatigue.
Subjects in the sleep study did worse on the PVT after their sleep-deprived week, and continued to do poorly even after two nights of catch-up sleep. Vgontzas says he doesn't know why this is. But apparently some function in people's brains hadn't recovered fully by the end of the experiment, even though they felt well rested.
It's worth noting that because there was a 24-hour testing period after each stage of the experiment, subjects actually had a sixth night of poor sleep before their "weekend." And some champion snooze-button users can sleep well past 10 hours on their real makeup days. Still, Vgontzas's findings suggest our brains are slow to catch up after losing sleep—specifically, our ability to pay attention suffers—and we might not know when we're mentally fatigued.
Vgontzas also doesn't know what the cumulative effect might be of living this way every week. On average, he writes, we need seven hours of sleep a night. (Though if you really can't sleep any later, a nap during the day will also help you recover.)
Image: by Phae (via Flickr)
Pejovic S, Basta M, Vgontzas AN, Kritikou I, Shaffer ML, Tsaoussoglou M, Stiffler D, Stefanakis Z, Bixler EO, & Chrousos GP (2013). Effects of recovery sleep after one work week of mild sleep restriction on interleukin-6 and cortisol secretion and daytime sleepiness and performance. American journal of physiology. Endocrinology and metabolism, 305 (7) PMID: 23941878
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Pejovic S, Basta M, Vgontzas AN, Kritikou I, Shaffer ML, Tsaoussoglou M, Stiffler D, Stefanakis Z, Bixler EO, & Chrousos GP. (2013) Effects of recovery sleep after one work week of mild sleep restriction on interleukin-6 and cortisol secretion and daytime sleepiness and performance. American journal of physiology. Endocrinology and metabolism, 305(7). PMID: 23941878
The term MAR autism - maternal autoantibody-related autism - whilst still a relatively new addition to the autism research vocabulary, has nevertheless already courted some controversy. This follows a decision to try and commercialise the growing research base in this area (see here) which raised a few eyebrows in various quarters.Speculating on a dead cat bounce? @ Wikipedia As I indicated on my previous post about said commercialisation, there are a few questions which perhaps need answering before this work starts down the path of becoming any sort of reliable 'autism test'. Some of these questions being particularly important if one is to learn the lessons from another proposed autism test which came across a few problems in replication recently (see here).Away from such discussions, the notion that a proportion of mums of children with autism spectrum disorder (ASD) "have antibodies in their bloodstream that react with proteins in the brain of their babies" is potentially a very important finding. The evidence for such a process is actually becoming quite consistent (see here) following on from other investigations pointing at some role for the maternal immune system when it comes to at least some cases of autism (see here).The paper by Lior Brimberg and colleagues* adds to the autism - maternal anti-brain antibodies story with their findings suggesting that "Mothers of an ASD child were four times more likely to harbor anti-brain antibodies than unselected women of child-bearing age (10.5 vs 2.6%)" based on the analysis of collected data from one or two quite large autism study initiatives (Simons Simplex Collection and Autism Genetic Exchange Resource). This in itself would be a worthy confirmatory research finding bearing in mind the number of plasma samples that were analysed as part of the study.But of perhaps equal importance was the observation that "The analysis of ASD mothers with brain-reactive antibodies also revealed an increased prevalence of autoimmune diseases, especially rheumatoid arthritis and systemic lupus erythematosus". This point was covered by other commentary of this study (see here) including findings related to the detection of anti-nuclear antibodies (ANAs) (53% vs 13.4%) in autism mums with and without the anti-brain antibodies respectively.Those who regularly visit this blog might know about my interest in all things autoimmunity with autism in mind (see here). The suggestion that the presence of brain reactive antibodies seemed to correlate with an increased frequency of maternal autoimmune conditions or their biological links represents yet another possible connection between autoimmunity and autism, at least some cases of autism.With my speculating hat firmly in place, I wondered about a couple of things as a result of these findings. I wondered for example, whether the anti-nuclear antibodies were also present in offspring of those mums who tested positive for both brain reactive antibodies and ANAs. I note that ANAs have been previously reported in cases of autism as per the findings of Mostafa and Kitchener** who observed: "Children with autism had a significantly higher percent seropositivity of anti-nuclear antibodies (20%) than healthy children (2.5%; P < 0.01)". That and their suggestion: "Anti-nuclear antibody seropositivity was significantly higher in autistic children with a family history of autoimmunity than those without such history (36.8% and 5%, respectively; P < 0.001)" makes for some interesting connections.Harking back to the ScienceDaily piece on the Brimberg study (see here) I was also intrigued by the suggestion that a 'leaky' blood-brain barrier may "allow the "anti-brain" antibodies to pass through to the babies' brains, possibly causing autism".Now just before I get too carried away with this, there has been a bit of debate down the years about just when the blood-brain barrier (BBB) actually becomes effective in the foetus and infant. The more recent discussions suggest that there is a "well developed barrier mechanisms in the developing brain". This contrasts with other reports such as the study by Volodin and colleagues*** suggesting that the final establishment of the foetal BBB, under typical circumstances, is carried out in the latter stages of gestation. I'll leave readers to draw their own conclusions on which is the correct position.This barrier however, partly physical and partly biochemical, is susceptible to 'damage' under certain circumstances as reported in an older post on this topic (see here). That alongside some of the gatekeeper molecules such as P-glycoprotein which help transport things through the BBB (see here) being potentially susceptible to 'alteration' as a function of various factors, means that BBB permeability is influenced by quite a few fluidic variables.If one assumes that, as in the example of a potential link between maternal SSRI use during the first trimester of pregnancy and offspring autism risk (see here**** and here for my post), early stage pre-completed formation of the infant BBB is a 'risk' time for the developing foetus and its susceptibility to things like anti-brain antibodies and/or ANAs, one might get a sense of how and when such a process "possibly causing autism" may come about. I hasten to add that I'm still speculating at this point.With leaky membranes in mind and the still-awaited peer-review publication of some conference proceedings from the lab of Paul Patterson (see here) on the suggestion of leaky gut present in their maternal immune activation offspring mouse model, I'm also wondering whether there may be another connection to be had here too. Various autoimmune conditions have been talked about with gut hyperpermeability in mind; ranging from gastrointestinal conditions such as coeliac disease (see here*****) to type 1 diabetes (see here******). It's not necessarily an all-or-nothing relationship but leaky gut and autoimmunity (with other factors such as gut bacteria also in the mix) is certainly on the scientific map.In a similar vein to the ANA story, I'm wondering whether there may be m... Read more »
Brimberg L, Sadiq A, Gregersen PK, & Diamond B. (2013) Brain-reactive IgG correlates with autoimmunity in mothers of a child with an autism spectrum disorder. Molecular psychiatry. PMID: 23958959
Everyone knows that too much sugar is bad for you, but how much is too much? According to a study …Continue reading »... Read more »
Ruff JS, Suchy AK, Hugentobler SA, Sosa MM, Schwartz BL, Morrison LC, Gieng SH, Shigenaga MK, & Potts WK. (2013) Human-relevant levels of added sugar consumption increase female mortality and lower male fitness in mice. Nature communications, 2245. PMID: 23941916
So just last night my twitter feed was abuzz with bacterial infection drama. The Frontline PBS show was doing a whole episode called “Hunting the Nightmare Bacteria” and based on the chatter I’d say they struck a nerve. Our antibiotic arsenal is failing us, and it’s crucial to figure out new ways to battle these […]... Read more »
Gillespie J. J., Wattam A. R., Cammer S. A., Gabbard J. L., Shukla M. P., Dalay O., Driscoll T., Hix D., Mane S. P., & Mao C. (2011) PATRIC: the Comprehensive Bacterial Bioinformatics Resource with a Focus on Human Pathogenic Species. Infection and Immunity, 79(11), 4286-4298. DOI: 10.1128/IAI.00207-11
Replication is one of the most important processes in those things we call science and the scientific method. Outside of conjuring up images of a certain 'Make it so' Captain with his "Earl Grey, Hot", scientific replication provides the community at large with some degree of reassurance that a research finding was not just a fluke or an artefact of a particular sample of people or a method used or an interpretation of results. As per the recent BBC article on vitamin use: "Looking at any one individual study won't be very revealing to answer the question of whether vitamin supplementation is good for you."Uncanny likeness @ Wikipedia With the issue of replication in mind, I was interested to read the Letter to the Editor from Robinson and colleagues* (open-access) who set about trying to replicate the findings from Skafidas and colleagues** (open-access) and their notion that science might be making some in-roads into the detection of "genetic biomarkers [that] can correctly classify ASD from non-ASD individuals". I posted about the Skafidas study at the time also (see here) and their analysis of single-nucleotide polymorphisms (SNPs) in relation to autism spectrum disorder (ASD).The Robinson letter reports an attempt to replicate the Skafidas findings based on an independent analysis of data from the Psychiatric Genomics Consortium (PGC) "which includes ~5400 cases, more than three times the number used in the original [Skafidas] report". I'm not on this occasions going to get the fine-toothed comb out on both papers because they're open-access so free for anyone to read.The conclusions from Robinson et al are pretty clear: "We find no evidence that the implicated SNPs, the classifier or the pathways named in Skafidas et al.1 are associated with ASDs. We therefore conclude that the classifier, as presented, cannot be used in a general way to predict ASDs, and consequently is unlikely to have any translational value."Obviously such findings are both a blow to autism research and also the original authors who first proposed the classifier model, who I don't doubt probably invested quite a lot of time, effort and funds into getting their experiments done and results published (and published in a Nature journal). The ego also takes a bit of a knock under such circumstances, believe me (see here and here and here).The Robinson data however re-emphasize the importance of replication in autism research. Perhaps just as important, they also reaffirm that autism is a tremendously difficult set of conditions to study. As is often the case when it comes to a heterogeneous condition like autism (or should that be the autisms) often carrying more than its fair share of comorbidity (see here) including risk of certain somatic conditions (see here), consistent findings are often few and far between. Indeed, that the use of the label autism, whilst providing a way of classifying certain types of behaviour and their impact on a person's life, is not necessarily the best thing for research purposes, as was vocalised through the grudge match that was DSM V vs. RDoC (see here).The added realisation that outside of no one single SNP being linked to all autism (see here) there may be a significant degree of overlap when it comes to the genetics of the autisms with other developmental and psychiatrically defined conditions (see here) implies that it's going to be some time yet before any genetic biomarkers or test is going to be able to accurately classify autism, sorry the autisms with any great accuracy. Then there is the question of what such a test would accomplish. I've not even mentioned the fact that autism, whilst having a genetic component, is probably not without it's [variable] partner in crime, environment (however you want to define this) when it comes to aetiology. And don't even mention that other area of increasing interest, epigenomics (see here)... which in recent days has seen some interesting papers published (see here and see here).I suppose in the spirit of all this talk on replication, the last question should be: who next is going to try and replicate the Robinson results? Indeed, does science any longer need the 'Letter to the Editor' in light of the rolling out of PubMed Commons?----------* Robinson EB. et al. Response to ‘Predicting the diagnosis of autism spectrum disorder using gene pathway analysis’. Molecular Pyschiatry. 2013: Oct 22. doi: 10.1038/mp.2013.125** Skafidas E. et al. Predicting the diagnosis of autism spectrum disorder using gene pathway analysis. Molecular Psychiatry. 2013; Sep 11. doi: 10.1038/mp.2012.126----------E B Robinson, D Howrigan, J Yang, S Ripke, V Anttila, L E Duncan, L Jostins, J C Barrett, S E Medland, D G MacArthur, G Breen, M C O'Donovan, N R Wray, B Devlin, M J Daly, P M Visscher, P F Sullivan, B M Neale (2013). Response to ‘Predicting the diagnosis of autism spectrum disorder using gene pathway analysis’ Molecular Psychiatry DOI: 10.1038/mp.2013.125... Read more »
E B Robinson, D Howrigan, J Yang, S Ripke, V Anttila, L E Duncan, L Jostins, J C Barrett, S E Medland, D G MacArthur, G Breen, M C O'Donovan, N R Wray, B Devlin, M J Daly, P M Visscher, P F Sullivan, B M Neale. (2013) Response to ‘Predicting the diagnosis of autism spectrum disorder using gene pathway analysis’. Molecular Psychiatry. DOI: 10.1038/mp.2013.125
If you watch the 2013 World Series that opens tomorrow night, you are likely to see pitchers using ice on their pitching arms between innings.The use of ice on key muscles between use seems counterintuitive. Isn't it best to key a muscloskeletal region warm? After all, we "warm-up" before using muscles all the time in a variety of activities.I had thought that icing was designed primarily to reduce muscle stiffness and soreness during the recover period.However, I recently ran into a controlled research study of the effects of arm and shoulder icing and pitching performance.Bishop and colleagues from the University of Alabama conducted a study on a group of eight college age pitchers. In this study they used a game-type simulation for the participants. Pitchers threw 12 pitches over four minutes followed by a rest period. Five total pitching cycles were completed simulating five innings of a baseball game.Each pitcher completed two five inning pitching simulation on separate days. On one day, they received intermittent cryotherapy to their pitching arm and shoulder and on the other day no cooling was provided. The key findings from the study included:Pitch velocity: Pitchers had higher mean pitch velocity with icing compared to non-icing in the 4th and 5th simulated inningsSubjective exertion and subjective recovery: Pitchers rated their subjective exertion lower during the icing series and also reported feeling better recovery prior to their next pitching sequenceThe increase in pitching velocity during icing was found to be about 1.3 meters/second and this translates into about 3 miles per hour. This is a significant velocity difference in pitching performance and represents not just a statistically signficant finding.One problem with this study is the difficulty or inability to blind the pitchers regarding their ice versus non-cooling periods. It is possible that a significant placebo effect may have factored into the ice period performance if the study group anticipated an effect with icing.It might have been valuable to have a sham intervention where the off-ice control period had a similar possible "intervention" effect. For example, covering the arm with a similar wrap and telling subjects another new performance aiding intervention was being tested and that it could not be detected by the subject. This study does suggest that icing may not only be beneficial after completion of a pitching outing, but may actually contribute to pitching outing duration and performance.Readers with more interest in this topic can access the citation by clicking on the PMID link below.Photo of Carlos Zambrano pitching for the Chicago Cubs is from the author's files.Bishop SH, Herron R, Ryan G, Katica C, & Bishop P (2013). THE EFFECT OF INTERMITTENT ARM AND SHOULDER COOLING ON BASEBALL PITCHING VELOCITY. Journal of strength and conditioning research / National Strength & Conditioning Association PMID: 24077378... Read more »
Bishop SH, Herron R, Ryan G, Katica C, & Bishop P. (2013) THE EFFECT OF INTERMITTENT ARM AND SHOULDER COOLING ON BASEBALL PITCHING VELOCITY. Journal of strength and conditioning research / National Strength . PMID: 24077378
Depression may be caused by poor Serotonin handling Depression stinks. It hurts. And it hurts others too. Taking care of yourself, and your moods, is important. A positive outlook andThe post Masters Women’s Health: Does low estrogen make women unresponsive to anti-depressants? appeared first on WODMasters.... Read more »
Michopoulos V, Berga SL, & Wilson ME. (2011) Estradiol and progesterone modify the effects of the serotonin reuptake transporter polymorphism on serotonergic responsivity to citalopram. Experimental and clinical psychopharmacology, 19(6), 401-8. PMID: 21843009
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