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  • February 23, 2015
  • 10:06 AM

Effects of Iron Deficiency in Female Runners (A Guest Post)

by Miss Behavior in The Scorpion and the Frog

By Ana Breit When people think of nutritional deficiencies, they probably picture women with goiters due to lack of iodine or other newsworthy examples. In reality, the most common nutritional deficiency in the United States is iron deficiency. Iron Deficiency (ID) is especially common in endurance athletes, especially female athletes. Start of 2013 Roy Griak Invitational Cross Country Meet at the University of Minnesota. Photo courtesy of Jennifer Larson.Iron is the metal in humans that allows oxygen to be carried in our bloodstream to all of our other organs. Without enough iron, less oxygen is taken to the muscles and other organs that need it. People with anemia (iron deficiency) may experience fatigue, weakness, and dizziness. Scientists Irena Auersperger, from the University of Ljubljana in Slovenia, Branko Skof and Bojan Leskosek, both from the University Medical Centre in Ljubljana, Slovenia, Ales Jerin, from the University Clinic Golnik in Golnik, Slovenia, and finally Mitja Lainscak, from Campus Virchow-Klinikum in Berlin, Germany asked how iron levels affect performance levels in female runners and whether or not intensified training impacts various iron parameters. Fourteen moderately active women were chosen to participate in the study. In order to be enrolled they had to have regular menstrual cycles, eat animal products on a regular basis, and not be taking forms of medication except birth control. Each woman was put into one of two groups based on her ferritin levels. (Ferritin is a protein that stores iron). Anyone with ferritin levels greater than 20 micrograms per liter was put in the Normal group (for normal iron stores). Anyone with ferritin less than or at 20 micrograms per liter was put into the Depleted group (for depleted iron stores). The study took place during a training period leading up to the International Ljubljana Marathon. During the eight week training period, runners had routine tests consisting of a 2400 meter (1.5 miles) time trial on a standard 400 meter outdoor track. Blood samples were taken at three different times: once before the eight week training period, once after the training period, and once more ten days after the marathon. These measurement times will be referred to as baseline, training, and recovery, respectively. Height, weight, and body fat percentage were measured during baseline and at recovery. Each woman then ran on a treadmill so researchers could measure her maximum speed, maximum oxygen consumption (VO2 max), and heart rate. Blood samples were taken at baseline, training, and recovery points to measure various blood parameters and iron parameters. Both Normal and Depleted groups had similar body measurements, VO2 max, and heart rates. Both groups had improvements in their endurance measurements, however, only the Normal group had endurance improvements that could be documented as significant while the Iron Deficient group’s endurance improvements were less. By the end of the experiment, most of the runners were anemic. Both groups experienced a decrease in iron levels during the training and recovery periods compared with the baseline levels. Overall, both groups’ iron levels decreased in all areas during the training phase, even though they were both getting stronger and faster. The group that started out with lower iron levels did not show as great of an improvement as the group with the normal iron levels at baseline. Even after the 10 day recovery period, iron level parameters were still considered low. With this data, the researchers agree that Iron Deficiency decreases performance levels of female athletes. Even though most people consider running to be a very healthy pastime, it can have undesired negative effects as well. All endurance athletes, especially female athletes, should have their iron levels checked regularly, and should make a conscious effort to incorporate iron into their hopefully already healthy diet by eating any enriched grains and a healthy amount of red meat. With consent of a physician, iron supplements can also be a good way to keep iron levels in check. Bibliography Auersperger I, Škof B, Leskošek B, Knap B, Jerin A, & Lainscak M (2013). Exercise-induced changes in iron status and hepcidin response in female runners. PloS one, 8 (3) PMID: 23472137 ... Read more »

  • February 23, 2015
  • 04:34 AM

Late, delayed and mis-diagnosis of autism

by Paul Whiteley in Questioning Answers

It's inevitable that with all the mountains of autism research published on a daily basis, certain themes will occur at certain times. My post today is reflective of one of those themes and how, on occasion, the autism diagnostic process does not run as smoothly as we would all like to think.I start this post with a link to an article discussing some forthcoming research to be published titled: 'The autistic pupils ‘traumatised’ by delayed diagnosis'. Describing the results of a survey of parents included as part of a scheme of work (see here) where experiences of the diagnostic process were gauged, researchers reported that over half of parents were "unhappy with the diagnostic process" for their children. The observation that children were waiting an average of 3.5 years from initial contact with healthcare professionals to final receipt of a diagnosis is a pretty eye-watering statistic too, albeit a step up from previous research in this area [1].Next up is the paper from Davidovitch and colleagues [2] reporting that: "Subsequent late diagnosis of ASD [autism spectrum disorder] after an initial ASD-negative comprehensive assessment is a common clinical experience." Based on an: "Extensive chart review of patients' electronic medical records" from "a representative population-based registry of patients seen during 2004 to 2011" researchers reported that over 200 children were diagnosed with an ASD after their 6th birthday "although their initial comprehensive developmental evaluations before the age of 6 were negative for ASD." The authors discuss possible reasons for the reversal of diagnosis including "evolving diagnosis as well as missed and overdiagnosed cases of ASD."Finally, is the paper from Aggarwal & Angus [3] with the conclusion: "ASDs can go undetected during childhood and these clients can sometimes present during adolescence to mental health services for a psychiatric comorbidity." This followed their experiences of a diagnosis of autism being potentially missed or masked during childhood, only to be picked up during adolescence when a referral was made "for a psychiatric comorbidity."Taken as a collection, these articles/features reiterate that the diagnosis and diagnostic process of autism is often a very complicated thing even before one starts to talk about politics, the availability of resources to undertake such a task and on occasion, actually getting someone to take notice of the need for a referral (see here). I've talked before on this blog about the various factors than can influence the age of autism diagnosis (see here) stressing for example, the fluidity in behavioural expression particularly during the early years (see here) and even into adulthood (see here). Outside of the idea that there may be a number of diverse developmental trajectories when it comes to autism (see here) impacting on presentation, including the idea of regression potentially being present for some (see here), even the most seasoned autism professionals are not error-free when it comes to something like autism screening and diagnosis (see here).Insofar as the Aggarwal/Angus results, and the idea that the label of autism may only come to diagnostic attention when other psychiatric comorbidity lead, this is something discussed previously on this blog (see here and see here). The overlap between the autism and for example, the schizophrenia spectrums (see here) is an area crying out for further research attention and how intersecting with the idea of ESSENCE in autism (lots of different labels/symptoms potentially following a diagnosis of autism), symptom masking can be a real issues (see here). That also goes for the potential appearance of autism in other conditions such as Down's syndrome for example (see here).With the growing tide of research suggesting that early (sometimes very early) intervention may be able to make a real impact on the course of autism for some (see here and see here), late, delayed or even mis-diagnosis should be viewed not only as a source of significant stress for those on the autism spectrum and their loved ones, but also as an area of vital importance to autism research on the ways and means of minimising such issues.Music then. I've probably linked to this before but here is Blondie and One Way Or Another.----------[1] Howlin P. & Asgharian A. The diagnosis of autism and Asperger syndrome: findings from a survey of 770 families. Dev Med Child Neurol. 1999 Dec;41(12):834-9.[2] Davidovitch M. et al. Late Diagnosis of Autism Spectrum Disorder After Initial Negative Assessment by a Multidisciplinary Team. J Dev Behav Pediatr. 2015 Feb 2.[3] Aggarwal S. & Angus B. Misdiagnosis versus missed diagnosis: diagnosing autism spectrum disorder in adolescents. Australas Psychiatry. 2015 Feb 4. pii: 1039856214568214.----------Davidovitch M, Levit-Binnun N, Golan D, & Manning-Courtney P (2015). Late Diagnosis of Autism Spectrum Disorder After Initial Negative Assessment by a Multidisciplinary Team. Journal of developmental and behavioral pediatrics : JDBP PMID: 25651066... Read more »

Aggarwal S, & Angus B. (2015) Misdiagnosis versus missed diagnosis: diagnosing autism spectrum disorder in adolescents. Australasian psychiatry : bulletin of Royal Australian and New Zealand College of Psychiatrists. PMID: 25653302  

  • February 23, 2015
  • 12:38 AM

Yes, autism is on the rise. Read this before blaming vaccines.

by EE Giorgi in CHIMERAS

Waiting for the rain, © EEGBecause I work on HIV vaccine design, lately I've often been involved in debates concerning the safety of vaccines. I have the greatest respect for parents who struggle with disabilities of any kind, especially in children. I'm a parent too and can't even imagine what life is like when your child has a permanent disability. But I'm also a scientist, and I believe in the good cause of my work. My boss has been working day and night for thirty years on a vaccine against HIV because her best friend died of AIDS. We have pictures of AIDS orphans on our desks. We are not monsters, we are not part of a conspiracy, we are not paid by companies to fool people.In fact, because we do basic research, our salary will be paid whether or not we do succeed in finding a vaccine. It's just our job, and we have no financial gain in this. If you want to point fingers, do it at companies who do make a profit out of health care, or out of selling plastic (and hence bypassing necessary health testing), or out of selling food. As a parent, I am the first to be concerned about the health of our children. I don't accept anything blindly without doing research, be it a vaccine or a drug or a type of food.I've discussed aluminum in vaccines and why it's a good idea to spread out the shots during the first year of life; I've also discussed why I decided to wait before letting my daughter have the HPV shot. At the same time, parents concerned about autism are right to be alarmed: if you look at the latest numbers published by the CDC, the prevalence of autism in children has doubled. However, this trend has supposedly started in the last two decades whereas vaccines have been around much longer than that [1]. It's true that the US have an aggressive vaccine schedule for infants and I suspect it's tailored to reduce the number of office visits as copays are expensive and insurance companies need to make their profits. So yes, just like other parents, I am bitter at the system. I am bitter at companies profiting out of the health of my own children, not at researchers working hard at finding a cure for deadly diseases. My plea today is to separate the two: the cure, which, just like any other cure, should be used wisely and with good measure and balance, and the people making profits out of the cure.    For example, nobody argues that antibiotics save lives. Unfortunately, today you find antibacterial stuff in soaps, detergent, even toothpaste. Doctors overprescribe antibiotics all the time. And then of course, poultry, beef and pork come loaded with antibiotics. This has led to extremely aggressive, antibiotic resistant superbugs like CRE. Yet nobody dreams of refusing antibiotics when they are really needed. That's because we all know that if you don't take them you might in fact lose your life.What our society needs is stop pointing fingers, quit all the conspiracy crap, and instead sit at the table and discuss better health practices that don't put profits first but health and good care instead.How should we address the rise in autism cases? I don't have an answer to this, but I did find a bunch of papers that got me thinking. I list them below.DISCLAIMER: I'm not discussing these papers to point at a cause of autism. In fact, I believe that we will never find a cause, just like we will never find a cause of cancer. Like I stated in my post last week, we need to think of our lives as a complex orchestra where DNA, RNA, proteins and the environment all play together to create the beautiful symphony of our life. There never is one such thing as a direct cause. Often it's just genetics. Even more often is a genetic predisposition combined with multiple sets of environmental exposures, lifestyle, and diet. If your child has autism, please focus your energy in taking care of that child rather than trying to find a cause.1) This study [1] looked into the raising numbers of autism cases:"Diagnosed autism prevalence has risen dramatically in the U.S over the last several decades and continued to trend upward as of birth year 2005. The increase is mainly real and has occurred mostly since the late 1980s. In contrast, children's exposure to most of the top ten toxic compounds has remained flat or decreased over this same time frame. Environmental factors with increasing temporal trends can help suggest hypotheses for drivers of autism that merit further investigation [1]." So the threat is real. Yet vaccines have been around much longer than the 1980s.2) Studies have found a higher incidence of autism in California, in higher educated families. This may be biased by the fact that people with a higher education will be more inclined to have their children tested for autism. But one study in particular [2] found another possible association:"Our study adds to previous work in California showing a relation between traffic-related air pollution and autism, and adds similar findings in an eastern US state, with results consistent with increased susceptibility in the third-trimester [2]." The researchers monitored the air particulate at the birth address of the child starting from preconception through the child's first birthday.  3) Breast feeding may play a protective role against autism spectrum disorders [3].4) Inflammation may play a role. Le Belle et al. [4] used a mouse model to test the following hypothesis:"A period of mild brain overgrowth with an unknown etiology has been identified as one of the most common phenotypes in autism. Here, we test the hypothesis that maternal inflammation during critical periods of embryonic development can cause brain overgrowth and autism-associated behaviors as a result of altered neural stem cell function [4]."What they found supports the idea that, paired with genetic susceptibility, an infection in the pregnant mother could indeed higher the risk of developing autism in the child.5) But one of the most fascinating associations I found is between gut microbiome and autism. Newborns are born without any bacteria in their guts and colonization begins right after birth. Vaginal birth vs. cesarean, breast fed vs. formula seem to be factors associated to the gut microbiota found in infants."Over the first years of life the gut microbiome is changing and remodeling, ultimately resembling an adult gut microbiome by year 3. This suggests there is a “core microbiome” that is the hallmark of a healthy individual [5]." This is particularly important because the microbiota community carries millions of genes whose expression affects our own physiology. The type and number of bacteria in our guts can influence the health and good functioning of our immune system.Now, here's the worrisome bit:"Broad-spectrum antibiotics are often prescribed to infants in the Western world in an attempt to protect the developing child from disease. In addition to conferring antibiotic resistance in infancy, antibiotic over usage can significantly disrupt the overall ecology of the gut microbiota, alter the abundances of resident gut bacteria, and potentially bias the child toward certain diseases [6]."I'm not making a case that antibiotics are bad, just like I will never say that vaccines are bad. I'm just raising a flag that, like in all things, a good measure should be practiced. Antibiotics are a great means to fight infections. But is it safe to use them routinely to prevent infection?The following study [7] is from 2000, so maybe a bit outdated, and the sample number is awfully low. Still, this is what it had to say:"In most cases symptoms of autism begin in early infancy. However, a subset of children appears to develop normally until a clear deterioration is observed. Many parents of children with "regressive"-onset autism have noted antecedent antibiotic exposure followed by chronic diarrhea. We speculated that, in a subgroup of children, disruption of indigenous gut flora might promote colonization by one or more neurotoxin-producing bacteria, contributing, at least in part, to their autistic symptomatology [7]."The study has a huge limit: they tested their hypothesis on 11 child... Read more »

Kalkbrenner AE, Windham GC, Serre ML, Akita Y, Wang X, Hoffman K, Thayer BP, & Daniels JL. (2015) Particulate matter exposure, prenatal and postnatal windows of susceptibility, and autism spectrum disorders. Epidemiology (Cambridge, Mass.), 26(1), 30-42. PMID: 25286049  

Al-Farsi YM, Al-Sharbati MM, Waly MI, Al-Farsi OA, Al-Shafaee MA, Al-Khaduri MM, Trivedi MS, & Deth RC. (2012) Effect of suboptimal breast-feeding on occurrence of autism: a case-control study. Nutrition (Burbank, Los Angeles County, Calif.), 28(7-8). PMID: 22541054  

Mulle, J., Sharp, W., & Cubells, J. (2013) The Gut Microbiome: A New Frontier in Autism Research. Current Psychiatry Reports, 15(2). DOI: 10.1007/s11920-012-0337-0  

Arrieta, M., Stiemsma, L., Amenyogbe, N., Brown, E., & Finlay, B. (2014) The Intestinal Microbiome in Early Life: Health and Disease. Frontiers in Immunology. DOI: 10.3389/fimmu.2014.00427  

Sandler RH, Finegold SM, Bolte ER, Buchanan CP, Maxwell AP, Väisänen ML, Nelson MN, & Wexler HM. (2000) Short-term benefit from oral vancomycin treatment of regressive-onset autism. Journal of child neurology, 15(7), 429-35. PMID: 10921511  

  • February 22, 2015
  • 06:10 AM

Sick Of Stress: Is Fear Making Us Ill?

by Agnese Mariotti in United Academics

Is stress making us sick? Scientists found that fear of terror increases pulse, the risk of disease and subsequent death.... Read more »

Shenhar-Tsarfaty, S., Yayon, N., Waiskopf, N., Shapira, I., Toker, S., Zaltser, D., Berliner, S., Ritov, Y., & Soreq, H. (2015) Fear and C-reactive protein cosynergize annual pulse increases in healthy adults. Proceedings of the National Academy of Sciences, 112(5). DOI: 10.1073/pnas.1418264112  

  • February 21, 2015
  • 02:36 PM

Mental illness and ultradian rhythms

by Dr. Jekyll in Lunatic Laboratories

In the relatively new 24 hour, always on the go, digital lifestyle we live — might living a structured life with regularly established mealtimes and early bedtimes lead to a better life and perhaps even prevent the onset of mental illness? Well according to a new study, it might do just that, you could have a better quality of life just by being a little more structured thanks to our circadian rhythm.... Read more »

  • February 21, 2015
  • 12:53 PM

Pharmacy Shopping and Overlapping Prescriptions Linked To Opioid Overdose

by Marie Benz in Interview with: Dr. Zhou Yang Office of the Associate Director for Policy Centers for Disease Control and Prevention, Atlanta, GA Medical Research: What is the background for this study? Response: Prescription drug misuse and abuse, largely those involving opioid … Continue reading →... Read more » Interview with:, & Dr. Zhou Yang. (2015) Pharmacy Shopping and Overlapping Prescriptions Linked To Opioid Overdose. info:/

  • February 21, 2015
  • 08:57 AM

Rally Health Gamifies Digital Platform To Support and Engage Consumers

by Marie Benz in Interview with: Brian Dolan Chief Strategy and Partner Integration Officer Rally Health Editor’s note: On February 3, 2015, Rally Health launched a New HIPPA compliant Digital Engagement platform that gives consumers the support and tools they need to … Continue reading →... Read more » Interview with:, Brian Dolan, Chief Strategy and Partner Integration Officer, & Rally Health. (2015) Rally Health Gamifies Digital Platform To Support and Engage Consumers. info:/

  • February 21, 2015
  • 05:39 AM

Coeliac disease: genes, autoimmunity, gut bacteria and bafflement?

by Paul Whiteley in Questioning Answers

Some things in life really do baffle me. When it comes to this blog, nothing seems to baffle me more than some of the talk about the triad that is autoimmunity, coeliac disease and gluten (see here for an example).My bafflement continued upon reading the papers by Emilsson and colleagues [1] and by Olivares and colleagues [2]. Respectively suggesting that: "spouses of individuals with celiac disease are at increased risk of non-celiac autoimmune disease" and "a specific disease-biased host genotype may also select for the first gut colonisers and could contribute to determining disease risk" I admit that I had to do a double-take on both these papers.Accepting that this post is published at the weekend and readers don't necessarily want to listen to me droning on and on, a few quick pointers about each study...Emilsson et al including the name of Jonas Ludvigsson (he of the not-quote-coeliac-disease-but-something-in-cases-of-autism (see here)) looked to assess "the risk of non-celiac autoimmune disease [in] first-degree relatives and spouses of people with celiac disease."They did this by "searching computerized duodenal and jejunal biopsies, collected from 1969 through 2008, at 28 pathology departments in Sweden" to identify those with coeliac disease (CD) and further through "Swedish healthcare registries" identify first-degree relatives and spouses of those with CD. Hazard ratios (HRs) were calculated "for non-celiac autoimmune disease (Crohn's disease, type 1 diabetes mellitus, hypothyroidism, hyperthyroidism, psoriasis, rheumatoid arthritis, sarcoidosis, systemic lupus erythematosus, or ulcerative colitis) in relatives/spouses compared with controls."Results: over a median follow-up period of about 10 years, some 4% of first-degree relatives of those with CD were diagnosed with an autoimmune condition not CD. This compared with 3% of controls. When it came to calculating those HRs, this translated as a slightly increased likelihood of relatives being diagnosed with an autoimmune condition. Results also suggested something of a similar statistic for spouses (I assume an unrelated individual as a partner).Conclusion: "First-degree relatives and spouses of individuals with celiac disease are at increased risk of non-celiac autoimmune disease." Then to the Olivares paper:Drawing on an increasing interest in how those trillions of wee beasties which inhabit our inner depths (the gut microbiota) might do so much more than help us digest our food, researchers set out to look at "whether the human leukocyte antigen (HLA)-DQ2 genotype is an independent factor influencing the early gut microbiota composition of healthy infants at family risk of CD." HLA genotype by the way is all about the genetics of identification and communication and how the body distinguishes between 'self' and 'foreign' from an immune perspective (see here). HLA-DQ2 is a bit of a biggie when it comes to risk of CD.The gut bacterial composition of infants (exclusively breastfed) either at high or low risk of developing CD by virtue of their genotype (HLA-DQ2 carriers vs. non-HLA-DQ2/8 carriers) were analysed."Infants with a high genetic risk had significantly higher proportions of Firmicutes and Proteobacteria and lower proportions of Actinobacteria compared with low-risk infants" among other things. Conclusion: "The genotype of infants at family risk of developing CD, carrying the HLA-DQ2 haplotypes, influences the early gut microbiota composition."There are some pretty obvious issues potentially associated with these papers. Olivares and colleagues in particular, relied on a very small sample size and as far as I can see, were talking about high risk over and above actual diagnosis of CD yet. It will be interesting to see how this pans out. I might also add that whilst gut bacterial composition is a rising star in CD research circles, it would be a brave person/research team who suggested that we have a gut bacterial 'phenotype' of CD (see here). We don't (yet).The Emilsson findings are just down-right confusing. How can a diagnosis of CD - an autoimmune condition - translate into an increased risk of an autoimmune condition outside of CD for an unrelated spouse? It could be a chance finding; some else to add to the strange collection of results which seem to be emerging [3]. It could be that spouses were by chance also more likely to harbour some of the genetics of autoimmune related conditions as per the cross-over between genotype for CD and something like type 1 diabetes [4]. Now, there's a psychology / sociology experiment waiting to happen. Or it could be due to other factors [5]?I wonder however whether there may be other explanations for this finding. Short of suggesting that autoimmune conditions might be 'transmissible' I hark back to the peculiar findings reported by Kalliokoski and colleagues [6] and the idea of passive transference of CD "by serum or immunoglobulins" in mice. Granted this was work done with mice and said mice were athymic. But it does present a tantalising suggestion that we might not know as much about autoimmunity as we perhaps thought and even less when it comes to other factors potentially indicated by the results from Moon and colleagues [7] also described in accompanying media (see here) (I'm gonna be blogging about the Moon findings soon too). Think back also to my previous musings on how alcohol and head injury might also tie into sensitisation to gluten and CD respectively.I continue to be baffled...And while I remain baffled here is Teenage Fanclub with Star Sign.----------[1] Emilsson L. et al. Autoimmune Disease in First-degree Relatives and Spouses of Individuals with Celiac Disease. Clin Gastroenterol Hepatol. 2015 Jan 30. pii: S1542-3565(15)00112-3.[2] Olivares M. et al. The HLA-DQ2 genotype selects for early intestinal microbiota composition in infants at high risk of developing coeliac disease. Gut 2015; 64: 406-417.[3] Namatovu F. et al. Neighborhood conditions and celiac disease risk among children in Sweden. Scand J Public Health. 2014 Nov;42(7):572-80.[4] Bao F. et al. One third of HLA DQ2 homozygous patients with type 1 diabetes express celiac disease-associated transglutaminase autoantibodies. J Autoimmun. 1999 Aug;13(1):143-8.[5] Skaaby T. et al. Prospective population-based study of the association between vitamin D status and incidence of autoimmune disease. Endocrine. 2015 Feb 11.[6] Kalliokoski S. et al. Injection of celiac disease patient sera or immunoglobulins to mice reproduces a condition mimicking early developing celiac disease. J Mol Med (Berl). 2015 Jan;93(1):51-62.[7] Moon C. et al. Vertically transmitted faecal IgA levels determine extra-chromosomal phenotypic variation. Nature. 2015. Feb 16.----------... Read more »

Emilsson L, Wijmenga C, Murray JA, & Ludvigsson JF. (2015) Autoimmune Disease in First-degree Relatives and Spouses of Individuals with Celiac Disease. Clinical gastroenterology and hepatology : the official clinical practice journal of the American Gastroenterological Association. PMID: 25645875  

  • February 20, 2015
  • 11:08 PM

Getting your tonsils removed: A (sometimes) cure for bedwetting

by Megan Cartwright in Science-Based Writing

Kids who snore are more likely to wet the bed than kids who don’t. Strangely enough, the reason may be their too-big tonsils, which can cause the snoring and sleep apnea affecting 1 in 10 kids. In 2013, Michigan scientists … Continue reading →... Read more »

Kovacevic L, Wolfe-Christensen C, Lu H, Toton M, Mirkovic J, Thottam PJ, Abdulhamid I, Madgy D, & Lakshmanan Y. (2014) Why does adenotonsillectomy not correct enuresis in all children with sleep disordered breathing?. The Journal of urology, 191(5 Suppl), 1592-6. PMID: 24679871  

  • February 20, 2015
  • 05:41 PM

Even Low-Level Physical Activity Improves Cardiac Risk

by Marie Benz in Interview with: Thomas W. Buford, PhD Assistant Professor, Division of Clinical Research Department of Aging and Geriatric Research, University of Florida College of Medicine Director, Health Promotion Center University of Florida Institute on Aging Medical Research: What is the … Continue reading →... Read more » Interview with:, & Thomas W. Buford, PhD. (2015) Even Low-Level Physical Activity Improves Cardiac Risk. info:/

  • February 20, 2015
  • 04:59 PM

Overriding muscles’ energy efficiency to burn more fat

by Dr. Jekyll in Lunatic Laboratories

What started as an evolutionary protection against starvation has become a biological “bad joke” for people who need to lose weight. The human body doesn’t distinguish between dieting and possible starvation, so when there is a decrease in calories consumed, human metabolism increases its energy efficiency and weight loss is resisted.... Read more »

  • February 20, 2015
  • 03:43 AM

Behavioural sleep intervention for ADHD?

by Paul Whiteley in Questioning Answers

I was really quite interested to read about the study from Harriet Hiscock and colleagues [1] (open-access) suggesting that: "A brief behavioural sleep intervention modestly improves the severity of ADHD [attention deficit hyperactivity disorder] symptoms in a community sample of children with ADHD." I had heard that these results would be forthcoming based on the publication of the study trial protocol [2] a few years back, alongside the trial entry listed in the ISRCTN registry (see here). There is also the promise of more to come from this group [3].The Hiscock paper is open-access but a few pointers might be useful:Based on the idea that sleep issues have been reported in quite a large proportion of those diagnosed with ADHD [4], authors set about testing the idea that consultations with specialists on managing sleep issues might impact on said problems and "might have lasting benefits not only on sleep but on the ADHD itself."Participants were randomly assigned to sleep intervention or usual clinical care for such matters. As with these kinds of trials and the various issues of attrition (drop-outs) and loss at follow-up, although 122 children were initially allocated to each group, a mix of sample sizes were available at the 3 month and 6 month follow-up periods. Statistical analysis of the results was made on the basis of intention to treat.Various outcomes were measured during the study. The ADHD rating scale IV was the primary outcome for ADHD symptoms (something I have a little experience of in my own research). Various sleep related issues were also monitored including actigraphy to measure movement "and used to differentiate between sleep and wake times."Results: "The families reported greater improvements in their children’s ADHD symptoms, sleep, behaviour, health related quality of life, and daily functioning, and teachers reported improved behaviour" as a function of the sleep intervention. The effects for parents were also noticeable insofar as "intervention parents reported fewer days late for work as a result of their child’s behaviour than control parents."The more objective actigraphy results also suggested: "an improved sleep duration of around 70 minutes a week in the intervention group" bearing in mind researchers reporting a few 'practical issues' with this method.Accepting a few limitations associated with their study methods, authors highlight the positive effects of the intervention and how: "These benefits occur over and above the effects of stimulant medications." Further: "Effects are comparable to those seen with intensive behavioural interventions targeting ADHD symptoms, more wide reaching than those reported in studies of melatonin, and importantly seem to be sustained over six months." Not bad at all.Of course further research is implied from such results to "determine whether these benefits can be replicated when the sleep intervention is implemented by community based clinicians in a rigorous effectiveness trial." Translational medicine I think its called. But there is little doubt that there is much more to see when it comes to the presentation of ADHD and the very valuable resource called sleep.Just before I leave you, the paper from Papadopoulos and colleagues [5] potentially also indicates how the Hiscock results might translate into improvements for those with autism also diagnosed with ADHD (see here). Based on an analysis of a "subsample of children with ADHD-ASD [autism spectrum disorder]... participating in the Sleeping Sound With ADHD study" (the Hiscock study) authors reported that those in receipt of the behavioural sleep intervention "had large improvements in sleep problems and moderate improvements in child behavioral functioning 3 and 6 months post-randomization."Further food for thought perhaps, added to what is already known about sleep and [some] autism (see here). Oh, and remember, screen time whilst useful, might also impact on sleep time as we are perhaps already seeing...So: Primal Scream - Kill All Hippies ('though not literally I might add).----------[1] Hiscock H. et al. Impact of a behavioural sleep intervention on symptoms and sleep in children with attention deficit hyperactivity disorder, and parental mental health: randomised controlled trial. BMJ. 2015 Jan 20;350:h68.[2] Sciberras E. et al. Study protocol: the sleeping sound with attention-deficit/hyperactivity disorder project. BMC Pediatr. 2010 Dec 30;10:101.[3] Lycett K. et al. Behavioural sleep problems in children with attention-deficit/hyperactivity disorder (ADHD): protocol for a prospective cohort study. BMJ Open. 2014 Feb 12;4(2):e004070.[4] Silvestri R. et al. Sleep disorders in children with Attention-Deficit/Hyperactivity Disorder (ADHD) recorded overnight by video-polysomnography. Sleep Med. 2009 Dec;10(10):1132-8. [5] Papadopoulos N. et al. The Efficacy of a Brief Behavioral Sleep Intervention in School-Aged Children With ADHD and Comorbid Autism Spectrum Disorder. J Atten Disord. 2015 Feb 2. pii: 1087054714568565.----------Hiscock H, Sciberras E, Mensah F, Gerner B, Efron D, Khano S, & Oberklaid F (2015). Impact of a behavioural sleep intervention on symptoms and sleep in children with attention deficit hyperactivity disorder, and parental mental health: randomised controlled trial. BMJ (Clinical research ed.), 350 PMID: 25646809... Read more »

  • February 19, 2015
  • 03:31 PM

Predicting the effectiveness of cancer vaccines

by Dr. Jekyll in Lunatic Laboratories

Cancer vaccines, once they were science fiction and now they are designed to turn the body’s own immune system specifically against tumor cells. Particularly promising are vaccines that are directed against so-called neoantigens — which are proteins that have undergone a genetic mutation in tumor cells and, therefore, differ from their counterparts in healthy cells.... Read more »

Bunse, L., Schumacher, T., Sahm, F., Pusch, S., Oezen, I., Rauschenbach, K., Gonzalez, M., Solecki, G., Osswald, M., Capper, D.... (2015) Proximity ligation assay evaluates IDH1R132H presentation in gliomas. Journal of Clinical Investigation. DOI: 10.1172/JCI77780  

  • February 19, 2015
  • 10:53 AM

Physical Activity in Elders Increased By Pedometers and Nursing Input

by Marie Benz in Medical Research Interviews and News Interview with: Tess Harris St George’s University of London   MedicalResearch: What is the background for this study? Response: Physical activity is vital for both physical and mental health in older people, preventing at least 20 common health problems. … Continue reading →
The post Physical Activity in Elders Increased By Pedometers and Nursing Input appeared first on Medical Research Interviews and News .
... Read more » Interview with:, Tess Harris, & St George’s University of London. (2015) Physical Activity in Elders Increased By Pedometers and Nursing Input. info:/

  • February 19, 2015
  • 09:00 AM

Pull Up A Stool And Let's Talk About Your Microbiome

by Bill Sullivan in The 'Scope

Can the types of microbes in your gut control your weight? A woman who received a "fecal transplant" to treat a stubborn case of colitis rapidly gained weight since the donor was obese. Let's learn more about our microbiome.... Read more »

Lax S, Smith DP, Hampton-Marcell J, Owens SM, Handley KM, Scott NM, Gibbons SM, Larsen P, Shogan BD, Weiss S.... (2014) Longitudinal analysis of microbial interaction between humans and the indoor environment. Science (New York, N.Y.), 345(6200), 1048-52. PMID: 25170151  

Bisgaard, H., Li, N., Bonnelykke, K., Chawes, B., Skov, T., Paludan-Müller, G., Stokholm, J., Smith, B., & Krogfelt, K. (2011) Reduced diversity of the intestinal microbiota during infancy is associated with increased risk of allergic disease at school age. Journal of Allergy and Clinical Immunology, 128(3), 646-65200000. DOI: 10.1016/j.jaci.2011.04.060  

Stefka, A., Feehley, T., Tripathi, P., Qiu, J., McCoy, K., Mazmanian, S., Tjota, M., Seo, G., Cao, S., Theriault, B.... (2014) Commensal bacteria protect against food allergen sensitization. Proceedings of the National Academy of Sciences. DOI: 10.1073/pnas.1412008111  

Williams NT. (2010) Probiotics. American journal of health-system pharmacy : AJHP : official journal of the American Society of Health-System Pharmacists, 67(6), 449-58. PMID: 20208051  

Alang, N., & Kelly, C. (2015) Weight Gain After Fecal Microbiota Transplantation. Open Forum Infectious Diseases, 2(1). DOI: 10.1093/ofid/ofv004  

  • February 19, 2015
  • 03:39 AM

Metal sensitisation and chronic fatigue syndrome?

by Paul Whiteley in Questioning Answers

I have to admit that I pondered longer than usual over whether I should talk about the paper by Vera Stejskal [1] (open-access here) and the idea that: "Patients with CFS [chronic fatigue syndrome] and fibromyalgia are frequently sensitized to metals found in the environment or used in dentistry and surgery."It was't that I doubted that metals - certain types present in the wrong place or wrong concentration - can affect physical and psychological health and wellbeing as per the example of lead (see here). I was even happy to accept some mention of ASIA (‘autoimmune (auto-inflammatory) syndrome induced by adjuvants’) in the Stejskal paper given my previous exploration of this potentially tricky concept with chronic fatigue syndrome in mind (see here) and some more recent data [2]. The editor-in-chief of the publishing journal, I should add, knows a little more about this than I.It's just that when I read the paper in its entirety and then googled the analytical weapon of choice - MELISA (Memory Lymphocyte ImmunoStimulation Assay) or rather the lymphocyte transformation test (LTT) - I couldn't help but be a little unsettled at some of the results displayed. When I also found that Dr Stejskal "is the inventor of the MELISA test and holder of trademarks" (see here) without however seemingly any mention of this as a potential conflict of interest on her paper, my brow furrowed a little more.Putting those issues to one side and hopefully avoiding any terse replies from proponents of MELISA, I am actually quite interested in the findings reported as they were in a peer-reviewed journal. A paper by Kern and colleagues [3] potentially intersecting with the Stejskal results bolstered my decision to blog about this issue and the potential to offer something important for at least some people falling onto the ME/CFS spectrum, subject to further inquiry. Oh, and by the way, when I say ME/CFS I mean SEID...The Stejskal paper is open-access but that's never stopped me before...Based on a very, very small participant number - three subjects with CFS and two with fibromyalgia - where metal exposure was "as a trigger for their ill health", MELISA testing was undertaken to measure "delayed-type hypersensitivity to metals (metal allergy)".The assay involves culturing lymphocytes (white blood cells) with selected metals at various concentrations and then measuring lymphocyte proliferation and using something called the Stimulation Index (SI) to describe "reactivity to metals". Just in case you might be querying the method, it has been validated by others as per the paper from Valentine-Thon and colleagues [4].Results are presented in a case-by-case format. Control participant data (n=9) based on MELISA testing is also provided: "In the majority of controls, MELISA was negative, indicating non-responsiveness to metals at the lymphocyte level." The same could not however be said for the symptomatic participants who presented with a range of results suggestive of issues with metal allergy. Interestingly, data is presented at both initial testing and "follow-up" after removal of various metal sources and is also complemented in some cases by more traditional patch testing results.The author concludes: "In this study, reduction of inflammation-causing metals resulted in an alleviation of symptoms and long-term health improvement. The decrease of metal-specific lymphocyte responses in vitro after removal of sensitizing metals supports the clinical relevance of these findings."As per other discussions on this blog, CFS/ME is a condition which has seen it's fair share of discussion and debate down the years (see here). A few weeks back, part of those discussions 'kicked off' again focused on the paper by Chalder and colleagues [5] and headlines about 'fear of exercise'. I might also draw your attention to a pretty good critique on that Chalder paper too (see here) alongside what the Cochrane Library recently said about exercise 'therapy' and CFS [6]. In this context, the Stejskal paper talking about metals potentially perpetuating symptoms and even the notion that something else - "As a child she had received at least eight thimerosal and aluminium-containing vaccines" - *might* be implicated in cases, is never going to be particularly well-received in some quarters.I'm not falling hook, line and sinker for the Stejskal results by the way, based as they were, on case reports and with very little discussion of objective measures of symptom profiles for example, outside of sentences like: "Rapid health improvement followed and she became symptom free." I am however interested in research which talks about clinical improvement in cases of ME/CFS recognising how destructive an illness this can be and the stigma which still pervades some discussions of the condition. The Stejskal paper perhaps offers a template for the consideration of further, more controlled study is this area, expanding on our current understanding of metal allergy [7] outside of just a generalised reaction to jewellery and possibly contributing further to some of the biology potentially involved in at least some CFS/ME [8].Music then... One by Johnny Cash. Oh and happy birthday Questioning Answers (4 today and therefore ready for reception!)----------[1] Stejskal V. Metals as a common trigger of inflammation resulting in non-specific symptoms: diagnosis and treatment. Isr Med Assoc J. 2014 Dec;16(12):753-8.[2] Somers EC. et al. Mercury Exposure and Antinuclear Antibodies among Females of Reproductive Age in the United States: NHANES. Environ Health Perspect. 2015. Feb 10.[3] Kern JK. et al. Evidence supporting a link between dental amalgams and chronic illness, fatigue, depression, anxiety, and suicide. Neuro Endocrinol Lett. 2014 Dec 24;35(7):537-552.[4] Valentine-Thon E. et al. LTT-MELISA is clinically relevant for detecting and monitoring metal sensitivity. Neuro Endocrinol Lett. 2006 Dec;27 Suppl 1:17-24.[5] Chalder T. et al. Rehabilitative therapies for chronic fatigue syndrome: a secondary mediation analysis of the PACE trial. The Lancet Psychiatry. 2015. Jan 13.[6] Larun L. et al. Exercise therapy for chronic fatigue syndrome. Cochrane Database Syst Rev. 2015 Feb 10;2:CD003200.[7] Thyssen JP. & Menné T. Metal allergy--a review on exposures, penetration, genetic... Read more »

  • February 18, 2015
  • 03:13 PM

Scientists find anti-HIV agent and possible start for a vaccine

by Dr. Jekyll in Lunatic Laboratories

We may just have found a missing link in the fight towards an HIV vaccine. No, this is not an over-hyped headline, in a remarkable new advance against the virus that causes AIDS, scientists have announced the creation of a novel drug candidate that is so potent and universally effective, it might work as part of an unconventional vaccine.... Read more »

Gardner, M., Kattenhorn, L., Kondur, H., von Schaewen, M., Dorfman, T., Chiang, J., Haworth, K., Decker, J., Alpert, M., Bailey, C.... (2015) AAV-expressed eCD4-Ig provides durable protection from multiple SHIV challenges. Nature. DOI: 10.1038/nature14264  

  • February 18, 2015
  • 11:53 AM

Exercise Guidelines in Prevention of Alzheimer's Disease

by William Yates, M.D. in Brain Posts

A series of seven guidelines for the prevention of Alzheimer's disease (AD) has recently been published.These guidelines resulted from a conference of experts in nutrition and the brain.The guidelines included a recommendation for 40 minutes of aerobic exercise three times a week.Support for this exercise recommendation by experts was linked to 2 areas of research:Observational studies show lower rates of AD in regular exercise groups compared to sedentary groupsA single clinical trial found reduced brain atrophy and improved memory following an intervention where elderly adults were randomized to a 40 minute three times a week protocolI recently summarized another manuscript looking at the association of exercise and brain imaging in those with the APOE genotype linked to Alzheimer's disease. This study was published following the expert conference manuscript.There certainly need to be more randomized clinical trials of exercise therapy in groups at high risk for cognitive decline and Alzheimer's disease.Here is the list of all 7 prevention recommendations from the manuscript. Readers can access the free full-text manuscript by clicking on the PMID link below.Prevention Recommendations for Alzheimer's DiseaseMinimize dietary saturated and trans fatsIncrease intake of vegetables, fruits, legumes and grainsDaily vitamin E intake from foods of 15 mgDaily vitamin B12 in diet or supplement with blood B12 level monitoringDaily multivitamins not recommended but if used avoid those with iron and copperAluminum link to AD is controversial but avoid antacids and baking soda that contains aluminumAerobic exercise of 40 minutes at least 3 times per weekI have previously summarized 10 prevention strategies in AD that include non-nutrition based features that can be found here.Photo of butterfly is from the author's files.Follow the author on Twitter @WRY999Barnard ND, Bush AI, Ceccarelli A, Cooper J, de Jager CA, Erickson KI, Fraser G, Kesler S, Levin SM, Lucey B, Morris MC, & Squitti R (2014). Dietary and lifestyle guidelines for the prevention of Alzheimer's disease. Neurobiology of aging, 35 Suppl 2 PMID: 24913896... Read more »

Barnard ND, Bush AI, Ceccarelli A, Cooper J, de Jager CA, Erickson KI, Fraser G, Kesler S, Levin SM, Lucey B.... (2014) Dietary and lifestyle guidelines for the prevention of Alzheimer's disease. Neurobiology of aging. PMID: 24913896  

  • February 18, 2015
  • 05:02 AM

Fasting Fruit Flies: Improved Focus and Brain Power

by Pieter Carrière in United Academics

Fasting: solely a religious activity or is it also beneficial for focus and brain power? Research links fasting and hunger to formation of long-term memory.... Read more »

Hirano Y, Masuda T, Naganos S, Matsuno M, Ueno K, Miyashita T, Horiuchi J, & Saitoe M. (2013) Fasting launches CRTC to facilitate long-term memory formation in Drosophila. Science (New York, N.Y.), 339(6118), 443-6. PMID: 23349290  

Dubnau J. (2012) Neuroscience. Ode to the mushroom bodies. Science (New York, N.Y.), 335(6069), 664-5. PMID: 22323806  

Quinn, W., Harris, W., & Benzer, S. (1974) Conditioned Behavior in Drosophila melanogaster. Proceedings of the National Academy of Sciences, 71(3), 708-712. DOI: 10.1073/pnas.71.3.708  

  • February 18, 2015
  • 03:59 AM

Autism and the inter-pregnancy interval (again)

by Paul Whiteley in Questioning Answers

The paper from Maureen Durkin and colleagues [1] adds to something of a growing research evidence base suggesting that the temporal spacing between pregnancies / births - the inter-pregnancy interval (IPI) - may have something of an effect on the risk of receipt of a diagnosis of autism or autism spectrum disorder (ASD).We've been here before. In fact, a couple of times I've talked about the IPI in relation to autism risk (see here and see here) not including other, similar research findings in this area [2]. If I were to generalise from the collected data so far, it might be to say something like a short IPI (below 12 months) and a longer IPI (above about 5 years) seems to carry some elevated risk of offspring receipt of a diagnosis of autism or autism spectrum disorder (ASD). But remember risk is risk...Durkin et al looking through the records of almost 32,000 second-born children, reported that: "In adjusted analyses, both short (<12) and long (>84 month) IPIs were associated with a two-fold risk of ASD relative to IPIs of 24-47 months."I don't want to dwell too long on this topic outside of reiterating a suggestion made in the paper from Nina Gunnes and colleagues [3]: "A possible explanation is depletion of micronutrients in mothers with closely spaced pregnancies." That being said, there may be other factors influencing risk such as a heightened risk for preterm birth also being associated with a small IPI. The elevated risk associated with a longer IPI is slightly more difficult to explain away, assuming that is, that one doesn't include the variable of 'older mother' into proceedings (see here) and possibly some contribution from the young upstart discipline that is epigenetics (see here). More research is indicated although I might also throw into the research mix the idea that a longer IPI might also raise the risk of something like preeclampsia [4] and how this might also impact on offspring autism risk (see here).Patio Song to close (and some excellent interpretive dancing).----------[1] Durkin MS. et al. Inter-Pregnancy Intervals and the Risk of Autism Spectrum Disorder: Results of a Population-Based Study. J Autism Dev Disord. 2015 Feb 1.[2] Cheslack-Postava K. et al. Increased risk of autism spectrum disorders at short and long interpregnancy intervals in Finland. J Am Acad Child Adolesc Psychiatry. 2014 Oct;53(10):1074-81.e4.[3] Gunnes N. et al. Interpregnancy interval and risk of autistic disorder. Epidemiology. 2013 Nov;24(6):906-12.[4] Shachar BZ. & Lyell DJ. Interpregnancy interval and obstetrical complications. Obstet Gynecol Surv. 2012 Sep;67(9):584-96.----------Durkin MS, DuBois LA, & Maenner MJ (2015). Inter-Pregnancy Intervals and the Risk of Autism Spectrum Disorder: Results of a Population-Based Study. Journal of autism and developmental disorders PMID: 25636677... Read more »

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