Health posts
- February 3, 2013
- 09:00 PM
- 122 views
Is the Difference in Penetrating Trauma Mortality Truly Significant? Part I
by Rogue Medic in Rogue Medic
MV observed the following the lack of distinction in scene time for penetrating trauma mortality, which I did not give the proper attention in "EMS Time and Survival from Blunt and Penetrating Trauma." I will try to correct my mistake here.... Read more »
Lerner EB, & Moscati RM. (2001) The golden hour: scientific fact or medical "urban legend"?. Academic emergency medicine : official journal of the Society for Academic Emergency Medicine, 8(7), 758-60. PMID: 11435197
McCoy CE, Menchine M, Sampson S, Anderson C, & Kahn C. (2013) Emergency Medical Services Out-of-Hospital Scene and Transport Times and Their Association With Mortality in Trauma Patients Presenting to an Urban Level I Trauma Center. Annals of emergency medicine, 61(2), 167-74. PMID: 23142007
- February 3, 2013
- 05:34 PM
- 127 views
Antiepileptic exposure and offspring autism risk
by Paul Whiteley in Questioning Answers
The great autism research spotlight continues to focus its gazerbeam on the very earliest days of being for any clues governing why some children might go on to develop autism. I've kinda lost count of how many times I've talked about maternal exposure for this or that having been linked to an elevated risk of offspring autism; ranging from maternal inflammation to parental occupational exposure to the possibility that maternal medication history during pregnancy might singularly or cumulatively exert some potential effect on risk.Baby @ Wikipedia Indeed this last factor on medication during pregnancy has once again been the source of some speculation following the publication of a paper by Bromley and colleagues* suggesting an increased risk of offspring autism in cases of exposure to various antiepileptic drugs in-utero.A quick search of PubMed reveals that Dr Bromley has some history in looking at foetal antiepileptic exposure on developmental outcomes as per papers like this one and this one (open-access). There were a few clues in these papers that autism and other developmental disorders might well have been next on the list for investigation for this research group.Press attention for the current study? Er, yes, it goes without saying particularly in light of headlines like: Epilepsy drug linked to tenfold increase in autism (complete with picture of pregnant mums holding their tummy) and Epilepsy drug link to brain damage in 17,500 babies. Aside from thinking that there is probably lots of money to be made in stock photos of pregnant women and their bumps, if I were a pregnant mum with epilepsy taking such meds, I would probably be straight on the phone to my doctor/midwife to ask about these findings.So what did Bromley et al actually find and report:Based on an analysis of children born to 528 pregnant mums based here in Blighty, physical and cognitive abilities were assessed at various point during early infancy and childhood.Of the total cohort, data across various testing points were available for 415 children; of which 19 had been diagnosed with a "neurodevelopmental disorder" by the age of 6 years.Some of these neurodevelopmental disorders included autism (n=12); others had diagnoses of conditions like ADHD and dyspraxia (developmental coordination disorder, DCD).Looking through the kind of meds being taken by mum's during pregnancy, the authors reported a connection between greater offspring neurodevelopmental issues in those mothers who were taking anti-epileptic medication compared to those who weren't (7.4% vs. 1.8% respectively) as per the rate of epilepsy in mums-to-be (243/528; 46%).Sodium valproate was in particular singled out as part of the study as per the text: "children exposed to valproate alone in the womb were six times more likely to be diagnosed with a neurodevelopmental disorder". Indeed an even greater risk if a cocktail of other meds were also used during pregnancy.As one would expect, the authors have cautioned that pregnant women with epilepsy taking these medications does not automatically translate into offspring autism and on no account should pregnant women just stop taking the drug without appropriate medical advice. Risk, as I have discussed before, is risk not certainty and epilepsy can be a life-threatening condition.Valproate has already some history with regards to its possible effects on the developing infant as per the description of foetal valproate syndrome** (open-access) highlighting its potential teratogenicity. With autism in mind, this is also not the first time that valproate has appeared in the research texts. I note for example papers like this one from Bristot Silvestrin and colleagues*** which talked about an "animal model of autism induced by prenatal exposure to valproate", also bringing in words like 'glutamate' which has also seen its fair share of scientific inquiry in recent times (see this post). There are several other papers I could cite with a valproate-autism connection but I don't want to bore you.Valproate is also a compound I've become quite interested in recently as a result of being part of some very brief forays into the science writing domain and in particular on the topic of epigenetics (see here but now for PJ members only). Since doing a little bit of research in that area I've for example, read quite a bit on how valproate is now considered to be quite a potent HDAC inhibitor**** (open-access) with some potentially useful effects in cancer therapy. This HDAC inhibition quality - leading on to histone hyperacetylation - has also been questioned as a possible route towards some of the autism-like findings. To quote from the paper by Kataoka and colleagues***** "findings suggest that VPA-induced histone hyperacetylation plays a key role in cortical pathology and abnormal autism-like behaviours in mice". Bearing in mind mice are mice and not humans.The Bromley paper is an interesting paper and certainly invites a lot more study into how prenatal valproate exposure *might* show some connection to offspring risk of autism and other developmental conditions. Not trying to be anti-medication or anything, the study also highlights how little we actually know about the medicines we take and in particular their potential for things like trans-generational effects...----------* Bromley RL. et al. The prevalence of neurodevelopmental disorders in children prenatally exposed to antiepileptic drugs. J Neurol Neurosurg Psychiatry. January 2013.** Kini U. Fetal valproate syndrome: a review. Pediatric & Perinatal Drug Therapy. 2006; 7: 123-130.*** Bristot Silvestrin R. et al. Animal model of autism induced by prenatal exposure to valproate: Altered glutamate metabolism in the hippocampus. Brain Res. 2013; 1495: 52-60.**** Göttlicher M. et al. Valproic acid defines a novel class of HDAC inhibitors inducing differentiation of transformed cells. EMBO J. 2001;20:6969–6978.***** Kataoka S. et al. Autism-like behaviours with transient histone hyperacetylation in mice treated prenatally with valproic acid. Int J Neuropsychopharmacol. 2013; 16: 91-103.----------... Read more »
Bromley, R., Mawer, G., Briggs, M., Cheyne, C., Clayton-Smith, J., Garcia-Finana, M., Kneen, R., Lucas, S., Shallcross, R., Baker, G.... (2013) The prevalence of neurodevelopmental disorders in children prenatally exposed to antiepileptic drugs. Journal of Neurology, Neurosurgery . DOI: 10.1136/jnnp-2012-304270
- February 3, 2013
- 07:29 AM
- 157 views
Your heart health: Why a vegetarian diet could be good for you
by Ruth Stephen Whallett in Zellula Health
Western diets are predominantly meat dependent. But is non-vegetarianism good for you? A recent study by Oxford University's researchers explores the effect of our dietary preferences on heart health. New research from Oxford University indicates that a vegetarian diet could reduce the risk of Ischaemic heart disease (IHD). IHD is the UK's biggest killer, causing around 94,000 deaths in the UK each year. It occurs when there is disruption in blood supply to the heart muscle causing insufficient oxygen supply, leading to angina or a heart attack. It is normally caused by atherosclerosis, a condition where the arteries that supply the heart are furred up with fatty deposits and are narrowed, impeding normal blood flow to the heart muscle.The study involved 44,651 men and women, of whom 34 % were vegetarian, living in England and Scotland, who were followed up for 11.6 years. 1235 of those enrolled in the study developed IHD. The researchers examined hospital records and death records to find possible causes of disease and/or death and found that a vegetarian diet resulted in a massive 32% reduced risk of IHD. Vegetarians enrolled in the study consumed more cheese, fruit, vegetables, and whole grains but low amounts of milk when compared to their counterparts and had a lower mean Body Mass Index -BMI (BMI were highest among non-vegetarian men and lowest in vegetarian women) and lower non-HDL-cholesterol concentration and lower blood pressure when compared to non-vegetarians. Another interesting observation was that at the time of recruitment of people into the study, the non-vegetarians were found to be more likely to require long term medical treatment, accounting to a quarter of them, when compared to less than 20% of vegetarians meaning the veggie eaters are more healthier.The researchers speculate that the low IHD in vegetarians is probably due to the vegetarian diet and lifestyle leading to lowering of bad cholesterol levels and blood pressure. A vegetarian diet has been shown to be beneficial to heart health in many previous studies, though this study is the first of its kind in the UK population. The overwhelming evidence against meat should spur us on to pass the meat counter next time in the supermarket, at least in the interest of our hearts.References:http://www.nhs.uk/Conditions/Coronary-heart-disease/Pages/Introduction.aspx<span class="Z3988" title="ctx_ver=Z39.88-2004&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.jtitle=The American journal of clinical nutrition&rft_id=info:pmid/23364007&rfr_id=info:sid/researchblogging.org&rft.atitle=Risk of hospitalization or death from ischemic heart disease among British vegetarians and nonvegetarians: results from the EPIC-Oxford cohort study.&rft.issn=0002-9165&rft.date=2013&rft.volume=&rft.issue=&rft.spage=&rft.epage=&rft.artnum=&rft.au=Crowe FL&rft.au=Appleby PN&rft.au=Travis RC&rft.au=Key TJ&rfe_dat=bpr3.included=1;bpr3.tags=Medicine,Health,Public Health, Nutrition, Epidemiology, Cardiovascular, Clinical Research">Crowe FL, Appleby PN, Travis RC, & Key TJ (2013). Risk of hospitalization or death from ischemic heart disease among British vegetarians and nonvegetarians: results from the EPIC-Oxford cohort study. <span style="font-style: italic;">The American journal of clinical nutrition</span> PMID: <a rev="review" href="http://www.ncbi.nlm.nih.gov/pubmed/23364007">23364007</a></span>... Read more »
Crowe FL, Appleby PN, Travis RC, & Key TJ. (2013) Risk of hospitalization or death from ischemic heart disease among British vegetarians and nonvegetarians: results from the EPIC-Oxford cohort study. The American journal of clinical nutrition. PMID: 23364007
- February 2, 2013
- 06:37 AM
- 123 views
Imagery rehearsal therapy for post-trauma nightmares
by Eva Alisic in Trauma Recovery
Sleep problems are a central component of posttraumatic stress, both in children and adults, with 72% experiencing nightmares. Imagery rehearsal (IR) therapy has a cognitive behavioral background and is used more and more to overcome sleep problems after trauma. How effective is IR? ... Read more »
Casement MD, & Swanson LM. (2012) A meta-analysis of imagery rehearsal for post-trauma nightmares: effects on nightmare frequency, sleep quality, and posttraumatic stress. Clinical psychology review, 566-74. PMID: 22819998
- February 2, 2013
- 12:04 AM
- 111 views
The "human" genome?
by zacharoo in Lawn Chair Anthropology
The topic this week in my Intro to Bioanthro course is genetics, with the subtheme being the mechanisms getting us from a genotype to "the" human phenotype (next week is variation and population genetics). Of course we talked about things like DNA, simple Mendelian inheritance (even though many traits/diseases probably aren't really Mendelian), and even epigenetics and genomic imprinting. But I also wanted to point out the many ways that our very existence relies of life extrinsic to that encoded by our personal genomes (this was inspired by the intriguingly titled, "A symbiotic view of life: We have never been individuals," [Gilbert et al., 2012; free pdf]).Mitochondria are classic examples. These "powerhouses of the cell" or "cellular powerplants" (thanks, Wikipedia!) seem to have once been, at least a billion years ago, their own unicellular organisms that somehow came under the employ of early enterprising eukaryotes. These little organelles are indispensable players in cell metabolism, implicated also in ageing and certain diseases.In addition, there's been a lot of research lately on the human 'microbiome' - the specific set of bacteria living in and on our bodies, which aren't incorporated into our individual cells like mitochondria, but are nevertheless requisite for us to thrive. Analyses of poop, of all things (a scatological lecture is always a good one), have revealed that the bacterial composition of human digestive tracts varies between geographical regions, but also that age-related changes in the microbiome are similar between regions (Yatsunenko et al., 2012; see the review by Ed Yong). These bacteria are crucial to our ability to digest certain foods, and some variation in gut flora probably underlies some diseases (Smith et al., 2013); this is why you may have read about a rise in poop transplants lately (van Nood et al., 2013).Finally, and I think perhaps most intriguingly, there is evidence that our own genes may be commandeered by the the RNA produced by the things we eat. Now, the regulation of gene expression is bewilderingly complex, and one important player in this are various types of non-coding RNA, including micro RNA (miRNA), piwi-interacting RNA, etc. (I grew up under the paradigm 'a gene codes for a protein and our genomes contain all this "junk" DNA,' so RNA-interference and the like blow my mind). Recently, Lin Zhang and colleagues (2012) have found that some miRNA produced by plants can not only survive cooking and digestion, but that these miRNAs can actually interact with, and alter the expression of, at least one human gene (involved in removing bad cholesterol in this case). WHAT?!One of the most exciting areas of modern biology is the discovery of the various genetic and developmental mechanisms and processes that literally make us human. Of course the genetics of human uniqueness and variation are, to use a phrase I hate, 'much more complex than previously thought' (such a pervasive mantra in any field of research...). Not only that, but being human, arguably the most successful complex organism in recent history, is something we cannot even do on our own.ReferencesGilbert, S., Sapp, J., & Tauber, A. (2012). A Symbiotic View of Life: We Have Never Been Individuals The Quarterly Review of Biology, 87 (4), 325-341 DOI: 10.1086/668166Smith MI, Yatsunenko T, Manary MJ, Trehan I, Mkakosya R, Cheng J, Kau AL, Rich SS, Concannon P, Mychaleckyj JC, Liu J, Houpt E, Li JV, Holmes E, Nicholson J, Knights D, Ursell LK, Knight R, & Gordon JI (2013). Gut Microbiomes of Malawian Twin Pairs Discordant for Kwashiorkor. Science PMID: 23363771van Nood E, Vrieze A, Nieuwdorp M, Fuentes S, Zoetendal EG, de Vos WM, Visser CE, Kuijper EJ, Bartelsman JF, Tijssen JG, Speelman P, Dijkgraaf MG, & Keller JJ (2013). Duodenal infusion of donor feces for recurrent Clostridium difficile. The New England Journal of Medicine, 368 (5), 407-15 PMID: 23323867Yatsunenko T, Rey FE, Manary MJ, Trehan I, Dominguez-Bello MG, Contreras M, Magris M, Hidalgo G, Baldassano RN, Anokhin AP, Heath AC, Warner B, Reeder J, Kuczynski J, Caporaso JG, Lozupone CA, Lauber C, Clemente JC, Knights D, Knight R, & Gordon JI (2012). Human gut microbiome viewed across age and geography. Nature, 486 (7402), 222-7 PMID: 22699611... Read more »
Gilbert, S., Sapp, J., & Tauber, A. (2012) A Symbiotic View of Life: We Have Never Been Individuals. The Quarterly Review of Biology, 87(4), 325-341. DOI: 10.1086/668166
Smith MI, Yatsunenko T, Manary MJ, Trehan I, Mkakosya R, Cheng J, Kau AL, Rich SS, Concannon P, Mychaleckyj JC.... (2013) Gut Microbiomes of Malawian Twin Pairs Discordant for Kwashiorkor. Science. PMID: 23363771
van Nood E, Vrieze A, Nieuwdorp M, Fuentes S, Zoetendal EG, de Vos WM, Visser CE, Kuijper EJ, Bartelsman JF, Tijssen JG.... (2013) Duodenal infusion of donor feces for recurrent Clostridium difficile. The New England Journal of Medicine, 368(5), 407-15. PMID: 23323867
Yatsunenko T, Rey FE, Manary MJ, Trehan I, Dominguez-Bello MG, Contreras M, Magris M, Hidalgo G, Baldassano RN, Anokhin AP.... (2012) Human gut microbiome viewed across age and geography. Nature, 486(7402), 222-7. PMID: 22699611
Zhang L, Hou D, Chen X, Li D, Zhu L, Zhang Y, Li J, Bian Z, Liang X, Cai X.... (2012) Exogenous plant MIR168a specifically targets mammalian LDLRAP1: evidence of cross-kingdom regulation by microRNA. Cell Research, 22(1), 107-26. PMID: 21931358
- February 1, 2013
- 05:00 PM
- 151 views
Aging, Poor Sleep, and Bad Memory
by Allison in Dormivigilia
A friend of mine has studied the functional relationships between brain anatomy, sleep/wake architecture, and performance on a memory-related task. I wonder how this relationship would hold in individuals with a predisposition to Alzheimer's or chronic traumatic encephalitis... Read more »
Mander BA, Rao V, Lu B, Saletin JM, Lindquist JR, Ancoli-Israel S, Jagust W, & Walker MP. (2013) Prefrontal atrophy, disrupted NREM slow waves and impaired hippocampal-dependent memory in aging. Nature neuroscience. PMID: 23354332
- February 1, 2013
- 03:04 PM
- 44 views
Taking a Kidney While Removing Gall Bladder an Ethical Quagmire
by Cristy at Living Donor 101 in Living Donors Are People Too
In 2009, a certain transplant surgeon *cough*Testa*cough* authored an article in 2009 which suggested that folks undergoing a gall bladder removal (Cholecystectomy) be used as living kidney donors. Let me repeat that: Testa and his co-authors were suggesting that since these folks were having surgery anyway, we should ask them if they’d like to relinquish … Continue reading »... Read more »
Gordon EJ, Frader J, Goldberg AM, Penrod D, McNatt G, Franklin J, & Chicago Transplant Ethics Consortium. (2010) In response to: Testa et al. 'Elective surgical patients as living organ donors: a clinical and ethical innovation'. American journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons, 10(3), 704. PMID: 20041861
- February 1, 2013
- 12:31 PM
- 8 views
Predatory Prawns
by Emarkham in GeneticCuckoo
A new ecological method of control for an African parasitic disease, an analysis of the benefits and limitations of this approach. ... Read more »
E Markham. (2013) Predatory Prawns. Blogspot. info:/
- February 1, 2013
- 11:44 AM
- 172 views
Oxytocin and Human Attachment
by William Yates, M.D. in Brain Posts
In a previous post, I summarized a recent review on the neuroscience of human attachment. This review highlighted research related to the human bonding and social interactions. Attachment ability shows significant variability in humans with insecure attachment styles contributing to risk for some mental disorders. The neuroanatomical framework for social processing is being investigated with brain imaging techniques.Hormonal factors including the role of oxytocin also play a key role in social processing. Kai MacDonald recently published a review of the prosocial role of oxytocin in attachment. This review highlighted individual factors that influence variability in oxytocin response.Molecular Model of OxytocinOxytocin is a central nervous system nine amino acid peptide that has both central and peripheral effects. Oxytocin can be administered through intranasal mist administration.The biological effects of oxytocin are complex and include stimulation of uterine contraction during labor, stimulation of breast milk letdown during nursing and modulation of sexual arousal and response.The effects of oxytocin in social interactions include:increases in strength of human bondingdecreases in anxiety in social situationsincreases in the trust in others increases in calmness and contentment in the presence of a mateMacDonald notes that individuality in response to oxytocin can be separated into three categories.Gender: Women appear to be more responsive to the effects of oxytocin. This may be due to the role of estrogen. The presence of estrogen upregulates oxytocin and oxytocin receptor production. Oxytocin response in women is dependent on female hormonal phase with more response during periods of higher estrogen levels. Administration of intranasal oxytocin has a stronger effect on increasing prosocial behavior in women compared to men. Genetic Variation in Oxytocin Receptor Gene and CD38: Genetic variability in the oxytocin receptor gene modulate response to oxytocin with some alleles linked to stronger and weaker responses. Additionally, genetic variation in the ectoenzyme CD38 have similar effects. CD38 contributes to the biologic process of oxytocin secretion. Specific combinations of oxytocin receptor and CD38 genes may contribute to clinical deficits in attachment, stress response and anxiety.Early Childhood Attachment Environment: Early traumatic experiences appear to impair the development of the oxytocin system. This may be due to more general adverse effects on neuroplasticity. Parents with a personal history of childhood abuse are less responsive to the prosocial effects of intranasal oxytocin. Early traumatic experience may unfortunately contribute to lifelong attachment impairment through this epigenetic effect.Future research in the role of oxytocin and the oxytocin receptor in a variety of mental disorders will be important. Intranasal oxytocin clinical trials will be coming in anxiety disorders, stress disorders and disorders of social interaction such as autism and schizophrenia. Understanding the factors associated with variability in oxytocin response will be key in interpreting the results of future research.Readers with more interest in this topic can access the free full-text manuscript by clicking the PMID link below. Photo of blue heron from the author's files.Molecular model from the Wikipedia Commons File authored by MindZiper.Macdonald KS (2012). Sex, receptors, and attachment: a review of individual factors influencing response to oxytocin. Frontiers in neuroscience, 6 PMID: 23335876... Read more »
Macdonald KS. (2012) Sex, receptors, and attachment: a review of individual factors influencing response to oxytocin. Frontiers in neuroscience, 194. PMID: 23335876
- February 1, 2013
- 06:24 AM
- 184 views
Acyl-carnitine profiles and autism
by Paul Whiteley in Questioning Answers
No doubt alongside quite a few others, I was interested to read the latest paper from Richard Frye and colleagues* (open-access) discussing the potential links between an animal model of autism spectrum disorder (ASD) and real-world ASD in a particular cohort of participants.This is not the first time that I've talked about (a) the work of Dr Frye - as per my [don't panic] post on folate receptor autoantibodies in cases of autism (see here) and (b) some of the difficulties attached to translating rat/mouse model findings in autism research into 'real-world' findings (see here). Indeed this last point might also tie into my recent musings on the use of LPS in autism research (see here).Daddy o' microbiology @ Wikipedia My interest in the latest Frye paper was further piqued upon realising that Derrick MacFabe was also part of the authorship team given his insightful work on how administration of propionic acid - a short chain fatty acid - to rodents might provide some interesting perspectives overlapping with various findings noted in cases of autism (see my previous post here).The Frye paper is open-access and available to all but here are a few points worth mentioning:Based on the animal model work looking at propionic acid (PPA) infusions and some of the collected effects (presentation of autism-type behaviours**, mitochondrial issues***, abnormal measures of glutathione, etc.), the aim of the current study was to map out whether some of the observations in the PPA rodent model were also present in real-life autism.Based on a clinic-based sample of children with autism (N=326), acyl-carnitine panels were conducted on about two-thirds of participants (n=213).Acyl-carnitines, as their name suggests, are related to carnitine which has previously been tied back to autism (see here) and represent a number of different compounds - complexes of carnitine and various fatty acids - involved in the transport of fatty acids into the mitochondrial matrix.The previous PPA rodent model indicated some disturbance in the amount of various acyl-carnitines, particularly with regards to short- and long-chain fatty acids (not so much in the medium-chain fatty acids) reflective of some mitochondrial dysfunction.So the authors looked at short-, medium- and long-chain acyl-carnitines in their autism cohort to see if there were any overlaps compared with the PPA treated animals.Results: 35% of the autism cohort showed "an increase in three or more acyl-carnitines when initially measured". When further testing were conducted on some of these participants showing elevation, this figure was revised to 17% of the cohort who "demonstrated consistent elevations in short-chain and long-chain, but not medium-chain, acyl-carnitines". You'll note the similarity with PPA animal model in terms of the short- and long-chain acyl-carnitines.Furthermore, four participants were also examined with regards to glutathione and oxidative stress markers. As per the quite consistent literature on things like total- and free-reduced glutathione (see this post), compared with controls, there were some familiar trends emerging.And relax.There is a lot to take in from this paper both in the protocol and testing undertaken and the possible interpretation of findings. A quote best sums up the results: "This study has demonstrated that ~17% of children with ASD manifest biomarkers of abnormal mitochondrial fatty-acid metabolism that parallel similar biomarkers in the PPA rodent model of ASD".As perhaps expected, there has been some press attention following the publication of this paper. The headline: Researchers discover link between certain types of autism and gut bacteria has been a common one, reflective of the fact that when it comes to the production of PPA outside of injecting the stuff directly into the rodent brain, the gut and in particular, certain types of gut bacteria, have been suggested as a route to PPA production in cases of autism. Indeed, I'm taken back to the findings by Wang and colleagues from Oz (see this post) on levels of fecal short chain fatty acids (SCFAs) in their cohort of children with autism which included propionic acid (propionate). I'm also reliably informed that there is 'more to come' from the Australian research group in the coming months.There are a few final aspects to the Frye study which I should have mentioned earlier. This includes the notion that "it is very likely that MD [mitochondrial dysfunction] is acquired" given that in the most part, both nuclear and mitochondrial DNA examinations in their cohort were negative for anything that might genetically account for the results. I'll be coming to DNA and mitochondrial issues in a subsequent 'training' post scheduled quite soon but one can perhaps see how this might strengthen any argument of disruptions to gut bacteria/microflora facilitating the production of elevated PPA onwards to disrupting acyl-carnitine chemistry. Additionally there is the implication based on the PPA rodent model that affecting PPA production could be a potential therapeutic route for some cases of autism at some point. I don't really want to go too far into the hows and whys of this suggestion at the current time given the current lack of evidence for any effect. Aside that is, from drawing your attention to a related field of inquiry into how disrupting PPA-producing gut bacteria might have some important implications for those suffering from conditions like propionic acidaemia****.I'm not going to get too carried away with the Frye results as they stand. As per my previous post on PPA, there is still a bit of a stretch from injecting rodent brains with PPA and recording outcomes to suggesting that gut bacteria will be able to produce enough PPA so as to exert a similar effect in humans. At least one group is asking the same question***** (open-access). That being said, I am still interested in the details of this study and how the authors have at least tried to model animal findings into real-life autism. Indeed how we really should be putting a lot more research effort into looking at mitochondria and autism as we potentially also should gut bacteria and autism.A song to finish... something mellow yet catchy.... Lovefool by the Cardigans.----------* Frye RE. et al. Unique acyl-carnitine profiles are potential biomarkers for acquired mitochondrial disease in autism spectrum disorder. Translational Psychiatry. 2013; 3: e220.** MacFabe DF. et al. Effects of the enteric bacterial metabolic product propionic acid on object-directed behavior, social behavior, cognition, and neuroinflammation in adolescent rats: Relevance to autism spectrum disorder. Behav Brain Res. 2011; 217: 47-54.*** Thomas RH. et al. Altered brain phospholipid and acylcarnitine profiles in propionic acid infused rodents: further development of a potential model of autism spectrum disorders. J Neurochem. 2010; 113: 515-529.**** Mellon AF. et al. Effect of oral antibiotics on intestinal production of propionic acid. Arch Dis Child 2000; 82: 169-172.***** El-Ansary AK. et al. C... Read more »
Frye RE, Melnyk S, & Macfabe DF. (2013) Unique acyl-carnitine profiles are potential biomarkers for acquired mitochondrial disease in autism spectrum disorder. Translational psychiatry. PMID: 23340503
- January 31, 2013
- 10:00 PM
- 135 views
EMS Time and Survival from Blunt and Penetrating Trauma
by Rogue Medic in Rogue Medic
People will tell you that they just know the we need to load and go. Some even claim that the mythological Golden Hour is real. Maybe there will be an episode of Ancient Aliens about R Adams Cowley identifying the meaning of trauma and writing it on a cocktail napkin in a bar.
... Read more »
McCoy CE, Menchine M, Sampson S, Anderson C, & Kahn C. (2013) Emergency Medical Services Out-of-Hospital Scene and Transport Times and Their Association With Mortality in Trauma Patients Presenting to an Urban Level I Trauma Center. Annals of emergency medicine, 61(2), 167-74. PMID: 23142007
- January 31, 2013
- 12:47 PM
- 163 views
Neuroscience of Human Attachment
by William Yates, M.D. in Brain Posts
Attachment is the ability to form human relationship bonds. Individuals vary in their ability to develop social relationships. The ability to form secure human relationships plays a key role in successful personal and occupational development.Attachment theory evolved over 50 years ago. This theory proposes all humans have an innate biological mechanism that supports social engagement. This engagement is necessary during infancy to encourage nurturance and provision of a safe environment.Bowlby is credited with describing attachment theory and he proposed three developmental styles of attachment. These three attachment styles included:Secure attachment: an ability to easily seek and obtain support from others. This style promotes strong bonds with parents, siblings, friends and later in life allows for bonding with a mate.Anxious attachment: a insecure attachment style where emotional support has often been inconsistent during childhood. Individuals with anxious attachment develop hypersensitivity to interpersonal rejection and have anxiety in social environments. They may develop a needy approach to relationships constantly seeking reassurance of the strength of social supports.Avoidant attachment: an insecure attachment style that may have been characterized by early social adverse environments. Individuals with insecure attachment style built a wall around their life denying a need or interest in human interactions.Emerging research in social neuroscience is providing a better understanding of brain mechanisms related to human attachment. Vrticka and Vuilleumier of the University of Geneva in Switzerland recently published an excellent review of the neuroscience of human attachment in the journal Frontiers in Human Neuroscience.The authors of this review begin by noting research showing attachment has profound effects in the domains of emotion processing, selective attention and memory. Insecure attachment individuals are hypersensitive to changes in the expression of emotions in others. Anxious attachments individuals have enhanced attention to threatening cues. Avoidant attachment individuals inhibit the memory processing of distressful information.The authors note social approach behavior appears regulated in specific brain regions including the ventral tegmental area, pituitary, striatum and ventral medial orbitofrontal cortex. Social aversion appears to be regulated through the amygdala, hypothalamus, insula, anterior cingulate and anterior temporal poles.Social behavior appears to regulated through both affective evaluation (emotional mentalization) and cognitive control systems (cognitive mentalizations). These systems interact with hormonal and neurotransmitter domains in influencing social interactions.The neuroscience of human attachment includes emerging research showing the importance of mental state representation of others (theory of mind). Mothers with high sensitivity to the cries of their own infants during the post partum period show increased gray matter and fMRI BOLD responses in the prefrontal cortex, superior temporal sulcus and fusiform gyrus. These regions have been identified as key components engaged in being aware of the emotional states of others. The authors conclude that the neuroscience of human attachment is beginning to outline key common and distinct elements in avoidant and anxious attachment styles. Attachment styles appear to be influenced by both environmental history as well as neurobiological factors, some of which may have strong genetic contributions.Future neuroscience of research will need to move experiments into the "real world" and not be limited to task in brain scanners. Additionally, future research needs to target early intervention studies in children with attachment problems to find the most effective methods to improve social outcomes.Readers with more interest in this review are directed to the DOI link below where the free full text manuscript can be found.Photo of great white egret from the author's files.Vrtička, P., & Vuilleumier, P. (2012). Neuroscience of human social interactions and adult attachment style Frontiers in Human Neuroscience, 6 DOI: 10.3389/fnhum.2012.00212... Read more »
Vrtička, P., & Vuilleumier, P. (2012) Neuroscience of human social interactions and adult attachment style. Frontiers in Human Neuroscience. DOI: 10.3389/fnhum.2012.00212
- January 30, 2013
- 09:32 AM
- 161 views
Video Tip of the Week: ScienceGameCenter #edtech
Could you help Gregor Mendel obtain a plant with its coloring specified by recessive genes? Would you want to try to solve crime with some forensic DNA analysis? The ScienceGameCenter can give you the chance to do those things, and learn concepts of biology (and other sciences too!) at the same time. This week’s video tip of the week will focus on what they offer.... Read more »
Khalili, N., Sheridan, K., Williams, A., Clark, K., & Stegman, M. (2011) Students Designing Video Games about Immunology: Insights for Science Learning. Computers in the Schools, 28(3), 228-240. DOI: 10.1080/07380569.2011.594988
Schneider, M., & Jimenez, R. (2012) Teaching the Fundamentals of Biological Data Integration Using Classroom Games. PLoS Computational Biology, 8(12). DOI: 10.1371/journal.pcbi.1002789
- January 30, 2013
- 07:14 AM
- 140 views
Autism and the criminal justice system
by Paul Whiteley in Questioning Answers
I assume most people with a connection to autism, either personal or professional, will have heard about the case of Gary McKinnon and his long-running battle against extradition from the UK to the United States to face charges of alleged hacking into various US Government systems.Order @ Wikipedia The politics have, over the 10-year period of this saga, tended to focus more on the extradition arrangements between the UK and US over and above the actual person, his Asperger syndrome diagnosis (and some possibly conflicting reports about his mental state) and the reasons given for his alleged actions.I'm sure, like me, many people (but not all apparently) were happy to hear that this ordeal for Gary has now come to some kind of end with the news that he will not face charges here in the UK. When however it comes to other people such as Syed Talha Ahsan, also diagnosed with Asperger syndrome but nonetheless extradited to the US, things have not turned out so well. Indeed there has also been some debate about possible double-standards.I'm not here to talk politics and political decisions but I did wonder if it might be time to revisit autism, or rather the autism spectrum, and the law in light of the Gary McKinnon news (and it was big news) and also the paper by Catherine Cheely and colleagues* on the prevalence of youth with an autism spectrum disorder in the criminal justice system.Regular readers of this blog might remember a post I wrote a while back on autistic symptoms and offending. The crux of that entry was the quite generalised assertion being raised by Geluk et al** detailing autistic symptoms as being "more prevalent in childhood arrestees compared to the general population and are uniquely associated with future delinquent behavior". I hasten to add that, as in the last post, I'm not intending to generalise, demonise or any other -ise in this entry on this quite delicate topic particularly with other recent tragic events still very much in mind.Back to the paper by Cheely:The aim of the study was three-fold: (i) look at the types of charges against youths with an autism spectrum disorder (ASD), (ii) examine adjudication outcome compared with a control cohort and (iii) see what was different about those with ASD charged compared with a cohort not charged.Six hundred and nine youths with an ASD were identified from the South Carolina Autism and Developmental Disabilities Monitoring Project (SC-ADDM). That's right, one of the CDC surveillance sites used to formulate things like their prevalence estimates (see the 1 in 88 post) based on 8-year olds.Five percent (32/609) of the cohort had contact with the criminal justice system and were charged with 103 offences (mean 3.3 offences per child).Compared with non-ASD control youths, there was a tendency for more crimes to be committed against a person over property and generally more likely to be school-based.Adjudication-wise, youths with ASD were significantly more likely to have their cases diverted and less likely to be prosecuted; indeed none of the cohort were sentenced to detainment.The differences between charged youths with ASD vs. controls ASD participants? Well, the presence of intellectual disability (ID) (learning disability if you will) was less likely to occur in ASD youths committing offences.As the authors point out, there is a feeling that most of the charges made against the youths with ASD in their study seem to eminate from spontineity over pre-meditation; something perhaps reflected in the zero percent detainment rate.That and the fact that school seemed to be a focal point for such behaviours perhaps offers further clues about factors such as stress and anxiety as being involved and combining with anger (see the study by Quek and colleagues***), even whether inclusion might be part and parcel of the issue here (see this blog post by Zoe on a recent paper published in the autism special edition of Pediatrics).One could try and get really technical and start talking about issues with empathy and inferring mental states as also being involved in such behaviours too, but to tell you the truth I doubt any adolescent, whether diagnosed with autism or not, truly uses such functions in this type of scenario which seems more probably like 'lashing out'. I must also make mention of the issue of bullying as potentially being related to offences highlighted by the authors in light of what has been discussed in this area in recent times and continues to be talked about.I don't want to come across as an apologist or anything like that in this post given that an individual's diagnosis of ASD has (rightly or wrongly) been discussed in relation to some very serious crimes**** (open-access) down the years, bearing in mind that we cannot tar everyone with ASD with the same brush. One also needs to put the numbers of offences linked to ASD into context with all the other crimes carried out by non-autistic people, which I'm sure impact on many, many more people and indeed the number of occasions where people with autism themselves are a victim of crime, even in some cases by those who are meant to protect and serve.In terms of where next with this topic of research, I'd actually like to see more done in a few areas. Things like looking at long-term outcome for that 5% who committed offences in terms of developmental course, any additional comorbidity which developed and were identified and importantly whether there was any further contact with the criminal justice system would be a good start. At least then we might get some ideas about whether we are indeed talking more about individual lapses in behaviour over something more chronic as per the literature so far on this topic*****.----------Additional note: The majority of this post was conceived and written in November 2012 based on the peer-reviewed research literature available at that time. I would kindly ask that any comments or opinions posted about this entry be confined to discussions about the scientific papers mentioned. Thanks.----------* Cheely CA. et al. The prevalence of youth with autism spectrum disorders in the criminal justice system. J Autism Dev Disord. 2012; 42: 1856-1862.** Geluk CA. et al. Autistic symptoms in childhood arrestees: longitudinal association with delinquent behavior. J Child Psychol Psychiatry. 2012; 53: 160-167.*** Quek LH. et al. Co-occurring anger in young people with Asperger's syndrome. J Clin Psychol. 2012; 68: 1142-1148.**** Haskins BG. & Arturo Silva J. Asperger's disorder and criminal behavior: forensic-psychiatric considerations. J Am Acad Psychiatry Law 2006; 34: 374-384.***** Hippler K. et al. No increase in criminal convictions in Hans Asperger's original cohort. J Autism Dev Disord. 2010; 40: 774-780.----------... Read more »
Cheely CA, Carpenter LA, Letourneau EJ, Nicholas JS, Charles J, & King LB. (2012) The prevalence of youth with autism spectrum disorders in the criminal justice system. Journal of autism and developmental disorders, 42(9), 1856-62. PMID: 22187108
- January 30, 2013
- 01:12 AM
- 271 views
Dr. David H. Barlow and Aversion Therapy for Gays
by The Neurocritic in The Neurocritic
Should a professional society honor a highly accomplished investigator who conducted studies in the past that would now be considered unethical? Distinguished professor and clinical psychologist Dr. David H. Barlow was recognized for his achievements by the Association for Psychological Science (APS) last year as the recipient of the 2012 James McKeen Cattell Fellow Award:David H. Barlow has made enormous theoretical and empirical contributions in many areas of clinical psychology. He is best known for his efforts to develop psychological treatments for anxiety disorders. His early work on the treatment of agoraphobia laid the groundwork for exposure-based treatments that are today regarded as the gold standard. As we learned more about the relationship of agoraphobic avoidance to the occurrence of panic attacks, Barlow led the way in the development of treatments for the remediation of panic symptoms.Much of Barlow’s research is based on the notion that anxiety is a disorder of emotion. He holds this to be the case regardless of the specific emotional disorder, and this has led him in the later years of his career toward the development and testing of a unified protocol for the transdiagnostic treatment of such disorders....What you might not have known is that such disorders have included homosexuality and transsexualism. Barlow advocated and practiced aversion and conversion therapies to "cure" gay and transgendered people of their "deviant" sexuality.While I do not wish to detract from Dr. Barlow's many positive accomplishments, I feel it is important to expose the questionable practices of the past and to hold people accountable for their actions. I looked far and wide to find a mea culpa from Dr. Barlow, much like Dr. Robert Spitzer's public apology for his published work on reparative therapy as a "cure" for homosexuality (Spitzer, 2003).1 But I did not find such a statement anywhere. Should we question the judgment of APS in honoring Dr. Barlow with the Cattell Award? 2 Are they tacitly condoning exorcism in transsexuals (Barlow et al., 1977) and aversion therapy in gay men (Barlow et al., 1969; Hayes et al., 1983)? At the very least, APS did not publicly acknowledge or condemn these former practices, which remain secretly buried in the past.I contacted two divergent experts to ask their opinions. Psychologist Dr. John Grohol, who founded the mental health networking and education site Psych Central, turned the question around:"Should we honor professionals who may have made questionable judgments in their early career? I would ask a question in return -- Should we forever withhold such honors for the poor judgments one makes in one's early career?"On the other hand, Professor Lynn Conway, the pioneering computer scientist, electrical engineer, and transgender activist, was surprised about the award. She felt an appropriate course of action is..."... to expose these old miscreants and get their misdeeds on the record. That way they'll all have to run for cover in the years ahead..." Let's examine some of these practices below so you can decide for yourself.Exorcism for Transsexualism?As some of you might have gathered, I came across this paper during my exorcism research. Barlow and colleagues (1977) didn't actually perform the exorcism themselves, but observed the resulting change in behavior "fortuitously" and used it as an example of how atypical gender identity could be modified, if not prevented all together:Although the prevention of transsexualism is the ideal, work in this area has been fraught with ethical problems... The authors reported the detailed case history of "John", a 21 year old patient who had a clear identity as female and wished to transition. Before doing so, John was persuaded to visit a Fundamentalist Christian doctor, who performed an exorcism:The physician administered a total physical exam and said that he could live quite well as a woman, but the real problem was possession by evil spirits. After some discussion of this, John reported a session which lasted 2-3 hr and involved exhortations and prayers over John by the physician and laying on a hands on John's head and shoulders. During this period, John reported fainting several times and arising to the continuing of the prayers and exhortations, resulting in the exorcism of 22 evil spirits which the physician called by name as they left his body. ... The physician noted ... that he showed John that his life was a fake and that Jesus could redeem him and that a standard prescription of Scripture readings caused the spirit of the woman in John to disappear.Immediately after the session John announced he was a man, discarded his female clothes (hiding his breasts as best he could), and went to the barber shop to have his long hair cut into his current short, masculine style...Rather than condemn the outlandish and unethical behavior of this physician, and counsel John (who had identified as Judy) on her previously excellent adjustment as female and readiness for surgery, they considered this a successful change in gender identity. An even more questionable event was a visit to a faith healer. After the laying on of hands, John reported that his breasts (size 36B) had disappeared immediately. Personally, I think a psychiatric assessment would have been in order.Very worth reading in regard to this paper is the text on Rogue Theories of Transsexualism written by Professor Conway. She says that "By seeing a collection of such theories side-by-side, we grasp the strangeness of them all."Aversion Therapy to Cure Sexual Deviance Even more outrageous were the papers on aversion therapy. As a prelude to the actual practices described by Barlow et al. (1969), I will use American Horror Story: Asylum as a near-exemplar.The year is 1964. Lana Winters is a reporter investigating the unethical practices at Briarcliff Manor, a mental institution for the criminally insane. She's caught snooping around and is committed against her will to keep her quiet, with the ostensible reason being that she is gay. She is forced to have shock treatment. Sympathetic psychiatrist Dr. Oliver Thredson tries to persuade her to undergo aversion therapy, which is presented as more "humane." She eventually agrees because she thinks it'll get released her from Briarcliff once Thredson pronounces her "cured."Under the direction of Dr. Thredson, Winters views a slide show of erotic pictures of women. She has an iv drip going into her left arm. She starts to get physically ill while viewing the slides and then throws up into a metal bucket.... Read more »
Barlow DH, Abel GG, & Blanchard EB. (1977) Gender identity change in a transsexual: an exorcism. Archives of sexual behavior, 6(5), 387-95. PMID: 921523
Barlow DH, Agras WS, & Leitenberg H. (1972) The contribution of therapeutic instruction of covert sensitization. Behaviour research and therapy, 10(4), 411-5. PMID: 4637499
Barlow DH, Leitenberg H, & Agras WS. (1969) Experimental control of sexual deviation through manipulation of the noxious scene in covert sensitization. Journal of abnormal psychology, 74(5), 597-601. PMID: 5349402
Hayes SC, Brownell KD, & Barlow DH. (1983) Heterosocial-skills training and covert sensitization. Effects on social skills and sexual arousal in sexual deviants. Behaviour research and therapy, 21(4), 383-92. PMID: 6138027
- January 29, 2013
- 07:58 PM
- 151 views
Antidepressants could cause moderate heart-beat problems
by Usman Paracha in SayPeople
Researchers have found that some anti-depressants could cause heartbeat problems.
This research has been published online in BMJ.
In this study, researchers worked on the electronic health record of 38,397 adult patients, from a large New England healthcare system, who underwent ECG following the prescription of antidepressant or methadone between February 1990 and August 2011.
Some anti-depressants though partially or completely solve the problem of depression but, could also create the problem of the heart-rhythm. Researchers have found that a class of anti-depressants known as selective serotonin reuptake inhibitors (SSRIs) could result in long QT interval showing heart rhythm abnormalities.
Researchers noted that "nearly one in five patients treated with these antidepressants who underwent electrocardiography had QT intervals which would be considered abnormal" but the clinical significance of this is unknown.
These recent findings are strengthening the US Food & Drug Administration (FDA)’s recommended safety communication released in 2011, according to which citalopram, a very popular anti-depressant, could not be used in doses greater than 40 mg/day as it may result in serious cardiac arrhythmias due to the prolongation of QT interval.
Methadone has also been found to increase the QT interval. According to the authors, despite some limitations, this study "confirmed a modest prolongation of QT interval with citalopram, and identified additional antidepressants with similar observed risk.” This modest prolongation is such that for many patients, the risk of abnormal heart rhythm is very less than the benefits of treatment of depression or anxiety.
Researchers also noted that “the question of whether patients for whom antidepressants will be prescribed should routinely have electrocardiograms before and/or after treatment starts cannot be addressed directly by this study.”
Reference:
Castro, V., Clements, C., Murphy, S., Gainer, V., Fava, M., Weilburg, J., Erb, J., Churchill, S., Kohane, I., Iosifescu, D., Smoller, J., & Perlis, R. (2013). QT interval and antidepressant use: a cross sectional study of electronic health records BMJ, 346 (jan29 3) DOI: 10.1136/bmj.f288... Read more »
Castro, V., Clements, C., Murphy, S., Gainer, V., Fava, M., Weilburg, J., Erb, J., Churchill, S., Kohane, I., Iosifescu, D.... (2013) QT interval and antidepressant use: a cross sectional study of electronic health records. BMJ, 346(jan29 3). DOI: 10.1136/bmj.f288
- January 29, 2013
- 07:31 PM
- 42 views
Microstructure of Film Coated Tablets
by Axel Zeitler in Pharmaceutical Solid State Research Cluster (PSSRC)
Since 2007 when terahertz pulsed imaging (TPI) was first developed to non-destructively measure the coating thickness of pharmaceutical tablets there has been intense research in the PSSRC into how this technique can help improve the quality of pharmaceutical coatings and thus make controlled release technology based on coatings of single dosage forms attractive to industry.... Read more »
Zeitler, J., Shen, Y., Baker, C., Taday, P., Pepper, M., & Rades, T. (2007) Analysis of coating structures and interfaces in solid oral dosage forms by three dimensional terahertz pulsed imaging. Journal of Pharmaceutical Sciences, 96(2), 330-340. DOI: 10.1002/jps.20789
Brock, D., Zeitler, J., Funke, A., Knop, K., & Kleinebudde, P. (2012) A comparison of quality control methods for active coating processes. International Journal of Pharmaceutics, 439(1-2), 289-295. DOI: 10.1016/j.ijpharm.2012.09.021
- January 28, 2013
- 07:00 PM
- 108 views
You Can Turn Healthy by Quiting at 40
by Katja Keuchenius in United Academics
Smokers, it’s not too late. Researchers showed that quiting before fourty gets you back almost the whole ten years usually lost by smoking.... Read more »
Jha, P., Ramasundarahettige, C., Landsman, V., Rostron, B., Thun, M., Anderson, R., McAfee, T., & Peto, R. (2013) 21st-Century Hazards of Smoking and Benefits of Cessation in the United States. New England Journal of Medicine, 368(4), 341-350. DOI: 10.1056/NEJMsa1211128
- January 28, 2013
- 09:09 AM
- 429 views
Identifying Samples from Genomic Data
by Daniel Koboldt in Massgenomics
In last week's issue of Science, Melissa Gymrek and colleagues from the lab of Yaniv Erlich (Whitehead) report a method for the triangulation the identity of a sample donor using genomic data and public databases.
As a proof-of-principle, they uncovered the identities of about 50 sample donors from the CEPH Utah collection, perhaps the best-studied collection of "anonymous" samples to date. Their approach exploits several facts of this "information age" we live in.... Read more »
Gymrek M, McGuire AL, Golan D, Halperin E, & Erlich Y. (2013) Identifying personal genomes by surname inference. Science (New York, N.Y.), 339(6117), 321-4. PMID: 23329047
- January 27, 2013
- 04:59 PM
- 179 views
CrossFit Training Post: On Creatine Supplements
by Andrea Kirk in WODMasters
What is Creatine?
In terms of athletics, Creatine is a molecule needed for muscle function. It helps keep you from running out of ATP during short, intense bursts of activity. Energy in ATP (high school biology refresher) ultimately fuels most life processes. Skeletal muscle uses a lot of ATP during intense exercise. Creatine helps recycle used ATP so it continues to be available. Creatine supplements increase muscle force and power. At least in the short term. And that's the very short of it. Creatine also interacts with other cellular processes. It appears to increase production of insulin-like growth factor (IGF). IGF works with Growth Hormone and Insulin to increase cell division and growth. Creatine supplements may cause this Creatine/Growth Hormone system to step up growth.
CrossFit Seven inadvertently advertises for Fuzzy's Taco Stand.
Will being on Creatine Supplements help me gain muscle mass?
Probably yes. This may be especially the case for vegetarians. In average Westerners your body produces half its own creatine. Diet (meat) supplies the other half. Vegetarians have lower levels of creatine than meat eaters. Masters Athletes may also benefit. Creatine may help preserve muscle mass as well.
Can Creatine Supplements help me during CrossFit Competition?
CrossFit involves intense burst of energy from many different muscle groups. So CrossFit might be the poster child for creatine supplements.
Can being on Creatine Supplements help me with endurance sports?
Creatine probably won't help with endurance. And it might slow you down if you have to carry more weight. That can be muscle mass or it might simply be retained water.
What else can Creatine Supplements do?
Creatine supplements are being studied as treatments for people with muscle disorders. They are also being studied for use in treating major depression. Creatine seems to increase the effectiveness of anti-depressants.
What are side effects or dangers?
One potential problem with Creatine Supplements is the increased activity of the IGF/Growth Hormone axis. While this might help with muscle growth, increased IGF and Growth Hormone can increase risk of cancer. Most studies of creatine supplementation have involved small numbers of subjects. And have been for short periods of time. This means that the effects of taking creatine for a long time are not known.
Another possible problem with creatine supplements is that they can reduce flexibility. This might be because of increased muscle mass. Or it might be because of fluid build-up in muscle tissue.
Should I be on Creatine Supplements all the time?
There is concern that taking creatine for a long time or in great amounts can cause kidney damage. "More" is often not "better." Another thing to keep in mind is that the body tends to seek balance. If you give it more of something it may respond by producing less of it itself. This happens, for example, with testosterone. Testosterone will increase muscle growth, but the testes will figure out that there is enough testosterone in circulation. And it will stop making so much. Hence the shrinking testes and reduced fertility in men who take testosterone supplements. It is possible that taking creatine supplements will eventually result in less creatine synthesis. If you are going to take creatine you should take it for short periods of time. And take breaks. Until more research is done.
Safdar A, Yardley NJ, Snow R, Melov S, & Tarnopolsky MA (2008). Global and targeted gene expression and protein content in skeletal muscle of young men following short-term creatine monohydrate supplementation. Physiological genomics, 32 (2), 219-28 PMID: 17957000
Candow DG, Forbes SC, Little JP, Cornish SM, Pinkoski C, & Chilibeck PD (2012). Effect of nutritional interventions and resistance exercise on aging muscle mass and strength. Biogerontology, 13 (4), 345-58 PMID: 22684187
Lyoo IK, Yoon S, Kim TS, Hwang J, Kim JE, Won W, Bae S, & Renshaw PF (2012). A randomized, double-blind placebo-controlled trial of oral creatine monohydrate augmentation for enhanced response to a selective serotonin reuptake inhibitor in women with major depressive disorder. The American journal of psychiatry, 169 (9), 937-45 PMID: 22864465
... Read more »
Safdar A, Yardley NJ, Snow R, Melov S, & Tarnopolsky MA. (2008) Global and targeted gene expression and protein content in skeletal muscle of young men following short-term creatine monohydrate supplementation. Physiological genomics, 32(2), 219-28. PMID: 17957000
Candow DG, Forbes SC, Little JP, Cornish SM, Pinkoski C, & Chilibeck PD. (2012) Effect of nutritional interventions and resistance exercise on aging muscle mass and strength. Biogerontology, 13(4), 345-58. PMID: 22684187
Lyoo IK, Yoon S, Kim TS, Hwang J, Kim JE, Won W, Bae S, & Renshaw PF. (2012) A randomized, double-blind placebo-controlled trial of oral creatine monohydrate augmentation for enhanced response to a selective serotonin reuptake inhibitor in women with major depressive disorder. The American journal of psychiatry, 169(9), 937-45. PMID: 22864465
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