Recently, claims have surfaced surrounding a Belgian coma victim - Rom Houben - who spent 23 years 'locked in', conscious but paralysed. It was only recently discovered that he had been conscious, and efforts were made to enable him to communicate using a controversial technique called 'Facilitated Communication'. As The Times report; "Mr Houben is now seemingly able to express himself in remarkably lucid messages while [his 'facilitator'] Mrs [Linda] Wouters guides his hand over a computer screen." This sounds all very good, until you watch the following video, and in particular the section around 1m 17s:
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The facilitator is moving the finger at an incredible rate of knots, but Houben is not even looking at the screen, or the keypad - his eyes are firmly shut. Now, yes, I can touch-type, but try touch-typing with your eyes closed, and directing somebody else's finger. It's a bloody big ask.
It sounds even more unlikely when you look at the scientific evidence for facilitated communication - or rather, the lack of evidence, since - as James Randi has pointed out in a gloriously annoyed blog - the technique has about as much support as Nick Griffin at an ACLU meeting. Wikipedia note that:
The majority of peer reviewed scientific studies conclude that the typed language output attributed to the clients is directed or systematically determined by the therapists who provide facilitated assistance.
In other words, as Randi points out, FC is most likely a case of the "Clever Hans Effect", a psychological quirk in which "a person's or an animal's behaviour can be influenced by subtle and unintentional cueing on the part of a questioner," notorious for its destructive influence on poorly controlled trials of this kind. The facilitator may not be doing it consciously, but it seems far more likely that the words are coming from her mind.
The Times, one of the few papers to question the findings, notes:
The novel method of communication has not convinced all medical experts, however. "It’s Ouija board stuff. It’s been discredited time and again when people look at it. It’s usually the person who is doing the pointing who is doing the messages," Arthur Caplan, Professor of Bioethics at the University of Pennsylvania, said after watching a video of the pair.
In a comment to Wired, Caplan has drawn attention to the unlikely language being expressed by Houben via his facilitator:
"You’re going to lie for 23 years in a hospital bed with almost no stimuli, and then sound completely coherent and cogent?" he said. "Something is wrong with that picture. The messages are almost poetic. It sounds too lucid, like someone prepared these things to say. I’m not saying it’s all a fraud, but I want to hear a lot more."
Caplan's disdain for Facilitated Communication (FC) is well justified. Mark Mostert published a systematic review of the literature in 2001  [pdf], painting a bleak picture for proponents. Of 29 studies reviewed, 19 had one or more control procedures and refuted FC claims, 6 had one or more control procedures and supported FC claims but were often riddled with methodological problems, while 4 had no controls and supported FC claims.
Mostert concluded with a statement that should sound all too familiar to anyone who has ever read meta-studies of treatments like homeopathy or chiropractic:
The results of the review support and confirm the conclusions reached by previous reviewers of the empirical FC literature. The divide between the results of studies incorporating control procedures find very little to no support for the efficacy of FC, studies employing fewer control procedures produce mixed results, and studies ignoring control procedures almost universally find FC to be effective. In the cases of the few, tentative positive results emerging from studies reporting some form of control procedures, as in the cases of Cardinal et al.  and Weiss et al. , these results are much more likely the artifact of methodological problems than an accurate representation of persuasive evidence.
Professor Laureys, the patient's neurologist claims to have performed a simple test to establish the truth, as The Times report:
The spectacle is so incredible that even Steven Laureys, the neurologist who discovered Mr Houben’s potential, had doubts about its authenticity. He decided to put it to the test.
"I showed him objects when I was alone with him in the room and then, later, with his aide, he was able to give the right answers," Professor Laureys said. "It is true."
The problem is that these claims are extraordinary, and therefore require extraordinary evidence to back up. Laureys cannot be considered an unbiased observer, given his emotional investment in the case. That isn't an accusation of fraud or wrong-doing - it is incredibly easy to deceive yourself in such situations.
Given what we know then, Professor Laureys and other medical staff working with Houben need to back up their extraordinary claims with much more solid evidence than the anecdata presented so far. After all, if it turns out that in fact the results produced by FC aren't real, they could be causing their patient even more stress than he has experienced so far.
And there's a further reward on offer. The James Randi Foundation have offered a one million dollar prize to anyone who can provide a valid demonstration of facilitated communication, and Randi has told Wired that the offer "is still there."
The gauntlet has been thrown. Will Professor Laureys be willing to put his claims to the test?
 Mostert, M. (2001). Facilitated Communication Since 1995: A Review of Published Studies Journal of Autism and Developmental Disorders, 31 (3), 287-313 DOI: 10.1023/A:1010795219886
 Cardinal DN, Hanson D, & Wakeham J (1996). Investigation of authorship in facilitated communication. Mental retardation, 34 (4), 231-42 PMID: 8828342
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Mostert MP. (2001) Facilitated communication since 1995: a review of published studies. Journal of autism and developmental disorders, 31(3), 287-313. PMID: 11518483
Cardinal DN, Hanson D, & Wakeham J. (1996) Investigation of authorship in facilitated communication. Mental retardation, 34(4), 231-42. PMID: 8828342
Weiss MJ, Wagner SH, & Bauman ML. (1996) A validated case study of facilitated communication. Mental retardation, 34(4), 220-30. PMID: 8828341
In a recent previous post the topic was the neuroanatomy of depression, or which sites of the brain can play a role in depression. Which parts of the brain show the dysfunction underlying depression. MRI scans can link neurobiology of depression with clinical findings through brain imaging studies that examine regional structure, regional function or [...]
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MacQueen GM. (2009) Magnetic resonance imaging and prediction of outcome in patients with major depressive disorder. Journal of psychiatry , 34(5), 343-9. PMID: 19721844
One of the most frightening symptoms of advanced cancer is "cachexia", or severe, unintentional weight-loss and wasting. It's a terrible prognostic sign, and the only truly effective treatment is removal of the cancer. Treatment of this syndrome has the potential to improve quality of life in patients with advanced cancers. Various types of medications, including antidepressants, hormones, and cannabis derivatives have been tried with little effect. Treating the symptoms of incurable cancers is difficult and although we're pretty good at it, we sometimes fail. Cannabis seems a plausible intervention, given the anecdotal and clinical data associating it with increased appetite, although appetite in normal, healthy individuals may be mediated by different pathways than the cachexia in cancer patients. Still, it's worthy of investigation. Read the rest of this post... | Read the comments on this post...... Read more »
Strasser, F. (2006) Comparison of Orally Administered Cannabis Extract and Delta-9-Tetrahydrocannabinol in Treating Patients With Cancer-Related Anorexia-Cachexia Syndrome: A Multicenter, Phase III, Randomized, Double-Blind, Placebo-Controlled Clinical Trial From the Cannabi. Journal of Clinical Oncology, 24(21), 3394-3400. DOI: 10.1200/JCO.2005.05.1847
As mentioned in a prior post, the exact mechanism of neurotoxicity in prion diseases in unknown. Two possibilities, which are not mutually exclusive, include a loss-of-function of the native prion protein and an acquired neurotoxic effect of the pathologic prion protein. PRNP knockout mice have previously exhibited memory impairment, disruption in circadian rhythms and sleep, behavioral, and neurotransmission changes. Also, excitatory glutamatergic, GABAa receptor-mediated fast inhibition and late afterhyperpolarization have been shown to be reduced or absent in PRNP knockout mice. Rangel and colleagues released a recent study looking at role of the native prion protein specifically in the context of neurotransmission and neuroexcitability. This is the second such in vivo study and the researchers used three populations of mice: 1) wild-type, 2) prion protein gene (PRNP) knock-outs, and PrPc-overexpressing Tg20 mice. In their study, they examined several responses to kainate (KA): seizure activity, electrophysiology, cell death, and gene expression. Both PRNP knockout and Tg20 mice showed susceptibility to KA in the form of onset, frequency, severity, and length of seizures. None of the wildtype mice died whereas one PRNP knockout and two Tg20 mice had severe seizures and expired. Hippocampal cell death was also noted in these two samples. Cell death was restricted to the CA1 and CA3 regions of the hippocampus in PRNP knockout mice and was more global in Tg20 mice. Reactive astrogliosis accompanied neurodegeneration in both samples. No cell death was observed in wild-type mice. Electrophysiological profiles also differed between the groups. There was a strong increase in paired-pulse facilitation and a disappearance of homeostasis in the PRNP knockout and Tg20 mice compared to wild-type mice. detected differences in gene expression profiles between groups. 336 genes were deregulated in the Tg20 mice compared to wild-type mice and PRNP knockouts demonstrated 404 de-regulated genes compared to wild-type mice. 129 genes in the following pathways were co-regulated in PRNP knockout and Tg20 mice: protein ubiquitination, glycerolphospholipid metabolism, nitrogen metabolism, GABA receptor signaling, D-glutamine and D-glutamate metabolism, glutamate receptor signaling, B-cell receptor signaling, hypoxia signaling in the cardiovascular system, and calcium signaling. RT-qPCR studies showed that GABAa and AMPA-kainate receptors were also co-regulated in PRNP knockout and Tg20 mice. In summary, this study shows the importance of the native prion protein in the homeostasis of hippocampal circuits and neuronal transmission, particularly in regards to neuronal excitability. However, too much and too little native prion protein were found to have negative effects in this study. Of note, overexpression of PrPc was performed in PrPres infected mice, which would have altered PrPc amounts. Unfortunately, PrPc levels was not measured in this study. Rangel, A., Madroñal, N., Massó, A., Gavín, R., Llorens, F., Sumoy, L., Torres, J., Delgado-García, J., & Río, J. (2009). Regulation of GABAA and Glutamate Receptor Expression, Synaptic Facilitation and Long-Term Potentiation in the Hippocampus of Prion Mutant Mice PLoS ONE, 4 (10) DOI: 10.1371/journal.pone.0007592 del.icio.us Tags: neuroscience,prion,genetics,molecular biology,biochemistry,research,biology ... Read more »
Rangel, A., Madroñal, N., Massó, A., Gavín, R., Llorens, F., Sumoy, L., Torres, J., Delgado-García, J., & Río, J. (2009) Regulation of GABAA and Glutamate Receptor Expression, Synaptic Facilitation and Long-Term Potentiation in the Hippocampus of Prion Mutant Mice. PLoS ONE, 4(10). DOI: 10.1371/journal.pone.0007592
The paper I'm about to present was written in 2002, and in the fast-paced world of the internet may seem out of date - after all, Youtube hadn't even been invented then, and Wikipedia and Google were shiny new businesses. But in fact, Davies et al's study of anti-vaccination websites is as relevant today as it was then - perhaps even more so .
"The internet has provided antivaccinationists with unprecedented opportunities for exposure. In the USA, 55% of adults with internet access use it to seek health related information. For all its benefits, the internet has great potential to
disseminate health information that is incorrect and potentially dangerous."
The scale of the internet in 2009 is of course orders of magnitude larger than it was seven years ago, reaching more of the population in a greater part of the world. Additionally, new ways of putting information across have been developed: in 2002, Youtube and the age of viral videos were still three years in the future, podcasts were a rarity, and mainstream blogging was still in its infancy. The scale of the problem is doubtless larger today, but what's remarkable is how quickly anti-vaccination activists came to dominate this scene in the early days of the web.
The researchers look at a hundred anti-vaccination websites, including the tone of their content, and also looked at search results from the leading search engines of the day (back then, you could still use the plural of 'search engine'). The table below shows the number of anti-vaccination pages in the top ten search results for 'vaccination' for each search engine:
So while AltaVista, Yahoo and Netscape produce a couple of dodgy sites each, Google's 'superior' technology failed spectacularly, with all of the top ten search results for 'vaccination' leading to anti-vaccination sites. The situation now is improved, but even today, a search on Google.co.uk brings up whale.to and naturalnews.com in the top ten results (Wikipedia, naturally, is first).
This for me raises interesting ethical questions about the role of search engines. If a parent was five times more likely to see an anti-vaccination result on Google than searching with AltaVista, what responsibility - if any - do Google (motto: "Do No Evil") have for the public health consequences of their abysmal rankings in 2002?
Moving on to the types of sites around, a distinct set of patterns emerged from their results that still sounds familiar today.
"Antivaccination groups sought to present themselves as legitimate authorities with scientific credibility: about one in four websites implied official status at national or international level."
There's an odd Cargo Cult mentality that exists in the alternative medicine and anti-science communities, in that they reject the institutions and research of modern medicine and science, yet seek to appropriate their titles, language and superficial aspects of their methodology, setting up 'clinics', calling each other 'doctor', and attempting to cite references from the literature...
"A majority of sites propounded the scientific validity of their claims by referencing from extensive literature dominated by self published works and the alternative medicine press. Allegedly damning research was often quoted, but without citation of its source. Referencing was frequently incomplete and often indiscriminate, including letters to editors of newspapers and television interviews. Research published in indexed medical journals was also quoted; however, the conclusions drawn were often inconsistent with those of the authors. Overall this produced a spectre of the existence of masses of data on the dangers of vaccination."
This of course is the same sort of behaviour we saw with the British Chiropractic Association's pitiful attempts to produce a 'plethora of evidence' for the use of chiropractic in treating childhood illnesses. But the psychology of this is complex and confusing - if you despise modern medicine, if you want to work against it, why are you so obsessed with imitating your enemy? It almost suggests a sort of authority-envy.
Over half of all sites cited rank breaking doctors speaking out against vaccination. Implied division within the medical community reinforced the notion of a debate among authorities. One third of sites promoted themselves as sources of non-partisan information on both sides of the immunisation 'debate'. Despite these claims a mere 15% contained any information supportive of vaccination. Only a third of sites had links to such sites.
This of course is the classic 'teach the controversy' approach. It follows the time-honoured Tobacco company trick that if you can't directly refute the science, you can wage a war of obfuscation that leaves the public with the impression of a scientific debate where in fact none still exists, something we've seen with tobacco harm, climate change, vaccination, and a dozen other areas.
The problem with all of the above is that it seems to result in a sort of cognitive dissonance. If you believe that the research is inconclusive, and that the 'real' picture of climate change, vaccination, smoking or whatever is not getting out to the public, then the only way to rationalize this is by inventing some sort of conspiracy. In fact, virtually all denialist beliefs seem to eventually come down to a conspiracy theory. Even when this isn't explicitly stated, it is often implied.
"Nearly all sites referred to the antivaccination struggle as a search for truth against a background of cover up and denial. Antivaccinationists portrayed themselves as crusaders excavating hidden truths. The vaccination hoax was a vehicle for the generation of limitless profit and which would produce epidemics of chronic illness, requiring billions of dollars worth of drugs and medical care. To many groups, compulsory vaccination represented the beginning of the slippery slope towards totalitarianism."
That 'nearly all' sites resorted to conspiracy theory is unsurprising then - it's a necessary leap to make since you can't believe that doctors are knowingly giving people dangerous vaccines without some element of conspiracy present. What's perhaps more interesting though is the depersonalization or dehumanization of 'the enemy'.
"Almost all sites featured the adversarial notion of 'us versus them' whereby parents and antivaccinationists stood against the depersonalised 'them' of doctors, health bodies, governments, and pharmaceutical companies. Doctors were presented as either willing conspirators cashing in on the vaccine 'fraud', or pawns manipulated by the shadowy vaccine combine; parents' love and compassion whose intuition about vaccination harms was considered a stronger force than cold, analytical science.
I couldn't have but read that and be reminded of the classic radio clash between Richard Littlejohn and Will Self, in which Self referred to Littlejohn's characterization of John Prescott as a 'chimp' with the observation:
"Well he doesn't say he's a human being, does he? He uses the classic form of demonisation which is to say he's a chimp, in other words he's bestial. So he's actually dehumanised the subject of his abuse before he even moves on to piling on the pejoratives, and I think that's very psychologically interesting, of course we're all familiar with the kind of people who demonise other human beings by turning them into bestiary..."
Which, while a bit strong, is interesting. Again, anti-vaccine propaganda requires that people believe doctors are behaving in an inhuman way, so this would seem to be the logical consequence of rationalizing that. The results of this dehumanization are deeply disturbing since, like the people Self alludes to, it allows people to resort to rabid abuse and attacks on those disagreeing with their ideological view. Paul Offit of course has been a target of concerted hate campaigns, and recently journalist Amy Wallace was subjected to extraordinary attacks, some involving vile misogynistic abuse, for an article she wrote in Wired.
This also seems to touch on people's fears of doctors and science in general, and it's unsurprising to see what follows:
"The answer to disease prevention was not the 'artificial' process of vaccination but the pursuit of natural lifestyle. Many sites asserted that infectious disease was a consequence of lifestyle, not microorganisms."
"Being unnatural, vaccinations deranged the function of the immune system. The natural immunity provided by infection was considered superior. Many sites urged parents to intentionally expose their children to infectious diseases alleging health benefits."
Yes the natural fallacy, the misguided notion that something 'natural' is healthier for you than something 'artificial.' The terrifying result of this sort of broken thinking is that parents may intentionally expose their children to infectious diseases. It begs the question, how many have fallen seriously ill or died as a result o... Read more »
A review of the literature connecting morphine and cancer growth in clinical trials.... Read more »
Exadaktylos AK, Buggy DJ, Moriarty DC, Mascha E, & Sessler DI. (2006) Can anesthetic technique for primary breast cancer surgery affect recurrence or metastasis?. Anesthesiology, 105(4), 660-4. PMID: 17006061
Biki B, Mascha E, Moriarty DC, Fitzpatrick JM, Sessler DI, & Buggy DJ. (2008) Anesthetic technique for radical prostatectomy surgery affects cancer recurrence: a retrospective analysis. Anesthesiology, 109(2), 180-7. PMID: 18648226
Kuru is an acquired prion disease, transmitted through ritualistic cannibalism, that reached epidemic proportions in the Fore tribe of Papua New Guinea. In a previous post, I presented an article by John Collinge’s group on the selection process of heterozygosity at codon 129 of the prion protein gene (PRNP). The research group has gone a step further by recently describing a new polymorphism of the PRNP gene, G129V. The authors performed PRNP genotyping of 3,000 individuals from the Eastern Highland population, which included 709 individuals who had participated in cannabalistic rituals. They looked specifically at the codons 127 and 129 among geographic regions and among individuals that were stratified by risk exposure (i.e., high, medium, and low risk). The G127V variant was only found in those regions where kuru was prevalent. 127V was present in half of the women who had the highest exposure to kuru and who were homozygous for methionine at codon 129 (MM). Interesting, although 129V was present in kuru exposed populations, it was not found in those who succumbed to kuru or in unexposed population groups around the world. 127V was also invariably linked to a 129M allele and predominately found in 129MM homozygotes in contrast to 129MV heterozygotes. Heterozygosity at codon 127 thus conveyed resistance to kuru in others susceptible 129MM homozygotes. Thus the newly described G127V polymorphism was naturally selected among populations exposed to kuru as a resistance factor. Both codon 129V and codon 127V are examples of natural selection that have occurred recently. Once again, prion diseases teach us a lot about biology in general…hence another important factor for studying them. Mead S, Whitfield J, Poulter M, Shah P, Uphill J, Campbell T, Al-Dujaily H, Hummerich H, Beck J, Mein CA, Verzilli C, Whittaker J, Alpers MP, & Collinge J (2009). A Novel Protective Prion Protein Variant that Colocalizes with Kuru Exposure. The New England journal of medicine, 361 (21), 2056-2065 PMID: 19923577 del.icio.us Tags: kuru,evolution,epidemiology,prion diseases,research,biology,genetics,risk ... Read more »
Mead S, Whitfield J, Poulter M, Shah P, Uphill J, Campbell T, Al-Dujaily H, Hummerich H, Beck J, Mein CA.... (2009) A Novel Protective Prion Protein Variant that Colocalizes with Kuru Exposure. The New England journal of medicine, 361(21), 2056-2065. PMID: 19923577
Chocolate, like many of the things we eat regularly, is a potentially fatal poison, and so it should come as no surprise that a study by the unimaginatively-named John Johnston (at the USDA National Wildlife Research Center) shows that our favourite sweet could prove to be an effective pesticide, for use against coyotes .
Chocolate, or rather the theobromine and caffiene it contains, is potentially fatal to many creatures, but of course "the poison is the dose." Humans are particularly efficient metabolizers of theobromine, but the same isn't true for dogs or cats. Whereas it would take dozens of pounds of chocolate to kill a human (probably more than you could physically eat), just 20 mg per kg of theobromine is enough to cause symptoms, while more than 60mg per kg can induce seizures (see the Merck Veterinary Manual).
To put those figures into perspective, milk chocolate contains around 60mg of theobromine per ounce, so if you have a dog weighing 20kg (44lbs), about a pound and a quarter (or half a kilo) of milk chocolate could bring on seizures.
The full set of symptoms for chocolate toxicosis are described in the manual thus:
Clinical signs of chocolate toxicosis usually occur within 6-12 hr of ingestion. Initial signs may include polydipsia, vomiting, diarrhea, abdominal distention, and restlessness. Signs may progress to hyperactivity, polyuria, ataxia, tremors, and seizures. Tachycardia, premature ventricular contractions, tachypnea, cyanosis, hypertension, hyperthermia, bradycardia, hypotension, or coma may occur. Hypokalemia may occur late in the course of the toxicosis, contributing to cardiac dysfunction. Death is generally due to cardiac arrhythmias, hyperthermia, or respiratory failure. The high fat content of chocolate products may trigger pancreatitis in susceptible animals.
Cats are actually somewhat more sensitive than dogs, but they have a useful defense - cats don't find chocolate tasty. Dogs on the other hand love it, which is bad for dogs, but handy if you're a farmer with a major coyote problem that you'd like to deal with without introducing too many nasty chemicals into the environment. And that brings us to the device below - a CLOD, or as only Americans would call it, a Coyote Lure Operative Device.
Coyotes are to American agriculture what Professor Nutt is to the Daily Mail or Katie Price is to people who want to read a newspaper without being confronted by giant fake breasts every two minutes. As well as being responsible for around three-quarters of all livestock losses due to animal predators (costing some US$44m in losses), other damage caused by coyotes apparently includes:
"...collisions with aircraft, attacks on pets and children, damage to fruit and vegetable crops, predation on game species such as elk and deer, and predation on poultry. In addition to directly damaging fruit and vegetable crops, coyotes also contribute to crop losses via damage to hose irrigation systems. Coyotes have also been implicated in the transmission and spread of epizootic rabies in the United States."
In short, coyotes are responsible for pretty much everything from the global recession to 9/11. If you're living in America and you can't find a pen, the chances are that a coyote has nicked it. Clearly it's time for some mass extermination. We're talking US$40m here. That's, like, Arnie's fuel budget for a month.
Leaving skepticism about the need for this aside, chocolate - or rather the engineered chocolate-mimic used in the trial has a number of advantages as a pesticide. It's safe for humans and many other animals while fatal to coyotes, who love it. Better yet, by carefully adjusting the ratio of theobromine to caffeine in their chocolate mimic (to 5:1), the USDA researchers were able to pretty much remove pre-mortality symptons - the coyotes ate the chocolate, and then later they died. As the researchers point out:
"The results from this research clearly demonstrate that theobromine/caffeine mixtures have potential as a pest coyote toxicant that is effective, selective, and potentially more socially acceptable than fluoroacetate or sodium cyanide."
Of course, numerous coyotes were killed in the course of establishing the 5:1 ratio as the best proportion of theobromine to caffeine to use. " Coyotes dosed with the 1:1 and 1:2 mixtures exhibited undesirable symptoms of toxicosis and were euthanized. " The search for safer pesticides is always a noble one, but personally I'd like to see evidence of a larger problem than a measly US$44m of damage caused before we start breaking out the toxic Mars Bars.
 Johnston, J. (2005). Evaluation of Cocoa- and Coffee-Derived Methylxanthines as Toxicants for the Control of Pest Coyotes Journal of Agricultural and Food Chemistry, 53 (10), 4069-4075 DOI: 10.1021/jf050166p
Martin is the editor of layscience.net.
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Johnston, J. (2005) Evaluation of Cocoa- and Coffee-Derived Methylxanthines as Toxicants for the Control of Pest Coyotes. Journal of Agricultural and Food Chemistry, 53(10), 4069-4075. DOI: 10.1021/jf050166p
The amount of arthroscopic rotator cuff repairs being performed has skyrocketed in recent years. The last 20 years or so have seen the transition from a full open approach, to a combined arthroscopic and mini-open technique, to the current all-arthroscopic technique. The implications on rehabilitation are enormous, as patients are recovering faster with less pain and surrounding tissue involvement. Initially, the strength of these arthroscopic rotator cuff repairs was in question and still lagged behind the strength of the mini-open procedure. But recently, more and more studies are being published that show the strength of the new techniques are comparable. A recent study in AJSM prospectively evaluated the integrity of the rotator cuff repair in 127 patients at the 1-year and 2-year postoperative marks. The authors used ultrasound to evaluate the tendons. Results showed that: At one year, 68% had an intact rotator cuff. 32% had a full thickness tear again. All the tendons that were intact at 1-year were still intact at 2-years. Interestingly, 8% of the tendons that were not intact at 1-year were intact at 2-years. All patients demonstrated significant improvement in ASES scores from baseline to 2-year follow-up. Patients with intact cuffs had ASES scores of ~95 in comparison to ~86 with tendon defects. Clinical Implications The finding that all patients with an intact cuff at 1 year still were intact at 2-years is significant, showing that the repairs are providing good results over a decent amount of time. In general, characteristics that led to more cases of intact rotator cuffs were: Age – the younger the better. All patients with cuff defects were > 60 years old. Tear size – the smaller the better. All patients with cuff defects had tears > 4cm. Tendon involvement – the less the better. 75% of patients with cuff defects had more than one rotator cuff tendon intact. It should also be noted that patients with an intact cuff demonstrated significantly great external rotation strength. The finding that 32% had cuff tears sounds alarming at first but is in line with past reports on rotator cuff repairs. This is a little known secret that we don't promote to our patients, because, as this study and several other studies have shown, patients improve regardless of whether or not the cuff is intact. The key comes down to rehab after surgery, as usual! Nho SJ, Adler RS, Tomlinson DP, Allen AA, Cordasco FA, Warren RF, Altchek DW, & MacGillivray JD (2009). Arthroscopic rotator cuff repair: prospective evaluation with sequential ultrasonography. The American journal of sports medicine, 37 (10), 1938-45 PMID: 19531660 ***************************
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Nho SJ, Adler RS, Tomlinson DP, Allen AA, Cordasco FA, Warren RF, Altchek DW, & MacGillivray JD. (2009) Arthroscopic rotator cuff repair: prospective evaluation with sequential ultrasonography. The American journal of sports medicine, 37(10), 1938-45. PMID: 19531660
Based on the results from functional neuroimaging studies, lesion patient studies and brain stimulation studies two important brain areas play an important role in the pathophysiology of depression. These two brain area s are the ventromedial prefrontal cortex and the dorsolateral prefrontal cortex. The ventromedial prefrontal cortex is depicted in red on the picture above [...]
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Koenigs, M., & Grafman, J. (2009) The functional neuroanatomy of depression: Distinct roles for ventromedial and dorsolateral prefrontal cortex. Behavioural Brain Research, 201(2), 239-243. DOI: 10.1016/j.bbr.2009.03.004
Lui, S., Parkes, L., Huang, X., Zou, K., Chan, R., Yang, H., Zou, L., Li, D., Tang, H., Zhang, T.... (2009) Depressive Disorders: Focally Altered Cerebral Perfusion Measured with Arterial Spin-labeling MR Imaging. Radiology, 251(2), 476-484. DOI: 10.1148/radiol.2512081548
Costafreda, S., Chu, C., Ashburner, J., & Fu, C. (2009) Prognostic and Diagnostic Potential of the Structural Neuroanatomy of Depression. PLoS ONE, 4(7). DOI: 10.1371/journal.pone.0006353
A nice complement to the one paper (Ng et al) I detailed last week is a paper that actually came out just before hand (Choi et al). Whereas the Ng paper used whole exome targeted sequencing to find the mutation for a previously unexplained rare genetic disease, the Choi et al paper used a similar scheme (though with a different choice of targeting platform) to find a known mutation in a patient, thereby diagnosing the patient.The patient in question has a tightly interlocked pedigree (Figure 2), with two different consanguineous marriages shown. Put another way, this person could trace 3 paths back to one set of great-great-grandparents. Hence, they had quite a bit of DNA which was identical-by-descent, which meant that in these regions any low-frequency variant call could be safely ignored as noise. A separate scan with a SNP chip was used to identify such regions independently of the sequencing.The patient was a 5 month old male, born prematurely at 30 weeks and with "failure to thrive and dehydration". Two spontaneous abortions and a death of another premature sibling at day 4 also characterized this family; a litany of miserable suffering. Due to imbalances in the standard blood chemistry (which, I wish the reviewers had insisted on further explanation for those of us who don't frequent that world), a kidney defect was suspected but other causes (such as infection) were not excluded.The exome capture was this time on the Nimblegen platform, followed by Illumina sequenicng. This is not radically different from the Ng paper, which used Agilent capture and Illumina sequencing. At the moment Illumina & Agilent appear to be the only practical options for whole exome-scale capture, though there are many capture schemes published and quite a few available commercially. Lots of variants were found. One that immediately grabbed attention was a novel missense mutation which was homozygous and in a known chloride transporter, SLC26A3. This missense mutation (D652N)targets a position which is almost utterly conserved across the family, and is making a significant change in side chain (acid group to polar non-charged). Most importantly, SLC26A3 has already been shown to cause "congenital chloride-losing diarrhea" (CLD) when mutated in other positions. Clinical follow-up confirmed that fluid loss was through the intestines and not the kidneys.One of the genetic diseases of the kidney that had been considered was Bartter syndrome, which the more precise blood chemistry did not match. Given that one patient had been suspected of Bartter but instead had CLD, the group screened 39 more patients with Bartter but lacking mutations in 4 different genes linked to this syndrome. 5 of these patients had homozygous mutations in SLC26A3, 2 of which were novel. 190 control chromosomes were also sequenced; none had mutations. 3 of these patients had further follow-up & confirmation of water loss through the gastrointestinal tract.This study again illustrates the utility of targeted sequencing for clinical diagnosis of difficult cases. While a whole exome scan is currently in the neighborhood of $20K, more focused searches could be run far cheaper. The challenge will be in designing economical panels which will allow scanning the most important genes at low cost and designing such panels well. Presumably one could go through OMIM and find all diseases & syndromes which alter electrolyte levels and known causative gene(s). Such panels might be doable for perhaps as low as $1-5K per sample; too expensive for routine newborn screening but far better than a endless stream of tests. Of course, such panels would miss novel genes or really odd presentations, so follow-up of negative results with whole exome sequencing might be required. With newer sequencing platforms available, the costs for this may plummet to a few hundred dollars per test, which is probably on par with what the current screening of newborns for inborn errors runs. One impediment to commercial development in this field may well be the rapid evolution of platforms; companies may be hesitant that they will bet on a technology that will not last.Of course, to some degree the distinction between the two papers is artificial. The Ng et al paper actually, as I noted, did diagnose some of their patients with known genetic disease. Similarly, the patients in this study who are now negative for known Bartter syndrome genes and for CLD would be candidates for whole exome sequencing. In the end, what matters is to make the right diagnosis for each patient so that the best treatment or supportive care can be selected.Choi M, Scholl UI, Ji W, Liu T, Tikhonova IR, Zumbo P, Nayir A, Bakkaloğlu A, Ozen S, Sanjad S, Nelson-Williams C, Farhi A, Mane S, & Lifton RP (2009). Genetic diagnosis by whole exome capture and massively parallel DNA sequencing. Proceedings of the National Academy of Sciences of the United States of America, 106 (45), 19096-101 PMID: 19861545... Read more »
Choi M, Scholl UI, Ji W, Liu T, Tikhonova IR, Zumbo P, Nayir A, Bakkaloğlu A, Ozen S, Sanjad S.... (2009) Genetic diagnosis by whole exome capture and massively parallel DNA sequencing. Proceedings of the National Academy of Sciences of the United States of America, 106(45), 19096-101. PMID: 19861545
Contour Drawing Rating Scale (Thompson & Gray, 1995) - established as a reliable and valid measure of body size perception.Anorexia nervosa, an obsessive and unrelenting quest for thinness, is one of the most deadly psychiatric disorders. The documented mortality rate ranges from 3.3% to 18% in different studies (Herzog et al., 2000), and those with the disorder are ten times more likely to die from their illness than a comparable healthy population. A severe distortion of body image is a cardinal feature of anorexia:Disturbance in the way in which one's body weight or shape is experienced, undue influence of body weight or shape on self-evaluation, or denial of the seriousness of the current low body weight.An excellent recent review covered the alterations in widespread neural circuits observed in those with anorexia, along with abnormalities in the neurotransmitters serotonin and dopamine (Kaye et al., 2009):New brain imaging technology provides insights into ventral and dorsal neural circuit dysfunction — perhaps related to altered serotonin and dopamine metabolism — that contributes to the puzzling symptoms found in people with eating disorders. For example, altered insula activity could explain interoceptive dysfunction, and altered striatal activity might shed light on altered reward modulation in people with anorexia nervosa.Another angle to examine is the reason for such pervasive distortions of self-image. Are there literally changes in visual cortex function that correlate with this symptom?But first, a few words on some confusing neuroanatomical terminology. The striatum is a subcortical structure that consists of the caudate nucleus and the putamen. As mentioned above, the striatum is involved in reward processing (among other things). On the other hand, the primary visual cortex, or V1 (at the back of the occipital lobe) is sometimes referred to as striate cortex. Higher levels of visual cortex beyond V1 are known as extrastriate cortex. And there is where our story begins.In 2001, an fMRI study demonstrated that a specific region in extrastriate cortex, in the lateral occipitotemporal cortex, showed selective responses to pictures of bodies and body parts relative to other types of visual stimuli (Downing et al., 2001). The authors dubbed this region the "extrastriate body area" (EBA). An earlier study in epileptic patients (McCarthy et al., 1999) found regions that showed selective responses to hands, relative to faces and objects (they didn't test other body parts). Instead of using fMRI, McCarthy and colleagues recorded from electrode grids placed directly on the cortical surface for the purpose of monitoring for seizures, prior to surgical resection of the epileptogenic tissue. They observed a specific electrophysiological response, which was evoked 230 msec after the subjects viewed pictures of hands.So the question arises, are there neuroanatomical and functional changes in the extrastriate body area of individuals with anorexia? Suchan et al. (2009) quantified the structural MRIs of 15 women with anorexia and 15 healthy control women. They also localized the EBA using functional MRI -- participants viewed the stimuli used in the study of Downing et al. (freely available for download). The participants also completed the Contour Drawing Rating Scale, and the scores were compared to those given by 10 independent female raters who viewed photos of the subjects.Not surprisingly, the women with anorexia (BMI=16.0, see images of Christian Bale in Anorexia, Insomnia, and Paranoia for an example) overestimated their body size. Conversely, the healthy women (BM=22.0) underestimated their body size. And using a whole-brain voxel-based morphometric analysis, gray matter density was indeed reduced in the left EBA of the anorexic participants.Fig. 2 (Suchan et al. (2009). Activation of the extrastriate body area (EBA) localizer scans from healthy age matched controls (blue), women with anorexia nervosa (AN; green) and reduction of gray matter in the EBA of the AN group (white). Overlap between EBA activation of healthy, age matched controls and AN is coloured in light-blue.Of course, whether the neuroanatomical change is a cause or an effect of the disease is unknown, as acknowledged by the authors:Although the present study is the first to demonstrate focused gray matter volume reduction in the EBA, several open questions remain. First, the causality is unclear. Future studies using a longitudinal design should focus on the question of whether the EBA volume reductions precede the onset of the AN and therefore might be of etiological relevance or whether they are a result of the disorder.Nevertheless, preliminary evidence supports a role for visual perceptual deficits contributing to body image distortion in anorexia nervosa.I'll leave you with the music video for Tunic (Song for Karen) by Sonic Youth. It's a weirdly arty but touching depiction of Karen Carpenter's struggle with anorexia and bulimia, with Kim Gordon as Karen.dreaming, dreaming of a girl like mehey what are you waiting for - feeding, feeding meI feel like I'm disappearing - getting smaller every daybut I look in the mirror - I'm bigger in every wayTunic (Song for Karen) ------Sonic YouthReferencesDowning PE, Jiang Y, Shuman M, Kanwisher N. (2001). A cortical area selective for visual processing of the human body. Science 293:2470-3.Herzog DB, Greenwood DN, Dorer DJ, Flores AT, Ekeblad... Read more »
Suchan, B., Busch, M., Schulte, D., Grönermeyer, D., Herpertz, S., & Vocks, S. (2010) Reduction of gray matter density in the extrastriate body area in women with anorexia nervosa. Behavioural Brain Research, 206(1), 63-67. DOI: 10.1016/j.bbr.2009.08.035
Today I was going to blog this paper, which says that you can predict which kids will grow up and be criminals by measuring their Pavlovian fear conditioning at age 8. In Mauritius. But The Last Psychiatrist already said everything I was going to.Luckily, there's another article in the American Journal of Psychiatry about crime in a tropical country for me to write about - Randomized, Double-Blind, Placebo-Controlled Trial of Vigabatrin for the Treatment of Cocaine Dependence in Mexican Parolees.The study found that a drug called vigabatrin helped Mexican cocaine users to stay clean. The addicts were all on parole from jail. They "were poor and unemployed or underemployed, and none had permanent telephone numbers", had a mean age of 30, and had been using cocaine, including crack, for 9 years on average. A difficult population, then.They were given either vigabatrin, or placebo, every morning for 7 weeks, and their cocaine use was measured with urine samples twice a week. If they managed to stay clean for 3 straight weeks, that was counted as successful treatment. What happened? In the placebo group, almost no-one managed to get clean - just 4 out of 53 (7.5%). But in the people on vigabatrin, 14 out of 50 made it (28%):Now there's two ways of describing this result. You could say, as the authors did, that "nearly four times as many subjects taking vigabatrin achieved full end-of-trial abstinence", which makes it sound amazing. Four times as many, woo! Or you could say that only 1 in 5 people were helped by the drug - not so good. But hey, it's still a result. And it's a lot more impressive than the "cocaine vaccine".Interestingly, many of the cocaine addicts were alcoholics too, and in the vigabatrin group 10 of them (43%) also achieved abstinence from alcohol, vs just 1 (6%) in the placebo group.What's vigabatrin? It's an anticonvulsant used in some countries - including Mexico but not the U.S. - to treat severe forms of epilepsy. Like most anticonvulsants, it works on the neurotransmitter GABA which inhibits neural firing; specifically, vigabatrin prevents GABA from being broken down by an enzyme in the brain. In laboratory experiments, it stops rats and mice from enjoying the effects of cocaine, probably because it blocks the ability of cocaine to increase dopamine levels.That all sounds promising, but there's a catch. Vigabatrin causes "a tardive peripheral visual field defect that is typically asymptomatic and neither progresses nor resolves upon treatment cessation" as the paper tells us. In other words, prolonged use causes permanent loss of peripheral vision, i.e. "tunnel vision". This can be severe in some cases. They tested for it, and it didn't happen to anyone in this study, but that's probably because it was a short trial and the cumulative total dose was about 10% of the amount that's thought to cause problems: 130g vs. 1,500g. Long-term treatment might be more of an issue.So why use vigabatrin, when there are plenty of other anticonvulsants that don't permanently damage your eyes? This is the first placebo-controlled trial of vigabatrin but there have been many trials of other anticonvulsants for cocaine dependence and they generally didn't work. So maybe vigabatrin is unique and more effective than other drugs of its kind. Only time, and bigger trials, will tell.Brodie, J., Case, B., Figueroa, E., Dewey, S., Robinson, J., Wanderling, J., & Laska, E. (2009). Randomized, Double-Blind, Placebo-Controlled Trial of Vigabatrin for the Treatment of Cocaine Dependence in Mexican Parolees American Journal of Psychiatry, 166 (11), 1269-1277 DOI: 10.1176/appi.ajp.2009.08121811... Read more »
Brodie, J., Case, B., Figueroa, E., Dewey, S., Robinson, J., Wanderling, J., & Laska, E. (2009) Randomized, Double-Blind, Placebo-Controlled Trial of Vigabatrin for the Treatment of Cocaine Dependence in Mexican Parolees. American Journal of Psychiatry, 166(11), 1269-1277. DOI: 10.1176/appi.ajp.2009.08121811
Travis and I often remind our readers that adopting healthy behaviours is the goal, even if weight loss does not occur. That is, simply by improving your current diet and increasing your daily physical activity will make you healthier and reduce your chance of countless diseases regardless of whether or not the number on your scale budges. However, the huge caveat to this notion is that individuals who adopt these healthy behaviours AND manage to lose at least 5-10% of their weight will benefit the most.Additionally, while we often suggest that people look beyond the bathroom scale when adopting a healthy lifestyle, a number of studies have shown that the regular use of a scale may actually be helpful when it comes to losing weight.For example, Vanwormer and colleagues nicely summarized the effect of regular weighing on weight loss in a systematic review of the literature published just last year. They included a total of 12 individual studies in their final analysis and found a number of interesting trends.Evidence from 11 of the 12 studies suggested that more frequent self-weighing was associated with greater weight loss or weight gain prevention, with those individuals who weighed themselves daily or weekly having about a 1-3kg weight loss lead on their non-weighing counterparts. A more recent prospective cohort study (2009) by the same authors provides further evidence of the positive effect of regular self-weighing on weight-loss success. In this study, 100 obese subjects were enrolled in a 6 month behavioural weight-loss program (consisting of telephone counseling and a written manual) which encouraged subjects to regularly weigh themselves. The study found that participants lost an additional 1 pound of weight for every 11 days they weighed-themselves. Looking at the data another way, individuals who weighed themselves at least weekly were more than 10 times as likely to reach a weight-loss of 5% (considered the cut-point for clinically significant weight loss) at the end of the 6 month intervention.Thus, self-monitoring of your weight may be helpful if weight-loss is your goal.While it is a VERY rare occurrence that we actually like a product, a new gadget I came across online while in Vancouver actually struck me as rather neat – especially given what I described above. The gadget I am alluding to is the Withings WiFi Body Scale, a bathroom scale which can do the following:1) Assess your body fat percentage using bioimpedance (albeit pretty inaccurately)2) Via WiFi connection, it can upload your daily body weight, % body fat, and BMI to a secure online tracking website or a specifically made iPhone app. That’s right – everytime you step on the scale it automatically tracks your information via whatever means you choose.3) It allows you to set up profiles for up to 8 different people, so that all can individually track their weight on a regular basis.4) Lastly (and this may be a bit much), for those on Twitter, and who like to be publically accountable for their progress, you can set up the WiFi Body Scale to automatically tweet your weight to all your followers.If you’d like to purchase the Withings WiFi Body Scale, you can click here to purchase for 159.00 at Amazon.com.While the price is a bit outside of my budget, this falls into the very small category of gadgets which I would actually like to own. You can also view a brief video below on how the WiFi Body Scale works (email subscribers please log onto Obesity Panacea to view).Have a great weekend,Peter Vanwormer JJ, French SA, Pereira MA, & Welsh EM (2008). The Impact of Regular Self-weighing on Weight Management: A Systematic Literature Review. The international journal of behavioral nutrition and physical activity, 5 PMID: 18983667VanWormer JJ, Martinez AM, Martinson BC, Crain AL, Benson GA, Cosentino DL, & Pronk NP (2009). Self-weighing promotes weight loss for obese adults. American journal of preventive medicine, 36 (1), 70-3 PMID: 18976879... Read more »
VanWormer JJ, Martinez AM, Martinson BC, Crain AL, Benson GA, Cosentino DL, & Pronk NP. (2009) Self-weighing promotes weight loss for obese adults. American journal of preventive medicine, 36(1), 70-3. PMID: 18976879
There is a very important paper due to be published in the Annals of Emergency Medicine. I expect that there will be a lot of criticism of this paper. There will be many reasons for being cautious in implementing the suggestions of the authors, but bad research is not one of them. One of the difficult things about this paper is that the authors are very good about identifying potential confounding influences. They explain that there are many factors that may have affected the results. They are thorough in pointing out the many different ways they analyzed the data to try to minimize any potential confounding influences. While many may look at this study, see the amount of doubt the authors express throughout the study, and conclude that there is too much uncertainty to pay any attention to this study, they would be wrong to do so.Trusting in the certainty of those promoting the Golden Hour is the true error. Anxious exhortations to Panic! and Faster! and Panic faster! are not substitutes for good patient care.The Golden Hour has been around for decades. This is the idea that seriously injured patients need to receive definitive care within 60 minutes of that serious injury. The amount of information used by Dr. R Adams Cowley to concoct the Golden Hour could fit onto a cocktail napkin. According to legend, it was dreamed up in a bar, so maybe it did fit onto a cocktail napkin. The Golden Hour is not science. The Golden Hour is marketing, and very successful marketing. There are still plenty of people citing the Golden Hour as their excuse for all sorts of mistreatment of patients - But we have to get them to the trauma center inside the Golden Hour. A more appropriate term is the Bogus Hour.The commonly used 8 minute response time (or 8 minutes 59 second response time in some places) limit (in at least 90% of responses) is based on the AHA's (American Heart Association's) Chain of Survival. The interesting thing is that cardiac arrest survival appears to be the only condition that has good science supporting a short response time.To date, patients with out-of-hospital cardiac arrest remain the only ﬁeld-based patient population with a consistent association between time (response interval) and survival.18,19The authors of this study probably looked at far more data on trauma time intervals than any other study. They evaluated the data in as many different ways as they could think of, to see if there were any ways that there could be a connection between prehospital time and survival. In spite of all of these different ways of evaluating the data, the conclusion based on all of the evidence is - time does not make a significant difference in survival for unstable trauma patients.This was not a study just looking at all trauma patients, the patients meeting only anatomic criteria were not included. The same is true for patients only meeting mechanism criteria. In other words, they excluded most of the patients transported to trauma centers. Why? Because these patients do not have serious enough injuries to expect time to make a difference. Even though these patients are rushed to trauma centers, their injuries have not resulted in unstable vital signs/level of consciousness. Therefore, they are not considered to have significant injuries for the purposes of this study.Here are some representative anatomic criteria and mechanism criteria for trauma triage - Anatomic Criteria:• Penetrating injury to head, neck, torso and extremities proximal to elbow or knee (unless obviously superficial)• Chest injuries with respiratory distress (for example, flail chest)• Two or more proximal long-bone (humerus or femur) fractures• Pelvic fractures• Limb paralysis (spinal cord injury)• Amputation proximal to wrist or ankleNone of these qualify to get the patient into the study - shooting, stabbing, nibbled at by a lion, - unless the patient has signs of being unstable. Mechanism of Injury:• Death of another occupant in same vehicle• Auto vs. pedestrian (bicycle) injury with significant impact• Pedestrian thrown or run over• Extrication time 20 minutes• Falls from 20 feet• Ejection from vehicle• Vehicle rollover• High-energy vehicle crash (e.g. significant intrusion intopassenger compartment)• Motorcycle crash with separation of rider from motorcycleOther factors combined with traumatic injuries:• Age 55 years• Combination of trauma with burns• Known heart disease, CHF, or COPD• Known bleeding disorder or taking coumadin/ heparin• Pregnancy (20 weeks)• Rigid or diffusely tender abdomen• Amputation of fingers with possibility of reattachmentThese are the kind of criteria that Maryland was using to fly patients. When they had their fatal crash last year, these mechanism criteria required permission from medical command to fly patients. Flights dropped by about two thirds and outcomes do not appear to have changed. Few of these criteria are useful for predicting instability. This study was only concerned with patients who really are unstable, not those with significant damage to their cars or trucks.So, what is unstable in the study?The criteria from the study - Injured patients with one or more of the following criteria were included: systolic blood pressure (SBP) less than or equal to 90 mmHg, Glasgow Coma Scale (GCS) score less than or equal to 12, respiratory rate less than 10 or greater than 29 breaths/min, or advanced airway intervention (tracheal intubation, supraglottic airway, or cricothyrotomy). “Injury” was broadly deﬁned as any blunt, penetrating, or burn mechanism for which the EMS provider(s) believed trauma to be the primary clinical insult.And still they have 10 physiologically unstable patients per day, if averaged over a year - with a few left over. Remember, this is after excluding most of the patients who would automatically be flown to trauma centers, because the authors do not believe that those patients are injured enough for time to make a difference in their outcomes.Editor’s Capsule SummaryWhat is already known on this topic The “golden hour” concept in trauma is pervasive despite little evidence to support it.What question this study addressedIs there an association between various emergency medical services (EMS) intervals and in hospital mortality in seriously injured adults?What this study adds to our knowledgeIn 3,656 injured patients with substantial perturbations of vital signs or mental status, transported by 146 EMS agencies to 51 trauma centers across North America, no association was found among any EMS interval and mortality.How this might change clinical practiceThis study suggests that in our current out-of-hospital and emergency care system time may be less crucial than once thought. Routine lights-and-sirens transport for trauma patients, with its inherent risks, may not be warranted.So, if time is not making a difference in survival, maybe we should stop killing people just to get patients to the hospital a little bit faster. Some more details from the paper - . . . total EMS time was not associated with mortality . . . for every minute of total time . . . When the sample was assessed with 10-minute increments for total EMS time, there was no evidence of increased mortality with increasing ﬁeld times . . . Similar results were obtained when total times were grouped by quartile . . . We were also unable to demonstrate independent associations between mortality and any other EMS interval for the overall sample . . . No matter how they broke down the time intervals, there was no detectable change in outcome.For categorized response interval, there was no association with mortality for patients with a 4- to 8-minute interval . . . or greater than 8-minute interval . . . compared with patients with a response less than 4 minutes.The same for response times.In multivariable logistic regression models, there was no demonstrable association between time and mortality for any subgroup.Although some seriously injured individuals may require time-dependent EMS interventions to survive (eg, airway obstruction, respiratory arrest, external hemorrhage at a compressible site), faster application of such interventions may not have a measureable effect on outcomes ... Read more »
Newgard CD, Schmicker RH, Hedges JR, Trickett JP, Davis DP, Bulger EM, Aufderheide TP, Minei JP, Hata JS, Gubler KD.... (2009) Emergency Medical Services Intervals and Survival in Trauma: Assessment of the "Golden Hour" in a North American Prospective Cohort. Annals of emergency medicine. PMID: 19783323
As promised, here's the second part of my look at the myth of drink spiking. Last time, we saw that the idea that drink-spiking is a widespread problem is a myth, with the evidence showing that in fact in the vast majority of cases where people believe their drinks have been spiked, this simply isn't the case - the symptoms they experience have been down to alcohol poisoning. In this post, we'll look at the reasons why this myth has become so widespread, as discussed in Burgess et al's "Embodying Uncertainty?: Understanding Heightened Risk Perception of Drink 'Spiking'" .
Their study found that those students showing a high degree of concern about drink spiking were almost exclusively female. To explain this, they propose a two-pronged explanation based on the hundreds of in-depth interviews they conducted:
"A need to explain feelings of vulnerability associated with ‘big nights’ may well impel young female students to assimilate the discourse of drink-spiking awareness, whilst the desire to find a way of framing the masculine practice of binge-drinking in feminine terms may well make the same discourse particularly appealing."
Their questioning of female university students revealed a great deal of anxiety about the drinking culture in universities, in particular the problem of being drunk while exposed to the 'false intimacy' of events like Fresher parties, or 'Flirt nights'.
In the UK interviews, female first-year students commonly saw nights out as risky affairs,
and often implied — although rarely conceded — that alcohol introduced an element of uncertainty into an already difficult social situation.
'Rarely conceded' is the key point, and in fact the interviews conducted showed what can only be described as denialism over drinking, as the following fascinating discussion describes:
Interviewee: I’m always quite precautionary, ’ cos when you’re drunk you’ve got to be, you can’t ... you’ve always got to be aware of things. But I think there is always [the threat of drink-spiking] in the back of your mind now. And I don’t necessarily think that’s a bad thing, it just means you’re more cautious ... it’s a slight paranoia. I mean, I wouldn’t get paranoid to the extent that it ruins a night, but it’s a concern. Especially because I don’t really drink bottled drinks ... I mean, you don’t always want to carry [your drink] around everywhere but, really, that’s inevitable .... Like, before, in the Venue you could leave your drinks and go for a dance. But not so much now. I only leave [my drink] with friends, but even then … [hesitates].
Interviewer: You wouldn’t leave it with a friend?
Interviewee: No, I do trust my friends, I don’t know why I said that...
What is interesting about this conversation, beyond the student’s marked level of distrust, is that concern about alcohol is quickly elided by concern about drink-spiking. Alcohol makes it necessary to be cautious, this young woman suggests, but it is the more specific threat of DFSA — of a drink being spiked rather than the drink itself — that becomes the focus of attention.
Whilst a few students give up drinking altogether, most continue to drink and increasing numbers drink heavily, and, for those in the last two categories — the drinking majority — alcohol is deemed to be less of a problem than drink-spiking. In fact, often, in US respondents’ accounts of suspected drink-spiking incidents, rhere was a distinctly defensive view negating the role of alcohol in producing the events or symptoms. This was accomplished either by identifying symptoms with a specific drink (n = 21) rather than ‘drinking’ or by including information about how little alcohol the victim had consumed (n = 12).
Interestingly, respondents apparently felt the need to address the contribution of alcohol in their stories, but this was often to deny its role. As the authors remark: "There appears to be widespread disbelief, or active denial, that excess alcohol could cause the same incoherence, physical distress and incapacity associated with ‘date rape’ drugs."
Why the denialism? Because of the immense pressure students feel to drink. Indeed, respondents suggested that it was "almost impossible' not to drink, and described "unrelenting pressure", as one response highlights:
"Before every night out there’s a drinking circle at the bar .... And last night I couldn’t go ... and this morning I had loads of text messages saying ‘where were you? It’s terrible, you’re a Fresher, you should be out’. Now I don’t drink that much, but it’s definitely seen as a bonding thing, like the Freshers should get to know the Seniors by going out and drinking .... There are a few people who don’t really drink in the club, and after a while they’ve been forced into doing it. Like I’ve been offered a drink, and when I said ‘No’ I’ve been given very funny looks... "
In other words, there is a deep conflict here. On the one hand, female students in particular describe feelings of vulnerability associated with nights out that involve heavy drinking; but on the other intense peer pressure prevents them from addressing the real cause of the problem. The authors suggest that "'Drink-spiking awareness' ... might perform just such a role."
Before I conclude, it's important to make clear that the mugging, assault or rape of an intoxicated individual is the responsibility of the mugger, attacker or rapist, and the state of their victim in no way absolves them of guilt. In fact in my opinion it makes the crime that much more cynical. Being drunk does not mean you should take the blame when somebody takes advantage of your state to commit a crime against you.
However, we have to confront a culture in which young women and men are abusing alcohol to the extent that they are losing all control over their actions and their situation. Town centres on a Saturday night are like war zones, and it's only thanks to heavy policing at a huge cost to taxpayers that the results of this aren't even worse than they already are in terms of violence, medical problems, and sexual assault.
Alcohol abuse in Britain and elsewhere is at epidemic proportions, and it's something that we seem to be in deep denial about. When something goes wrong on a night out we'll blame spiking, our mood, our friends, anything but the drink itself. The myth of the date rape drug is in many ways a construct of our cultural denial of the harm that alcohol is causing. In many ways, the same denial contributed to Professor Nutt's sacking as he dared to question the idea that alcohol and tobacco are somehow more acceptable than drugs like cannabis or ecstacy.
Don't tell us we're drinking to much; we don't want to hear it.
 Burgess, A., Donovan, P., & Moore, S. (2009). Embodying Uncertainty?: Understanding Heightened Risk Perception of Drink 'Spiking' British Journal of Criminology, 49 (6), 848-862 DOI: 10.1093/bjc/azp049
Martin is the editor of layscience.net.
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Burgess, A., Donovan, P., & Moore, S. (2009) Embodying Uncertainty?: Understanding Heightened Risk Perception of Drink 'Spiking'. British Journal of Criminology, 49(6), 848-862. DOI: 10.1093/bjc/azp049
Ever look up your symptoms on the internet? Ever have a friend diagnose you with something they have had previously?With the internet today more and more people are taking initiative to diagnose themselves. New research shows there is some merit in telling your doctor what you believe you may have. The British Medical Journal recently published an article discussing the new phenomenon of “Self Diagnosis” or “Self Labeling”.Reports have been made that “Self Diagnosis” can initiate a correct finding in 18% of consultations. Furthermore, the “presenting complaint” of a patient may guide the diagnosing process 70% of the time. This indicates the importance of a patient communication to their doctor. If you have multiple symptoms a diagnosis may be established by your initial complaint.Conditions accurately diagnosed by self labeling: Urinary tract infections, recurrent uveitis, schistosomiasis and head lice.However, don't over estimate the power of self diagnosis. Wrongful incidence of self diagnosis can occur when treatment is initiated by the patient before consulting their doctor. Women who purchase over the counter antifungal treatment with the suspicion of having an infection are a great example. A high percentage of these women actually have a bacterial form of infection not fungal.In addition, self diagnosis can be at times very unsafe. Cases have been reported of a heart attack being mistaken as indigestion and rectal bleeding thought to be due to haemorrhoids only to be discovered as colon cancer.Conditions often misdiagnosed by self labeling: pregnancy, yeast infections and scabies. Normal 0 false false false EN-CA X-NONE X-NONE MicrosoftInternetExplorer4 ... Read more »
One of the better research outcomes a biologist can hope for is to find that a particular mechanism, disease, or benefit has a single point of control somewhere in its web of interlinked genes and feedback loops. A single gene or protein that acts as a switch or a dial, and has no or few entanglements with other biological systems. That lack of entanglements is important - a switch that turns one thing off and three other things on isn't of much use, at least for those of us who like our medicine without potentially lethal side-effects, but human biochemistry contains far more multi-switches than examples of any simpler construction. Evolution is based upon the promiscuous reuse of components, and almost any protein of note involved in regulating metabolism has more than one duty to perform. In any case, researchers engaged in picking apart the mechanisms underlying calorie restriction might still manage to uncover a simple switch somewhere in amidst the all complexity and chains of genes and proteins turning one another on and off. They've been hacking away the brush for some years now, but there's no shortage of undergrowth yet to be cleared. You might see hints of...... Read more »
Zhang, M., Poplawski, M., Yen, K., Cheng, H., Bloss, E., Zhu, X., Patel, H., & Mobbs, C. (2009) Role of CBP and SATB-1 in Aging, Dietary Restriction, and Insulin-Like Signaling. PLoS Biology, 7(11). DOI: 10.1371/journal.pbio.1000245_id
Multilevel (or hierarchical) regression modeling is very popular in the social sciences. So what I want to do is a hierarchical quantile regression of the 75% quantile of time spent in jail. And that was my question for Andrew Gelman.... Read more »
Carmichael SL, Witte JS, & Shaw GM. (2009) Nutrient pathways and neural tube defects: a semi-Bayesian hierarchical analysis. Epidemiology (Cambridge, Mass.), 20(1), 67-73. PMID: 19234400
PGC-1alpha is my favorite gene/protein to study, as it is essential for mitochondrial regulation, influential on many diseases and ageing. I also am fascinated by the relatively new field of epigenetics and its relation to nutrition and health. So you can understand my geeky giddiness when I found that a study by Barrès et al. (1) shows [...]... Read more »
Barrès R, Osler ME, Yan J, Rune A, Fritz T, Caidahl K, Krook A, & Zierath JR. (2009) Non-CpG methylation of the PGC-1alpha promoter through DNMT3B controls mitochondrial density. Cell metabolism, 10(3), 189-98. PMID: 19723495
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