Minocycline, the tetracycline antibiotic, is probably not something that most people would traditionally link with autism or conditions presenting with autism-like behaviours. Indeed, the suggestion that antibiotics or antimicrobials if you prefer, may be able to modify either the behaviour or linked biochemistry of the autism spectrum disorders (ASDs) or even influence the onset and expression of ASD is quite frankly a little bit unusual.Minocycline (for chemists) @ Wikipedia But unusual is what often crops up on this blog. And how if one assumes that autism, sorry the autisms, are not just conditions solely pertaining to the grey-pinkish matter floating inside our skull, one starts to see how behaviour and physiology might provide some interesting perspectives. Say for example, when one starts to look at the gut microbiome...On today's post I'm considering a few reports which recently cropped up on the research radar including the results of placebo-controlled trial of minocycline for Fragile X syndrome (FXS) published by Mary Jacena Leigh and colleagues* (open-access), a small open-trial of minocycline reported by Carlos Pardo and colleagues** (open-access) and although not autism-related, the results of a study by Parvin Ataie-Kachoie and colleagues*** (open-access) on what happened to an ovarian cancer cell line when minocycline was added, specifically with the cytokine IL-6 in mind. A bit of a mixed bag of studies by all accounts but with some potential common threads.The Leigh study has already been covered by some media (see here) so no grand description needed from me. Suffice to say that there is a suggestion from this MIND Institute study, that minocycline might have some modest positive impact on various aspects of behaviour in paediatric cases of FXS with the requirement for further research. As per some previous chatter on this blog, this is not necessarily new news for FXS as per studies like the one by Paribello and colleagues**** (open-access). Interestingly, the Paribello results also mention something called matrix metalloproteinase-9 (MMP-9) as a particular target of minocycline which has also been discussed on this blog (see here). So, potentially (potentially!) there may be some merit in looking at minocycline for cases of FXS; although as per my blog caveat, I'm not recommending anything.Moving on. The Pardo study (see here for the trial record), whilst small in participant numbers, looked more directly at the use of minocycline - and vitamin B6 - with ten children diagnosed with an ASD. The focus was on autism with a regressive aetiology linked to presentation, and alongside various behavioural measures, there was also analyses of various biological fluids for "markers of neuroinflammation". The study was open and unblinded so not exactly the same calibre as the Leigh trial.The main result of the trial, er... no clinical improvements following minocycline use, even after six months of use. Indeed not only were no significant changes to behaviour reported but a variety of respiratory and gastrointestinal (GI) side-effects correlated with minocycline use. The efficacy and safety profile was not particularly great based on these study results allowing for the lack of any control group and the dosage used.There were however, a few reported changes to some of the biochemistry under investigation, specifically with brain derived neurotrophic factor (BDNF) and hepatocyte growth factor (HGF) in mind but not in the more classically related parameters such as that MMP-9 connection. This lack of effect of minocycline on MMP-9 is slightly unusual but potentially revealing. Certainly the review by Siller & Broadie***** (open-access) hints that MMP inhibition might be a key part of the effects of minocycline in FXS. It's possible a few scenarios might pertain with regards to the biological/genetic differences between autism and FXS. One might even speculate that there is some involvement for the TIMPs (tissue inhibitors of metalloproteinases) in that non MMP inhibitory effect noted from minocycline in autism, but much more work is perhaps needed.Indeed the authors very overtly noted that "minocycline exerted biological effects that were not translated into behavioral or neurological changes" which certainly questions the link between some of the biochemistry that was seemingly affected and presented symptoms assuming there wasn't more subtle behavioural changes.Finally, there is the Ataie-Kachoie study on minocycline application to ovarian cancer cell lines. I'll freely admit that I know even less about cancer cell lines than I do about autism so please excuse any widely inaccurate statements that I might make. The long-and-short of it was that in the lab, minocycline seems to have an interesting effect on "the IL-6 signaling pathway" at least in ovarian cancer cells such that minocycline might reduce IL-6 or at least prevent increases after certain events. As part of my learning jounrney through this paper I did not know that IL-6 was for example being linked to cancer metastasis as discussed by Tawara and colleagues****** for example. Seemingly this metastasis might correlate with those MMPs (particularly MMP-2 and MMP-9).I know I'm moving further and further away from my autism and FXS purpose with the Ataie-Kachoie data, but there may be some lessons to be learned. That for example minocycline might affect cases of FXS by means of impacting on MMP-9 is already under discussion. The added suggestion that minocycline might also be working on cytokines like IL-6 in an anti-inflammatory fashion is certainly another source of discussion. Indeed, I note from the Pardo autism study, that in Table 3 showing the pre- and post-treatment effects on biochemistry, the value reduction for serum IL-6 just managed to escape that magical significance point coming in at p=0.08. The change in another interesting cytokine, TNF-alpha, was even closer (p=0.074).This has been a post comparing apples and pears to a large extent and reiterating my earlier caveat, I am by no means advocating minocycline for anything other than it's intended use with appropriate medical physician support and supervision. Outside of the discussions already included, what this post does serve to show is that (a) the actions of medicines are not necessarily restricted to what's printed on the patient information leaflet, an... Read more »
Leigh, M., Nguyen, D., Mu, Y., Winarni, T., Schneider, A., Chechi, T., Polussa, J., Doucet, P., Tassone, F., Rivera, S.... (2013) A Randomized Double-Blind, Placebo-Controlled Trial of Minocycline in Children and Adolescents with Fragile X Syndrome. Journal of Developmental , 34(3), 147-155. DOI: 10.1097/DBP.0b013e318287cd17
Shakespeare wasn't kidding about the "winter of our discontent." In the colder and darker months, people do more internet searches for mental health terms, from anxiety and ADHD all the way to suicide. Search patterns also promise that like a refreshed browser window, better times are due to arrive soon.
John Ayers, of the Center for Behavioral Epidemiology and Community Health in San Diego, and other researchers dove into Google Trends to explore whether certain searches vary by season. "Seasonal affective disorder is one of the most studied phenomena in mental health," Ayers says, "with many individuals suffering mood changes from summer to winter due to changes in solar intensity." He wanted to find out whether any other mental health complaints changed with the seasons, as some studies had hinted.
Since Google Trends breaks down searches by category, the researchers started in the "mental health" section. Looking at all mental health searches in the United States between 2006 and 2011, they saw a consistent cycle with peaks in the winter and troughs in the summer. (If you do this search yourself, you'll see that there's also a dip around the December holidays—but the curve reliably bottoms out in July of each year.)
The team did some statistical smoothing and found that mental health searches overall were about 14% higher in the winter than in the summer. To confirm that the difference was due to the season, they ran the same analysis on data from Australia. Searches cycled in the same way—about 11% higher in winter than summer—but the peaks in the southern-hemisphere country were almost exactly 6 months out of sync with the United States.
When the scientists broke down searches by specific symptoms or illnesses, the seasonal cycle remained—and in some cases got much stronger. "We were very surprised" to see this, Ayers says. Searches including the terms ADHD, anxiety, bipolar, depression, anorexia or bulimia, OCD, schizophrenia, and suicide all rose in the winter and fell in the summer.
One of the most dramatically cycling search terms was schizophrenia, at 37% higher in the winter. Eating disorder terms varied just as strongly. (The smallest seasonal difference was for anxiety, which was just 7% higher in the winter in the United States, and 15% in Australia.)
Some of this seasonality might be due to the schedule of the school year, Ayers points out. Referrals for kids with ADHD and eating disorders may come from their schools.
Other explanations involve winter itself. The effect of shorter days on our circadian rhythms and hormone levels might be a factor, the authors write, as in seasonal affective disorder. They speculate that a lack of vitamin D (which we make using sunlight) in the winter might contribute. Even omega 3 fatty acids might matter: we consume less of them in winter, and omega 3 deficiency has been linked to some mental illnesses.
There's also the question of what we're doing all season. People hunkered indoors during the colder months may have fewer chances for socializing, which is "a well-known health emollient," the authors write. The same goes for physical activity.
"There is a lot more we need to learn about mental health and seasonality," Ayers says. "For instance, is there a universal mechanism that impacts our mental health?"
Of course, sometimes our malaise isn't about the season.
Whatever portion of mental health is predictable, though, doctors would love to know about it and use that information to help.
This study doesn't give reveal much about low-income or elderly populations who aren't online. And knowing what people are searching for isn't exactly the same as knowing what symptoms they're experiencing. "We are actively working to address these limitations," Ayers says. Working with Google.org, the charitable branch of Google, he hopes to develop systems similar to Google Flu Trends that can track a population's mental health.
"Intuition suggests that these results are reflective of an important link between the seasons and mental health," Ayers says. For now, we have the reassurance of computer algorithms that skies will be clearer soon.
Ayers, J., Althouse, B., Allem, J., Rosenquist, J., & Ford, D. (2013). Seasonality in Seeking Mental Health Information on Google American Journal of Preventive Medicine, 44 (5), 520-525 DOI: 10.1016/j.amepre.2013.01.012
Image: Skaneateles, NY, by me.
... Read more »
Ayers, J., Althouse, B., Allem, J., Rosenquist, J., & Ford, D. (2013) Seasonality in Seeking Mental Health Information on Google. American Journal of Preventive Medicine, 44(5), 520-525. DOI: 10.1016/j.amepre.2013.01.012
In a recent essay by Gary
Taubes in BMJ he discusses the issues with the current scientific
approach to weight loss and how this can be remedied. Gary Taubes is
an exceptional writer, he is eloquent and articulate, and this fact
alone makes what he claims believable. The problem I find is he does
such a good job refuting the 'calories matter' hypothesis that you
tend to just believe what he says afterwards. But what he fails to do
is shine the same light of criticism on his own cherished hypothesis,
and under this light it also tends to look more like fallacy than
fact. Let me explain.
Gary Taubes convincingly,
and correctly, argues that a calorie restriction approach to weight
loss is incorrect. I remember one of my favourite quotes from Gary
Taubes (and I am basing this off memory) “if you spend a century
testing a hypothesis, spend millions of dollars to prove that
hypothesis, have millions of people try what you propose, and yet you
don't get any results that prove your claim then it's time to look
for a new hypothesis”. He is right.....after all this time calorie
restricted weight loss studies simply don't work. No study has been
able to show permanent and substantial weight loss. Calories is a
simplistic, and reductionist, way of viewing things and it does not
account for the complex organism that we are. Many animal studies
such as ones that observe squirrels putting on weight as they go into
hibernation, despite severe calorie restriction, indicate that weight
gain is a bit more complex.
He then argues that a
competing hypothesis, one that was mainstream within Germany and
Austria in the first half of the 20th century, took this
into account and opposed the calorie restriction hypothesis held
generally by English and American scientists. This was all pre-WWII
and after the war people tended to have a bit of a grudge against
anything German sounding, and so they simply stopped paying attention
to the theory. What this alternative hypothesis proposes is that fat
deposition is a hormonal issue and just like hormones determine where
hair grows, they also determine where fat is stored. Because insulin
is the grandaddy of fat storage hormones it is logical then that
insulin is what needs to be lowered to prevent fat gain. Thus, Gary
Taubes, and all proponents of the insulin hypothesis, propose that
consuming a diet low in carbohydrates will lead to weight loss.
The problem he says is
history. After WWII calorie restriction became the norm and was
institutionilised. Anyone who tried to say that fat was not
unhealthy, and that calorie restriction was a waste of time was
shunned by academics, funding agencies, and the general public at
large. I don't disagree with this. But here is where me and Gary go
our seperate ways. This is where I feel he needs to look at the
insulin hypothesis with the same criticisms he did for calorie
restriction. Firstly, the fact that calorie restriction is wrong does
not make the alternative true. So just because his theory was
oppressed by those evil calorie restriction monsters does not mean it
However, my main point is
this. He admits that this insulin theory has been around for almost a
century, if not longer. He admits that it was mainstream, and then
was lost until Atkins hit the scene in the 60's. So a relatively small hiatus of 20 years. Low carbohydrate
diets then existed in one form or another until this current day. So
these diets have been tried by millions of people and yet have had
little success. I'm sure everyone has heard of weight loss success
stories, but that is the fun thing about stories they are fiction and
you get to make stuff up. The fact is if low carbohydrate diets
worked, and caused substantial weight loss permanently, we would know
about it and be doing it. Enough people have tried!!! The reason I
know this is because when I heard about all the 'success' I also
jumped the bandwagon and gave it a go. We know that no government
agency, or grant funding agency, or mass media hype is going to
prevent the public from trying what seems like a whacky fad diet if
that diet takes a hold, and by god did Atkins take a hold.
My last point is that he
states clinical trials have shown that low carbohydrate diets
convincingly beat low calorie diets in terms of weight loss. Again
this is true but it doesn't make them effective. Low calorie diets
are shockingly ineffective, so all that is required is for low
carbohydrate diets to be less shockingly ineffective. In a recent
study on low carbohydrate diets the authors looked at over 23 clinical trials on over 1000 obese
patients and they found that the mean weight loss was 7kg. Even if you
considered that everyone of those patients was merely borderline
obese, weighing in at 200 pounds, this is only 15 pounds, or a 7.5%
weight loss. For the majority of obese people, and for nearly all the
obese people in those studies, this weight loss percentage would be
much less, and not nearly enough to move them from obese to even just
fat. It is a minimal amount of weight loss and it is still failure.
Low carbohydrate diets simply do not work.
If I was to bump into
Gary Taubes, and after I had told him how I do appreciate his work I
would like to ask him this one question “if after almost a century
of study, with millions of dollars and people thrown at the insulin
hypothesis with little result, isn't it high time that we just admit
that diets don't goddam work!”Taubes, G. (2013). The science of obesity: what do we really know about what makes us fat? An essay by Gary Taubes BMJ, 346 (apr15 5) DOI: 10.1136/bmj.f1050Santos FL, Esteves SS, da Costa Pereira A, Yancy WS Jr, & Nunes JP (2012). Systematic review and meta-analysis of clinical trials of the effects of low carbohydrate diets on cardiovascular risk factors. Obesity reviews : an official journal of the International Association for the Study of Obesity, 13 (11), 1048-66 PMID: 22905670... Read more »
Taubes, G. (2013) The science of obesity: what do we really know about what makes us fat? An essay by Gary Taubes. BMJ, 346(apr15 5). DOI: 10.1136/bmj.f1050
Santos FL, Esteves SS, da Costa Pereira A, Yancy WS Jr, & Nunes JP. (2012) Systematic review and meta-analysis of clinical trials of the effects of low carbohydrate diets on cardiovascular risk factors. Obesity reviews : an official journal of the International Association for the Study of Obesity, 13(11), 1048-66. PMID: 22905670
T’is the season of finals again, and with it, a surging interest in prescription “smart drugs” (see Fig 1). High school and college students are increasingly turning to ADHD medicine (Ritalin, Adderall) in hopes of enhancing school and test performance. Intuitively this makes sense: drugs that increase energy, attention and concentration should inevitably lead to [...]... Read more »
Lakhan SE, & Kirchgessner A. (2012) Prescription stimulants in individuals with and without attention deficit hyperactivity disorder: misuse, cognitive impact, and adverse effects. Brain and behavior, 2(5), 661-77. PMID: 23139911
Smith ME, & Farah MJ. (2011) Are prescription stimulants "smart pills"? The epidemiology and cognitive neuroscience of prescription stimulant use by normal healthy individuals. Psychological bulletin, 137(5), 717-41. PMID: 21859174
Last March, Dr. Deborah Persaud, from the John's Hopkins Children Center, presented a stunning finding at the conference CROI, receiving great resonance across several newscasts: Persaud reported the first case of infant functionally cured of HIV. You can watch Persaud's presentation by downloading the podcast here, it's the seventh talk of the session "Is there hope for HIV eradication?"Up until this finding, the only living person cured from HIV was the Berlin Patient, who was cured after receiving gene therapy for his underlying leukemia condition. Despite this one successful case, gene therapy is not a feasible way to cure HIV. What does it mean to be functionally cured?Once in the host, the HIV virus establishes reservoirs of latent virus: these are viral particles that stay dormant in cells and tissues and have the ability to quickly rebound in the event that therapy is discontinued. That's why it's so important for an HIV infected person to never discontinue the drug regimen, as the rebound virus may be drug resistant. HIV is so efficient at escaping the immune system and therapy that standard practice these days is a lifetime of not just one, but a cocktail of 3-4 antiretroviral drugs. To be functionally cured means that drugs are no longer needed to keep the viral load in check (close or below detection), something that until now had only been achieved by an extremely low number of HIV-positive individuals (less than 1% of infected adults), the so-called "elite controllers." In all other subjects, the reservoirs are never completely weakened and they enable the virus to bounce back once therapy is interrupted. So, what was different with this child?The mother went into labor without prenatal care. An HIV test was done during labor and normally, when the test is positive, antiretroviral drugs are administered. This is highly effective in preventing mother-to-infant infections as the only moment when the infant is exposed to the mother's blood is at birth. The antiretroviral drugs keep the viral load so low that the risk of infection becomes very small (around 2%). Unfortunately, in this particular case, the birth was so precipitous that there was no time to administer such drugs. The newborn baby was immediately tested for HIV. This is my understanding of what was unique about this case: normally a first test is done and, if positive, a second follow-up test is performed and prophylaxis is started once the infection is confirmed. In this case, though, two independent tests were done at the same time and, since both confirmed the HIV infection, prophylactic treatment was started very early, when the baby was 31 hours of age. Also, unique to this case was the fact that a regimen of three drugs, of which one at the therapeutic level instead of the standard prophylactic dosage, was administered during the first week of life. After that, the baby was switched to a standard treatment of antiretroviral drugs (again, my understanding from the CROI talk). Such regimen successfully brought the child's viral load down to undetectable, which is normal in these cases. Despite this, because of HIV's ability to establish reservoirs, antiretroviral therapy is never discontinued. Like I said before, it is a lifetime therapy. So called "drug holidays" result in more virulent and drug-resistant HIV quasispecies. However, this child was lost to follow-up at 18 months of age and was once again seen by the doctors at 25 months of age, when the caregiver reported discontinuing the therapy. Immediate testing was done to assess the child's viral loads. The child was tested not once, but many times. Genetic testing was also done to make sure it was the same child treated before. The doctors must have been in disbelief as for the first time they were seeing the incredible: after 5 months since discontinuing antiretroviral therapy, the viral load in this child was still undetectable. What are the consequences? As Dr. Persaud repeated many times during her talk, this is a single case and a proof of concept. We need more cases to be able to generalize (as statistics teach us). However, it points to something that indeed needs to be explored: how early in the infection can we (and should we) intervene? In a 2012 paper , Persaud and colleagues studied the dynamics of the latent HIV reservoirs in 17 infants on very early antiretroviral drug therapy (median start age 8 weeks) and found that the size of the reservoirs at age 2 was associated to how early undetectable viral loads were achieved during therapy. The earlier viral load was suppressed through therapy, the smaller the HIV reservoir at age 2. Is there a point, very early into the infection, when the virus is vulnerable and all reservoirs can be not just reduced in size, but actually completely eradicated through potent and prompt intervention? In rare cases, HIV-infected patients are able to spontaneously maintain their viral load at a very low level without the need of drugs, the so called "elite controllers." What if, when administered early enough, antiretroviral drugs could transfer this type of spontaneous protection to every HIV-infected person? Shortly after the CROI conference, a French study published in PLoS Pathogens  reported 14 cases of what they call "post-treatment controllers," in other words, people whose viral loads remained very low after interrupting treatment. With the exception of mother-to-infant transmissions at birth, it's extremely hard to catch this virus early because people often don't realize they've been infected: symptoms, if any, appear 3-4 weeks later and are often mistaken for a common cold. Twelve of the 14 cases reported in  had symptoms that prompted early intervention and start of therapy during the primary infection."Post-treatment controllers (PTCs) had a more severe primary infection with higher viral loads and were frequently symptomatic, which may have prompted the early treatment in some cases [. . .] Therefore, our results strongly suggest that the infection control in the PTCs was not achieved spontaneously and was favored by the early onset of therapy. Because the interruption of long-term antiretroviral therapy initiated early during primary infection is not recommended, only a very small proportion (~2%) of the patients in the French Hospital Database on HIV Infection experienced such an interruption, which may explain the rarity of PTCs worldwide ." Persaud, D., Palumbo, P., Ziemniak, C., Hughes, M., Alvero, C., Luzuriaga, K., Yogev, R., Capparelli, E., & Chadwick, E. (2012). Dynamics of the resting CD4+ T-cell latent HIV reservoir in infants initiating HAART less than 6 months of age AIDS, 26 (12), 1483-1490 DOI: 10.1097/QAD.0b013e3283553638 Sáez-Cirión, A., Bacchus, C., Hocqueloux, L., Avettand-Fenoel, V., Girault, I., Lecuroux, C., Potard, V., Versmisse, P., Melard, A., Prazuck, T., Descours, B., G... Read more »
Persaud, D., Palumbo, P., Ziemniak, C., Hughes, M., Alvero, C., Luzuriaga, K., Yogev, R., Capparelli, E., & Chadwick, E. (2012) Dynamics of the resting CD4 T-cell latent HIV reservoir in infants initiating HAART less than 6 months of age. AIDS, 26(12), 1483-1490. DOI: 10.1097/QAD.0b013e3283553638
Sáez-Cirión, A., Bacchus, C., Hocqueloux, L., Avettand-Fenoel, V., Girault, I., Lecuroux, C., Potard, V., Versmisse, P., Melard, A., Prazuck, T.... (2013) Post-Treatment HIV-1 Controllers with a Long-Term Virological Remission after the Interruption of Early Initiated Antiretroviral Therapy ANRS VISCONTI Study. PLoS Pathogens, 9(3). DOI: 10.1371/journal.ppat.1003211
What causes fatigue? And why is it sometimes so hard to push through it? Few people enjoy the sensations of fatigue and pain that accompany intense exercise. While endurance athletesThe post What causes fatigue? Why is it different in CrossFit? appeared first on WODMasters Stiff Competition.... Read more »
Bassini A, Magalhães-Neto AM, Sweet E, Bottino A, Veiga C, Tozzi MB, Pickard MB, & Cameron LC. (2013) Caffeine Decreases Systemic Urea in Elite Soccer Players during Intermittent Exercise. Medicine and science in sports and exercise, 45(4), 683-690. PMID: 23135367
Wilkinson DJ, Smeeton NJ, & Watt PW. (2010) Ammonia metabolism, the brain and fatigue; revisiting the link. Progress in neurobiology, 91(3), 200-19. PMID: 20138956
Bassini-Cameron, A., Monteiro, A., Gomes, A., Werneck-de-Castro, J., & Cameron, L. (2008) Glutamine protects against increases in blood ammonia in football players in an exercise intensity-dependent way. British Journal of Sports Medicine, 42(4), 260-266. DOI: 10.1136/bjsm.2007.040378
A study done at the University of Leeds suggests that the risk of hospital infection could dramatically increase when the windows in the ward are closed.... Read more »
Gilkeson, C., Camargo-Valero, M., Pickin, L., & Noakes, C. (2013) Measurement of Ventilation and Airborne Infection Risk in Large Naturally Ventilated Hospital Wards. Building and Environment. DOI: 10.1016/j.buildenv.2013.03.006
Researchers found that the patients with heart problems, known as STEMI, already admitted in the hospital have 10 times more chances of dying from heart attack as compared to the patients, who get heart attack outside of the hospital and taken to the hospital quickly.
Journal of the American Heart Association
World is full of strange events but humanity is even more strange. Researchers from University of North Carolina (UNC) School of Medicine, in this study, worked on a type of heart attack known as ST elevation myocardial infarction (STEMI) in the hospital inpatients (who are already admitted to the hospital).
"We found that the survival rate for outpatients brought to UNC Hospitals for STEMI treatment was slightly more than 96 percent," said George A. Stouffer, MD, distinguished professor in the UNC School of Medicine and senior author of the study. "But the survival rate for inpatients who suffered a STEMI was much lower, only 60 percent."
Although, this may in-part occurs due to the age difference of the people i.e. people already admitted to the hospital were older and sicker as compared to the people taken from the outside but according to Stouffer, there are still important differences.
Another possible explanation for this could be the effective training of the hospital team in the emergency departments, so that when a STEMI patient brought in from outside, the time of starting the treatment with angioplasty is fast i.e. about 45 minutes at UNC hospitals.
"In contrast, when patients who are in the hospital for a non-cardiac condition have a STEMI, the onset is not usually heralded by chest pain and thus health care providers may not suspect that a coronary artery has occluded. As a result, the time it takes for restoration of coronary blood flow for inpatients is much slower and more variable," Stouffer said.
“Inpatient STEMIs are a major health care problem, suggesting that efforts aimed at improving care of this patient population would have a large impact,” Researcher wrote, “We found that the incidence of inpatient STEMI in our institution was 3.4 per 10 000 hospital discharges and was associated with an in‐hospital mortality of 40%.”
Dai X, Bumgarner J, Spangler A, Meredith D, Smith SC, & Stouffer GA (2013). Acute ST-Elevation Myocardial Infarction in Patients Hospitalized for Noncardiac Conditions. Journal of the American Heart Association, 2 (2) PMID: 23557748... Read more »
Dai X, Bumgarner J, Spangler A, Meredith D, Smith SC, & Stouffer GA. (2013) Acute ST-Elevation Myocardial Infarction in Patients Hospitalized for Noncardiac Conditions. Journal of the American Heart Association, 2(2). PMID: 23557748
Researchers found that the U.S. hospitals get more profit when the surgery goes wrong as compared to the condition when all the tasks go well and patients go home without any complications.
The Journal of the American Medical Association (JAMA)
Quite disturbing report but one of the points to consider in healthcare system is that the finances spent on that industry have to be properly planned.
Do you know nearly $400 billion is spent on the surgical procedures annually, in U.S. only?
For the past few years, effective methods and ways to cut the complications have been introduced in so many researches but hospitals were found slow in getting and implementing those ways. Now researchers have found that finances could be one of the reasons.
“We found clear evidence that reducing harm and improving quality is perversely penalized in our current health care system,” Sunil Eappen, study author and chief medical officer of Massachusetts Eye and Ear Infirmary, said in a statement.
Researchers found that privately insured surgical patients with complications provided hospitals nearly 330% more profit as compared to the patients with no complications. Medicare patients with some complications provided more than 190% margin.
“It’s been known that hospitals are not rewarded for quality. But it hadn’t been recognized exactly how much more money they make when harm is done,” said senior author Atul Gawande, director of Ariadne Labs, professor in the Department of Health Policy and Management at HSPH and a surgeon at BWH.
It means reducing complications decreases financial achievements of the hospitals.
“This is clear indication that health care payment reform is necessary,” said Gawande. “Hospitals should gain, not lose, financially from reducing harm.”
I think we have to study the same thing in other developed countries.
Harvard University, The Raw Story
Eappen, S. (2013). Relationship Between Occurrence of Surgical Complications and Hospital Finances JAMA, 309 (15) DOI: 10.1001/jama.2013.2773... Read more »
Eappen, S. (2013) Relationship Between Occurrence of Surgical Complications and Hospital Finances. JAMA, 309(15), 1599. DOI: 10.1001/jama.2013.2773
In a new study on mice, researchers from the RIKEN Institute, Japan have discovered a compound that could be used to prevent cancer relapse in acute myeloid leukaemia (AML) patients, especially the ones carrying the FLT3-ITD mutation.Read More... Read more »
Saito, Y., Yuki, H., Kuratani, M., Hashizume, Y., Takagi, S., Honma, T., Tanaka, A., Shirouzu, M., Mikuni, J., Handa, N.... (2013) A Pyrrolo-Pyrimidine Derivative Targets Human Primary AML Stem Cells in Vivo. Science Translational Medicine, 5(181), 181-181. DOI: 10.1126/scitranslmed.3004387
Researchers from the Massachusetts General Hospital in the US have grown rat kidneys in the laboratory that produced urine when transplanted into living animals. This is an important step towards the production of customised organs for transplantation into people with kidney failure, which could replace donor organ transplants. Patients with kidney failure can be treated with dialysis, but can only be cured with a kidney transplant. About 15,000 people are waiting for a donor kidney in the Eurotransplant region, but only 7,000 kidney transplants take place each year. Patients may wait up to five years for a donor kidney and many lose their lives during that time. A few research groups have attempted to make artificial kidneys, and some are trying to genetically modify pigs so their kidneys can be used in human transplants, but Harald Ott and his team take a different approach: they hope to grow kidneys in the laboratory using the patient’s own cells. This would put an end to donor organ shortage and immune rejection problems. “If this works, there wouldn’t be any need for immunosuppression or dialysis anymore, it would ... Read more »
Song Jeremy J, Guyette Jacques P, Gilpin Sarah E, Gonzalez Gabriel, Vacanti Joseph P, & Ott Harald C. (2013) Regeneration and experimental orthotopic transplantation of a bioengineered kidney. Nature Medicine. DOI: 10.1038/nm.3154
Yesterday at "The Paramedic's Edge," this was the topic of discussion of a possible use of NTG (NiTroGlycerin – GTN GlycerylTriNitrate in Commonwealth countries).
NTG is a vasodilator and sepsis is a vasodialtion problem. There are other problems with sepsis, but vasodilation may be the primary problem.... Read more »
Guglin, M., & Postler, G. (2009) High dose nitroglycerin treatment in a patient with cardiac arrest: a case report. Journal of Medical Case Reports, 3(1), 8782. DOI: 10.4076/1752-1947-3-8782
Spronk, P., Ince, C., Gardien, M., Mathura, K., Straaten, H., & Zandstra, D. (2002) Nitroglycerin in septic shock after intravascular volume resuscitation. The Lancet, 360(9343), 1395-1396. DOI: 10.1016/S0140-6736(02)11393-6
A key element in discovering valid mental disorder categories is to differentiate a mental disorder from other valid mental disorder categories.Biological markers for mental disorders have been slow to develop. Functional brain imaging techniques and other research tools are evolving to help in the important task of improving the validity of clinical neuroscience disorders.Adjustment disorder is a relatively common condition that has lagged in research attention. Adjustment disorder is defined as an abnormal and excessive response to a stressor that produce significant distress and impairment. The response may include elements of anxiety, depression or abnormal behavior.Adjustment disorder with depressive symptoms may be difficult to distinguish from major depression and other types of mood disorder. However, a recent study of the technique of quantitative electroencephalogram (qEEG) supports adjustment disorder as a distinct condition different from major depressive disorder.The key elements of the design of this study included the following:Subjects: 31 subjects with adjustment disorder with depressed mood and 51 subjects with major depressive disorder using DSM-IV criteriaqEEG: Standard qEEG techniques were employed including calculation of absolute power and coherence for delta, theta, alpha and beta band widthsStatistical analysis: Independent t-test comparison of absolute power and coherence using Neurostat softwareThe key findings from the study included:Absolute power means were lower for the adjustment disorder group in the frontal regionsInterhemispheric coherence values for the delta and beta bands involving the right posterior region were lower in the adjustment disorder groupIntrahemispheric coherence was lower in the alpha bandwidth in the frontal and temporal areas in the adjustment disorder groupThe authors note the findings support adjustment disorder being a relatively less severe mood disorder. However, they noted that the differences may be explained by different patterns of anxiety disorder comorbidity between the two groups.Weaknesses in this study included not including a no mental disorder control group. Additionally, the adjustment disorder group had a statistically higher percentage of male subjects so the two groups were not gender matched.It would be interesting to see if this difference between adjustment disorder and major depression could be replicated in default network connectivity analysis using functional MRI.However, this study is important as it presents a novel biological marker candidate for adjustment disorder with depressed mood. It may stimulate additional biological marker studies is patients suffering significant stress-related anxiety and mood responses.Individuals with more interest in this study can access the free full-text article in the link below.Photo of great white heron from the Venice, FL rookery is from the author's files.Jeong HG, Ko YH, Han C, Kim YK, & Joe SH (2013). Distinguishing Quantitative Electroencephalogram Findings between Adjustment Disorder and Major Depressive Disorder. Psychiatry investigation, 10 (1), 62-8 PMID: 23482820... Read more »
Jeong HG, Ko YH, Han C, Kim YK, & Joe SH. (2013) Distinguishing Quantitative Electroencephalogram Findings between Adjustment Disorder and Major Depressive Disorder. Psychiatry investigation, 10(1), 62-8. PMID: 23482820
This week’s video Tip of the Week offers you a quick tour of GISAID’s resources and their EpiFlu™ database. This is the database you might be hearing about in the news—the one to which researchers submit the new H7N9 influenza sequence data that they are collecting. Originally this initiative was seeded as the “Global Initiative [...]... Read more »
Gao, R., Cao, B., Hu, Y., Feng, Z., Wang, D., Hu, W., Chen, J., Jie, Z., Qiu, H., Xu, K.... (2013) Human Infection with a Novel Avian-Origin Influenza A (H7N9) Virus. New England Journal of Medicine, 2147483647. DOI: 10.1056/NEJMoa1304459
"If you've met one person with autism, you've met one person with autism" so the oft-cited phrase goes. The implication is that whilst unified under the label of presenting with the triad/dyad characteristics of an autism spectrum condition, the heterogeneity present across the spectrum coupled with other comorbidity, allied to factors such as genes, personality, temperament, maturation, environment et al, mean that everyone is different and importantly everyone is dynamic.Umbrella under an umbrella? @ Wikipedia Another term used by some people (including researchers) is that of 'neurotypical' to somehow denote not-autism. For me however, that's always been a little too simplistic. It implied (a) that there is a definite line between autism and not-autism which kinda over-simplifies things including the broader autism phenotype (BAP), and (b) that there is such as thing as 'neurotypical' and indeed is counter to the phrase: 'if you've met one person, you've met one person' which should surely be as pertinent to not-autism as it is to autism; if you get me?These concepts are relevant as today I'm talking about two papers: a paper by Whitehouse & Stanley* (open-access) questioning whether autism is one condition or multiple conditions, and a paper by Moreno-De-Luca and colleagues** which implies that we should even be doing away with behaviourally-defined labels such as autism and schizophrenia in favour of an altogether broader definition of 'developmental brain dysfunction' or DBD.Regular readers might recognise the name Andrew Whitehouse as being one and the same researcher who has talked about various autism-related results from the Raine study (see here and here and here). His latest opinion piece builds on the fact that despite the 70 year anniversary since the first description of autism was published by Kanner (with appropriate consideration for Hans Asperger too), alongside huge amounts of time, money and research efforts, we are really still only scratching the research surface of the condition(s) known as autism. Certainly science hasn't yet come up with many defining 'universal' reasons to account for the appearance of the the clustering of symptoms and as for intervention options, well take a look at the recent draft guidance from NICE to see what I mean. One of the main stumbling blocks he and his colleague opine on is the "phenotypic variability" and how moves should be made towards defining smaller subgroups on the autism spectrum. In effect talking about the autisms over autism as per another very interesting paper by Poot*** (open-access).To many people this is not new news. That the search for an 'autism gene' or 'autism genetic mutation' (sorry about the cold science term) or indeed 'autism environmental variable' has so far been underwhelming in terms of results coupled to the cost/benefit ratio of such research for example, is testament to the variability present in both autism and not-autism. This demonstrates also how complex a continuum the autism spectrum is. Indeed how complex a thing the human spectrum is****.Likewise when it comes to intervention, I've talked before on this blog about how we should perhaps be re-assessing the way we look at proposed interventions and in particular focusing on subgroup responses rather than some almighty universal spectrum response to denote intervention success of not. Without equating autism with cancer or vice-versa, the recent opinion paper by Stewart & Kurzrock***** (open-access) might inform this methodological discussion somewhat further.Whitehouse and Stanley also talk about the lessons learned from cerebral palsy (CP) and how where once CP was thought of as "a unitary disorder", the more contemporary view is somewhat more "umbrella" like. I've covered CP on this blog before so won't say much more about that; I think many people might agree that autism is similarly an umbrella term; even more so when the DSM-V comes into force in literally weeks time (Monday 20th May 2013 apparently).The Moreno-De-Luca paper goes one stage further. As per the paper and some associated media attention (see here) the suggestion is that not only is there the autisms, but that because of the various overlapping genetic features between the autisms and conditions such as schizophrenia (the schizophrenias), we should be looking at using an even more over-arching concept to group these collected diagnoses together: developmental brain dysfunction (DBD). A sort of umbrella for the umbrella if you like. It's not a new suggestion by the way****** (open-access).I can imagine that your view of autism - be that a personal perspective of autism, a parental perspective or just an observer looking in - is probably going to influence how you receive this suggestion to some degree. For a researcher looking at the possibility of shared genetics or even epigenetics between conditions which might overlap, there is some sense in looking at the bigger picture. My recent post on common ground (see here) based on the 'five psychiatric disorders linked' paper******* kinda reiterates this position alongside other papers including this one from Caamaño and colleagues******** on subclinical comorbid psychopathology. That and the fact that there might be some convergence when it comes to the autism and schizophrenia spectrums for example (see here) also makes a case. The authors sum it up well: "genes don't respect our diagnostic classification boundaries, but that really isn't surprising given the overlapping symptoms and frequent co-existence of neurodevelopmental disorders".Other perspectives - and I am only speculating on such viewpoints - might not necessarily share the same sentiments. Aside from leaving out any important relationship that genes might have with little things like the environment, as in ... Read more »
Moreno-De-Luca A, Myers SM, Challman TD, Moreno-De-Luca D, Evans DW, & Ledbetter DH. (2013) Developmental brain dysfunction: revival and expansion of old concepts based on new genetic evidence. Lancet neurology, 12(4), 406-14. PMID: 23518333
How would you feel if you would have an eternal liver, a liver that lasts forever? Recently, researchers have found gene targets which will boost the regenerative capacity of your liver cells. This means a complete cure for all your liver related problems!... Read more »
Wuestefeld, T., Pesic, M., Rudalska, R., Dauch, D., Longerich, T., Kang, T., Yevsa,T.,, Heinzmann, F., Hoenicke, L., Hohmeyer,A., Potapova,A., Rittelmeier, I., Jarek,M., Geffers,R.,, Scharfe, M., Klawonn, F., Schirmacher, P., Malek, N., Ott, M., Nordheim, A., Vogel, A.,, & Manns, M. . (2013) A Direct In Vivo RNAi Screen Identifies MKK4 as a Key Regulator of Liver Regeneration. Cell, 153(2). info:/
Everybody remembers the kind captain in Titanic, drowning in his own guilt when he realises he has comprised safety regulations for fame, and his decision to go down with the ship. Before meeting his demise, he first makes sure the women and children make it off the ship. Surely this is the proper thing to do in such situations – women and children first- right? Research suggests otherwise.... Read more »
Bruno S. Frey, David A. Savage, and Benno Torgler. (2010) Behavior under Extreme Conditions: The Titanic Disaster. Journal of Economic Perspective. info:/
Bush SP. (2004) Snakebite suction devices don't remove venom: they just suck. Annals of emergency medicine, 43(2), 187-8. PMID: 14747806
Engineers at the University of California, San Diego have invented a “nanosponge” capable of safely removing a broad class of dangerous toxins from the bloodstream – including toxins produced by MRSA, E. coli, poisonous snakes and bees.... Read more »
Catherine Hockmuth, & Daniel Kane. (2013) Nanosponges Soak Up Toxins Released by Bacterial Infections and Venom. UC San Diego News Center. info:/
An #openaccess link to a 2013 review in Advances in Parasitology on recent developments in Blastocystis research.... Read more »
Beer can be an acquired taste, but the taste of beer can still affect your brain's reward center and may increase alcohol cravings.... Read more »
Oberlin, B., Dzemidzic, M., Tran, S., Soeurt, C., Albrecht, D., Yoder, K., & Kareken, D. (2013) Beer Flavor Provokes Striatal Dopamine Release in Male Drinkers: Mediation by Family History of Alcoholism. Neuropsychopharmacology. DOI: 10.1038/npp.2013.91
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