Health posts

January 2, 2010
01:48 AM
1,965 views

how to speak your mind, literally.

Talking brains have been a staple of science fiction and comic books, usually taking the role of villains using their considerable intellect to destroy or conquer the world and implying that nerds with access to money and weapons can be really dangerous. The Brain from the DC Comics’ series Doom Patrol was essentially a raw [...]... Read more »

Guenther, F., Brumberg, J., Wright, E., Nieto-Castanon, A., Tourville, J., Panko, M., Law, R., Siebert, S., Bartels, J., Andreasen, D.... (2009) A Wireless Brain-Machine Interface for Real-Time Speech Synthesis. PLoS ONE, 4(12). DOI: 10.1371/journal.pone.0008218

January 1, 2010
02:51 PM
672 views

2009’s Top Threat To Science In Medicine

by Rogue Medic in Rogue Medic

Science-Based Medicine, has a post by Dr. Val Jones - 2009’s Top 5 Threats To Science In Medicine.I do not disagree with the list except, and what would one of my posts be without an except, the number one threat to science in medicine is much more of a problem. Our science education in grade school is where we fail our children. Before they even become adults, they are exposed to all sorts of magical thinking.Full moons, speaking about something bad increasing the chances it will occur (a jinx), believing that something natural is safer than something manufactured - just because it is not man made, or just a belief in the stereotypical mad scientist bringing about horrors by using the scientific method of inquiry. That is what science is. Science is a method of inquiry. Science is a tool we use to find out how the world works. We see something that makes us think. Most people may form an opinion, but not look at this with a method designed to minimize the effect of our biases. And we all have biases.It seems that there are more patients during a full moon. With a full moon falling at 19:15 GMT (Greenwich Mean Time) this past New Years Eve, this must have been a horrible night of death and destruction. Or was it?We formulate a hypothesis. The full moon causes accidents and/or illnesses, or makes accidents and/or illnesses even worse than they would be if there were no full moon.We figure out what we need to control for to limit our variable to just the possible influence of the full moon. So, let's look at a study that investigated the effect of a full moon on something that would be very difficult to misinterpret.We postulated that on full moon days there would be more available moonlight, thus influencing individuals’ activities, and in turn, the propensity for cardiac arrest.[1]Interesting. They are not really assuming that the cause of an increase in cardiac arrests would be due to some mystical property of the moon, but that it would be due to more moonlight. fortunately, it does not matter what the actual cause would be for an increase in cardiac arrests, if they set the experiment up properly.What do they need to do?This study was a retrospective analysis of a computerized billing database of ED visits.[1]The study population consisted of CPR (CardioPulmonary Resuscitation) occurring daily at a cohort of seven hospital ED in northern New Jersey, USA, during the period of 1 January 1988 to 31 December 1998, comprising 4018 days over 11 years. Consecutive patients seen by an emergency physician were included. Emergency physicians see 80–95% of all ED patient visits and the vast majority of cardiac arrest patients. Private physicians see the remainder of the patients.[1]Their theory was that the increased moonlight would lead to more activity; more activity would lead to more cardiac arrests; thus there would be more cardiac arrests during a full moon.Did the investigators prove their hypothesis?Table 2 Time series regression modeling resultsModel variablevariable estimatetP valueFull moon–0.002–0.030.97New moon–0.12–2.290.02Saturday 0.288 4.710.0001Sunday 0.139 2.270.02Monday 0.172 2.810.005Winter 0.205 4.650.0001Long-term trend–0.00004–2.410.02Fdf=7 =8.71, P =0.0001.Durbin–Watson d= 1.96, r =0.018[1]According to this table, there is no increase in cardiac arrest incidence during a full moon. They actually recorded a decrease, but the difference is not statistically significant. The reported statistically significant difference in incidence of cardiac arrest is this. During the new moon, there is less likely to be a cardiac arrest treated by an emergency physician. There were 2370233 patient visits in the database during the 4018-day (11year) period of study, with 6827 having the primary ICD-9 diagnosis of cardiac arrest.[2] Table 2 contains the time series regression results. Full moon days were not significantly different from other days (P=0.97). We had an 80% power to identify a difference of 4.5%. However, on average 0.12 fewer CPR occurred on new moon days than on other days (P=0.02). This translates into an average of 6.5% fewer CPR (95% confidence interval 1.3–11.7%) on new moon days than other days. In addition, the results for the potentially confounding variables are presented in Table 2.[1]I left part of their original hypothesis off of the initial quote. The stated objective of the study is - Objective To determine the effect of the phase of the full and new moon on the variation in the number of daily cardiopulmonary resuscitations.[1]In the discussion, they elaborate on their purpose - Our results show a small but statistically significant decrease in the incidence of CPR with new moon days. We speculate that this may be secondary to a decrease in activity because of less available light on these days, as it has been shown that increased activity is a risk factor for sudden death[39]. Our initial rationale sought to identify and determine the size of any effect on the occurrence of cardiac arrest and its attempted resuscitation (‘CPR’) by lunar influence as a potential insight into an aspect of the occurrence of cardiac arrest. In addition, we sought to identify patient volume variation by lunar cycle potentially to allow for staffing modifications; however, the effect identified did not warrant this.[1]This - We postulated that on full moon days there would be more available moonlight, thus influencing individuals’ activities, and in turn, the propensity for cardiac arrest.[1]Becomes - We speculate that this may be secondary to a decrease in activity because of less available light on these days, as it has been shown that increased activity is a risk factor for sudden death[39][1]They have found a way to stick with their initial hypothesis by reversing it. More moonlight does not appear to lead to more cardiac arrests. Why this lack of correlation does not need to be explained is not in the paper. However, the correlation between fewer deaths during a new moon is something that they feel needs to be explained. Haven't they just misappropriated a Willy Wonka quote? Strike that. Reverse it. Willy Wonka was reversing the meaning of what he was saying. That was the reason he needed to reverse the order.The authors have not really changed the meaning, only the way they express it. More light/less light leads to more activity/less activity. This leads to more/fewer cardiac arrests.While I do not dispute the results of this study, I do have a problem with the way they get from Point A to Point C. They seem to travel there by way of a study that shows that more activity leads to more cardiac arrest. Actually the study is of vigorous exertion, not just more activity, but the authors seem to have interpreted the study as couch potatoes live longer. The vigorous exertion study did show - As expected, the base-line level of habitual exercise significantly attenuated the increase in the risk of sudden death that was associated with an episode of vigorous exertion in both the primary analysis and the three sensitivity analyses. Habitually active men had a much lower ri... 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Alves, D., Allegra, J., Cochrane, D., & Cable, G. (2003) Effect of lunar cycle on temporal variation in cardiopulmonary arrest in seven emergency departments during 11 years. European Journal of Emergency Medicine, 10(3), 225-228. DOI: 10.1097/00063110-200309000-00013

December 31, 2009
09:00 AM
1,747 views

Radiation from CT scans: Balancing risks and benefits

by Orac in Respectful Insolence

NOTE: Orac is on semi-vacation this week, trying very hard to recharge his Tarial cells. Actually, although he is at home, he is spending much of his time in his Sanctum Sanctorum (i.e., his home office) working on an R01 for the February submission cycle. Given that the week between Christmas and New Years Day tends to be pretty boring, both from a blogging and blog traffic standpoint, he's scaling back the new, original stuff and mixing in some "best of" reruns, as well as some more recent stuff that appeared in a different form elsewhere, modified a bit to be more appropriate to this blog. Why? Because he likes them enough that he wants to make sure that as many people as possible see them.

Fear not, though. If something sufficiently interesting happens, Orac will welcome a break from the drudgery of grant writing to apply some appropriate not-so-Respectful Insolence to it. Oh, wait. He already did break his "vacation" to post two or three times....

Science-based medicine consists of a balancing of risks and benefits for various interventions. This is sometimes a difficult topic for the lay public to understand, and sometimes physicians even forget it. My anecdotal experience suggests to me that surgeons are probably more aware of this basic fact. Of course, that isn't because we're better than other doctors or anything like that; rather, it's because our interventions generally involve taking sharp objects to people's bodies and using steel to remove or rearrange parts of people's anatomy for (hopefully) therapeutic effect. Ditto oncologists, who prescribe highly toxic substances to treat cancer, the idea being that these substances are more toxic to the cancer than they are to the patient. Often they are only marginally more toxic to the cancer than to the patient. However, if there's one area where even physicians tend to forget that there is potential risk involved, it's the area of diagnostic tests, in particular radiological diagnostic tests, such as X-rays, fluoroscopy, computed tomography (CT) scans, and the variety of ever more powerful diagnostic studies that have proliferated over since CT scans first entered medical practice in the 1970s. Since then, the crude images that the first CT scans produced have evolved, thanks to technology and ever greater computing power, to breathtaking three dimensional-views of the internal organs. Indeed, just since I finished medical school back in the late 1980s, I'm continually amazed at what these new imaging modalities can accomplish.

The downside of these imaging modalities is that most of them require the use of X-rays to produce their images. True, over the last 15 years or so MRI, which uses very strong magnetic fields and radiofrequency radiation rather than ionizing radiation to produce its images, has become increasingly prevalent. MRI is great because it produces more contrast between different kinds of soft tissue than CT scans do. However, CT tends to be superior for examining calcified organs, such as bone. (The breast surgeon in me notes that breast MRI is pretty much useless for detecting microcalcifications, an important possible indicator for cancer.) Also, MRI scans require a prolonged period of laying still in a very tight tube, which is a problem for patients with any degree of claustrophobia, although "open" MRIs are becoming increasingly available. More importantly for the quality of images, because they require a patient to lie more still than a CT, MRIs tend to be prone to more motion artifacts, which is perhaps why CT is more frequently used to image the abdomen other than large solid organs such as the liver. The point is that, although MRI is becoming more prevalent, CT scans aren't going away any time soon. They have different strengths and weaknesses as imaging modalities and are therefore best suited for different, albeit overlapping, sets of indications. Read the rest of this post... | Read the comments on this post...... Read more »

Berrington de Gonzalez, A., Mahesh, M., Kim, K., Bhargavan, M., Lewis, R., Mettler, F., & Land, C. (2009) Projected Cancer Risks From Computed Tomographic Scans Performed in the United States in 2007. Archives of Internal Medicine_id, 169(22), 2071-2077. http://archinte.ama-assn.org/cgi/doi/10.1001/archinternmed.2009.440

Smith-Bindman, R., Lipson, J., Marcus, R., Kim, K., Mahesh, M., Gould, R., Berrington de Gonzalez, A., & Miglioretti, D. (2009) Radiation Dose Associated With Common Computed Tomography Examinations and the Associated Lifetime Attributable Risk of Cancer. Archives of Internal Medicine, 169(22), 2078-2086. DOI: 10.1001/archinternmed.2009.427

Redberg RF. (2009) Cancer risks and radiation exposure from computed tomographic scans: how can we be sure that the benefits outweigh the risks?. Archives of internal medicine, 169(22), 2049-50. PMID: 20008685

Brenner DJ, & Hall EJ. (2007) Computed tomography--an increasing source of radiation exposure. The New England journal of medicine, 357(22), 2277-84. PMID: 18046031

December 30, 2009
06:11 PM
796 views

Death and Taxes: It's Shaping Up to be a Busy Year

by Eric Widera in GeriPal

Death elasticity and the estate tax.... Read more »

Kopczuk, W., & Slemrod, J. (2003) Dying to Save Taxes: Evidence from Estate-Tax Returns on the Death Elasticity. Review of Economics and Statistics, 85(2), 256-265. DOI: 10.1162/003465303765299783

Gans, J., & Leigh, A. (2006) Did the Death of Australian Inheritance Taxes Affect Deaths?. Topics in Economic Analysis , 6(1). DOI: 10.2202/1538-0653.1654

December 30, 2009
10:05 AM
958 views

Escaping the "poverty trap" of infectious disease

by Jeremy Yoder in Denim and Tweed

Even in the twenty-first century, infectious diseases such as malaria, dengue fever, cholera, and AIDS remain widespread in much of the developing world, at tremendous cost to human life and economic productivity. Poorer nations lack the resources for more effective public health measures; but widespread infectious disease may slow or prevent the economic development that can provide those resources. A new paper in Proceedings of the Royal Society tries to sort out this chicken-and-egg problem, and finds that economic development is the fastest route out of the "poverty trap" [$a].

The paper's authors, Bonds et al. start with a classic model of infectious disease, in which susceptible (healthy) members of a population have a chance of becoming infected whenever they encounter an infected person, and infected people have a chance to recover to susceptible condition if they survive the effects of the disease. The first probability is the rate of transmission from person to person; the second is the rate of recovery from disease caused by the infection.

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A woman receives tetanus vaccine in the Central African Republic. Photo by hdptcar.Bonds et al. insert economics into this basic model by reasoning that the rate of recovery is a function of per-capita income – well-fed people are better able to fight off infection – and that income is a function of the proportion of the population that remains uninfected at any given time. This yields a mathematical version of the poverty trap I outlined above: high-income populations are easily able to fight off infection and remain near 100 percent susceptible, but highly infected societies are unable to increase their per-capita income to reduce their rate of infection. However, there is an internal equilibrium point – a level of income and infection from which a population could easily move in either direction, towards high income and low infection or high infection and low income.

The question then becomes how best to push a developing nation's population toward that threshold condition – or how best to bring the threshold closer. Bonds et al. compare two options: reducing the rate of disease transmission, and boosting individual economic productivity. The former captures the effect of boosting public health – vaccination, better sewage treatment, food aid. The latter captures the effect of improving infrastructure or financial institutions – making the economy more developed. They found that the threshold condition is more sensitive to economic productivity. Even at low transmission rates, a society can be caught in the poverty trap if its productivity is low enough, but at high enough productivity levels, societies can avoid the trap created by even highly transmissible diseases.

This suggests that, although medical aid can help the acute problem of infectious disease, it's investment in economic development that can ultimately solve it.

Reference

Bonds, M., Keenan, D., Rohani, P., & Sachs, J. (2009). Poverty trap formed by the ecology of infectious diseases Proc. R. Soc. B DOI: 10.1098/rspb.2009.1778

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Bonds, M., Keenan, D., Rohani, P., & Sachs, J. (2009) Poverty trap formed by the ecology of infectious diseases. Proc. R. Soc. B. DOI: 10.1098/rspb.2009.1778

December 28, 2009
05:42 PM
569 views

Antipodean Pharmaceuticals and their Mitochondrially Targeted Antioxidant

by Reason in Fight Aging!

You might recall the work of Skulachev's research group in producing an ingested antioxidant compound that targets the mitochondria and extends life span in mice. Similarly, mice genetically engineered to produce more naturally-occurring antioxidants in their mitochondria also live longer. By way of comparison, all other forms of antioxidant examined to date generally do nothing for life span, and may even harm your health and longevity. The plausible explanation for the effects of mitochondrially targeted antioxidants rests on the mitochondrial free radical theory of aging. In short, your mitochondria are powerplants, thousands of them in each cell of your body. They convert food into the chemicals used to power cellular processes, but emit damaging free radicals as a byproduct. Some fraction of aging is caused by the chain of events that occur as mitochondria progressively damage themselves with their own emissions. Thus anything that can soak up these free radicals at the source, before they cause any harm, should lower the rate at which biochemical damage occurs, and extend life span. Now let me direct your attention to Antipodean Pharmaceuticals, a New Zealand based research group working to develop an antioxidant targeted to mitochondria. Their compound, called MitoQ, appears similar...... Read more »

Rodriguez-Cuenca S, Cochemé HM, Logan A, Abakumova I, Prime TA, Rose C, Vidal-Puig A, Smith AC, Rubinsztein DC, Fearnley IM.... (2009) Consequences of long-term oral administration of the mitochondria-targeted antioxidant MitoQ to wild-type mice. Free radical biology . PMID: 19854266_id

December 28, 2009
08:00 AM
1,634 views

The revenge of cell phones and cancer strikes back yet again in the never-ending controversy...

by Orac in Respectful Insolence

NOTE: Orac is on semi-vacation this week, trying very hard to recharge his Tarial cells. Actually, although he is at home, he is spending much of his time in his Sanctum Sanctorum (i.e., his home office) working on an R01 for the February submission cycle. Given that the week between Christmas and New Years Day tends to be pretty boring, both from a blogging and blog traffic standpoint, he's scaling back the new, original stuff and mixing in some "best of" reruns, as well as some more recent stuff that appeared in a different form elsewhere, modified a bit to be more appropriate to this blog. Why? Because he likes them enough that he wants to make sure that as many people as possible see them.

Fear not, though. If something sufficiently interesting happens, Orac will welcome a break from the drudgery of grant writing to apply some appropriate not-so-Respectful Insolence to it. (Yes, I'm referring to Deepak Chopra, who, I'm told, returned over the weekend after Christmas, surpassing even his own usual level of vitriol towards "skeptics.")

It's been about a year and a half since I've written about this topic; so I thought I'd better update the disclaimer that I wrote at the beginning:

Before I start into the meat of this post, I feel the need to emphasize, as strongly as I can, four things:

I do not receive any funding from the telecommunications industry in general, or wireless phone companies in particular. None at all. In other words, I'm not in the pocket of "big mobile" any more than I am in the pocket of big pharma.
I don't own any stock in telecommunications companies, other than as parts of mutual funds in which my retirement funds are invested that purchase shares in many, many different companies, some of which may or may not be telecommunications companies.
None of my friends or family work for cell phone companies.
I don't have a dog in this hunt. I really don't.

There. That's better. Hopefully that will, as it did last time, serve as a shield against the "shill" argument, which is among the frequent accusations I hear whenever I venture into this particular topic area. So, as I did back in 2008, I just thought I'd clear that up right away in order (hopefully) to preempt any similar comments after this post. Unfortunately, as I have known for a long time, I'm sure someone will probably show his or her lack of reading comprehension and post one of those very criticisms of me. It's almost inevitable, either here or elsewhere. Posting such disclaimers never seems to work against the "pharma shill" gambit when I write about vaccines or dubious cancer cures. Even so, even after nearly ten years involved in skepticism and promoting science-based medicine, hope still springs eternal.

There are two reasons that I think the issue of mobile phones and cancer needs an update on our blog: First, it has been a year and a half since I last wrote about it. At that time I castigated Dr. Ronald B. Herberman, who at that time was director of the University of Pittsburgh Cancer Institute for what I viewed as fear mongering over cell phones and cancer based on at best flimsy evidence. Second, there have been two fairly high profile studies looking at whether there is a link between mobile phone use and cancer. One of these my colleague and friend Steve Novella has already discussed, but there was another one that he didn't see because it didn't get quite as much publicity, possibly because the corresponding author is based in Korea. I will take this opportunity to discuss them both. Read the rest of this post... | Read the comments on this post...... Read more »

Myung, S., Ju, W., McDonnell, D., Lee, Y., Kazinets, G., Cheng, C., & Moskowitz, J. (2009) Mobile Phone Use and Risk of Tumors: A Meta-Analysis. Journal of Clinical Oncology, 27(33), 5565-5572. DOI: 10.1200/JCO.2008.21.6366

Deltour, I., Johansen, C., Auvinen, A., Feychting, M., Klaeboe, L., & Schuz, J. (2009) Time Trends in Brain Tumor Incidence Rates in Denmark, Finland, Norway, and Sweden, 1974-2003. JNCI Journal of the National Cancer Institute. DOI: 10.1093/jnci/djp415

December 27, 2009
03:24 PM
724 views

The Genetics of Living To 100

by Neuroskeptic in Neuroskeptic

Is there a gene for long life?Boston-based group Sebastiani et al say they've found not one but two, in RNA Editing Genes Associated with Extreme Old Age in Humans and with Lifespan in C. elegans.They took 4 groups of "oldest old" people: from New England, Italy, and Japan, and American Ashkenazi Jews. All were aged 90 or more, and many of them were 100, centenarians. As control groups, they used random healthy people who weren't especially old. The total sample size was an impressive 2105 old vs. 3044 controls.On the basis of a pilot study, they chose to look at two candidate genes, ADARB1 and ADARB2. Both are involved in post-transcriptional RNA editing, one of the steps in the process by which genetic material, DNA, controls protein synthesis. It's something every cell in the body needs to do in order to function.What happened? Their abstract makes the exciting claim that18 single nucleotide polymorphisms (SNPs) in the RNA editing genes ADARB1 and ADARB2 are associated with extreme old age in a U.S. based study ... We describe replications of these findings in three independently conducted centenarian studies with different genetic backgrounds (Italian, Ashkenazi Jewish and Japanese) that collectively support an association of ADARB1 and ADARB2 with longevity.But read the whole paper and the picture is a little more complex. For ADARB1, they looked at 31 variants (SNPs). In the New England sample, which was the largest, 5 of them were statistically significantly more common in old people compared to the controls. However, none of these were significantly associated in any of the other samples, although for 3 of the 5 variants, there was some evidence of an effect in the same direction in the other samples.In ADARB2, out of 114 variants, 10 were significantly associated in the New England sample. Of these, 4 were independently significant in the Italian sample, and in the combined New England/Italian sample all 10 were still associated. But the Jewish and the Japanese samples showed a rather different picture: only 1 of the 10 associations was significant in the Jews, although several were weakly associated in the same direction, and in a pooled New England/Italian/Jewish analysis 9 were still significant. In the Japanese sample, one association was replicated but another variant was associated in the wrong direction.They also did some lab work and found that in nematode worms (C. Elegans), mutants lacking the worm equivalent of the ADARB1 and ADARB2 genes had a 50% reduced lifespan - 10 days, instead of the normal 20 - despite no obvious symptoms of illness. Hmm.I'm not quite sure what to make of this data. They looked at 4 separate, large samples, which is an excellent size by the standards of candidate gene association studies. The evidence implicating ADARB1 and (especially) ADARB2 variants in longevity is fairly convincing, although the most consistent effects came from the European-ancestry samples, suggesting that different things might be going on in other populations. This is the first research looking at these genes; ultimately, we won't know for sure until we get more. The worm data is a nice touch, but I'd like to see evidence from animals with a bit more similarity to humans, say mice.Still, suppose that these genes are associated with long life; suppose they they control the rate of the ageing process, protecting you from dying from "natural causes" too early. That doesn't mean that you'll live to an old age - it just makes it possible. If you get hit a truck or fall of a cliff, you're dead, anti-ageing genes or not.Frenchwoman Jeanne Calment, born 1875, died 1997, is the oldest person on record, at 122 years. But we'll never know whether someone with the genetic potential to outlive her died in WW2, or the Cultural Revolution, or just got hit by a truck. Calment presumably had the right genes, but she was also lucky.So a trait's being genetically heritable doesn't make it pre-ordained and immutable. IQ, for example, most likely has a heritability of around 50% - some people likely have a higher potential for intellectual achievement than others. But if you're born into an abusive family, or deep poverty, or you never get a chance to go to school, you may never reach that potential. There's always that truck.Sebastiani P, Montano M, Puca A, Solovieff N, Kojima T, Wang MC, Melista E, Meltzer M, Fischer SE, Andersen S, Hartley SH, Sedgewick A, Arai Y, Bergman A, Barzilai N, Terry DF, Riva A, Anselmi CV, Malovini A, Kitamoto A, Sawabe M, Arai T, Gondo Y, Steinberg MH, Hirose N, Atzmon G, Ruvkun G, Baldwin CT, & Perls TT (2009). RNA editing genes associated with extreme old age in humans and with lifespan in C. elegans. PloS one, 4 (12) PMID: 20011587... Read more »

Sebastiani P, Montano M, Puca A, Solovieff N, Kojima T, Wang MC, Melista E, Meltzer M, Fischer SE, Andersen S.... (2009) RNA editing genes associated with extreme old age in humans and with lifespan in C. elegans. PloS one, 4(12). PMID: 20011587

December 26, 2009
01:13 PM
972 views

Christmas Cheer from BMJ

by The Neurocritic in The Neurocritic

Fig 1 (Firth et al., 2009). X ray pictures can easily detect an ingested coin. Position of coin on lateral view (left), relative to anterior (right) or posterior picture affects size of image on film.Every year, BMJ has a special Christmas issue with spoof articles and silly studies. Today's feature examines the relationship between the Dow Jones Industrial Average and the value of coins swallowed by children (Firth et al., 2009):Main outcome measures Total value of coins ingested and number of incidents of coins versus other objects swallowed, measured before and after the stock market crash of October 2008.The authors reviewed computerized records from the endoscopy suite at Massachusetts General Hospital:...we compiled data on all numismatic and sundry detritus acquired (NASDAQ composite index) from children’s gastrointestinal tracts by the paediatric gastroenterology service at our hospital between August 2006 and July 2009. ... We calculated the financial total swallowed and extracted as a fraction of the US$ or 100 cents (FTSE 100 index), and the ratio of patients with coins versus all those with foreign objects removed (pecuniary extraction ratio, PE ratio). We calculated the mean end-of-month closing value of the Dow Jones Industrial Average. We examined whether there was a change in the monthly mean NASDAQ, FTSE, and PE ratio before and after the collapse of the Dow Jones Industrial Average of October 2008.What did they find? There was no relationship between the value of the stock market and the value of coins swallowed by children, as one might intuitively expect from a population that has no idea that the Dow Jones Industrial Average even exists [except for maybe the 15 (!) year old]:The patients were aged 1 to 15 years. The NASDAQ composite index was 18. Eleven coins were retrieved from nine patients: three pennies (or cents), five nickels (1 nickel=5 cents), no dimes (1 dime=10 cents), and three quarters (1 quarter=25 cents), giving a total return on ingestment for the period, or FTSE 100 index, of $1.03. Seven other objects in seven children included an unsafe safety pin (open), a battery, a marble, a ballbearing, a magnet, a dentist’s guard, and a rubber doorstopper. The PE ratio was therefore 0.57 (9/16)....We found no change in the FTSE 100 index (2.3 v 3.1, P=0.77) or PE ratio (0.54 v 0.66, P=0.5) during a period of dramatic Dow Jones (12 537 v 8388, P less than 0.0001), despite the NASDAQ composite index remaining stable (0.4 v 0.5, P=0.75). In other words, despite a massive swing in the stock market there was no concomitant absolute or relative change in paediatric wealth intake against an unaltered background rate of foreign body ingestion.Nonetheless, the authors bemoan the paucity of gastropecuniary studies and call for further investigations in the numismedical field.Brain Blogger covers another article from the 2009 issue, Santa Claus: a public health pariah? in their post, Is a Slim Santa Claus Coming to Town? My personal favorite, though, is this announcement from BMJ editor Tony Delamothe: "Anaesthetists’ brains differ markedly from surgeons’. Who would have thought?"Classics from Christmases past include Are Surgeons Taller And Better Looking Than Other Doctors?, Sword Swallowing And Its Side Effects, Sneezing etiquette and the efficacy of masks, Sex, aggression, and humour: responses to unicycling, and Rage Against the Machine Syncope and the Texting Sign. Happy reading!ReferenceFirth, P., Zheng, H., & Biller, J. (2009). Ingested foreign bodies and societal wealth: three year observational study of swallowed coins. BMJ, 339 (dec04 1). DOI: 10.1136/bmj.b5066

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Firth, P., Zheng, H., & Biller, J. (2009) Ingested foreign bodies and societal wealth: three year observational study of swallowed coins. BMJ, 339(dec04 1). DOI: 10.1136/bmj.b5066

December 24, 2009
06:59 PM
746 views

Intravenous drug administration during out-of-hospital cardiac arrest: a randomized trial.

by Rogue Medic in Rogue Medic

Also posted over at Paramedicine 101. Go check out the rest of what is there.This study has received a lot of attention. I will interchangeably use the terms the IV (IntraVenous) group and the epinephrine group depending on the terminology I think is more relevant at the time. The distinction is not one that I believe is important. This is a study of IV medication in cardiac arrest. Epinephrine is the stated focus of the study.There has never been any evidence to suggest that medication leads improved resuscitation outcomes. Unless your idea of an improved resuscitation outcome has nothing to do with quality of life.Beneficial short-term effects of epinephrine have been shown in animal studies,3-5 but there is increasing concern for increased myocardial dysfunction6,7 and disturbed cerebral microcirculation after cardiac arrest.8[1]Some people argue that the short-term effects are important. If we do not get a pulse back, we will not resuscitate anyone. This is true, but the problem is how much long-term damage do we inflict just to obtain that short-term improvement? High-dose epinephrine is no longer recommended, even though it was better than standard-dose epinephrine at producing ROSC (Return Of Spontaneous Circulation). The current recommendation for epinephrine is based on this same misconception. More ROSC = better outcomes - except that the dogma is not supported by any evidence.CONCLUSIONS--High-dose epinephrine (HDE) significantly improves the rate of return of spontaneous circulation and hospital admission in patients who are in prehospital cardiac arrest without increasing complications. However, the increase in hospital discharge rate is not statistically significant, and no significant trend could be determined for neurological outcome. No benefit of NE compared with HDE was identified. Further study is needed to determine the optimal role of epinephrine in prehospital cardiac arrest.[2]That study was 17 years ago. That was far from the first study of epinephrine. There has been many studies of epinephrine in cardiac arrest since then. We still do not have any research to show improved outcomes with any dose of epinephrine to treat cardiac arrest, but rather than admit that epinephrine should only be used in well controlled studies, we continue to make excuses. We are practicing alternative medicine, not real medicine. Absence of evidence of benefit does not mean an absence of benefit, but when does it become enough evidence to insist that we stop using this ineffective and potentially harmful drug as the standard treatment? Back to the current study. Because there are no randomized controlled studies showing improved survival to hospital discharge with any drugs routinely administered during CPR, we concluded such a study was warranted.[1]This study is possible because these researchers are outside of the US. In the US, the IRBs (Institutional Review Boards) seem to have concluded that it is unethical to deviate from the standard treatment, even if the standard treatment is harmful. Of course, we can never learn if the standard treatment is harmful, or even if it is beneficial, if we are prohibited from studying the treatment. However, the IRBs' definition of ethics seems to have been arrived at while consuming hallucinogens and reading Lewis Carroll.Epinephrine in cardiac arrest is also firmly established outside of the US. Here is a part of their explanation of the study design.In this prospective, randomized controlled trial of intravenous drug administration during out-of-hospital cardiac arrest, we compared outcomes for patients receiving standard ACLS with intravenous drug administration (control) and patients receiving ACLS without intravenous drug administration (intervention).[1]ACLS is Advanced Cardiac Life Support - almost all of the treatments that would be given in the ED (Emergency Department). Not giving the drug is the intervention. Giving the drug is considered the non-intervention - the control against the effects of the treatment, which is the non-treatment.Defibrillation was attempted in more patients in the intravenous group compared with the no intravenous group (47% vs 37%, respectively; OR, 1.16 [95% CI, 0.74-1.82]). More defibrillation shocks were delivered to those who received defibrillation in the intravenous group compared with the no intravenous group (median, 3 [range, 1-22] vs 2 [range, 1-26], respectively; P = .008). Both groups had adequate and similar CPR quality with few chest compression pauses (median hands-off ratio, 0.15 for the intravenous group and 0.14 for the no intravenous group) and the compression and ventilation rates were within the guideline recommendations (Table1).[1]While there were no apparent differences in the quality of CPR, the more frequent defibrillations might be worth looking at. One of the important aspects of this study, as opposed to most prehospital research, is the recognition of a need to control for quality.The explanation for the more frequent defibrillations that seems most likely is that the epinephrine produced a shockable rhythm more often than CPR alone produced a shockable rhythm. Since a shockable rhythm appears to be the next best thing to ROSC, this would not be a surprise. Many patients will change from a shockable rhythm to asystole when defibrillated. Defibrillation is a profound vagal stimulus and asystole is the ultimate vagal state. Even with similar initial rates of shockable rhythms, some of both groups would be expected to be shocked into asystole. The epinephrine, being a huge cardiac stimulus, would be expected to lead to a return of a shockable rhythm more often than just CPR. In other words, if the epinephrine is expected to produce ROSC more often, it should also produce a shockable rhythm more often. The authors came to a similar conclusion.Without differences in the predefined primary outcome, patients in the intravenous group received more defibrillations, were resuscitated for a longer period, and more frequently had ROSC. With similar and adequate CPR quality, this is likely due to the pharmacological effects of the drugs used (epinephrine, atropine, and/or amiodarone). This finding is consistent with previous animal studies with epinephrine,6,7 and clinical studies evaluating the effects of amiodarone,23 atropine,24 and even high-dose epinephrine,25 all of which documented improved short-term effects without improving long-term outcomes.[1]One major criticism of the methods is that they did not have a placebo to be given to keep the EMS crews blinded to the actual treatment. The authors do admit that this is a limitation. Of course, this placebo would probably not be called a placebo, since the epinephrine arm is the placebo arm, while the non-treatment arm is the active intervention arm, but that is really only an amusing problem of terminology and attitude. When the epinephrine group is the group with an IV line in place during resuscitation and the no epinephrine group is the one that does not have an IV until after return of pulses, there is not even an attempt at blinding. Did this lead to any detectable difference in the way patients were treated by EMS, other than other than the differences intended by the study design?Our study has several limitations. First, ambulance personnel could not be blinded to the randomization. Closely related to this, only patients who were randomized to the no intravenous group could be monitored with regard to protocol compliance. If intravenous drugs were administered to a patient in the no intravenous group, violation of the study protocol could be documented. If intravenous drugs were not administered to a patient in the intravenous group, several valid reasons could exist, such as rapid ROSC. We have no reason to believe that personnel refrained from establishing intravenous access under the pretense that the procedure was unsuccessful. The ambulance personnel involved were strongly committed to testing the hypothesis presented, but we cannot totally rule out possible bias toward procedures such as intravenous access and ad... Read more »

Olasveengen TM, Sunde K, Brunborg C, Thowsen J, Steen PA, & Wik L. (2009) Intravenous drug administration during out-of-hospital cardiac arrest: a randomized trial. JAMA : the journal of the American Medical Association, 302(20), 2222-9. PMID: 19934423

December 23, 2009
06:10 PM
545 views

Good News for Armchair Neuropathologists

by Neuroskeptic in Neuroskeptic

Ever wanted to crack the mysteries of the brain? Dreamed of discovering the cause of mental illness?Well, now, you can - or, at any rate, you can try - and you can do it from the comfort of your own home, thanks to the new Stanley Neuropathology Consortium Integrative Database.Just register (it's free and instant) and you get access to a pool of data derived from the Stanley Neuropathology Consortium brain collection. The collection comprises 60 frozen brains - 15 each from people with schizophrenia, bipolar disorder, and clinical depression, and 15 "normals".In a Neuropsychopharmacology paper announcing the project, administrators Sanghyeon Kim and Maree Webster point out thatData sharing has become more important than ever in the biomedical sciences with the advance of high-throughput technology and web-based databases are one of the most efficient available resources to share datasets.The Institute's 60 brains have long been the leading source of human brain tissue for researchers in biological psychiatry. Whenever you read about a new discovery relating to schizophrenia or bipolar disorder, chances are the Stanley brains were involved. The Institute provide slices of the brains free of charge to scientists who request them, and they've sent out over 200,000 to date.Until now, if you wanted to find out what these scientists discovered about the brains, you'd have to look up the results in the many hundreds of scientific papers where the various results were published. If you knew where to look, and if you had a lot of time on your hands. The database collates all of the findings. That's a good idea. To ensure that they get all of the results, the Institute have another good idea:Coded specimens are sent to researchers with the code varying from researcher to researcher to ensure that all studies are blinded. The code is released to the researcher only when the data have been collected and submitted to the Institute.The data we're provided get about these brains is quite exciting, if you like molecules, comprising 1749 markers from 12 different parts of the brain. Markers include levels of proteins, RNA, and the number and shape of various types of cells.It's easy to use. While waiting for my coffee to brew, I compared the amount of the protein GFAP76 in the frontal cortex between the four groups. There was no significant difference. I guess GFAP76 doesn't cause mental illness - so darn. So much for my Nobel Prize bid theory. But then I found that levels of GFAP76 were very strongly correlated with levels of another protein, "phosphirylated" (I think they mean "phosphorylated") PRKCA.In the paper, Kim and Webster used the Database to find many differences between normal brains and diseased brains, including increased levels of dopamine in schizophrenia, and increased levels of glutamate in depression and bipolar. And decreased GAD67 proteins in the frontal cortex in bipolar and schizophrenia. And decreased reelin mRNA in the frontal cortex and cerebellum in bipolar and schizophrenia. And...This leaves open the vital questions of what these differences mean, as I have complained before. And the problem with giving everyone in the world the results of 1749 different tests, and letting us cross-correlate them with each other and look for differences between 4 patient groups, is that you're making possible an awful lot of comparisons. With only 15 brains per group, none of the results can be considered anything more than provisional, anyway - what we really need are lots more brains.But this database is still a welcome move. This kind of data pooling is the only sensible approach to doing modern science, and it's something people are advocating in other fields of neuroscience as well. It just makes sense to share results rather than leaving everyone to do there own thing in near-isolation from each other, now that we have the technology to do so. In fact, I'd say it's a... no-brainer.Kim, S., & Webster, M. (2009). The Stanley Neuropathology Consortium Integrative Database: a Novel, Web-Based Tool for Exploring Neuropathological Markers in Psychiatric Disorders and the Biological Processes Associated with Abnormalities of Those Markers Neuropsychopharmacology, 35 (2), 473-482 DOI: 10.1038/npp.2009.151... Read more »

Kim, S., & Webster, M. (2009) The Stanley Neuropathology Consortium Integrative Database: a Novel, Web-Based Tool for Exploring Neuropathological Markers in Psychiatric Disorders and the Biological Processes Associated with Abnormalities of Those Markers. Neuropsychopharmacology, 35(2), 473-482. DOI: 10.1038/npp.2009.151

December 23, 2009
10:05 AM
784 views

Why aren't there more sickle-cell anemics in the Mediterranean?

by Jeremy Yoder in Denim and Tweed

The story of sickle-cell anemia and its malaria-protective effects is a textbook case how environmental context determines the fitness of a given genetic profile. However, the evolution of human blood disorders in response to selection from malaria parasites might be more complicated than that textbook story.

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Malaria-causing parasites (dark-stained) among human red blood cells (top), and "sickled" red blood cells (bottom). Photos via WikiMedia Commons.Malaria is caused by mosquito-spread parasites that attack their hosts' oxygen-bearing red blood cells. A particular mutation in the gene that codes for part of the hemoglobin molecule – the molecule that actually stores oxygen inside red blood cells – leads to deformed, sickle-shaped, blood cells. People who carry two copies of the sickle cell gene develop sickle-cell disease, in which the sickle-shaped cells reduce oxygen transport efficiency and interfere with blood circulation. People with only one copy of the sickle-cell gene are healthy, and better able to resist malaria infection than those with no copies. The textbook story is that, in regions where malaria is common, such as sub-Saharan Africa, the advantage of malaria resistance is enough to offset the fitness risk of carrying the sickle-cell gene – that one-fourth of children born to parents who each have one copy of the gene will themselves have two copies and develop sickle-cell disease.

However, there are regions like the Mediterranean where malaria has historically been prevalent, but in which the human population hasn't evolved the higher frequency of sickle-cell genes that you'd expect from the scenario outlined above. A new paper in PNAS demonstrates that this may be because of interactions between the sickle-cell gene and another genetic blood disorder, thalassemia [$a].

Thalassemia is a class of genetic disorders affecting the protein subunits that comprise hemoglobin. Each hemoglobin molecule is formed by binding together two "alpha"-type subunits, and two "beta"-type subunits. If there is a shortage of correctly-formed subunits of either type, then hemoglobin formation is impaired, resulting in anemia or (if the mutation stops subunit production altogether) death. However, like sickle-cell genes, thalassemic mutations can confer resistance to malaria; and if alpha-thalassemia is paired with beta-thalassemia, the reduced production of both subunits can balance out.

As it happens, in combination with alpha-thalassemia, the sickle-cell gene's malaria protection is neutralized. Using population genetic models, the new study's authors show that this effect may have actively prevented the sickle-cell gene from establishing in the Mediterranean, where alpha- and beta-thalassemias are more common than in Africa. In the Mediterranean, the presence of beta-thalassemia genes reduces the fitness cost of (mild) alpha-thalassemia genes; and in the presence of alpha-thalassemia genes, the sickle-cell gene confers no protection to people with one copy but still induces sickle-cell disease in people with two copies.

These interactions between genes are called epistasis, and they can have dramatic impacts on evolution. Although I haven't seen many cases as well-characterized as this one, epistasis is probably widespread in the complex systems of genomes, where thousands of regulatory and protein-coding genes interact to build living things.

References

Penman, B., Pybus, O., Weatherall, D., & Gupta, S. (2009). Epistatic interactions between genetic disorders of hemoglobin can explain why the sickle-cell gene is uncommon in the Mediterranean Proc. Nat. Acad. Sci. USA, 106 (50), 21242-6 DOI: 10.1073/pnas.0910840106

... Read more »

Penman, B., Pybus, O., Weatherall, D., & Gupta, S. (2009) Epistatic interactions between genetic disorders of hemoglobin can explain why the sickle-cell gene is uncommon in the Mediterranean. Proc. Nat. Acad. Sci. USA, 106(50), 21242-6. DOI: 10.1073/pnas.0910840106

December 23, 2009
08:00 AM
731 views

Insulin resistance as a protective mechanism, a paradigm shift?

by Colby in nutsci.org

Oxidative stress has been implicated implicated in insulin resistance, and a new study by Hoehn et al. (1) adds some convincing evidence that one specific radical, superoxide generated in the mitochondria, may be a unifying cause. But the findings suggest that we may need to reconsider how we treat it.

The authors begin by suggesting that [...]... Read more »

Hoehn KL, Salmon AB, Hohnen-Behrens C, Turner N, Hoy AJ, Maghzal GJ, Stocker R, Van Remmen H, Kraegen EW, Cooney GJ.... (2009) Insulin resistance is a cellular antioxidant defense mechanism. Proceedings of the National Academy of Sciences of the United States of America, 106(42), 17787-92. PMID: 19805130

December 23, 2009
02:30 AM
1,828 views

Deep Brain Stimulation for Schizophrenia?

by Dr Shock in Dr Shock MD PhD

In short, a recent article proposed to do deep brain stimulation for schizophenia. Schizophrenia has positive-, negative- and cognitive symptoms (see the figure above). The authors propose the DBS for positive symptoms. Their approach is based on current models of the neurocircuitry of psychosis .
They hypothesize:
that chronic, high frequency electrical stimulation (HFS) of [...]

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Mikell, C., McKhann, G., Segal, S., McGovern, R., Wallenstein, M., & Moore, H. (2009) The Hippocampus and Nucleus Accumbens as Potential Therapeutic Targets for Neurosurgical Intervention in Schizophrenia. Stereotactic and Functional Neurosurgery, 87(4), 256-265. DOI: 10.1159/000225979

Bakay, R. (2009) Deep Brain Stimulation for Schizophrenia. Stereotactic and Functional Neurosurgery, 87(4), 266-266. DOI: 10.1159/000225980

December 22, 2009
12:40 PM
504 views

Revisiting the Cause of the Black Death

by Michael Long in Phased

Mark Welford and Brian Bossak (Georgia Southern University) shed doubt on the long-held conclusion that the Black Death was caused by bubonic and pneumonic plague. This news feature was written on December 22, 2009.... Read more »

Welford, M. R., & Bossak, B. H. (2009) Validation of Inverse Seasonal Peak Mortality in Medieval Plagues, Including the Black Death, in Comparison to Modern Yersinia pestis-Variant Diseases. PLoS ONE, 4(12). DOI: 10.1371/journal.pone.0008401

December 22, 2009
12:00 PM
657 views

The Truth About Organic Farming

by Christie Wilcox in Nutrition Wonderland

In the past year or two, certified organic sales have jumped around 30% to about $52 billion (2008 dollars) worldwide despite the fact that organic foods cost up to three times as much as those produced by conventional methods. More and more, people are shelling out their hard-earned cash for Certified Organic. Imagine, people say: you can improve your nutrition while helping save the planet from the evils of conventional agriculture – a complete win-win. And who wouldn’t buy organic, when it just sounds so good?

Here’s the thing: here are a lot of myths out there about organic foods, and a lot of propaganda supporting methods that are rarely understood. It’s like your mother used to say: just because everyone is jumping off a bridge doesn’t mean you should do it, too. Now, before I get yelled at too much, let me state that I’m not trying to say that organic farming is bad – far from it. There are some definite upsides and benefits that come from many organic farming methods. For example, the efforts of organic farmers to move away from monocultures, where crops are farmed in single-species plots, are fantastic; crop rotations and mixed planting are much better for the soil and environment than conventional monocultures. Instead, I only want to point out that not everything is as it seems. So here are som... Read more »

Gold, L., Slone, T., Stern, B., Manley, N., & Ames, B. (1992) Rodent carcinogens: setting priorities. Science, 258(5080), 261-265. DOI: 10.1126/science.1411524

Caboni, P., Sherer, T., Zhang, N., Taylor, G., Na, H., Greenamyre, J., & Casida, J. (2004) Rotenone, Deguelin, Their Metabolites, and the Rat Model of Parkinson's Disease. Chemical Research in Toxicology, 17(11), 1540-1548. DOI: 10.1021/tx049867r

Mukherjee A, Speh D, Dyck E, & Diez-Gonzalez F. (2004) Preharvest evaluation of coliforms, Escherichia coli, Salmonella, and Escherichia coli O157:H7 in organic and conventional produce grown by Minnesota farmers. Journal of food protection, 67(5), 894-900. PMID: 15151224

Fillion, L., & Arazi, S. (2002) Does organic food taste better? A claim substantiation approach. Nutrition , 32(4), 153-157. DOI: 10.1108/00346650210436262

Health

December 22, 2009
11:29 AM
1,089 views

A closer look at the new CDC autism prevalence rates

by Nestor Lopez-Duran PhD in Child-Psych

By now most people interested in autism have read the CDC report, or at least read the news, regarding the new estimated prevalence rates of autism in the United States. Today I finally was able to read the full original report and have some brief general thoughts.
The report is based on the findings by the [...]... Read more »

Kogan, M., Blumberg, S., Schieve, L., Boyle, C., Perrin, J., Ghandour, R., Singh, G., Strickland, B., Trevathan, E., & van Dyck, P. (2009) Prevalence of Parent-Reported Diagnosis of Autism Spectrum Disorder Among Children in the US, 2007. PEDIATRICS, 124(5), 1395-1403. DOI: 10.1542/peds.2009-1522

December 22, 2009
10:05 AM
596 views

Cancer genomes

by Joe Dunckley in Cotch

Since sequencing the human genome, the Sanger Institute in the UK and the US National Human Genome Research Institute have turned their sights -- and their vast sequencing capacities -- to cancer. Cancers can be thought of as genomic diseases, caused by somatic mutations, and progressing by the accumulation of further mutations. Last week, Nature published online the papers describing two new cancer genomes, bringing the total number of human cancer genome sequences published to five...... Read more »

Pleasance, E., Stephens, P., O’Meara, S., McBride, D., Meynert, A., Jones, D., Lin, M., Beare, D., Lau, K., Greenman, C.... (2009) A small-cell lung cancer genome with complex signatures of tobacco exposure. Nature. DOI: 10.1038/nature08629

December 21, 2009
02:35 PM
606 views

Multiple Sclerosis and Irrational Exuberance

by PalMD in White Coat Underground

Multiple sclerosis (MS) is fascinating illness that can range from mild annoyance to debilitating nightmare. The frightening nature and unclear cause of the disease makes it a magnet for questionable medical therapies (i.e. quackery). A piece published last week in (surprise!) the Huffington Post helps fuel the fires of suspicion and paranoia while failing to shed any light on the future of MS research.

Multiple sclerosis is a disease of the nervous system. Its victims develop symptoms based on what part of the nervous system is affected. For example, if MS attacks the optic nerve, a patient may experience blurry vision or blindness. If it affects the motor areas of the brain that controls the left leg, the patient will develop weakness in the left leg. Typically, the symptoms will last a certain period of time and then improve, but often not completely back to normal. The exact initial cause of the disease isn't known, but we do have a good understanding of of how the disease works. In MS, the immune system attacks the sheath surrounding certain types of nerve cells. This leads to "plaques" in nervous tissue such as the brain, and these plaques correspond to the symptoms of MS. The disease appears to result from a combination of a genetic predisposition and some sort of environmental insult, such as a viral infection. Many people have T-cells in their immune system that recognize myelin, the substance attacked in MS, but in MS these T-cells are more capable of attacking myelin. In order to do this effectively they must breach the "blood-brain barrier", a system that keeps the circulation in the brain protected from toxins, infections, and the immune system. In MS, this barrier is breached, perhaps by infection, allowing T-cells into the brain to coordinate an attack on the nerve cells. Based on our still-incomplete knowledge of the disease, we have developed some pretty-effective treatments over the last decade or so. These treatments are based on drugs that affect the immune system. All of these drugs have significant side-effects and none is completely effective. There are probably many different "kinds" of MS based on different genetics and different environmental triggers, so we have a long way to go in understanding the disease and developing treatments.Given the fear and debility associated with the disease, and our still-incomplete knowledge, it's natural for people to look for (and see) patterns where none exist. Diseases like MS attract quackery (such as bee-sting therapy) and conspiracy theories, such as the one in the Huffington Post. It started with an article in the Globe and Mail, Canada's national newspaper. This article detailed new MS research by an Italian doctor named (I kid you not) Zamboni. Dr. Zamboni hypothesizes that MS may be at least partly due to a problem with venous blood flow in the brain, and that a surgical procedure can correct this blood flow and improve MS symptoms. He has done some small studies to evaluate these claims. These studies have not yet been replicated by other researchers, and it isn't clear (at least to me) how plausible his hypothesis is. Still, it is interesting, and the Globe and Mail article was fairly well-written, providing a counter-balance to Zamboni's exuberance:"I am confident that this could be a revolution for the research and diagnosis of multiple sclerosis," Dr. Zamboni said in an interview. Not everyone is so bullish: Skeptics warn the evidence is too scant and speculative to start rewriting medical textbooks. Even those intrigued by the theory caution that MS sufferers should not rush off to get the surgery - nicknamed the "liberation procedure" - until more research is done.The National MS Society (US) is also taking a cautious approach and is facilitating further research into this new theory. "Cautious" is not a word that ever applies to medical reporting in the Huffington Post. Erika Milva vilifies the American press and the MS society blaming entrenched interests for failing to jump on Zamboni's ideas. Of the MS society's statement, Dr. Lorne Brandes, an oncologist who blogs for CTV News' Health Blog, wrote, "If their official response to Dr. Zamboni's research was any cooler, icicles would form on their spokespersons' lips. Why am I not surprised? These organizations are big money operations, run by risk-adverse professionals and fundraisers who are absolutely petrified of making a mistake and prematurely backing a losing horse. Their interests are also heavily intertwined with those of Big Pharma."This is absurd. Advocate groups such as the NMMS are often supported by patients and their families and others who are strongly motivated to get results. The MS society is actively seeking researchers to help investigate these new findings but is cautioning patients not to jump to quickly after unproven therapies. It is important for researchers to think outside the box and we believe Dr. Zamboni has done this. His hypothesis is a pat... Read more »

Frohman EM, Racke MK, & Raine CS. (2006) Multiple sclerosis--the plaque and its pathogenesis. The New England journal of medicine, 354(9), 942-55. PMID: 16510748

Zamboni, P., Galeotti, R., Menegatti, E., Malagoni, A., Tacconi, G., Dall'Ara, S., Bartolomei, I., & Salvi, F. (2008) Chronic cerebrospinal venous insufficiency in patients with multiple sclerosis. Journal of Neurology, Neurosurgery , 80(4), 392-399. DOI: 10.1136/jnnp.2008.157164

Zamboni, P., Galeotti, R., Menegatti, E., Malagoni, A., Gianesini, S., Bartolomei, I., Mascoli, F., & Salvi, F. (2009) A prospective open-label study of endovascular treatment of chronic cerebrospinal venous insufficiency. Journal of Vascular Surgery, 50(6), 1348-1358000. DOI: 10.1016/j.jvs.2009.07.096

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