tag:blogger.com,1999:blog-51375780942882071702024-03-12T22:52:31.575-07:00Where's the beef?A blog about how we know what we know and why we believe what we believe with a focus on anatomy & physiology, especially of runningmiddle.professorhttp://www.blogger.com/profile/02370737843957507859noreply@blogger.comBlogger21125tag:blogger.com,1999:blog-5137578094288207170.post-10982038025221763262012-03-01T06:04:00.000-08:002012-03-01T06:04:36.690-08:00Links<a href="http://www.sciencebasedmedicine.org/index.php/milk-thistle-and-mushroom-poisoning/">herbal medicine/mushroom poisioning/milk thistle</a><br />
<br />
<a href="http://www.sciencebasedmedicine.org/index.php/high-fructose-corn-syrup/">HFCS</a><br />
<br />
<a href="http://www.sciencebasedmedicine.org/index.php/more-breast-cancer-awareness-month-quackery/">Adams/Mercola/breast cancer/IGF-1/Bovine growth hormone/cow's milk</a>middle.professorhttp://www.blogger.com/profile/02370737843957507859noreply@blogger.com0tag:blogger.com,1999:blog-5137578094288207170.post-53543175783582804422010-11-26T14:51:00.000-08:002010-11-26T17:19:17.831-08:00Anecdoctal evidence and the Problem of inferring CauseI'm finally back running after taking a nearly 5 week hiatus due to a self-diagnosed metatarsal stress fracture. The fracture came on quite suddenly during a run at Twin Brook. I completed the run, hoping it would go away. It didn't and I took a break, which was easy enough since all my major fall races were over.<br /><br />I'm quite confident that the cause of the stress fracture was racing the 5K XC race 6 days after my first marathon and then the PT8k a week after that. The body is very good at adapting to stresses and the stress that I was giving my body all summer and fall was running at a steady, marathon (6:40-6:50) pace. Other than the few fun "sprints" (really about 400-800 meters) at Twin Brook, I hadn't run faster than 6:30 for three months, and faster than about 6:05 since Spring. My average pace at the 5K XC race was about 6:15 and the flat and especially downhill sections were significantly faster. My average pace at the 8K was 5:58. My feet weren't adapted for this pounding and the result was the stress fracture.<br /><br />Wait, scratch that paragraph and read this instead:<br /><br />I'm quite confident that the cause of the stress fracture was due to low bone density because of Vitamin D deficiency, as I've unintentionally cut back on the amount of milk that I drink at dinner (replaced largely with wine). Vitamin D deficiency is very, very common and Vitamin D fortified milk is a great source. Vitamin D increases Calcium absorption in the gut. With lower gut absorption, my low blood Calcium levels triggered Parathyroid hormone release, which activates the cells (osteoclasts) that remove the bony matrix from bones, releasing calcium to the other tissues.<br /><br />Wait, scratch that and read this instead:<br /><br />I'm quite confident that the cause of the stress fracture was due to running a road marathon two weeks before the bone finally fractured. I run mostly trails. Indeed, in training for the marathon I only ran two long runs (one 16 miler one 18 miler) on the roads. All my other long runs were on trail. I did run a weekly 10 mile marathon-pace run on the roads. But that was it. Our body is very good at adapting to the stresses we give it and I made the mistake of running a road marathon without training enough on the roads. While I made it through the marathon without incident, I clearly stressed my metatarsals enough that all it took was a little more running to give me the stress fracture.<br /><br />Wait, scratch that and read this instead.<br /><br />I'm quite confident that the cause of the stress fracture was due to changing my form only three weeks before running my first marathon. I was watching good running video and reading some literature on efficient running kinematics and decided that I didn't let my trailing leg extend enough before toe off (actually it's extension at the hip). I worked on this new form both before and during the marathon and two post-marathon races. The more more extended hip places additional stresses on the more dorsiflexed foot. Our body is very good at adapting to the stresses we give it and I made the mistake of racing the marathon and two post-marathon races using my new form without giving my body enough time to adapt.<br /><br />Wait, scratch that and read this instead.<br /><br />I'm quite confident that the cause of the stress fracture was due to trying out a new, minimalist shoe that I had received for review. I typically run in racing flats of various sorts, such as the NB 790 and 100 on the trail and the Asics Piranha and Hyperspeed on the road. Prior to this year, I also typically did 1-2 barefoot cooldowns per week but because of a bruised left forefoot (from landing on a rock while running downhill) I had not done any barefoot runs at all this summer or fall. The new minimalist shoes have zero cushion - they are simply a vibram sole with some cloth that wraps that foot. After receiving the shoes, I immediately went out and did some 5-8 mile runs. Our body is very good at adapting to the stresses we give it but I made the mistake of running in the cushionless, minimalist shoes without properly building up to the novel stresses that these placed on my foot.<br /><br />Wait, scratch that and read this instead<br /><br />I'm quite confident that the cause of the stress fracture was running with tight calf muscles following my first marathon. This calf tightness was new to me, so I was surprised to have it persist for over two weeks - up until the day that I stopped running in fact. I have no idea what the connection between tight calves and metatarsal stress fracture is, but I've repeatedly read that tight calves is a risk for metatarsal stress fracture on the web.<br /><br />OK, ok. What is the point of all of this? Quite simple - all of these explanations make plausible stories. And importantly, that's what humans do, <a href="http://www.nytimes.com/2007/08/21/science/21magic.html?8dpc=&pagewanted=all">we create stories to explain events</a>. The actual cause of my stress fracture may be one of these that I've listed, or some combination, or none. I simply don't know. Running injuries have complex causes and there are always numerous, plausibly causal antecedents. Why do people tend to assign cause to a single antecedent? I would argue it's the antecedent most consistent with the person's world view. So we often hear: "this hip muscle imbalance gave me this knee injury" or "this drink made me recover faster" or "this workout made me run faster." Quite remarkably, world view often trumps plausibility.<br /><br />I don't really care that individuals make up stories to explain events in their life. We all do this. <a href="http://www.nytimes.com/2007/08/21/science/21magic.html?8dpc=&pagewanted=all">It's part of being human</a>. The problem is when these anecdotal stories determine how professionals in the health sciences - broadly and liberally defined - practice health care.middle.professorhttp://www.blogger.com/profile/02370737843957507859noreply@blogger.com4tag:blogger.com,1999:blog-5137578094288207170.post-28940923630475515452010-11-22T19:13:00.001-08:002010-11-23T13:39:26.097-08:00Is high fructose corn syrup (HFCS) eviler than sugar?This is a long critique of Bocarsly et al 2010 “High-fructose corn syrup causes characteristics of obesity in rats: Increased body weight, body fat and triglyceride levels” published in Pharmacology, Biochemistry, and Behavior, which is edited by G.F. Koobs (full paper <a href="http://www.foodpolitics.com/wp-content/uploads/HFCS_Rats_10.pdf">here</a>).<br /><br />I am moved to write this critique not because I have a dog in this fight but because I teach Human Anatomy & Physiology to students who come in with very rigid misconceptions about health and disease and who will communicate these misconception to their patients/clients/athletes unless the misconceptions are addressed in the classroom and on the web.<br /><br />The title of the paper should not raise an eyebrow among physiologists. Indeed, the role of carbohydrates and especially sugars regulating appetite and satiation would seem to be a fascinating and important field of study. Even the abstract is not at all controversial. But the paper doesn’t simply claim that access to HFCS makes rats fat but that this effect is found only in HFCS and not sucrose. And it is this claim that was promoted in the first sentence of the <a href="http://www.princeton.edu/main/news/archive/S26/91/22K07/index.xml?section=topstories">Princeton University press release</a> “A Princeton University research team has demonstrated that all sweeteners are not equal when it comes to weight gain: Rats with access to high-fructose corn syrup gained significantly more weight than those with access to table sugar, even when their overall caloric intake was the same” and emphasized by the PI, Bart Hoebel (from the same release): "Some people have claimed that high-fructose corn syrup is no different than other sweeteners when it comes to weight gain and obesity, but our results make it clear that this just isn't true, at least under the conditions of our tests," said psychology professor Bart Hoebel.<br /><br />The claim that the metabolic consequences of HFCS and sucrose differ radically should raise eyebrows among physiologists. While I’d be skeptical of any results that find a difference, I would find good evidence for differences fascinating and it would make a great conversation in my A&P class. I’m not a carbohydrate physiologist but I can, nevertheless, come up with three hypotheses that might explain differences between HFCS and sucrose. Differences between sucrose and HFCS on oral receptors or the small differences in the proportions of glucose to fructose in the stomach and small intestine have (1) large effects on carbohydrate and lipid metabolism or (2) the hormonal regulation of appetite or (3) the hormonal regulation of activity metabolism. Hypotheses (1) and (2) seem unlikely given that the authors also claim that the total caloric intake did not differ between rats given access to HFCS and sucrose. So if I were a metabolic physiologist, I might be tempted to look into how HFCS makes rats less active.<br /><br />Except that I wouldn’t because after reading the paper, I would note that the experimental design, statistical analysis, and interpretation of the results in Bocarsly et al 2010 are deeply flawed. Indeed, the elementary flaws in the statistical analysis and the absence of any discussion of the glaring paradoxes in the results combined with a much higher rigor of analysis and interpretation in the senior authors’ previous papers raises several ethical questions that will be addressed at the end.<br /><br />Finally, I am not taking any time to better organize this critique because it has taken far too long to simply comment on all of the errors. There are also numerous small errors in presentation, analysis, and interpretation that I do not raise here because of time and space. It's also written as if I were asked to peer review it for the journal. Which is a good thing because while the ms may have been peer read and okayed, it certainly wasn't peer reviewed.<br /><br /><b>Flaws in the design and statistical analysis of Experiment 1<br /></b><br />Experimental Design. The experiment lacks a 24-h Sucrose treatment and thus any interpretation of the 24-h HFCS treatment confounds two potential factors, time (12-h v. 24-h) and sugar (HFCS v. sucrose).<br /><br />Statistical Analysis<br />Result 1. “Animals with 12-h 8% HFCS access gained significantly more weight in 8 weeks than animals with 12-h 10% sucrose access (F(2,25) = 3.42; P less than 0.05).” The authors do not give test results for any of the other comparisons. The authors do not give either the effect size or the raw or percent increase in weight in any of the treatment levels. The authors do not provide a chart showing the response by treatment level. The authors do give a table of the final weight of the four treatment levels, which is worth looking at here, but will be discussed in more detail below.<br /><a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEhhS1pDA87wFK9KLsF9q76nasYt4-pOyUNJprRPDSlaMFYHzfpHsMd94aKZQLLOZzeHfLQNJs3_MGUaEO7JAtHKO-9QdoH_yO5D97j49kuda76jNxeJL7MrKg_nInn7YhDk9WjdyWDTyKrP/s1600/Picture+667.png"><img style="margin: 0px auto 10px; display: block; text-align: center; cursor: pointer; width: 400px; height: 244px;" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEhhS1pDA87wFK9KLsF9q76nasYt4-pOyUNJprRPDSlaMFYHzfpHsMd94aKZQLLOZzeHfLQNJs3_MGUaEO7JAtHKO-9QdoH_yO5D97j49kuda76jNxeJL7MrKg_nInn7YhDk9WjdyWDTyKrP/s400/Picture+667.png" alt="" id="BLOGGER_PHOTO_ID_5542595375808936738" border="0" /></a>We are not given what the errors are (Given the one reported F statistic, I think it’s safe to assume that these are one standard error of the mean). Of course, to analyze or interpret this table, we would need either the initial mean weights or make the assumption that the initial mean weights were exactly the same. The authors do state that the intial groups were weight matched, so we’ll have to assume that the match was close enough to not effect the statistics. The asterisk for the 12-h HFCS treatment level indicates <i>P</i> less than 0.05 for the comparison with the chow only treatment level. Note also that the asterisk signifies a different comparison than the significant result reported in the text (and quoted above).<br /><br />For the one comparison with statistics given (12-h HFCS v. 12-h Sucrose), the actual P value for F(2,25) is 0.049, which is, indeed, less than the traditional acceptable type I error rate (0.05) but doesn’t give me much confidence in the conclusions given the claim that 55% fructose has a metabolic effect while 45% fructose does not. Given that table one is the raw endpoint weight, I also have less than perfect confidence that the statistics were computed on the actual weight gain (or percent weight gain) and not simply on the endpoints. Were the P-value really low, this wouldn’t matter. Given that the P-value is 0.049, my concern matters.<br /><br />Regardless, there are two egregious errors with the F statistic and the interpretation of the associate P-value. First, the F statistic is compared to a distribution using 2 and 25 degrees of freedom (df) but given two means and 10 animals per group the correct df should be 1 and 18. Assuming F = 3.42, the correct P-value, with 1 and 18 df, is 0.081, which fails to reject the null hypothesis if we follow the traditional frequentist interpretation. Given the author’s report of 2 and 25 df, I’m not confident in the value of the F statistic (3.42) itself as the df suggests that some other combination of individuals might have been used. Here’s one interpretation: the F statistic is based on an ANOVA with both HFCS treatments and the Sucrose treatment in the model and there is missing data. If this is what was done, then the P value says nothing about which one of the treatment levels differs, only that there is a difference somewhere. This is what posthoc tests are for. This is textbook Stats 101. But maybe I’ve guessed incorrectly how they came up with a F test with 2 and 25 df.<br /><br />Second, and most importantly, because this is relevant to all of their results, the authors either fail or make no mention of controlling for type I error using something like a Tukey-HSD test, <a href="http://scholar.google.com/scholar?as_q=tukey&num=10&btnG=Search+Scholar&as_epq=&as_oq=&as_eq=&as_occt=any&as_sauthors=hoebel&as_publication=&as_ylo=&as_yhi=&as_sdt=1.&as_sdtp=on&as_sdts=20&hl=en">a test the authors have used previously</a>. Given four means, there are six possible pairwise comparisons, all of which are orthogonal and all of which are of interest. The type I error rate given six orthogonal comparisons is 26.5%, well above the 5% assumed by the authors.<br /><br /><br />From table 1, I have computed the Tukey’s HSD for each comparison, as well as the more powerful Ryan’s Q, the Games & Howell modification of Tukey HSD for heterogenous variances, and a simple (naive) t-test with the SE and df computed for that comparison only. These computations assumed a sample size of 10 rats per group, even though there are several statistics that the authors report that suggest that they have missing data (not 10 rats per group), so my P-values will be liberal.<br /><a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEhZ28aXdlWmAjm7ndb23NPphJUrRL0YXJE8ZynB-lcC8okmGGEOKTO6UXK4l7-a-89N36Ks-n72mlRaf8Oi8Xasqt9iE8RdevvGrt7Tt_admZ4SO41w0Xz5wGjIVbLqLcjpwF4uPKwbzta2/s1600/Picture+669.png"><img style="margin: 0px auto 10px; display: block; text-align: center; cursor: pointer; width: 345px; height: 400px;" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEhZ28aXdlWmAjm7ndb23NPphJUrRL0YXJE8ZynB-lcC8okmGGEOKTO6UXK4l7-a-89N36Ks-n72mlRaf8Oi8Xasqt9iE8RdevvGrt7Tt_admZ4SO41w0Xz5wGjIVbLqLcjpwF4uPKwbzta2/s400/Picture+669.png" alt="" id="BLOGGER_PHOTO_ID_5542598332186680034" border="0" /></a>I’ll discuss more of this table later but I want to focus on the single comparison reported by the authors, which was 12h-HFCS v. 12h-Sucrose. My simple t-test P-value is slightly less than that computed by the authors, although as discussed above, I’m not sure how they computed F or why they used 2 and 25 df. Regardless, this P-value is less than 0.05, the traditionally acceptable type I error rate. Importantly, the Tukey HSD test and the more powerful Ryan’s Q test fail to reject the hypothesis of no difference between 12h-HFCS and 12h-Sucrose.<br /><br />At best, we can conclude from experiment 1 that there is some evidence that the rats with 12 hour access to HFCS gained more wait than rats in the chow only treatment level. We cannot make this conclusion for the 24h-HFCS rats nor can we conclude that there was a difference in gained wait between the 12h-HFCS and 12h-Sucrose rats. I discuss various interpretations of these results below. While the source of the mistake in the df of the F statistic is a mystery, the failure to account for multiple post-hoc tests is disturbing, especially given the prior use of this adjustment in previous papers by the first author (a graduate student), the 3rd author (a post-doc), and the last author (the PI of the lab). The inflation of type I error with multiple tests and the methods to control this error are not esoteric minutiae only known to the statistical cognoscenti but are covered, often in great detail, in all undergraduate textbooks. The authors cannot claim ignorance<a href="http://scholar.google.com/scholar?as_q=tukey&num=10&btnG=Search+Scholar&as_epq=&as_oq=&as_eq=&as_occt=any&as_sauthors=hoebel&as_publication=&as_ylo=&as_yhi=&as_sdt=1.&as_sdtp=on&as_sdts=20&hl=en"> given their prior use of the Tukey-HSD</a>. I’ll leave it to the authors to explain why they ignored the Tukey-HSD in this paper.<br /><br />Result 2. “There was no overall difference in total caloric intake (sugar plus chow) among the sucrose group and two HFCS groups.” Remarkably, the authors do not give any statistics to support this. There is no P value, or test statistic, or effect size, or confidence limits, or group means, or a chart showing total caloric intake as a function of treatment level. No statistics are reported for any of the other sorts of comparisons. The statement is simply baldly asserted with no evidence. Given the author’s assertion that the HFCS rats gained more weight than the sucrose or chow only rats, the statement that the total caloric intake did not differ is a really extraordinary result (with emphasis on the extra). In his reply to Mari<a href="http://www.foodpolitics.com/2010/03/hfcs-makes-rats-fat/">on Nestle’s concern</a> with the study, the PI and last author states “As commonly done, we did not present the overall caloric intake since there was no difference between groups.” For some uncontroversial result, we might state something like “statistics not given) but the authors are arguing that the 12-hr HFCS rats gained more weight but consumed the same number of calories as the 12-hr Sucrose rats, which would be a remarkable result and suggest interesting differences in energetics. This statement begs for evidence. but the authors gave us no data to evaluate the claim. The reason why editors and reviewers (except apparently in this paper) ask for test statistics and sample size and effect sizes and standard errors is because careful readers need these to evaluate the results! Otherwise, we can say whatever fits our view of the way the world works. Was this paper even reviewed?<br /><br />Result 3. “Even though the 12-h HFCS group gained significantly more body weight, they were ingesting fewer calories from HFCS than the sucrose group was ingesting from sucrose (21.3 ± 2.0 kcal HFCS vs. 31.3 ± 0.3 kcal sucrose; F(1,16) = 12.14; <i>P</i> less than 0.01).” Again no attempt to control for Type I error rate. If this was the only comparison they were interested in, why do the other treatment levels? The F statistic here also suggests there are missing data, which supports my interpretation of the F(2,25) statistic above. The authors state that there were 10 rats per treatment level so there should be 18 df in the F test, not 16.<br /><br />Missing Results.<br /><br />The authors give almost no statistics about the other pairwise comparisons between the treatment levels in experiment 1 (that is other than the 12h-HFCS v. 12h Sucrose levels). They do give table one with endpoint weights and standard errors and the one asterisk for the 12h-HFCS vs. Control comparison, so I guess we can infer that the other sugar treatment levels do not differ from the Control but what about 24-h HFCS v. 12h Sucrose or 24-h HFCS v. 12-h HFCS? Where are these statistics? Again, there is no attempt to control for Type I error. Above, I give a table of all pairwise comparisons for endpoint weight, but the authors don’t give the data for me to do something similar for sugar calories or total calories. The relevant statistics are simply not given. Importantly, the authors discuss some of the pairwise comparisons in the discussion but the discussion is not based on any statistical evidence presented in the results!<br /><br />It is important to point out that the measured effect of HFCS effect seems to occur only in the 12-h HFCS rats and not the 24-h HFCS rats, which, if real, would raise some interesting physiological issues. It's also important to point out the opposite pattern is found in the long term experiment. The authors fail to report either of these paradoxes/contradictions, even though it jumps out of Table 1. <a href="http://www.foodpolitics.com/2010/03/hfcs-makes-rats-fat/">Marion Nestle also raises this concern</a>. Hoebel, the PI, responds to Nestle with the statement "Actually, it is well known that limited access to foods potentiates intake. There have been several studies showing that when rats are offered a palatable food on a limited basis, they consume as much or more of it than rats offered the same diet ad libitum, and in some cases this can produce an increase in body weight. So, it is incorrect to expect that just because the rats have a food available ad libitum, they should gain more weight than rats with food available on a limited basis.” First, why didn't the authors discuss this in the paper, since they have an obviously paradoxical pattern? Second, if it's so well known, why wasn't this a prediction or hypothesis from the beginning? Third, Hoebel doesn't address the contradictory, opposite patterns between the short term and long term results (which unfortunately also is confounded by sex, since we cannot compare the long term Sucrose males since this treatment was ignored).<br /><br /><b>Flaws in the design and statistical analysis of Experiment 2<br /></b><br />Design of the experiment.<br />Flaw 1. The authors do not have a 12-h sucrose treatment level in the males “since we did not see effects of sucrose on body weight in Experiment 1 with males.” Uh, there was also no treatment effect for the 24-h HFCS male rats but these were included in experiment two. And presumably there is a reason for conducting a longer term experiment, such as finding a long term effect in 12-h Sucrose males, but this possibility is precluded without including the level in the design. And, since the goal of the paper is to show that HFCS has different consequences than Sucrose, and no Sucrose treatment was done in Experiment two male rats, the whole experiment (on males at least) becomes irrelevant to the paper.<br /><br />Flaw 2. In the female experiment two, there are four treatment levels but the access to Chow differs between these levels (in two, rats have 24-h access to chow but in the other two, rats have only 12-h access to chow). So both sugar and chow are being manipulated but within a single factor design.<br /><br />Statistical Analysis<br /><br />In General. Again, the authors fail to control for type I error using Tukey HSD or similar method. I’ve re-analyzed the enpoint weight data from Table 1 (table above) using Tukey HSD, the more powerful Ryan’s Q, and the Game-Howell modification of Tukey to account for variance heterogeneity. I also add a simple t-test calculated assuming no other groups other than the two under comparison.<br /><br />Experiment 2 males.<br />Result 1. The authors report a difference in both HFCS treatment levels and the Control treatment. Interestingly, they only give one statistic to support this (F(1,14) = 5.07; <i>P</i> less than 0.05), so I’m not sure which comparison this applies to. The df are correct and suggest there are no missing data. Note also that in contrast to Experiment one, the 24-h HFCS rats gain more weight than the 12-h HFCS rats (this is not statistically significant).<br /><br />Result 2. “The difference in body weight was significant by week 3 (F(2,21) = 4.44; <i>P</i> less thant 0.05).” Again the authors report a single statistic for what should be two comparisons. The F statistic with 2 and 21 df suggests that this was based on an ANOVA with all three groups in the model (in which case the df are correct). Again, this P-value does not tell us which of the groups differ from which.<br /><br />Result 3. “As an indication of obesity, the rats with 24-h or 12-h HFCS had significantly heavier fat pads than control rats (F(4,35) = 13.01; <i>P</i> less than 0.01; Fig. 4).” Although all fat pads were heavier, this effect was most pronounced in the abdominal region (F(4,35) = 8.36; <i>P</i> less than 0.05; Fig. 2). It is not clear to me what test the authors did to get F with 4 and 35 df. Again, no post-hoc tests are done.<br /><br />Experiment 2 females<br /><br />Result 1. “female rats with 24-h access to HFCS for 7 months gained more body weight than chow- and sucrose-fed controls (F(1, 14) = 8. 74, <i>P</i> less than 0. 01).” Again there are two comparisons but one statistic. For the 24-h HFCS v. Sucrose, I did not find a statistically significant difference even using a simple t-test that doesn’t account for inflated Type I error (my table above). Using Tukey’s HSD, neither comparison is significant (my table above).<br /><br />Result 2. The authors do not report on other comparisons of weight and, importantly, ignore the result that the 12-h HFCS rats gained less weight than both Control and 12-h Sucrose (not statistically significant using any method). This pattern is the opposite of that in Experiment 1, as discussed above.<br /><br />Result 3. For the comparison of fat pad weight, I still do not know what test they used to get F with 4 and 35 df.<br /><br /><b>Repeated misrepresentation of results in the Discussion.<br /></b><br />The authors state in the introduction to the Discussion that the experiment 1 “male rats with access to HFCS drank less total volume and ingested fewer calories in the form of HFCS (mean = 18.0 kcal) than the animals with identical access to a sucrose solution (mean = 27.3 kcal), but the HFCS rats, never the less, became overweight.” Actually the HFCS rats didn’t ingest fewer calories in the form of HFCS than the Sucrose rats because the latter had none, by design. If the authors meant the HFCS rats ingested fewer calories from the sugar-water, they should have said this. More importantly, the take home message is that the HFCS rats became overweight but the Sucrose rats did not. If we fail to account for multiple tests, this is true only for the 12-h HFCS rats; indeed the 24-h HFCS rats gained less weight on average than the 12-h Sucrose rats. If we account for multiple tests, then none of the treatment levels had a statistically significant effect. But the authors are not simply cherry picking but are explicitly misrepresenting their results: “In these [experiment 1] males, both 24-h and 12-h access to HFCS led to increased body weight.” Actually, no. Even the author’s own table 1 shows this is not true for the 24-h HFCS treatment level. More disturbingly, this practice of cherry picking and misrepresentation is a consistent pattern throughout the discussion.<br /><br />“In Experiment 2 (long-term study, 6–7 months), HFCS caused obesity greater than that of chow in both male and female rats.” This is true only for the male rats. In fact, the 12-h HFCS female rats gained statistically insignifanctly less weight than the Control (chow only). Again, the authors select only the results that are consistent with one conclusion. Interestingly the authors do not compare the HFCS treatments to the sucrose treatment here. Except that they did in the originally published version, which had the same sentence but with “sucrose” instead of “chow”. Yes, in the originally published paper, the authors stated that the long-term HFCS male rats gained more weight than the long-term Sucrose rats, even though the latter weren’t even in the experimental design. The substitution of “chow” for “sucrose” avoids the embarrassing misrepresentation but still is empirically incorrect.<br /><br />“Rats with HFCS access gain more weight than sucrose-consuming rats, even when ingesting fewer calories from their respective sugars”. Again more selective cherry picking of the results.<br /><br /><b>Closing thoughts<br /></b><br />This paper has an unusually rich number of errors in statistical design and analysis, selective picking of results that match what can only be a preferred outcome, and outright misrepresentation of the design and results. The senior authors, the editor handling the paper, the editor-in-chief, the reviewers, the Princeton University press release team, and any science blogs and journalists that uncritically parroted the press release should simply be ashamed.middle.professorhttp://www.blogger.com/profile/02370737843957507859noreply@blogger.com3tag:blogger.com,1999:blog-5137578094288207170.post-76749498744297537022009-11-03T14:50:00.000-08:002009-11-03T15:36:02.258-08:00Injury and the running man theoryJohn Hawkes quite reasonably <a href="http://johnhawks.net/weblog/topics/energetics/endurance-running-parker-pope-2009.html">asked for critiques of Lieberman and Bramble's "endurance running" hypothesis</a> that persistence hunting was a significant factor on the evolution of the various functional systems that contribute to endurance running, and asked, if humans evolved to be long distance runners, why are we so prone to injury? I don't think we have enough data to ask this question, that is, are we prone to injury?<br />1. Injury rates may be high because racing and the training required to race (intervals, tempo runs) stresses the musculoskeletal system well above any safety factor that evolved in response to persistence hunting. High injury rates among racers, then, may not be relevant to the hypothesis.<br />2. I did a quick google scholar search of injury rates among race horses and found "<a href="http://www.ingentaconnect.com/content/evj/evj/2004/00000036/00000004/art00012">fractures and tendon injuries in National Hunt horses in training in the UK: a pilot study</a>" published in the Equine Veterinary Journal. The authors found that 25% of the National Hunt race horses sustained either a fracture or a tendon/ligament injury during a single race season. Should we conclude from these high rates of injury that horses didn't evolve to run?<br />3. What we need are injury rates among runners persistence hunters. Or at least populations that run long slow distance and only LSD. I'm not aware of any of the injury studies that decompose the data in this manner. And anecdotal stories about the tarahumara isn't data. But even the relevance of these injury data collected from people raised on concrete and cars is questionable.<br />4. I'd also be interested in chronic injury rates among endurance mammals such as wolves or wildebeest.<br />5. As with any evolved response, trade-offs occur. What is the fitness cost of plantar fascitis or IT band syndrome?middle.professorhttp://www.blogger.com/profile/02370737843957507859noreply@blogger.com0tag:blogger.com,1999:blog-5137578094288207170.post-73869121121735440692009-10-13T08:21:00.000-07:002009-10-13T08:40:58.996-07:00Red Meat > Fat > Colorectal cancer?I was alerted by google news to an article on the "<a href="http://www.foxnews.com/story/0,2933,562385,00.html">5 healthiest Meats</a>". The article begins with a statement about a recent study showing increased risk of colon cancer in those eating red meat compared to those do not eat red meat. The article then summarizes the "five healthy meats that won’t wreak havoc on your colon". The article gives no review of how these meats are related to risk of colon cancer but only discusses percent fat in each. Wait what? Where in the article did the author state a connection between dietary fat and risk of colon cancer? What absolute lazy science reporting. Five minutes with google scholar and the author could have written a much more informative article.<br /><br />The link between red meat and colon cancer is decades old and reviews of the evidence suggests a cautiously solid association. The association quickly led to the hypothesis that high dietary intake increases risk of colon cancer but recent reviews of both prospective and intervention studies do not support the hypothesis that high dietary fat increases risk of colorectal cancer. Interestingly, at least one intervention study found no decreased risk of colorectal cancer over a 10 year period after replacing meat with vegetables in the diet.<br /><br />The news article highlights the poor training of science journalists. The biomedical literature highlights the difficulty in assessing causation in complex functional systems.<br /><br />A good review is:<br /><span style="font-weight: bold;">Diet, nutrition and the prevention of cancer </span><br /><span style="font-weight: bold;">Timothy J Key, Arthur Schatzkin, Walter C Willett, Naomi E Allen, </span><br /><span style="font-weight: bold;">Elizabeth A Spencer and Ruth C Travis</span><br /><span style="font-weight: bold;">Public Health Nutrition: 7(1A), 187–200</span>middle.professorhttp://www.blogger.com/profile/02370737843957507859noreply@blogger.com0tag:blogger.com,1999:blog-5137578094288207170.post-46279808209854464002009-07-28T14:18:00.001-07:002009-07-28T14:18:47.852-07:00Must read<a href="http://www.csicop.org/si/2009-03/spector.html">http://www.csicop.org/si/2009-03/spector.html</a>middle.professorhttp://www.blogger.com/profile/02370737843957507859noreply@blogger.com0tag:blogger.com,1999:blog-5137578094288207170.post-60374385102912007742009-07-03T09:39:00.000-07:002009-07-03T09:46:55.263-07:00Will this be a weekly drama series?<object width="480" height="295"><param name="movie" value="http://www.youtube.com/v/HMGIbOGu8q0&hl=en&fs=1&"></param><param name="allowFullScreen" value="true"></param><param name="allowscriptaccess" value="always"></param><embed src="http://www.youtube.com/v/HMGIbOGu8q0&hl=en&fs=1&" type="application/x-shockwave-flash" allowscriptaccess="always" allowfullscreen="true" width="480" height="295"></embed></object>middle.professorhttp://www.blogger.com/profile/02370737843957507859noreply@blogger.com0tag:blogger.com,1999:blog-5137578094288207170.post-13840407223054142052009-07-02T13:02:00.000-07:002009-07-07T05:15:43.184-07:00The healing joke to end all healing jokesWith apologies to Joel Grus and his brilliant <a href="http://yrif.org/2009/03/24/the-religious-joke-to-end-all-religious-jokes/">religious joke to end all religious jokes</a>. I wanted to make a specific point to my class and stole his format...<br /><br />A Doctor of Osteopathy (DO), a chiropractor, a physical therapist, a massage therapist, an accupuncturist, a macrobiotic, an herbalist, a medieval court physician, a therapeutic touch practitioner, a scientologist, a Navaho medicine man, a homeopath, a podiatrist, a Christian scientist, a Catholic exorcist, a surgeon, and a physiologist walk into a bar. They overhear a man telling the bartender that his son's lungs are full of phlegm making it difficult to breath and the lungs are chronically infected. The child was also not growing well and had developed distal intestinal obstruction syndrome. Finally, the child is missing his vas deferens and his sweat is very salty.<div><br /></div><div>All the healers thought about the cause of such an odd assortment of symptoms and being betting men, they decided to bet. The DO said "I bet a dollar he has dysfunctional cranial rhythm", and the chiropractor said "I bet a dollar it's a vertebral subluxation", and the physical therapist said "I bet a dollar it's an imbalance between right and lift hip abductor strength”, and the massage therapist said “I bet a dollar it’s a myofascial trigger point”, and the acupuncturist said “I bet a dollar he’s disrupted the circulation of qi along his meridians”, and the macrobiotic said “I bet a dollar the child’s body is in decay because he’s living out of balance with nature and the cosmos”, and the herbalist said “I bet a dollar the kid’s yin and yang are out of balance”, and the medieval court physician said “I bet a dollar he has an imbalance in his four humours”, and the therapeutic touch practitioner said “I bet a dollar that his aura is out of tune” and the scientologist said “I bet a dollar it’s the body thetans”, and the Navaho medicine man said “I bet a dollar the child has a disrupted nilch’i hwii’siziinii”, and the homeopath said “I bet a dollar that the boy has a tubercular miasm”, and the podiatrist said “I bet a dollar the boy has excessive overpronation” , and the Christian scientist said “I bet a dollar the child is full of fear, ignorance, and sin”, and the Catholic exorcist said, “I bet a dollar an evil spirit has invaded the boy’s body”, and the surgeon said, “I don't know the cause but I bet a dollar I can remove the lungs and hook the child up to a lung machine and he'll be alright”, and the physiologist said “I bet a dollar the boy has a mutation in his CFTR gene.”<br /><br />So they went to the boy to search for dysfunctional cranial rhythms, and subluxed vertebrae, and hip muscle imbalances, and myofacial trigger points, and disrupted qi, and bodies out of balance with nature and the cosmos, and yin and yang, and the four humours, and an out of tune aura, and body thetans, and disrupted nilch’I hwii’siziinii, and tubercular miasms, and excessive overpronation, and fear, ignorance, and sin, and evil spirits but none could convince all the others that their prediction was true. Except the physiologist who correctly predicted the boy would have a mutated CFTR gene. She won $16 that day.</div>middle.professorhttp://www.blogger.com/profile/02370737843957507859noreply@blogger.com0tag:blogger.com,1999:blog-5137578094288207170.post-40917678773758059752009-07-02T11:50:00.001-07:002009-07-02T11:50:58.722-07:00Do naturopaths wear eyeglasses?well?middle.professorhttp://www.blogger.com/profile/02370737843957507859noreply@blogger.com0tag:blogger.com,1999:blog-5137578094288207170.post-68600762474395811722009-07-01T12:17:00.001-07:002009-07-02T13:19:32.513-07:00Dr. Rob Rinaldi on how to reduce running injuries<a onblur="try {parent.deselectBloggerImageGracefully();} catch(e) {}" href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEiX_ojwepXP1RS3AN-DCZ8Co38i5cJKPM7EsoJJ4hHoR_z4qF-7Y3eKF4fN2M9qhD97-dMUaS0XZ12bhYRsUbbuSIO0Q0hpfOel3Xy-y4BZTSAod0ZOzSNQGpTMmy7uQTi_y7u2WWooxIwx/s1600-h/+01*golden_ass_award.jpg"><img style="margin: 0pt 0pt 10px 10px; float: right; cursor: pointer; width: 233px; height: 320px;" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEiX_ojwepXP1RS3AN-DCZ8Co38i5cJKPM7EsoJJ4hHoR_z4qF-7Y3eKF4fN2M9qhD97-dMUaS0XZ12bhYRsUbbuSIO0Q0hpfOel3Xy-y4BZTSAod0ZOzSNQGpTMmy7uQTi_y7u2WWooxIwx/s320/+01*golden_ass_award.jpg" alt="" id="BLOGGER_PHOTO_ID_5353598277613325330" border="0" /></a>The <a href="http://blogs.discovermagazine.com/badastronomy/2009/02/07/did-the-founder-of-the-antivax-movement-fake-autism-vaccine-link/">Andrew Wakefield </a>golden ass award goes to Dr. Rob Rinaldi, DPM, for making the claim that <a href="http://www.vtsports.com/articles/prevent-85-percent-all-running-injuries">85% of all running injuries could be prevented</a> if we'd only run in the right shoes (that is matching our foot kinematics with the shoe). Where did mr. Rinaldi get the 85% figure? Not from any research because there isn't any that would support this claim. But alot of the beginning of his article talks about his <span style="font-weight: bold;">gut feeling,</span> so most likely, <a href="http://en.wikipedia.org/wiki/Anus">he pulled it from where he felt it</a>.<br /><br />Although there are <a href="http://where-is-the-beef.blogspot.com/2009/06/running-shoes.html">zero papers showing that correctly matched running shoes reduce injury rate</a>, there is a single paper, published in 2006 and available to Rinaldi when he did his 10 months of research for the article, showing that runners fit by the Sports Science Institute of South Africa Sports Medicine running shoe clinic had an equal frequency of injuries in the year following shoe purchase to matched runners that had not been to the clinic. Since some of the control group (those that had not been to the clinic) were getting professional advice on shoe fit, we might expect the difference in injury rate to be small. Indeed, if all of the control runners were getting professional advice, we expect the injury difference to be zero (assuming the advice was the same).<br /><br />So maybe both groups were just getting good advice and the frequency of injury in both groups was low? The authors do not report the percentage of runners who were injured in the year following running shoe purchase, only the raw number of total injuries. The shoe-clinic group had 93 injuries and 94 runners. The control group had 115 injuries and 83 runners (note that the control group ran more and the frequency of injury/running day were very close). Clearly some runners had multiple injuries. Regardless, these must reflect high injury rates (typical statistics are something like 50-80% or runners are injure per year). So there is no evidence from this one study that correctly matching foot kinematics to running shoe will reduce injury rates <span style="font-weight: bold;">at all</span> much less 85%.<br /><br />Schwellnus, MP and G Stubbs (2006). Does running shoe prescription alter the risk of developing a running injury? International SportMed Journal, Vol.7, pp. 138-153.middle.professorhttp://www.blogger.com/profile/02370737843957507859noreply@blogger.com0tag:blogger.com,1999:blog-5137578094288207170.post-66441109570690293162009-06-28T09:17:00.000-07:002009-07-02T13:19:12.321-07:00Engage Gluteus Maximus for Piriformis Injury?I was googling piriformis and roller skiing yesterday because I thought I might go out for an inline skate (don't have roller skis) instead of a run. I came across<a href="http://www.easyvigour.net.nz/fitness/h_gluteus_max_piriformis.htm"> this page</a>, a personal testimony of how one guy (thinks that he) solved his piriformis injury. His logic goes<div><br /></div><div>1. I never get butt soreness when I alpineer</div><div>2. I always wear a backpack when I alpineer</div><div>3. Wearing a backpack causes me to activate my gluteus maximus</div><div>4. Therefore, activating the gluteus maximus has allowed me to alpineer injury free</div><div>5. Consequently activating the gluteus maximus during activity<span class="Apple-style-span" style="font-style: italic;"> </span>will allow me to recover from piriformis injury and remain injury free in the future.</div><div><br /></div><div>Hmm? #4 simply doesn't follow from the premises (#1-3). Its a typical case of <span class="Apple-style-span" style="font-style: italic;"><a href="http://en.wikipedia.org/wiki/Post_hoc_ergo_propter_hoc">post hoc ergo propter hoc</a></span>. Lots of things occurred prior to his not getting injured. Maybe it was the pollen from the lovely alpine flowers. But I guess it allows us to start somewhere. But a problem is that the <a href="http://www.ncbi.nlm.nih.gov/pubmed/16709916">gluteus maximus is activated during running</a> but runners get piriformis injury. Lots of sights claim downhill running can aggravate the piriformis - is this because the g. maximus is not active?<br /></div>middle.professorhttp://www.blogger.com/profile/02370737843957507859noreply@blogger.com0tag:blogger.com,1999:blog-5137578094288207170.post-21722115847024778042009-06-26T17:45:00.000-07:002009-07-02T13:18:43.414-07:00Born to Run<a onblur="try {parent.deselectBloggerImageGracefully();} catch(e) {}" href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEhDzBI_jEHfYc1TGw4Xq1akZis22PcXOmjjqYcHKiseS8QZBQuVSnmZad-AMvd-PMk8tcASO9XMp4zGfcRDvdp8e_uWcMP0tRva_K4eDlDTzS9RhZ0zegU6lO2-L3XPSsoDxk4b3OeX841R/s1600-h/+41fpSM7oO2L._SS500_.jpg"><img style="margin: 0pt 0pt 10px 10px; float: right; cursor: pointer; width: 218px; height: 320px;" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEhDzBI_jEHfYc1TGw4Xq1akZis22PcXOmjjqYcHKiseS8QZBQuVSnmZad-AMvd-PMk8tcASO9XMp4zGfcRDvdp8e_uWcMP0tRva_K4eDlDTzS9RhZ0zegU6lO2-L3XPSsoDxk4b3OeX841R/s320/+41fpSM7oO2L._SS500_.jpg" alt="" id="BLOGGER_PHOTO_ID_5351821392970060610" border="0" /></a><a href="http://www.amazon.com/gp/product/0307266303?ie=UTF8&tag=whersthebeef-20&linkCode=as2&camp=1789&creative=390957&creativeASIN=0307266303">Born to Run: A Hidden Tribe, Superathletes, and the Greatest Race the World Has Never Seen</a><img src="http://www.assoc-amazon.com/e/ir?t=whersthebeef-20&l=as2&o=1&a=0307266303" alt="" style="border: medium none ! important; margin: 0px ! important;" border="0" height="1" width="1" /><br />by Chris McDougall has the difficult task of living up to its reputation. After the first few chapters, I had my doubts that it could. But doubt gave way to intrigue, then to fun, and then thrill. The book reads like a novel. It's hard to put down, because the short chapters end with little mysteries that are only uncovered in the next chapter. Kinda like The DaVinci Code, only better. Two chapters could be excerpted as stand-alone essays, one on running shoes and injury, and one on the <a href="http://www.nature.com/nature/journal/v432/n7015/full/nature03052.html">running man theory of human bipedalism</a>. The running man chapter should be nominated for the Best American Science Writing series.<br /><br />That said, I do have some criticisms. I'm skeptical of the romantic portrait of the tarahumara that McDougal paints, but that is a small issue. I'm also skeptical that the tarahumara do not get running injuries. McDougal states this several times but doesn't offer any evidence other than anecdote. Indeed, one of the tarahumara has a typical running injury during the Leadville race but this is dismissed as a function of running in running shoes for the first time. But he was also running in Colorado for the first time so maybe that was the cause? Or more likely, Tarahumara are humans like the rest of us and get injured. This is an important point because McDougal is building the case that there is way to run injury free, and this way includes both running techique and avoiding modern running shoes. McDougal quite correctly asks why running isn't like every other sport, that is, one requiring practice of a certain techniqe. Nevertheless, while the evidence that certain kinematics (such as "overpronation") cause injury is, essentially non-existent, there also isn't good evidence that running a certain way (such as chi or pose running) reduces injury. Ditto for shoes. McDougal makes the oft-heard claim among barefoot runners that running injuries have increased since the advent of the modern shoe. I've not found the citation documenting this but even if it is true, that doesn't necessarily implicate the modern running shoe. Since the 70s (when the first modern shoes started to appear), americans have also gained alot of weight and become more sedentary. We drive cars *everywhere*. And modern marathon advertisers have spent big money to get the couch-to-5K crowd running 26.2. So while I'm sympathetic to the idea that certain running kinematics and retro shoes are less likely to contribute to injury, I want to emphasize "contribute" because the one variable that we do know that causes an increased rate of running injury is running itself.<div><br /></div><div>But I shouldn't (and didn't) focus on the science. It is part of the message but not critical. What is the message? That running is fun (indeed it evolved to be fun). Mixed in with the message and the science are fun biographies/stories of some of the big names and personalities in the sport of ultrarunning. And fun histories of some of the big ultra races. But the story behind the story is the mysterious Caballo Blanco and his quest to get the best North American ultrarunners to race in his Copper Canyon ultramarathon with the turahumara runners. The science, the biographies, the histories weave in and out of this central story and the story doesn't close, as it should, until the final chapter. It's a fun run to the finish.</div>middle.professorhttp://www.blogger.com/profile/02370737843957507859noreply@blogger.com0tag:blogger.com,1999:blog-5137578094288207170.post-26856347717859758702009-06-17T13:44:00.000-07:002009-07-02T13:18:07.952-07:00Running ShoesI finally opened my May 2009 issue of Outside magazine and turned immediately to "Spectrum: different runners require different shoes. Our guide to your perfect fit". The single page highlights three shoes, one lightweight cushiony trainer for the neutral runner, one stability shoe, and one motion control shoe. Note that the lightweight trainer is 12 oz (341 grams). Note also that they state that, combined, 80-85% of runners need a shoe to deal with moderate to severe overpronation. I'm sure this statistic is accurate, but the immediate response should be, "wait what?" If 80% of overpronate, maybe overpronation is not so bad?<br /><br />I'm picking on Outside but they're just parroting the dogma from nearly every running shoe company, shoe store fit specialist, podiatrist, sports medicine M.D., chiropractor, and textbook. The only contrarians seem to be the loud-mouthed minimalists on letsrun.com, the hippy barefoot runners, and everyone who has recently read <a href="http://www.amazon.com/gp/product/0307266303?ie=UTF8&tag=whersthebeef-20&linkCode=xm2&camp=1789&creativeASIN=0307266303">Born to Run</a>. But given the universal acceptance of the "personally fit running shoes are necessary to reduce injury" model, you'd think there would be more evidence for this than something like, say, the <a href="http://www.skepdic.com/psychic.html">ability of psychics to predict the next bus bombing</a>. Here is the abstract of a recent paper from the British Medical Journal.<br /><br /><div class="slugline"> Published Online First: 18 April 2008. doi:10.1136/bjsm.2008.046680<br /> <i>British Journal of Sports Medicine</i> 2009;<b>43</b>:159-162 <div class="copyline">Copyright © 2009 BMJ Publishing Group Ltd & <a href="http://www.basem.co.uk/">British Association of Sport and Exercise Medicine</a>.</div> </div> <!--/slugline--> <h2 style="font-weight: normal;">Reviews</h2> <h3 style="font-weight: normal;"> Is your prescription of distance running shoes evidence-based?</h3> <p class="author_group"> C E Richards<strong><sup>1</sup><sup>,2</sup></strong>, P J Magin<strong><sup>1</sup></strong> and R Callister<strong><sup>2</sup></strong> </p> <p> <sup>1</sup> Discipline of General Practice, School of Medicine and Public Health, University of Newcastle, Australia<br /><sup>2</sup> School of Biomedical Sciences, University of Newcastle, Australia </p> <p>Correspondence to:<br />Dr C Richards, Discipline of General Practice, Bowman Building, School of Medicine and Public Health, University of Newcastle, University Drive, Callaghan 2308, Australia; <span id="em0"><a href="mailto:craig.richards@newcastle.edu.au">craig.richards@newcastle.edu.au</a></span><script type="text/javascript"><!-- var u = "craig.richards", d = "newcastle.edu.au"; document.getElementById("em0").innerHTML = '<a href="mailto:' + u + '@' + d + '">' + u + '@' + d + '<\/a>'//--></script></p> <!-- ABS --> <p> <b>Objectives: </b>To determine whether the current practice of prescribing distance<sup> </sup>running shoes featuring elevated cushioned heels and pronation<sup> </sup>control systems tailored to the individual’s foot type<sup> </sup>is evidence-based.<sup> </sup></p><p> <b>Data sources: </b>MEDLINE (1950–May 2007), CINAHL (1982–May 2007),<sup> </sup>EMBASE (1980–May 2007), PsychInfo (1806–May 2007),<sup> </sup>Cochrane Database of Systematic Reviews (2<sup>nd</sup> Quarter 2007),<sup> </sup>Cochrane Central Register of Controlled trials (2<sup>nd</sup> Quarter<sup> </sup>2007), SPORTSDiscus (1985–May 2007) and AMED (1985–May<sup> </sup>2007).<sup> </sup></p><p> <b>Review methods: </b>English language articles were identified via keyword and medical<sup> </sup>subject headings (MeSH) searches of the above electronic databases.<sup> </sup>With these searches and the subsequent review process, controlled<sup> </sup>trials or systematic reviews were sought in which the study<sup> </sup>population included adult recreational or competitive distance<sup> </sup>runners, the exposure was distance running, the intervention<sup> </sup>evaluated was a running shoe with an elevated cushioned heel<sup> </sup>and pronation control systems individualised to the wearer’s<sup> </sup>foot type, and the outcome measures included either running<sup> </sup>injury rates, distance running performance, osteoarthritis risk,<sup> </sup>physical activity levels, or overall health and wellbeing. The<sup> </sup>quality of these studies and their findings were then evaluated.<sup> </sup></p><p> <b>Results: </b>No original research that met the study criteria was identified<sup> </sup>either directly or via the findings of the six systematic reviews<sup> </sup>identified.<sup> </sup></p> <b>Conclusion: </b>The prescription of this shoe type to distance runners is not<sup> </sup>evidence-based.middle.professorhttp://www.blogger.com/profile/02370737843957507859noreply@blogger.com0tag:blogger.com,1999:blog-5137578094288207170.post-89532141079824401282009-06-16T11:58:00.000-07:002009-07-02T13:20:42.240-07:00Do any of us know what we're talking about?First, <a href="http://www.nytimes.com/2009/05/28/health/nutrition/28best.html">a link to a recent Gina Kolata article</a> on "bad advice" from sport health professionals. The problem is more insidious than bad advice. It's that the empirical evidence behind the efficacy of most everything in sport performance, health, injury, and recovery is, at best, weaker than than a <a href="http://en.wikipedia.org/wiki/Homeopathy">30c homoepathic dilution</a>*. I was searching the letsrun.com forum the other day to read people's experiences with piriformis pain. I wasn't looking for solutions, I just wanted to know if people had run through the injury successfully. But reading people's solutions to the injury was a microcosm of the problem outlined in Kolata's article.<br /><br />• Do these stretches (link to stretches) because the muscle needs to be loose and flexible to recovery and remain healthy. Definitely don't do strength exercises becaus tight, inflexible muscles are what's causing the pain in the first place<br />• Do these strength exercises (link to strength exercises). You need a strong core to allow the weakened muscle to recover and reduce future injury. Definitely do not stretch it because you will tear scar tissue in the weakened muscle.<br /><br />More generally, there is a huge industry of health care professionals and gadget makers throwing advice at us on how to reduce the probability of injury. Stretch! Orthotics! Core Strength! Pose (or Chi) running! Barefoot! Nike Free! Medial Posting! 300-500 Miles! Compression Shorts! The list is endless.<br /><br />Let me compare the sports medical advice with something like the advice to take vaccines. The flu vaccine has an efficacy of <a href="http://en.wikipedia.org/wiki/Influenza_vaccine">50-75%</a>. The polio vaccine has reduced the rate of polio cases from ><a href="http://en.wikipedia.org/wiki/Polio">100,000 year to ~1000/year</a>. The smallpox vaccine has reduced smallpox from ><a href="http://en.wikipedia.org/wiki/Smallpox">50,000,000/year to ZERO</a>.<br /><br />So my question to M.D.s, chiropractors, yoga gurus, podiatrists, sport shoe companies, physical therapists, and CW-X, is, if your advice reduces running injuries, how come we're not seeing fewer injured runners?**<br /><br />Finally, Kolata's article goes well with my post yesterday. Too few of us really challenge our own beliefs with hard data.<br /><br />*a 30C dilution is a solution that has been diluted 1/100, thirty times. The probability that a single molecule of the solute remains in the water is fantastically small. Now that is a weak solution!<br /><br />*There is good evidence that running less reduces the rate of injuries.middle.professorhttp://www.blogger.com/profile/02370737843957507859noreply@blogger.com0tag:blogger.com,1999:blog-5137578094288207170.post-40674672986438104242009-06-16T11:14:00.000-07:002009-06-16T11:58:41.645-07:00Quck Links<a href="http://www.skeptic.com/eskeptic/09-05-20#feature">On Placebo</a>. A great summary of the placebo effect with many implications in sport health and injury.<br /><br /><a href="http://www.nytimes.com/2009/06/16/health/16alco.html?ref=science">Does drinking a moderate amount of alcohol increase health?</a> A nice summary with a healthy dose of skepticism thrown at the moderate alcohol -> healthier body studies.middle.professorhttp://www.blogger.com/profile/02370737843957507859noreply@blogger.com0tag:blogger.com,1999:blog-5137578094288207170.post-14225864969069853472009-06-15T06:34:00.000-07:002009-06-15T11:14:21.696-07:00Inferring cause when there is a delay between cause and effectHumans have evolved mental tools to seek causation from complex patterns. But the identification of causation is difficult when the effect is temporally distant from the many potential causes. For example, I've had a mildly sore piriformis m. for the last month. Friday morning, the soreness was much worse than the previous few days. My inference engine went to work to understand why, so I could avoid the cause and not repeat the pain. This is what humans do. It's what all animals do, it's just that the process rises to consciousness in humans (if not some other animals).<br /><br />So what had I done to augment the soreness? Well, I <a href="http://www.pfitzinger.com/labreports/water.shtml">pool ran</a> for the first time in over a year on Wednesday, and pool ran again on thursday. To get a good workout pool running, you need to have very fast turnover. I ran Tuesday evening, 5 miles and easy, on grass. I hadn't run in 8 days prior to this. I went to the sports medicine doctor on Thursday morning, and in her series of diagnostic tests, she asked/facilitated various explosive jumps and deep stretches. And finally, I was reading about how letsrun.com posters had dealt with piriformis issues and I tried a few of the stretches that several posters swore by. There are many other antecedents that could effect pain (sleep patterns? stress? diet? sitting on the couch all day thursday? maybe just the way I slept or got out of bed that morning?) but this is a pretty good start. But how do I "know" which of these activities to avoid in the future to keep from aggravating my piriformis?<br /><br />Humans will combine experience with biases (preconceived ideas or beliefs) to infer cause. If a belief is strong enough, it probably would not even occur to the person that there are multiple potential independent and interacting causes. The one prior event that matches the belief is recalled to memory but the other events are left in the dustbin of the brain. This is an example of the well-known and pervasive "confirmation bias". Confirmation biases reinforce prior belief and make alternative causes even less likely to be believed.<br /><br />But I'm well trained to seek multiple potential causes - that's what I do for a living (although the discounting of some potential causes such as sleep, stress, and diet, and the complete refusal to even entertain planetary alignment & evil demons reflects my own set of beliefs). So I list out potential causal candidates, like I did above. But these causal candidates are a tiny fraction of the literally thousands of activities that I've engaged in over the last few days. The ones I listed reflect my own biases. Note that I put sleep, and stress, and diet in parentheses because I don't believe these as serious candidates for this case. Also note that I would never even entertain the possibility of an imbalance in my <a href="http://en.wikipedia.org/wiki/Humorism">humors</a>, <a href="http://en.wikipedia.org/wiki/Vertebral_subluxation">spinal misalignment</a>, or <a href="http://en.wikipedia.org/wiki/Qi">qi</a>, much less something like planetary alignment or evil spirits.<br /><br />So I turn to my experience (or maybe the experience of others). Of course it is these experiences that shape our biases, which in turn, shape our experiences (that is the strength of the memory of past events will be a function of our biases). But let's pretend my experience is objective. I've not had a sore piriformis before but I have had this injury wax and wane over the past month. What are the common activities that occurred prior to soreness feeling worse? Again, I simply cannot ask this objectively because the ability to recall activities in memory reflects my beliefs. So I turn to my logbook. But I write very little in my logbook with no notes at all on my diet, sleep, feeling of stress, etc., etc., etc. Regardless, certainly there are far too many common antecedents, most unrecognized, to infer causation with an confidence. My belief structure rejects most of these antecedents and narrows the list down to the few that fit my worldview (overuse and stretching) And now my inference engine looks for consistency; which of these consistantly preceded augmented soreness? That is our brain is searching for a pattern. Psychologists have a field day with freshman classes showing how humans frequently find patterns (associations between events) when non actually exist. There is too little data (coincidence between activity and increased soreness) and too much noise (all the spuriously correlated activities that have nothing to do with soreness and all of the un-recalled variables that might have contributed to the soreness). It's a futile exercise if the signal-to-noise ratio is low (I'll write about a case with a high signal-to-noise ratio later).<br /><br />The point of all of this is, our ability to infer causation using our own experience when the effects are temporally far removed from the cause is utterly confounded by our belief structure and our proclivity to find pattern when none exists. If we want to know what works (avoiding injury, recovering from injury, performing at peak ability) in sport, then we have to exploit the methods of inference that overcome the many cognitive biases and illusions. These methods are the manipulative experimental methods of science.<br /><br />Unfortunatly, we cannot do most of the manipulative experiments on humans that we'd really like to do. For example, I'd really like to know if running barefoot reduces injury. To do this, I'd need a population of humans that are cloned from a single genotype and raised in a common laboratory environment. They've each had the exact same diet, light, sleep, exercise, and education, all in their little cages. I'd then randomly assign 50 pairs to 50 different gyms with an indoor 200m track. Within each pair, one would always run with a modern running shoe and one barefoot. Same diet, same sleep schedule, same training schedule. And yes, they would never leave the gym. Then after two years, I'd stop the experiment and tabulate the rate of injury. Of course, maybe my shoe choice was particularly bad or maybe there is a genotype x shoe interaction (the shoe on the lab genotype caused more injury but wouldn't have on some other genotype). Or maybe there is no effect of shoes on a gym track but there is on a road or on a trail So I'd have to repeat the experiemnts using different genotypes, different shoes, and different surfaces. Not gonna happen.<br /><br />Anything other than a controlled, manipulative experiment will have confounding factors. Without much ability to manipulate, what the science of sport (and most modern medicine) is left with is the attempt to control these confounding factors using statistics and, hopefully, large sample sizes. This is "evidence-based medicine" and it's the only game in town for inferring what works and what doesn't. There are huge problems with every evidence-based medicine study, but the best studies are better than our many experiments of one.<br /><br />Note that <a href="http://www.sciencebasedmedicine.org/?p=527">Science Based Medicine</a> has a really nice blog post this morning on, essentially, how the sort of confirmation bias that I've discussed above, can lead to pseudoscience quackery among professionals in health related fields. It's a long post and he only gets to the confirmation bias part near the end, but it's a worthy read.middle.professorhttp://www.blogger.com/profile/02370737843957507859noreply@blogger.com2tag:blogger.com,1999:blog-5137578094288207170.post-39284210106633265742009-06-11T11:14:00.000-07:002009-06-11T18:41:59.404-07:00Why we cook<a onblur="try {parent.deselectBloggerImageGracefully();} catch(e) {}" href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEiTEQ5W8-orMQmVXRv138JRPgteDVeKKT4zSodkhYY-8rP-lsujt2ISZnY97DWGY7eVkXxpyx6ix4HIIJ32DM_5yF1d_zMBYlRn81nqjGSUEiEVJgT9dq2g90QyWzFLGBd7TaA8EbDzpe8x/s1600-h/+400000000000000160529_s4.jpg"><img style="margin: 0px auto 10px; display: block; text-align: center; cursor: pointer; width: 265px; height: 400px;" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEiTEQ5W8-orMQmVXRv138JRPgteDVeKKT4zSodkhYY-8rP-lsujt2ISZnY97DWGY7eVkXxpyx6ix4HIIJ32DM_5yF1d_zMBYlRn81nqjGSUEiEVJgT9dq2g90QyWzFLGBd7TaA8EbDzpe8x/s400/+400000000000000160529_s4.jpg" alt="" id="BLOGGER_PHOTO_ID_5346155369979089298" border="0" /></a><br />Middle class folk from industrial countries don't worry too much about the major <a href="http://emedicine.medscape.com/article/984496-overview">macronutritient</a> diseases that kill millions (mostly children) throughout the world. Instead, we continuously argue about the proper proportions of macronutrients - our carbohydrates, fats, and proteins - the form these should come in, and how best to prepare them. So we have low-fat diets, Atkins diets, various flavors of vegetarianism (those that consider fish vegetables and those that consider fish animals), various flavors of carnivorous diets (red meat v. no red meat), vegan diets, the paleo diet, raw food diet, etc., etc,. etc.<br /><br />Too much to blog about in one post but I will make one comment on any diet that purports to be "natural" or more in tune with our "nature" or "evolutionary past". The health claims of these diets assume that humans have not evolved since the pleistocene, that is, back when we were gathering nuts and scavenging lion kills on the African savannah. But there is a huge new research program in human evolutionary genetics that documents <a href="http://www.amazon.com/gp/product/0465002218?ie=UTF8&tag=whersthebeef-20&linkCode=xm2&camp=1789&creativeASIN=0465002218">pervasive genetic adaption over the last few <span style="font-style: italic;">thousand</span> years</a>. The poster child of this phenomenon is <a href="http://evolution.berkeley.edu/evolibrary/news/070401_lactose">the recent evolution of the regulation of the lactase gene</a>, which has allowed both northern europeans and some africans to adapt (via natural selection) to the behavior of drinking milk from farm animals, as adults. <a href="http://www.biology.ucr.edu/people/faculty/Zuk.html">Marlene Zuk</a> has a <a href="http://www.nytimes.com/2009/01/20/health/views/20essa.html?_r=2">nice essay from the NYT science section </a>from earlier in the year. Note that the recent, accelerated genetic evolution theory is not uncontroversial (although certain instances like the lactase regulation is, indeed, uncontroversial). If you are interested, <a href="http://www.anthropology.wisc.edu/people_hawks.html">John Hawkes</a> frequently<a href="http://johnhawks.net/weblog"> blogs about this stuff </a>and since he works in this field, his views merit close attention. In his most recent blog, John mentions Richard Wrangham's most recent book that is receiving a lot of interest: "<a href="http://www.amazon.com/gp/product/0465013627?ie=UTF8&tag=whersthebeef-20&linkCode=xm2&camp=1789&creativeASIN=0465013627">Catching Fire: How Cooking made us Human</a>". A <a href="http://seedmagazine.com/content/article/did_cooking_make_us_human/">seed interview with Wrangham</a> about his book is short and sweet.<br /><br />I've put this book on my list, but what I'm really curious is what (if any) selection has occurred in response to cooking?middle.professorhttp://www.blogger.com/profile/02370737843957507859noreply@blogger.com2tag:blogger.com,1999:blog-5137578094288207170.post-5896899805715581282009-06-07T18:56:00.000-07:002009-06-11T12:47:47.652-07:00got cramps?Does good hydration or eating a banana or taking an S-cap help prevent muscle cramps? Martin Schwellnus has a new review (citation below) that finds little evidence for these traditional explanations/therapies. Schwellnus also reviews the neuromuscular control model that he developed in the late 90s, which suggests that cramping is due to a spinal reflex in response to muscle fatigue during/following intense exercise.<br /><br />A good summary of the competing models (<a href="http://www.sportsscientists.com/2007/11/muscle-cramps-part-1-theories-and.html">part I</a>, <a href="http://www.sportsscientists.com/2007/11/muscle-cramps-part-ii.html">part II</a>, <a href="http://www.sportsscientists.com/2007/11/muscle-cramp-part-iii.html">part III</a>, <a href="http://www.sportsscientists.com/2007/12/muscle-cramps-part-v.html">part V</a>) is on the Science of Sport blog. Read these and the comments. If you only read one read, part V and the comments.<br /><br />Schwellnus also recommends passive stretching of the model to at least temporarily relieve the cramp since this causes a spinal reflex that relaxes the tensed (cramped) muscle. A recent chapter in the Olympic Textbook of Medicine in Sport, which includes Schwellnus as an author, recommends regular stretching of the muscles that generally cramp and proper carbohydrate and fluid intake prior to exercise (in order to delay muscle fatigue, not because this directly decreases probability of cramping).<br /><br /><span style="font-family:verdana,arial,helvetica,sans-serif;">Schwellnus, M P<br /><a href="http://bjsm.bmj.com/cgi/content/abstract/43/6/401"><strong>Cause of Exercise Associated Muscle Cramps (EAMC) -- altered neuromuscular control, dehydration or electrolyte depletion?</strong></a><br />Br J Sports Med 2009 43: 401-408 </span>middle.professorhttp://www.blogger.com/profile/02370737843957507859noreply@blogger.com0tag:blogger.com,1999:blog-5137578094288207170.post-48429965015762973772009-06-03T12:13:00.001-07:002009-06-03T18:29:06.858-07:00Runner's HighThe Wall Street Journal has a <a href="http://online.wsj.com/article/SB124269273787132707.html">nice, feel good running opinion</a> from May 19 that raises more than a few common folk ideas about running. Too little time to comment on them all but here is one:<br /><br />"But running is not just exercise. It's a great stress reliever and an inexpensive source of neurotransmitters like dopamine that wash the body with good feelings."<br /><br />That is, running makes us high. The general idea is that running long and fast signals the secretion of endogenous opioids, which are our own version of <a href="http://en.wikipedia.org/wiki/Morphine">morphine</a> (of which heroine is a derivative) and these endogenous opioids (or <a href="http://en.wikipedia.org/wiki/Endorphins">endorphins</a>), bind to receptors on cells in brain circuits that make us feel euphoric.<br /><br />Gina Kolata, a reporter for the New York Times, criticized the endorphin hypothesis of runner's high in her book <a href="http://www.amazon.com/gp/product/0312423225?ie=UTF8&tag=whersthebeef-20&linkCode=xm2&camp=1789&creativeASIN=0312423225">Ultimate Fitness</a>. I don't have the book but she also had an <a href="https://notes.utk.edu/bio/greenberg.nsf/0/218e0cb9e11ebe6285256c33004917d7?OpenDocument">article</a> in the Milwaukee Journal Sentinal that suggested that runner's high does not come from an "endorphin rush". Most recently, however, <a href="http://www.nytimes.com/2008/03/27/health/nutrition/27best.html?ex=1207281600&en=1c358177ac27ff29&ei=5070">she's changed her mind</a> based on a <a href="http://www.ncbi.nlm.nih.gov/pubmed/18296435">new study</a> that shows (according the the authors and Kolata) (1) endogenous opioid activity increases after a 2hr run compared to before the run and (2) perceived euphoria is greater after the 2hr run than before, and, importantly, (3) the level of opioid activity is positively correlated with perceived euphoria. Here is a <a href="http://www.sciencedaily.com/releases/2008/03/080303101110.htm">lay summary</a> of the paper.<br /><br />As I understand the original paper, the authors did not actually measure levels of the endogenous opiods but measured the levels of the binding of an radioactive opioid antagonist, which they could detect with PET. Since the antagonist and the endogenous opioids compete for the same binding sites, then if measured levels of the antagonist decrease, the conclusion from the authors is that endogenous opioid activity is increased (they quickly dismissed alternatives, such as downregulation of opioid receptors, but I didn't really spend enough time to evaluate these).<br /><br />One note - the authors note that runners were both (1) told that they were being treated with opioids ligands and (2) confirmed that they had previously experienced runner's high. Runner's tend to be a well educated group and I'm guessing that more than one figured out what the study was about. It's a nice study but I'm not completely confident that a placebo effect can be ruled out and it still isn't measuring endogenous opioid activity directly.<br /><br />Also note that there is a<a href="http://www.ncbi.nlm.nih.gov/pubmed/15388533?ordinalpos=12&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_DefaultReportPanel.Pubmed_RVDocSum"> group that argues</a> that runner's high is due to <a href="http://en.wikipedia.org/wiki/Cannabinoid">endogenous cannibinoids</a> and not opioids. Amby Burfoot has a <a href="http://www.runnersworld.com/article/0,7120,s6-243-297--1102-0,00.html">comment</a> on this.middle.professorhttp://www.blogger.com/profile/02370737843957507859noreply@blogger.com0tag:blogger.com,1999:blog-5137578094288207170.post-33049562642067747062009-06-02T13:08:00.000-07:002009-06-03T12:43:59.451-07:00Against chiropracticA <a href="http://www.newscientist.com/article/mg20227101.100-what-you-should-know-about-chiropractic.html?DCMP=OTC-rss&nsref=online-news">good, skeptical look at </a><a href="http://www.newscientist.com/article/mg20227101.100-what-you-should-know-about-chiropractic.html?DCMP=OTC-rss&nsref=online-news">chiropractic</a> by <a href="http://en.wikipedia.org/wiki/Edzard_Ernst">Edzard Ernst</a>, who has a long history working in complimentary and alternative medicine and who co-authored a recent <a href="http://www.amazon.com/gp/product/0393066614?ie=UTF8&tag=whersthebeef-20&linkCode=xm2&camp=1789&creativeASIN=0393066614">book</a> reviewing the evidence for many of the complimentary and alternative therapies.middle.professorhttp://www.blogger.com/profile/02370737843957507859noreply@blogger.com0tag:blogger.com,1999:blog-5137578094288207170.post-45234354176371943182009-06-02T13:04:00.000-07:002009-06-02T13:28:29.881-07:00Why this blog?Two reasons to start this blog:<br /><br />1) I teach Human Anatomy & Physiology to many kinds of pre-health students including nursing, athletic training, sports medicine, exercise physiology, the various therapies (occupational, physical), psychology, and a few pre-meds. We spend a year talking about how the different organ systems function in health (mostly) and disease (a little, since pathophysiology is an upper level class), generally at the molecular and cellular level. The students learn about enzyme function, and protein channels, and protein transporters, and cell signaling, and all that good stuff. I usually spend a full lecture on "how we know what we know and why we believe what we believe" which is a lecture on <a href="http://en.wikipedia.org/wiki/Evidence-based_medicine">evidence-based medicine</a> (in the broad sense) and especially how science (in the broad sense) is the only game in town that allows us to overcome the many <a href="http://en.wikipedia.org/wiki/List_of_cognitive_biases">cognitive biases</a> that get in the way of gaining <a href="http://www.freeinquiry.com/intro-to-sci.html">reliable knowledge</a>. A few students like the lecture but many don't because I really challenge many of their beliefs.<br /><br />2) I run and ski and there's lots of bad information out there on endurance physiology and on how to avoid injury in these sports and how to treat injuries.<br /><br />So this blog gives me space to draw attention to these areas. Since I don't have time to write a bunch of essays, mostly they will be links but sometimes I might write something longer.middle.professorhttp://www.blogger.com/profile/02370737843957507859noreply@blogger.com0