Paris Marathon: Splits and Commentary

Paris Marathon 2012: Live coverage, splits and comment

Stanley Biwott has won the 2012 Paris Marathon to kick off the spring marathon season, and it has started the same way that 2011 left off - with a course record 2:05:11 (unofficial, from TV times).  Biwott, who came into the race with a 2:07:03 PB, broke clear as early as 29km, when the group thinned dramatically and he was left with a solo pursuit for the finish line.

At that stage, he was on course for a sub-2:04 finish, courtesy a super fast first half (1:01:51), and an even quicker section from 25km to 30km (14:24 for the interval).  That surge, off that pace, saw a group of about ten become three within minutes, and soon after, Biwott went clear of his Ethiopian rivals Assefa and Jisa.

From that moment, it was Biwott against the clock, and though he slowed (15:30 from 30 to 35km, though I must confess I'm not confident in the splits I was getting on TV), the damage had been done and Biwott hung on to break the course record of 2:05:47 by 36 seconds, and smash his own PB by just under 2 minutes.

Behind, there were big gaps. Having been bunched at 25km, the time gaps illustrate how attritional the early pace was. First to second was 1:12, a gap created entirely in the final 12km.  Tenth place was over 2:09, so that's almost 5 minutes over the final 15km.  The closest athlete to an even split was Biwott, who went through halfway in 1:01:51, and closed in 1:03:20:  For everyone else in the top 10, the second half was over 3 minutes slower than the first.

Just as testament to the emergence of talent in these big city marathons, the man who finished third, Jisa, came into the race with a reported half-marathon PB of 64:33.  He ran 2:06:26 today, which means a 61:51 first half, followed by a 64:35 second half.  In other words, he basically equalled his previous half-marathon PB during the second half of a marathon, in which he broke it by almost three minutes in the first half.  Talk about a breakthrough day!

So a course record in Paris to go with course records galore in 2011, and now it's Rotterdam, and Mosop's (and other Kenyan's) assault on the world record!)

Comments and splits at 5km intervals are below...

Live splits as the race unfolded

The Paris Marathon kicks off what was recently called "8 days for Glory" by our Letsrun.com colleagues!  That's a reference to what could be one of the greatest weeks in the history of the marathon, driven by the intense competition between the Kenyans to nail down one of three spots on the Olympic team for London.  Either side of the Atlantic, the greatest marathon runners in history will be tackling, in order, Paris, Rotterdam, Boston and London.

Paris is first, and below are the splits and comments from the men's race.  Rotterdam comes later, and it has the better field with Moses Mosop touted to challenge the world record.  That race is not televised in SA, but I'm looking into live streams (which usually don't work in South Africa either!), but no matter what, I'll post those splits later today!

Paris splits

5km - 14:56

Conservative start by today's marathon standards, but that's probably par for the course in Paris - the field has some good names, but not the spectacular sub-60 min half marathoners or the 2:04-marathon men of the other races.  Paris has often been a springboard for first time big city marathon winners, and it's not a major, so perhaps the course record of 2:05:47 is a good target for today.  Although, there is a 2:05:25 man in Albert Matebor, but it's a sign of the times that we view him as "only" a 2:05 man in this era of marathon running!

10km - 29:21 (14:25 for the last 5km)

Super fast five kilometer split, which puts the projected pace below 2:04, so that is interesting.  Certainly we're seeing aggressive marathon running more and more.  Whether this is sustainable, we shall see!

15km - 43:58 (last 5km in 14:37)

Still very aggressive, a group of about 12 or 13, which doesn't include defending champion Benjamin Kiptoo, who dropped off at about 11km.

Half-Marathon - 1:01:51

The halfway split projects a 2:03:42, so it's not slowing down.  Yet.  The group is thinning out, down to about 10 men now, including three pace-makers still.  Some of the men have just run half-marathon PBs by more than 2 minutes, on route to running a marathon!  If wheels are going to come off, they'll start slowing now...

25km - 1:13:40 (29:42 last 10km)

The pace has slowed somewhat and it's now on course for a 2:04:20.  Two of the pacemakers are also gone, and the pace is at something of a dangerous crossroads, and may continue to slide to below 2:05 pace.

30km - 1:28:04 (14:24 for the last 5km)


The pace has increased again, and it's caused big splits in the lead pack.  In fact, it's now down to only one - Stanley Biwott, who is running towards a sub-2:04 again.  His projected time at 30km is 2:03:52, but he's now all alone with 12km to go.

Eric Ndiema has gone off the back.  He ran 2:06:07 in Amsterdam last year. Tariku Jefar, winner in Houston this year (2:06:51) is also losing contact with the lead group.  The final pacemaker dropped out at about 28km, and it became a race between three men over 12km.   Those mean were Biwott of Kenya, against Jisa and Assefa of Ethiopia.  Jisa is the man who came into the race with a reported half-marathon PB of 64:33, and he has improved that by almost 3 minutes, and is still running at 30km!

Just short of 30km, Stanley Biwott, who won the Paris Half Marathon, has moved clear and split the three.  Jisa is in second, about 20m back at the 30km, with another 30m to Assefa in third.

35km - 1:43:34 (last 5km in 15:30)

The pace has now slowed considerably - the last 5km in 15:30 is easily the slowest of the race.  So perhaps not surprisingly, the solo effort off the very fast pace is taking its toll.  Biwott still leads, the gap to Jisa in second is now around 30 seconds (a guess), so the race really has exploded since 25km.  That when the pace was ramped by to 14:24 for the 5km interval, off a pace much, much faster than all the men had ever run, so it is no surprise that having been bunched at 25km, there are now 2 minute gaps there!

The bigger challenge may come from those in third and fourth, Assefa and Cesar, who are together and chasing Jisa.  Stanley Biwott, incidentally, has a PB of 2:07:03, so he's looking at 2 to 3 minutes' improvement today.  If he can hang on for 7km.  At the current pace of 3:06/km, he'll come home in a 2:05:30

40km - 1:58:10 (last 5km in 14:36)

Biwott has now sped up, but I must confess I'm skeptical about the accuracy of these splits.  Nevertheless, the time at 40km is 1:58:10, and it means that Biwott can close in 6:30 and he'll run a mid-2:04, and so the course record in Paris is definitely going to fall, and now it is a race for Biwott to see if he can claim the world-leading time for 2012.  That's currently 2:04:23 from Dubai...

Behind him, Jisa is continuing to run an incredible race, and he's locked in a battle with Assefa for second.  Eric Ndiema has done a yo-yo, first catching and passing those two, and then being caught and passed with 3km to go.  He then fought back and reclaimed second at about 41km.

Finish line - 2:05:11

Biwott gets the course record, but not the sub-2:05 that seemed on at 40km.  He definitely slowed considerably, it was visible even on the coverage that he was grinding out the final kilometers, and he closed in 7 minutes.  Nevertheless, it's a course record by 36 seconds, a PB by almost 2 minutes, and a good start to the spring season.

Rotterdam later, join me after that one!  Not sure I'll be able to do live splits, but I'll certainly get something up later today

Ross

Around the rings: Weekly buzz

Ashenden, anti-doping and the impending marathon season and Olympic team selection

Ashenden steps down - "managing the message"

Michael Ashenden is one of the leading anti-doping advocates in the world as a result of a) his contribution to the development of the biological passport system and the detection of blood doping and EPO use, and b) his outspokenness about the process, including two interviews that will (and should) become part of the anti-doping folklore, but more on these shortly.

Ashenden last week stood down from the AMPU, a body that was recently created to manage the biological passport process, because he felt that the contract that its members were asked to sign was too restrictive, and would help foster a culture of "omerta", the pact of silence that characterizes the professional cycling peloton (originally a mafia term).

You can read a news piece on his resignation here for the details, but what was most interesting is Ashenden's description that the Athlete Passport Management Unit, formed recently to manage the biological passport system for cycling and athletics, is trying "manage the message".

I can see both sides of the story here - you can't have a person involved in the system, with intimate knowledge of the cases and processes, speaking out too much about ongoing cases, because it's potentially harmful (that is, slanderous and libelous) to the athlete involved.  So some form of "management" is non-negotiable to those bodies, it has to be in order to protect their credibility.

You may recall that the biological passport system was designed as "three strike" system, where a case is only opened against an athlete when they produce several unusual or suspicious results in a short period.  This is because for all its progress, the biological passport remains an imperfect method, which can, as shown by research, produce "false positives" (this fact is acknowledged by everyone on it, incidentally, and it will always be the case because physiological systems don't obey our best understanding at this stage).

For this reason, it was designed with multiple stages of evaluation, both legal and scientific, the first of which was the regular measurement of reticulocyte %, hemoglobin concentration and a calculated off-score, and the probability calculation of values occurring in an undoped individual.  The second level is evaluation by a panel, who assess the changes and evaluate whether a profile is suggestive of doping, and the third level is the opening of a legal proceeding.

The process is thus length and intensive, and I think it's fair to say that this is out of necessity, because the authorities have to "manage" the process, so that they don't pursue athletes unfairly.  Linked to this must be some form of "managing the message", at least while the case is ongoing.  But this is so obvious it feels almost foolish to point out, but I think that from some circles, criticism of Ashenden's resignation (and there is some) was based on the perception that Ashenden wanted to discuss individual cases while they were happening.  I certainly didn't see it this way.

Rather, my take is that the more transparency there is, the better.  The process should be explained so that the fans, the media and the athletes properly understand how the system works (the role of educator) and so that there is no chance whatsoever of anything being covered up (the whistleblower from inside).  The latter is so vital because in the last two years, so many allegations have emerged of preferential treatment for certain cyclists that the credibility and trust in the entire anti-doping system has been undermined.  There is a growing perception that some are untouchable, whereas others will be made examples of, because it's convenient to do so.  Exposing the champions is not as good for media coverage and sponsor perceptions (for example, remember that it's been media pressure that has exposed certain recent high profile cases). 

The only solution for this is transparency.  As Ashenden states, "there should be nothing to hide, so why stop experts from talking?" There are of course some reasons to stop experts from talking in certain situations - there may, at times, be "something to hide".  For example, when authorities were working with the pharmaceutical companies to develop the test for CERA, it was beneficial to be silent.  Again, this is obvious.  In most other situations, I agree with Ashenden - talk and educate and inform so that you build credibility through transparency.  The reverse is also true - if a system is broken and flawed, then preventing people from saying so, and refusing to accept criticism, halts that progress and fosters an environment where further cheating can prosper. 

Ashenden interview: Contador's CAS case and doping explained

Speaking of transparency, Ashenden had barely left the APMU and an interview appeared on nyvelocity.com, in which he described the scientific issues of the Contador CAS case.  This is the second interview Ashenden has done with Andy Shen of nyvelocity.com.  The first was a huge interview he gave in 1999, where he covered EPO testing and Lance Armstrong's failed EPO tests, and laid out why he believed Armstrong had doped.

Both interviews should be required reading, I think, because Ashenden explains the process from inside.  One can still disagree with Ashenden's final opinion, but it's the process by which he arrives at it, and the explanations of the anti-doping process that I found so interesting and valuable.  As mentioned, the first interview, and now this one, shed more light on the testing and anti-doping processes than the entire collection of news stories in the last decade, and this is the value of experts being accessible.

You can read the interview here - Ashenden typically pulls no punches, explains blood doping and EPO microdoping, plasticizers, and then his role in the CAS hearing.  As I say, it's well worth a read.

My thoughts, apart from interest at the anti-doping content, are that Ashenden was clearly frustrated at the narrow terms of the CAS hearing.  That seems typical of CAS hearings, incidentally (and perhaps law, for that matter), but what emerges from Ashenden is that there was a good deal of evidence against Contador but that the very narrow question being asked meant that it could not be covered and presented as evidence.   He was ordered not to answer certain questions and describes his frustration that some relatively simple matters which could have been resolved in 30 seconds took many hours to thrash out.  

This frustration seems typical for a scientist in a legal setting - reading the decision from the Pistorius case, for example, it was equally clear that CAS don't hear all the evidence, they rule only on a previously defined question and decision (the nature of arbitration, of course).  The result is that a decision gets made in arbitration that does not truly reflect the evidence - in the Contador case, the plasticizer and transfusion theory could never be fully advanced, whereas in the Pistorius case, the Weyand/Bundle theory of swing times was never even presented to the panel.  It seems a flawed system to me.  I'd have thought that the goal of the CAS as the final decision-maker should be to evaluate ALL the evidence, rather than to be bound up in dozens of boxes of legal arguments, but I guess such is life and legality.

Marathon season is here

Moving away from cycling to running, next week sees the start of the Spring Marathon season, and it's a loaded season, for many reasons.  Recall that 2011 was the most sensational year of marathon running ever seen, largely because of Kenyan runners - they occupied the Top 20 places in the world rankings, won every major marathon, broke every Major Marathon course record, and the world record.

It's almost inconceivable that the same could happen this year, but it's a loaded season because everything now points towards London in August.  The next three weeks will determine who even gets to start the Olympic Marathon, because Kenya and Ethiopia will pick their teams based on London, Rotterdam and Boston performances, and I can't think of a time when competition was so deep, at such a high quality, just to earn the right to represent a country in the Olympic Games.

First up are Paris and Rotterdam, followed on Monday by Boston.  Neither of the weekend's races is a Major, and Paris is unlikely to produce a scintillating time, though it has served as a springboard for future champions.  For now, however, it's Rotterdam on Sunday that should attract most attention, because Moses Mosop of Kenya will be aiming for a world record on Rotterdam's super fast course.  He's joined there by Peter Kirui, who is Kenya's 10,000m champion, and a man who recently won the New York Half Marathon looking extremely comfortable. If Rotterdam's weather plays along (and here, the wind has been the main culprit in recent years) then the world record is under threat, and Kenya's selection problems may multiply ahead of Boston (where Geoffrey Mutai races) and London (where just about all the others - Emmanuel Mutai, Patrick Makau, Wilson Kipsang, Abel Kirui and Martin Lel - are running).

It means that of all the Marathons, London has the most spectacular field, but may only provide one place for Kenyan runners, given that Geoffrey Mutai must surely be the first choice based on his Boston and New York wins last year.  Quite how Kenyan officials will select when athletes are running on different courses under different circumstances is anyone's guess, but it should make for good discussion.  Incidentally, on this note, the weather forecast for Boston is not favorable.  Last year, the weather helped make Boston the fastest marathon ever run - 2:03:02 beat 2:03:06.  This year, even with a strong tailwind, the forecast is for warm temperatures, and that means a repeat is unlikely.

Make the Olympic Marathon open to everyone?

Ethiopia, meanwhile, have similar selection problems, in that a host of young Ethiopians dominated the Dubai Marathon earlier this year, and seem to be front-runners for their three spots.  Whether it's wise to choose youth in a fast race (and a first-time performance) over the experience and proven pedigree of athletes like Tsegaye Kebede or Gebremariam, who may be a little slower, is a debatable point.

What I would say, however, is that I agree with Amby Burfoot who recently wrote that the Olympic Marathon should not restrict each country to selecting only three athletes.  His reasoning is that the Olympic Marathon should be the premier marathon in the world, and I agree with him.  As it stands, the London Marathon is clearly the deepest, highest quality race, but it is missing at least three of the best in the world, in Mosop, Mutai and Kirui.  The Olympic Marathon in August will be short of at least 10 Kenyans, and probably five Ethiopians, and that somewhat "dilutes" its value.

The downside is that opening the race up to every Kenyan with a 2:06 or faster means that the Olympic Marathon would start to resemble the World Cross Country Championships, which are really a Kenyan and Ethiopian procession, and which kind of turns many "less than passionate fans" away from the sport.  The reality is that for global reach and appeal, the chance that an Italian or American athlete, for example, can medal in the Olympic Marathon, is necessary.  

So it's a difficult one - there is almost zero chance that the London Marathon on the 22nd will be won by anyone NOT from Kenya or Ethiopia, and if the top 10 from each of these countries raced in the Olympics, the same would be true.  As it is, the top 3 from Kenya and Ethiopia look close to untouchable, but at least there's some hope!  Would love to hear your thoughts on this one!

The spillover from the marathon and Kenya's bizarre selection processes

And finally, related to this incredible depth and quality in the marathon, we're starting to see a potential "spill down" back to the half-marathon and possibly 10,000m event.  The last few years have seen the marathon explosion, and that has been to the detriment of the longest track event.  Not many high quality 10,000m races happen each year, and the result is that Kenenisa Bekele's world records have been untroubled for a long time.

That's unlikely to change, but what does seem to be happening, again driven by the Olympic Games, is that a lot of runners who would be heading towards the Marathon are now coming back down to the 10,000m distance.  Last week, a previously unknown Ethiopian, aged only 20, won the Prague half marathon in 58:47.  Atsedu Tsegay became the fifth fastest man in history, and declared afterwards that he'll now focus on making the Ethiopian team in the 10,000m for the Olympics.

Similarly, Dennis Koech won the Berlin half marathon in 59:14 and also stated his intent to qualify for the 10,000m event (he was not however named in a 30-man squad of athletes for the Kenyan pre-trial trial, as discussed below).  These are athletes who almost certainly will be running marathons by 2013, and they're on the way to that distance, because that's clearly where the prestige and hence biggest payday lies.

But, the depth of talent available to those countries, and the relatively late stage in the year means that for these men, the sensible approach is to look down, at the shorter 10,000m distance, for now.  As Letsrun.com pointed out, what this means is that the medal chances of their USA-based athletes take a hit as this talent comes back to the track, albeit for a few months only.

The good news, however, is that just today, Kenyan athletics announced a ridiculous ultimatum that will exclude many of their potential 10,000m medalists from even making their team.  They have arranged a 10,000m event in Nairobi on Saturday, and announced that anyone NOT participating in these trials will be ineligible for selection to the Olympic Team.

The result is that Geoffrey Mutai, who races in Boston on Sunday, as well as Mosop and Kirui who race Rotterdam on Sunday, are automatically excluded from the Kenyan 10,000m team.  Not that any of these three wanted to be in the 10,000m team, but all could be potential medalists in the event that they fail to make the Kenyan Marathon team.

The reality is that there is enough time post-Rotterdam/Boston/London for a talented and fast marathon runner to reassess their season's focus and come down to the 10,000m event.  This is particularly the case for Mutai and Kirui - Mutai was Kenya's Cross Country champion last year and Kirui, as mentioned, their 10,000m champion.  So both were options over 10,000m, in the event that they didn't make the Marathon team.  

Now, that option has also been taken away, and it's a foolish thing to do.  Why have two separate trial races?  As you may already know, the final Kenyan 10,000m trials have been "outsourced" to the USA in June, and will take place in Oregon on June 2nd.  This 'mini-trial' will feature 30 athletes, and the top 15 will qualify for the Oregon race. 

It's an unnecessary thing to do in the first place, but when it excludes some of your top runners, who happen to be focusing on the marathon at the time, it seems doubly foolish.  Kenya has not won a gold over 10000m in the Olympic Games since 1968, and with Mo Farah and a host of Ethiopians standing in their way, it may be ambitious to think that one of their top marathon runners could come down in distance and win that gold in London this year, but this kind of decision makes it even more unlikely, and that seems like a bad decision in sports management.

Again, your thoughts welcome!

Ross

If your NEAT is low, maybe you should chill

I wrote most of this post a while ago, and then forgot about it. The recent blogosphere storm of comments regarding cold-induced thermogenesis caught me by surprise (), and provided a motivation to get this post out. Contrary to popular perception, I guess, cold-induced thermogenesis is an extensively researched topic. Some reasonably well cited references are linked here.

Let us backtrack a bit. When people say that they want to lose weight, usually what they really want is to lose is body fat. However, they frequently do things that make them lose what they do not want – muscle glycogen, water, and even some muscle protein. Physical activity in general depletes muscle glycogen; even aerobic physical activity.

Walking, for example, depletes muscle glycogen; but slowly, and proportionally to how fast one walks. Weight training and sprints deplete muscle glycogen much faster. Whatever depletes muscle glycogen also lowers the amount of water stored in myocytes (muscle cells), effectively reducing muscle mass. Depleted muscle glycogen needs to be replenished; protein and carbohydrates are the sources. If you deplete muscle glycogen through strength training, this will provide a strong stimulus for glycogen replenishment and thus muscle growth, even beyond the original level – a phenomenon called supercompensation ().

In conjunction with strength training, situations in which one burns mostly fat, and very little glycogen, should be at the top of the list for those wishing to lose weight by losing body fat and nothing else. These are not very common though. One example is nonexercise activity thermogenesis (NEAT), or heat generation from nonexercise activities such as fidgeting (). There is a great deal of variation in NEAT across individuals; for some it is high, for others it is annoyingly low.

Walking slowly is almost as good as NEAT for body fat burning, when done in conjunction with strength training. Up the pace a bit though, and you’ll be burning more muscle glycogen. But if you walk slowly you don’t burn that much body fat per unit of time. If you walk a bit faster you’ll burn more fat, but also more glycogen. C’mon, there is no way to win in this game!

This is why being physically active, in a “non-exercise way”, seems to be so important for health; together with strength training, limiting calorie intake, and all the while having a nutritious diet. These are not very common things in modern urban environments. Long term, there isn’t a lot of margin for error. It is ultimately a game of small numbers in the short term, played over long periods of time.

But there is an alternative if your NEAT is low – just chill. That is, another situation in which one can burn mostly fat, and very little glycogen, is exposure to mildly cold temperatures, but above the level that induces shivering (mild cold: 16 degrees Celsius or so; about 60 degrees Fahrenheit). Shivering in general, and particularly intense shivering, is associated with levels of muscle activity that would induce glycogen depletion () (). If muscle glycogen depletion happens while one is fasting, liver glycogen will be used to replenish muscle glycogen, and also to supply the needs of the brain – which is always hungry for glucose.

As the liver glycogen tank goes down beyond a certain point, and no protein or carbohydrates are eaten, the body will use amino acids from muscle to produce glucose. Muscle glycogen will be locked until it is needed. Interesting eh!? The body sacrifices muscle protein but doesn’t tap into muscle glycogen, which is only used to fuel violent muscle contractions. We are talking about fight-or-flight responses here. From an evolutionary perspective, sacrificing some muscle beats losing a lot of it to a predator any day.

Cold-induced thermogenesis is a very interesting phenomenon. The figure below, where open circles represent lean and closed circles obese folks, shows that it leads to different responses in lean and obese folks, and also that it presents a lot of variation across different individuals (like NEAT). This type of thermogenesis actually seems to be strongly associated with an increase in NEAT (); although it seems to also be associated with futile cycles used by the body to generate heat without any movement, as in thermogenesis during hibernation in certain animals () (). Having more brown fat as an adult, or being able to make brown fat more easily, is associated with more cold-induced thermogenesis; and also with a lower obesity risk.

In fact, cold-induced thermogenesis leads to an increase in energy expenditure that is comparable with that of another major energy sinkhole – overfeeding () (). Unlike overfeeding though, cold-induced thermogenesis does not require calories to go in. And, no, you don’t burn more than you take in with overfeeding.

How can one burn fat via cold-induced thermogenesis? Here are some ideas. Set the home thermostat to a mildly cold temperature in the winter (this will also save you some money). When it is a little cooler than normal, don’t wear heavy clothes. Take mildly cold showers, or end a warm shower with some mildly cold water.

What about more extreme cold exposure? It should be no surprise that one would feel pretty good after a dip in ice-cold water; that is, if the person does not suffer from a glycogen storage disease (e.g., McArdle's disease). At least in theory, that type of cold exposure should induce whole-body muscle glycogen depletion, just like an intense whole-body exercise session, with the resulting hormonal changes ().

Growth hormone should be up after that, perhaps for hours. Done right after weight training, or intense exercise, it may have a boosting effect on the hormonal response. But if you do that in the recovery phase (e.g., several hours after the weight training session), it should impair muscle recovery. It would be a bit like doing another strength training session, when the body is trying to recover from the previous one.

The 2012 Arch Intern Med red meat-mortality study: Eating 234 g/d of red meat could reduce mortality by 23 percent

As we have seen in an earlier post on the China Study data (), which explored relationships hinted at by Denise Minger’s previous and highly perceptive analysis (), one can use a multivariate analysis tool like WarpPLS () to explore relationships based on data reported by others. This is true even when the dataset available is fairly small.

So I entered the data reported in the most recent (published online in March 2012) study looking at the relationship between red meat consumption and mortality into WarpPLS to do some exploratory analyses. I discussed the study in my previous post; it was conducted by Pan et al. (Frank B. Hu is the senior author) and published in the prestigious Archives of Internal Medicine (). The data I used is from Table 1 of the article; it reports figures on several variables along 5 quintiles, based on separate analyses of two samples, called “Health Professionals” and “Nurses Health” samples. The Health Professionals sample comprised males; the Nurses Health sample, females.

Below is an interesting exploratory model, with results. It includes a number of hypotheses, represented by arrows, which seem to make sense. This is helpful, because a model incorporating hypotheses that make sense allows for easy identification of nonsense results, and thus rejection of the model or the data. (Refutability is one of the most important characteristics of good theoretical models.) Keep in mind that the sample size here is very small (N=10), as the authors of the study reported data along 5 quintiles for the Health Professionals sample, together with 5 quintiles for the Nurses Health sample. In a sense, this is somewhat helpful, because a small sample tends to be “unstable”, leading nonsense results and other signs of problems to show up easily – one example would be multivariate coefficients of association (the beta coefficients reported near the arrows) greater than 1 due to collinearity ().

So what does the model above tell us? It tells us that smoking (Smokng) is associated with reduced physical activity (PhysAct); beta = -0.92. It tells us that smoking (Smokng) is associated with reduced food intake (FoodInt); beta = -0.36. It tells us that physical activity (PhysAct) is associated with reduced incidence of diabetes (Diabetes); beta = -0.25. It tells us that increased food intake (FoodInt) is associated with increased incidence of diabetes (Diabetes); beta = 0.93. It tells us that increased food intake (FoodInt) is associated with increased red meat intake (RedMeat); beta = 0.60. It tells us that increased incidence of diabetes (Diabetes) is associated with increased mortality (Mort); beta = 0.61. It tells us that being female (SexM1F2) is associated with reduced mortality (Mort); beta = -0.67.

Some of these betas are a bit too high (e.g., 0.93), due to the level of collinearity caused by such a small sample. Due to being quite high, they are statistically significant even in a small sample. Betas greater than 0.20 tend to become statistically significant when the sample size is 100 or greater; so all of the coefficients above would be statistically significant with a larger sample size. What is the common denominator of all of the associations above? The common denominator is that all of them make sense, qualitatively speaking; there is not a single case where the sign is the opposite of what we would expect. There is one association that is shown on the graph and that is missing from my summary of associations above; and it also makes sense, at least to me. The model also tells us that increased red meat intake (RedMeat) is associated with reduced mortality (Mort); beta = -0.25. More technically, it tells us that, when we control for biological sex (SexM1F2) and incidence of diabetes (Diabetes), increased red meat intake (RedMeat) is associated with reduced mortality (Mort).

How do we roughly estimate this effect in terms of amounts of red meat consumed? The -0.25 means that, for each standard deviation in the amount of red meat consumed, there is a corresponding 0.25 standard deviation reduction of mortality. (This interpretation is possible because I used WarpPLS’ linear analysis algorithm; a nonlinear algorithm would lead to a more complex interpretation.) The standard deviation for red meat consumption is 0.897 servings. Each serving has about 84 g. And the highest number of servings in the dataset is 3.1 servings, or 260 g/d (calculated as: 3.1*84). To stay a bit shy of this extreme, let us consider a slightly lower intake amount, which is 3.1 standard deviations, or 234 g/d (calculated as: 3.1*0.897*84). Since the standard deviation for mortality is 0.3 percentage points, we can conclude that an extra 234 g of red meat per day is associated with a reduction in mortality of approximately 23 percent (calculated as: 3.1*0.25*0.3).

Let me repeat for emphasis: the data reported by the authors suggests that, when we control for biological sex and incidence of diabetes, an extra 234 g of red meat per day is associated with a reduction in mortality of approximately 23 percent. This is exactly the opposite, qualitatively speaking, of what was reported by the authors in the article. I should note that this is also a minute effect, like the effect reported by the authors. (The mortality rates in the article are expressed as percentages, with the lowest being around 1 percent. So this 23 percent is a percentage of a percentage.) If you were to compare a group of 100 people who ate little red meat with another group of the same size that ate 234 g more of red meat every day, over a period of more than 20 years, you would not find a single additional death in either group. If you were to compare matched groups of 1,000 individuals, you would find only 2 additional deaths among the folks who ate little red meat.

At the same time, we can also see that excessive food intake is associated with increased mortality via its effect on diabetes. The product beta coefficient for the mediated effect FoodInt --> Diabetes --> Mort is 0.57. This means that, for each standard deviation of food intake in grams, there is a corresponding 0.57 standard deviation increase in mortality, via an increase in the incidence of diabetes. This is very likely at levels of food consumption where significantly more calories are consumed than spent, ultimately leading to many people becoming obese. The standard deviation for food intake is 355 calories. The highest daily food intake quintile reported in the article is 2,396 calories, which happens to be associated with the highest mortality (and is probably an underestimation); the lowest is 1,202 (also probably underestimated).

So, in summary, the data suggests that, for the particular sample studied (made up of two subsamples): (a) red meat intake is protective in terms of overall mortality, through a direct effect; and (b) the deleterious effect of overeating on mortality is stronger than the protective effect of red meat intake. These conclusions are consistent with those of my previous post on the same study (). The difference is that the previous post suggested a possible moderating protective effect; this post suggests a possible direct protective effect. Both effects are small, as was the negative effect reported by the authors of the study. Neither is statistically significant, due to sample size limitations (secondary data from an article; N=10). And all of this is based on a study that categorized various types of processed meat as red meat, and that did not distinguish grass-fed from non-grass-fed meat.

By the way, in discussions of red meat intake’s effect on health, often iron overload is mentioned. What many people don’t seem to realize is that iron overload is caused primarily by hereditary haemochromatosis. Another cause is “blood doping” to improve athletic performance (). Hereditary haemochromatosis is a very rare genetic disorder; rare enough to be statistically “invisible” in any study that does not specifically target people with this disorder.

The weekly Olympic Buzz: Around the rings

Weekly Olympic Buzz: Around the rings - sports news of interest

With only four months to go before the Olympic Games of 2012, there's so much going on in the world of sport that builds towards those amazing 2 weeks in London.  Sadly, much of this has flown by us at The Science of Sport, and we've been posting at insufficient frequency of two articles a month this year!

So to "force" myself to keep the momentum going a little more, I'm today starting a new weekly feature, which I'll call The Olympic Buzz: Around the rings.  Five rings, five news stories per week that grab my attention for their sports science, sports performance and sports management content!  Not a full analysis, but some quick thoughts and links to try to at least peel away some of the interesting stories as we build to the Games.

These are stories that will also come up on our Facebook page and our Twitter feed, where I have tried to keep the 'discussion' going when 'normal' work suffocates the longer posts, so if you haven't joined the social network for The Science of Sport yet, and want regular "thought droplets" in those barren patches, please do so now - Facebook and Twitter!  For now, let's kick of the Buzz...

This week, I'm looking at the recent World Indoor championships, Fabrice Muamba's cardiac arrest, Kenyan women's emergence, the women's 800m with Semenya and Jelimo, and the Olympic fashion 'controversy.


1.  World indoor champs - new names to watch for

The World Indoor championships results are often quite difficult to interpret, particularly in an Olympic year, because so many big names are absent, there are differences in racing strategy as a result of the track length, and the focus, even of those who are there, is often five months in the future.

But the recent World Indoor Championships in Istanbul did ask a few interesting questions for the rest of the year.  A few potential stars emerged - Helen Obiri outkicked Meseret Defar in one of her first ever races over 3,000m (she's a 1500m specialist), running the final 1500m in a shade outside 4:05.

Genzebe Dibaba served notice that she may be ready to emerge from her sister Tirunesh's lengthy shadow by dominating the 1500m event all season, being particularly spectacular in the World Championships, where she front-ran and got faster and faster on route to gold.  Front running is certainly made easier indoors because of the tighter bends and short straights which make overtaking a little more difficult.  But she is a name to look for.

Among the more established names, Kirani James had a poor semi-final and ended up in Lane 1 for the 400m final, and was never in the race on the tight inside lane, which adds a layer to the men's 400m, which seems incredibly open ahead of the outdoor season.

Mo Farah raced in the men's 3000m, and was outkicked in the final by Bernard Lagat, eventually finishing a shade outside the medals.  You could have thrown a blanket over silver, bronze and Farah, and so he was only just outside silver.  The British media have since dissected and analyzed this is a sign of the impending apocalypse, but the reality is that 3,000m is just a touch short in distance for Farah, and to be that within hundredths of a second of silver is hardly a disaster.  At worst, it's neutral, at best, encouraging.

This assumes, of course, that the media scrutiny as a result doesn't undermine Farah's preparation moving forward - as much of an honour as it is for an athlete to race in the Olympics for their home fans, the microscope on GB's athletes is intense!

One other interesting point re Farah - last year, Farah was preparing for his ultimate gold-silver combo by racing and winning the New York Half Marathon.  This year, a 3,000m season indoors.  That's a huge departure from a successful formula, which is not necessarily bad, but must carry some small risk.  The training may not be as radically different as one would think, but certainly one would not be racing 3,000m indoors and a half marathon on identical training in March.

With that change in training, however subtle, the dynamic of maintaining speed, doing the necessary endurance base, all change, and that's an interesting deviation from approach by Farah with his coach.  One would forgive an athlete coming off a really strong season for repeating exactly the same template.  Perhaps this is the small difference that turns a gold-silver to a gold-gold combo... only time will tell!

2. Fabrice Muamba and cardiac arrest

Another dramatic story in the last few weeks was the collapse of Bolton footballer Fabrice Muamba.  Thankfully, he received excellent care almost immediately, and is now seemingly on the way to recovery.  The media coverage after the event focused, as is typical after these incidents, on the fact that all sports people should be screened for these conditions before playing.

And while in theory this is attractive, there are some real challenges to overcome.  One is cost, and this sounds somewhat callous (because any life saved should be worth any expense), but it's fairly complicated.

One of the problems, for example, if that the heart muscle of an elite athlete is thickened as a result of the training they perform.  This is a favourable adaptation, but it can easily be confused with conditions including Hypertrophic cardiomyopathy, where the heart muscle thickens enough to compromise its blood flow.  The result is that normal screening processes can produce false positives between 2% and 5% of the time (it used to be 15%).

I hope it's not necessary to point out that if you falsely diagnose an elite athlete as being a "ticking time bomb", you are making an incorrect life changing diagnosis.  You have to be really sure that you can distinguish pathology from the normal changes and remodeling of the heart associated with training, otherwise you destroy players livelihoods, and lives, unnecessarily.  At that rate (2% to 5%), if you test a Super Rugby or professional football squad of 40 players, you could well identify two false positives, players who you'd tell they have a risk when there is none.

So the point is that physicians have to be very well qualified to read the signs, to make the correct interpretation because these are not normal screenings.  And I don't know if we have that level of expertise, certainly not here in South Africa.

On this note, if a problem is identified, it has to be managed - is the automatic response to force the player to retire?  This would depend on the case, of course, but it's an interesting ethical one.  Consider for example that some conditions, even when present, have a risk of death of only 1 in 10,000.  If I'm making $200,000 per week playing football (or any money, for that matter), I might well say that I'll take my chances when they're 1 in 10,000.  

But screening, if compulsory, may mean that disclosure and confidentiality issues arise - if you're the owner of a team, paying that salary, do you want the risk, however small, that your player collapses and dies while playing?  This is an interesting ethical debate also worth considering.  Of course, screening can provide management to reduce risk, which is only a good thing, but there's always a question of how medical information is handled, particularly if the testing goes the genetic route, because here, having a gene is often even less likely to produce a clinical outcome.

Another problem is the sensitivity of the tests - a physical examination (a basic screen) is really not sensitive enough to identify the common conditions, let alone the rare ones.  So physical exams are not particularly reliable, and it would need more comprehensive tests (ECG, both resting and stress), and this is where a cost-benefit question becomes relevant.  The cost, not only of doing the testing, but of providing the required follow up support and service would cripple many sports bodies.  

And this is important because there's a question of who is responsible for the athlete?  It's easier for Spurs or Bolton, or any professional team, to know that they are responsible for their contracted players.  It's less clear whether this drive to test also requires the Football Association (FA) or say the SA Rugby Union to take on the responsibility for all its players.  That would include club players, school players in sanctioned competition, and in the end, it spirals dramatically out of control and would destroy the sports organizations.

So I think that testing would help, undeniably, but it has to be implemented very sensibly, because blanket screening for everyone must mean everyone.  I think professional sports teams can offer comprehensive screening - the risk far outweighs the cost, however small that risk may be.  But the questions are who gets screened, and how often, and then who pays?  Because there has to be line somewhere, unfortunately.

For more on this, here is an excellent podcast and if you have the time, I'd highly encourage you to listen, because Jon Drezner is one of the world's authorities on cardiac screening, and he spells out some statistics and facts that are worth knowing in the aftermath of Muamba's incident.

Two points he makes that are most important:

1. First, the prevalence of these conditions is quite a bit higher than had been thought - it's easy to identify cases like Muamba's, less obvious are cases where media and immediate treatment are not documented.  So the prevalence, always thought to be 1 in 200,000, now seems to be more like 1 in 40,000 to 50,000.  That's definitely worth paying attention to.
2. The provision of adequate medical care when these events do occur makes an enormous difference to the prognosis and survival rate.  The chances of surviving cardiac arrest during sport goes from 5 to 8% when there is no emergency defibrillator within 3 to 5 minutes, to well over 50% (64% in one study) when a defibrillator is present.  That's an enormous improvement, and it points to the importance of providing that medical service at events, even if the person using the defibrillator is used by a lay person, and not necessarily a trained medical practitioner.
   
   I think given the complexity of screening, there is a bigger impact to be made by making sure that the treatment quality is improved through the provision of defibrillators - this is the secondary prevention concept.  Muamba's case was testament to outstanding medical provision.  And so I'd suggest that the money that people are saying should be spent screening, at least once you get down below the professional ranks, might be better spent on training and supporting medical care at events.  

3.  Kenyan women set to dominate in London


Here's a bit of a quiz  (answer below this post):  Name the first Kenyan woman to win a medal at the Olympic Games?  How about the first gold medal winner at the Olympic Games?

The hint is that you don't have to go too far back - while their men have long been dominant on the track, their women have only recently emerged at the same level.  But now, in 2012, they have potential gold medalists in every single track event from 800m to 10,000m, as well as in the marathon, and may even out-medal the men.

In the 800m, the re-emerging Jelimo (more on this later) runs with Jepkosgei, though Jepkosgei may not quite have the capacity to run the 1:57s it might take, so it will probably be up to Jelimo to win gold.  Over 1500m, Helen Obiri will race alongside defending champion Nancy Langat (assuming she makes the team after a fairly disappointing period since Beijing).  In the 5000m and 10000m, Vivian Cheruiyot is arguably the best distance runner in the world right now, and unless Ethiopia can find a way to get Dibaba or Defar back to their 2005/07 form, Cheruiyot should win double gold in London.  Then in the marathon they have an amazing squad, headed by Mary Keitany, and their team strength may be crucial in helping them overcome the challenge from Shobhukova.  The 3000m steeplechase sees Milcah Chemos, though she'll have a Russian challenge to overcome for gold.  Then of course there is a group who've yet to emerge, but don't be surprised to discover a new name or two by July.

So while nothing is certain, Kenya's women look good for a handful of medals, possibly all gold (though that would be extra-ordinary).  Their men are less 'secure' - I can't see them winning 5,000m or 10,000m gold (in fact, I'd be surprised if they pick up more than two minor medals here too, if Bekele is back in good condition).  Rudisha, the steeplechase and a marathon look "certain", and the men's 1500m is open, but Kenya have chances there too.

So the Kenyan women look set to contribute at least half Kenya's medals, and that would be a first.  There is no doubt a fascinating social, economic and cultural discussion to be held about why it has taken the women 40 years to reach the same level as their men did from 1968 onwards.  The floodgates may now have been opened, however, and perhaps the complexity of some of those answers help to further uncover the "secrets" of Kenyan distance running domination, which I believe is the most fascinating question in exercise performance physiology today.

4. Pamela Jelimo re-emerges.  And Caster Semenya kicks off 2012

Every event is of course a drama, but there will be few with as much human interest as the women's 800m.  In 2008, Pamelo Jelimo emerged from Kenya to dominate women's 800m like we've rarely seen before - her crushing, front-running displays and regular 1:56 or faster performances (I count six sub-1:56 times in 2008, including a best of 1:54.01) to win the Olympic Gold and the Diamond league jackpot that year (the only winner of a $1,000,000 jackpot).  All this at the age of 18, it was an unparalleled dominance of the event.

Over the course of the next three years, however, things slid dramatically - first a 1:59.49 failure to make it beyond the semi-finals of the World Championships in Berlin.  Then a best of 2:01.52 in 2010, and a failure to qualify for the African Championships.  2011 saw a best of 2:09.12.  An astonishing fall from the highest peak, fully 15 seconds off her consistent times from 2008.

And now she may be back - 2012 has seen Jelimo return to sub-2 minute territory for the first time since 2009, and that's been indoors.  She won the World Indoor title recently, in 1:58.83, a second sub-2 min clocking on the boards, and won the gold convincingly.  And yes, it is difficult to use indoors as a barometer for the Games, but it's nevertheless a good start and the talk from Jelimo has been promising.

She'll hopefully be back and ready for an event that has seen its fair share of drama, even without her.  There is no athlete in the world more "mysterious" (which is to say, not understood at all) as Caster Semenya.  Jelimo's "disappearance" in 2009 was barely noticed in the storm that gathered around the South African.  Also 18, she too exploded onto the scene, winning a few low key races before making her debut for the world in Berlin.  There, she won easily, and the heavens opened with accusations that she was male.  Controversy, gender verification tests, controversy and a return to the podium for silver in 2011 followed, amidst allegations of deliberately running slowly and losing on purpose to deflect attention, and of still being a man.  Semenaya runs under a microscope few others can imagine.

She'll do the same in 2012, until there is more transparency regarding what happened with regards to her treatment during 2009 and 2010 - the athletics fraternity will remain untrusting and the media will continue to cheer her defeats (as allegedly happened in Daegu when Savinova overhauled her).  She kicked her 2012 season off with a pretty slow 2:03.60 in a local meet here in SA.  That's fully 6.6% off her best, and is the equivalent of David Rudisha kicking off with a 1:51!

It would be "typical" for an elite athlete to start their season and improve by 2 to 3% (2 to 3.5 seconds over 800m), and 6.6% is a big jump to make.  But it's difficult to interpret, because an athlete like Semenya doesn't to be fast to win against weak local opposition, and has the 'luxury' of starting gradually.

So it will be interesting to see how she goes in the first few races of the European season.  Her large variability in performance (last year she was going from well outside 2 minutes to well inside fairly regularly), her racing strategy and apparent ease of running will attract more speculation.

All in all, there are few events with more intrigue than the women's 800m.

5.  The Olympic fashion show begins - why the kit is more important than one might think

If it's an Olympic year, and that means the race to unveil the latest in sports clothing is on.  Some nations have gone for designer kit, like Italy with Giorgio Armani, Great Britain with Stella McCartney.  The GB reviews were not great - not enough red, they said, even though it seemed to have about as much red as they always have.

I get the feeling you can never win with these high-profile kit launches - recently, in Australia, adidas launched the super lightweight kit and hurdler Sally Pearson commented that it was so light it was like being naked.  Of course, that's the quote that was sent around the world, and once taken out of context, "super light" no longer seems super complimentary!

This kit launch topic got a few people talking over on our Facebook and Twitter pages.  I can appreciate that people want to watch sport, and don't appreciate when it gets transformed into fashion.

But I think this fashion focus is good for two reasons.  One is that if the kit was low-key and understated, the sport would reach far fewer people.  The reality is that sport doesn't appeal to everyone, just as fashion doesn't appeal to everyone.  But by overlapping them, even if only for a day or two, it raises awareness of the athletes and the events.  If there are 100 people who have now seen Jessica Ennis or Phillips Idowu because they were shown on Sky News and in newspaper modeling McCartney's designs, then the sport of athletics is better off for it.

Secondly, I think the importance of good kit is undervalued as a performance enhancer.  Not for the obvious reason that it keeps athletes cool or light or any of the other "gimmicks" that are often sold with kit, but because it says to the athlete that "we invest in you".  This psychological factor is more obvious in the other direction - if you neglect to look after the athlete's image, then you undermine their professionalism.  I'm lucky (or unlucky, actually) to experience this in SA, where our Olympic Committee often bungle the kit - in Beijing, we got what the athletes themselves described as grandma's knitting, and many refused to wear it for training, saying it was just too hot, itchy and uncomfortable.  Ahead of London, nobody knows what we're getting, but among the athletes I'm involved with, nobody is exactly holding their breath.

I worked with SA Canoeing, who didn't even provide kit to their aspirant Olympic paddlers, other than a suit to race in.  No out of competition kit at all, and that contrast between us and the likes of Germany, GB and France at the World Championships I attended in Poznan in 2010 was stark - clothes don't necessarily make the man, but they help the athlete a heck of a lot, especially when he doesn't have any compared to rivals who have everything!  The clothes are a symptom of the system-wide attitude to excellence, and the reality is that if the powers that be shared a mindset of excellence, they'd recognize that kit fits into that ethos.  Some nations succeed despite their kit, which again points to a larger problem of professionalism and "elitism" of attitudes towards success and excellence.

And there's a snap reaction to that, where athletes (and me) can be labeled "primadonnas", but that's not fair either (in this case).  I have been lucky (and I mean it this time) to have worked with SA Sevens, where we've tried very hard to foster professionalism, and recognize that this kind of thing really matters.  So if I'm an Olympic athlete, racing in kit that has been commissioned by my management from Stella McCartney, made by adidas (or Armani, in the case of Italy, or Hilfiger for the USA), then that's worth a tiny bonus.  And who knows, perhaps those tiny bonuses add up to difference between reaching a final or not, between winning a medal or being fourth...?

That's a wrap for this week's Olympic Buzz around the Rings.  It was a long one - that's only because I had a month's worth of news to sum up!  From now on, a weekly Buzz should be shorter!

Bring on the Games!

Ross

Question answers:

The first woman to win an Olympic medal was Pauline Konga, who won silver in the 1996 Atlanta Olympic 5000m race.

The first Kenyan gold was as recently as 2008 - Pamela Jelimo in the 800m. She was followed only days later by Nancy Langat in the 1500m, but Beijing was the first time that a Kenyan gold medalist was female.  By the end of London, they may have doubled that number...

Vibram shoes named in lawsuit: The danger of barefoot running

Vibram Five-finger named in lawsuit - zealousness, unfiltered advice creates more problems than it fixes

I received this link from a reader yesterday, which explains how Vibram USA Inc and Vibram FiveFingers LLC are part of a lawsuit where it is being alleged that they made "deceptive and misleading statements about the benefits of barefoot running".

It is alleged that the company, which makes the now famous Five-Finger shoe (pic on the right) have made deceptive claims about their health benefits, and this is leading to increased injuries among runners who make the switch.

The problem - the "skill" of barefoot running was not recognized

There is even some research as part of the lawsuit - the American Council of Exercise is carrying a report of this study, which finds that many people who make the switch continue to land on their heel.

Why is this potentially bad?  Well, the graph below, taken from a study on the ACE website, shows the loading rate in three conditions - barefoot (blue column), in Vibrams (purple) and in normal running shoes (green).

What should be immediately clear is that when you look at runners who land on the forefoot (shown by the cluster on the left) the loading rate is lowest when barefoot and highest when forefoot.

However, when you look at runners who land on the heel (right cluster), their loading rate goes in the other direction - here, the barefoot runners who heel strike have loading rates that are about double those of shod runners who are landing on the heel.  This is the effect of the big cushion under the heel of modern running shoes, and it serves to dampen the impact and reduce the loading rate significantly.  Vibrams lack this cushioning, on so fare only marginally better than the pure barefoot condition in heel-strikers.

Those of you who have followed this barefoot running debate will immediately recognize that this finding of impact force differences is not new at all.  In fact, it was found by Daniel Lieberman in a paper published in Nature about 2 years ago.  Lieberman's differences were even more striking - he found that if you run barefoot and land on the heel, then your impact forces are seven times higher than if you land on the heel in shoes.

The graph below is one that I redrew using Lieberman's data and put on this website when I reviewed the barefoot running phenomenon last year.

Now, having said all this, it's important to find the balanced, evidence-based view and be transparent about some "limitations" in these studies.  The first is that the link between loading rates and injuries is not as tight as many would think.  Certainly, higher loading rates have been associated with certain conditions (bone stress injuries being the main one), but the precise aetiology of how injury develops is far more complex than simply saying "if you reduce loading rate, you won't get injured".  Truth is, you might just get a different injury, especially if you start running on the forefoot because you see these graphs!

Then secondly, I'd like to see the study above published in a peer-reviewed journal, only to see the methods in a bit more detail.  Lieberman found a pretty large difference (7-fold) whereas the latest study finds a 2-fold difference between shod and barefoot runners when heel-striking.  That, plus the exact percentage of runners who continue to heel-strike, as well the 'training' they did for the two-week training period, would be of interest to me in order to understand exactly what is being measured in the laboratory.

On that note, Lieberman found that 83% of habitually shod runners were still heel-striking when barefoot.  The ACE study is saying 50% are still heel-striking, even two weeks into running with the minimalist shoes.

Now, that flies in the face of the popular literature, which tells us that when you run barefoot, you switch automatically to an apparently amazing cushioned forefoot running style.  That doesn't seem to happen, though, and the vast majority of people seem to take a lot longer to make this transition than the books (Born to Run is the main one) suggest.

The skill component

In fact, I believe this leads to the most intriguing question of all - understanding the skill of barefoot running.  The ACE study, mentioned above, had the runners do a 2-week "familiarization" period in the Vibrams, where they were asked to run for 20 minutes a day in an attempt to get them accustomed to it.  It's easy to criticize this period as too short and insufficient (all the stuff those who've already made up their mind can say - no study is perfect, remember).

But this two-week adaptation period may partly explain why Lieberman found that 83% of his shod runners were heel-striking when barefoot, whereas the ACE study found that "approximately half" were heel-striking.  Perhaps two weeks of familiarization was responsible for the shift of more runners (1 in 2 rather than 1 in 6) to a forefoot strike, as they 'learned' how to run.

The real question, however, is why the other 50% didn't make this adaptation?  And whether they would given more time? Are there some runners who would never succeed?  Who are they, and what distinguishes them from those who do succeed?  I strongly suspect that some people CANNOT adapt to barefoot running, that they don't have the necessary "skill" to improve the way they run barefoot and change what is years of shod-running-induced motor patterns.

Of course, this is an unanswered question, but I think it's the most important one that needs to be answered right now.  Just as one would not expect anyone who picks up a tennis racquet or a golf club to even become competent at playing it (especially later in life), I don't think it should be expected that simply making the transition to barefoot running will be sufficient either.  Everyone can improve, certainly.  But can they good enough to overcome or avoid what are some pretty clear "risks" associated with the transition?  Remember, in running, unlike tennis or golf, it's not good enough to simply improve over time, because if you don't improve enough, you get injured, so there is a "minimum required improvement" to make the transition to barefoot or minimalist running viable in the first place.

Coaching - sound in theory, but another risk in practice

Here, one can begin to introduce the concept of coaching, that barefoot running (or any running, for that matter) should be taught as a skill.  And certainly, this would help.  In the same way that my tennis or golf game will improve faster if I'm guided, running ability will too.  However, I don't think this will overcome what, for some people, may be a "skill deficit" that will prevent them from succeeding at barefoot or minimalist running.  Again, this is an unanswered question, at least for now.

The other issue, which I raised above, is that there is substantial risk associated with making any change in running technique.  This distinguishes running from, say golf, where wrong technique means lots of lost balls and frustration.  In running, failure to find that apparently elusive "correct running technique" equals disaster.  And what makes it even more tricky is that there's no feedback until the injury - unless you have fancy high speed cameras and force plates to analyse how you run, the first sign of the mistake is often injury.

So if you are going to advocate that people should run barefoot and then coach them so that they learn the right way to do it, then you'd better be certain that you'll make them good enough to avoid the risk - there is a minimum threshold, and if a runner fails to reach it, you've led them to injury, despite good intentions.  And it's not fair to runners to say "Run barefoot" and then blame the runner for their failures.

It's not simply about forefoot landing - even more danger lurks there

To illustrate this, the one thing that many will take out of this study is that it's the forefoot landing that will make the difference.  That is, if you land on the forefoot, you'll be fine.  And in theory, this is borne out by the evidence shown in the two graphs above.

However, in reality, it's a little more complex.  One of the authors of this ACE study is quoted as saying "Buying these Vibrams and continuing to land your heels is probably worse than wearing shoes because the Vibrams don’t have any cushioning. … People may need very explicit instruction and time spent practicing how to land on the ball of the foot. Otherwise, they may be doing themselves more harm". 

I think this is advice is probably MORE DANGEROUS than not saying anything, because as soon as you give an explicit instruction, you put the runner into the compromised situation where they are now focused on a forefoot landing. How do this achieve this?  They planar flex - point the toe away from their body, and drop more than three times their body weight down onto a contracted calf muscle in a compromised shortened position, about 400 times every kilometer.  That's a recipe for disaster, and so the most common problem associated with barefoot running is Achilles and calf related injuries.

Therefore, you can't "instruct" a runner to avoid the risk.  If anything, you instruct them into risk.  Bad idea.  The key, I believe, is to let the skill be acquired gradually, using a few drills to guide the athlete without ever changing their technique "manually", so to speak.  But here again, nobody really knows what works and what doesn't.  We don't even know what constitutes "good technique", and so to simplify it down to which part of the foot hits the ground first is also wrong.  And that's why it's reckless to advocate anything.  At this stage, everyone is learning, and so advocacy has no place, in my opinion.  It's all about education for now.

Extremism:  the media are more to blame than Vibram

Final point re "responders" and "non-responders".  Because we don't yet know who belongs to each group, I think it's reckless and irresponsible to treat them all as potential responders.  The prudent thing to do would be to assume the "worst case scenario", that everyone is a non-responder who needs serious time and intense work and lots of practice.  And then start from this point, and if a runner adapts faster, so be it, that's good news.  Instead, the media and advocates of barefoot running assume that everyone should make the switch because everyone will benefit.  And the bodies left behind will be dealt with later.  It's just too aggressive, too extreme.

And on this note, the media have propagated the myth far more even than the shoe companies like Vibram have.  Vibram are trying to sell shoes, and so they make claims as part of marketing strategies to differentiate their product from their rivals'.  That's normal.  And I can't comment on the specifics of the lawsuit - maybe they're guilty.

But I do know that the media have done a poor job of providing education on this topic.  With a few notable exceptions, they have allowed themselves to become a platform for the advocates of barefoot running without providing the necessary education.  Lieberman's paper illustrates this - he titled that research study "Foot strike patterns and collision forces in habitually barefoot versus shod runners".  The word "habitually" was in there for a reason.

But when the media got hold of that study, they reported only that barefoot running was excellent because it reduced loading rates 7-fold.  This study "proved" the benefit of barefoot running.  Quickly, the "extremists" (my pet hate in all matters of sports science) jumped on this said "It proves our point" and the study's other findings were lost in the aggressive or uninformed interpretation of the data.

This is an eerily similar thing to what happens when it comes to dietary advice.  Recently, I've been involved in debate back here in SA about paleo diets, low carb diets, high carb diets and the like.  And once again, it's a situation where people seem to become over-zealous, finding a cause for which they appoint themselves the spokesperson.  Their success, which is either isolated (1 in 100) or common (1 in 2, perhaps, but never 100%) becomes their proof, and they start telling the world there is only one way to succeed.  "Follow me to change your life" is the message, whether it's barefoot running or eating like a caveman supposedly did.  They thus make the mistake they accuse others of making, by lumping everyone into the same group.

And here, those who succeed become loud, outspoken (and dare I say, obnoxious), whereas those who fail slink away into the background and remain quiet about their failure.  So those who tried barefoot running and got injured disappear, those who succeeded often find a soapbox, write a book, and shout about it.  Those who try low carbohydrate diets and fail revert back to routine with minimal fuss, whereas those who succeed feel the need to tell the world.  They dismiss any research study finding that challenges their position as "corrupt", "incompetent" and "garbage", and so debate goes nowhere.  Once again, this happens because of aggressive advocacy, when it should be about education.

Prescribing a treatment for a condition we don't understand, without knowledge of risk or benefit

Which brings me to the final point.  The big issue, I believe, is that people have become carried away with barefoot running as a way to treat injury and potentially improve performance without really appreciating how it might work (or, importantly, that it may not).

The result then is that barefoot running has taken on the characteristics of a medicine or a drug - it is dispensed by "experts" (who often change their names to "Barefoot X") as a "treatment", but unlike drugs, there are a few key things missing:

• We don't know which conditions (injuries) the treatment will be effective for.  And by definition, this means we can't say when it will be ineffective
• We don't know what the correct dosage is
• We don't know how to phase the dosage in over time for different people
• We don't know whether the "treatment" is effective for everyone, or whether there are responders and non-responders
• We don't recognize the possible "contra-indications".  When you take a powerful drug prescribed by a doctor, he knows to check for certain conditions - pregnancy, allergies etc.  For barefoot running, nobody has thought about this
• What is the effect of other factors on the success of the 'treatment'?  For example, how does fatigue, terrain, muscle weakness, flexibility, strength etc impact on the success of the outcome?
• As a result of all of the above, we are in a very poor position to quantify the risks, and the "cost-benefit" of barefoot running.

The point is, all the answers, which are pretty important, that you can read on the package insert when you get prescription medication, are unknown for barefoot running.  Yet it is still prescribed 'recklessly'.

And for this, I completely blame the polarization of the debate that allows extremist views to develop and thrive.  It's perfect for the media and the 'zealots' who try to force their success on large groups of people without being open to the other side.  And there are some who are more moderate - I apologize for lumping everyone together.  But there are many who are not.  They base their 'prescription' of barefoot running on their own success story, or at best, a group of runners who they have succeeded with, and suddenly, the entire running community is being told to take this "drug".  It works.  Maybe.  In some people.  If they get it right.  Possibly.  That's not good enough.

And what's worse is that when it doesn't work, when they get injured, then it's their fault.  To return to the medication analogy, this is like giving a drug out to a sick patient and then hoping they get the dosage right.  And even if they follow the instructions to the letter, they may fail, and then it's their doing.  They must have done something wrong.  That's not a viable drug.  It's not a viable "product", and until that is recognized, I would caution all runners to be a little more prudent about how they advise others, and about following advice they receive.

The golden rule in science should be that polarization should be regarded as highly suspicious.  There are very few things that are known with absolute certainty, and when you're dealing with incredibly complex human physiology, the individual differences that make us who we are, what we're good at, how we run and what we eat, for example, are so vast and complex that nothing can be polarized without being wrong!  So when someone says "It's all about training, genes don't matter", they're just as wrong as someone who says "It's all about genes, training is irrelevant".

Similarly, barefoot running is not "the answer", but nor is it bad.  Carbohydrates are not evil, but nor are they the best option for some people, as evidence is now showing.  An individual approach is the only accurate way to go - it's not great for the media who love the sensation, and it's not great news for the gold-diggers who want sensation to sell books, but that's the reality.

Barefoot running - where does it leave us? Opinion and exploration

And so for barefoot running, where does that leave us?  Again, this is my opinion, based on the evidence and my own current research (I have two research studies underway, looking at various aspects of what I've discussed in this and other posts - results in a year or so!).  However, I'd say the following:

In a group of 100 runners, every single one will benefit from barefoot running as a training method.  It changes muscle activation patterns, strengthens muscles and tendons that we don't activate nearly as well in shoes, may be an effective form of rehabilitation, and it's really enjoyable.  So I would say that everyone should incorporate some barefoot running into their training programme.  Whether it's a 2 minute warm-up, an easy 30 min jog once a week, or some sprints after training, I'd say try it out and feel the difference it makes.

However, it's probably not for everyone.  Practically, theoretically, logistically and for many other reasons, some people will not take to barefoot running well enough for them to become 100% barefoot runners.  However, for others, it may well work.  It may prove to be the answer to your prayers, and the secret to injury-free running for life.  That's fantastic, and so you should embrace it and do it with enjoyment.  But don't believe that because it helped you, it must be used in the same dosages by everyone else - they may not have the same "condition" as you, they may have an entirely different history and thus set of contra-indications, and your enthusiasm, however well intended, will cause more problems than it solves.

You may sit on one of the poles - either north or south, either a responder and great barefoot runner, or a non-responder, and classic shod runner.  Which is perfect for you, but remember, between those poles, there's a world of people who are different, and so your extreme position in the complex spread of physiology shouldn't produce an extreme advocate for anything.

Ross

The 2012 red meat-mortality study (Arch Intern Med): The data suggests that red meat is protective

I am not a big fan of using arguments such as “food questionnaires are unreliable” and “observational studies are worthless” to completely dismiss a study. There are many reasons for this. One of them is that, when people misreport certain diet and lifestyle patterns, but do that consistently (i.e., everybody underreports food intake), the biasing effect on coefficients of association is minor. Measurement errors may remain for this or other reasons, but regression methods (linear and nonlinear) assume the existence of such errors, and are designed to yield robust coefficients in their presence. Besides, for me to use these types of arguments would be hypocritical, since I myself have done several analyses on the China Study data (), and built what I think are valid arguments based on those analyses.

My approach is: Let us look at the data, any data, carefully, using appropriate analysis tools, and see what it tells us; maybe we will find evidence of measurement errors distorting the results and leading to mistaken conclusions, or maybe not. With this in mind, let us take a look at the top part of Table 3 of the most recent (published online in March 2012) study looking at the relationship between red meat consumption and mortality, authored by Pan et al. (Frank B. Hu is the senior author) and published in the prestigious Archives of Internal Medicine (). This is a prominent journal, with an average of over 270 citations per article according to Google Scholar. The study has received much media attention recently.

Take a look at the area highlighted in red, focusing on data from the Health Professionals sample. That is the multivariate-adjusted cardiovascular mortality rate, listed as a normalized percentage, in the highest quintile (Q5) of red meat consumption from the Health Professionals sample. The non-adjusted percentages are 1.4  percent mortality in Q5 and 1.13 in Q1 (from Table 1 of the same article); so the multivariate adjustment-normalization changed the values of the percentages somewhat, but not much. The highlighted 1.35 number suggests that for each group of 100 people who consumed a lot of red meat (Q5), when compared with a group of 100 people who consumed little red meat (Q1), there were on average 0.35  more deaths over the same period of time (more than 20 years).

The heavy red meat eaters in Q5 consumed 972.37 percent more red meat than those in Q1. This is calculated with data from Table 1 of the same article, as: (2.36-0.22)/0.22. In Q5, the 2.36 number refers to the number of servings of red meat per day, with each serving being approximately 84 g. So the heavy red meat eaters ate approximately 198 g per day (a bit less than 0.5 lb), while the light red meat eaters ate about 18 g per day. In other words, the heavy red meat eaters ate 9.7237 times more, or 972.37 percent more, red meat.

So, just to be clear, even though the folks in Q5 consumed 972.37 percent more red meat than the folks in Q1, in each matched group of 100 you would not find a single additional death over the same time period. If you looked at matched groups of 1,000 individuals, you would find 3 more deaths among the heavy red meat eaters. The same general pattern, of a minute difference, repeats itself throughout Table 3. As you can see, all of the reported mortality ratios are 1-point-something. In fact, this same pattern repeats itself in all mortality tables (all-cause, cardiovascular, cancer). This is all based on a multivariate analysis that according to the authors controlled for a large number of variables, including baseline history of diabetes.

Interestingly, looking at data from the same sample (Health Professionals), the incidence of diabetes is 75 percent higher in Q5 than in Q1. The same is true for the second sample (Nurses Health), where the Q5-Q1 difference in incidence of diabetes is even greater - 81 percent. This caught my eye, being diabetes such a prototypical “disease of affluence”. So I entered the whole data reported in the article into HCE () and WarpPLS (), and conducted some analyses. The graphs below are from HCE. The data includes both samples – Health Professionals and Nurses Health.

HCE calculates bivariate correlations, and so does WarpPLS. But WarpPLS stores numbers with a higher level of precision, so I used WarpPLS for calculating coefficients of association, including correlations. I also double-checked the numbers with other software, just in case (e.g., SPSS and MATLAB). Here are the correlations calculated by WarpPLS, which refer to the graphs above: 0.030 for red meat intake and mortality; 0.607 for diabetes and mortality; and 0.910 for food intake and diabetes. Yes, you read it right, the correlation between red meat intake and mortality is a very low and non-significant 0.030 in this dataset. Not a big surprise when you look at the related HCE graph, with the line going up and down almost at random. Note that I included the quintiles data from both the Health Professionals and Nurses Health samples in one dataset.

Those folks in Q5 had a much higher incidence of diabetes, and yet the increase in mortality for them was significantly lower, in percentage terms. A key difference between Q5 and Q1 being what? The Q5 folks ate a lot more red meat. This looks suspiciously suggestive of a finding that I came across before, based on an analysis of the China Study II data (). The finding was that animal food consumption (and red meat is an animal food) was protective, actually reducing the negative effect of wheat flour consumption on mortality. That analysis actually suggested that wheat flour consumption may not be so bad if you eat 221 g or more of animal food daily.

So, I built the model below in WarpPLS, where red meat intake (RedMeat) is hypothesized to moderate the relationship between diabetes incidence (Diabetes) and mortality (Mort). Below I am also including the graphs for the direct and moderating effects; the data is standardized, which reduces estimation error, particularly in moderating effects estimation. I used a standard linear algorithm for the calculation of the path coefficients (betas next to the arrows) and jackknifing for the calculation of the P values (confidence = 1 – P value). Jackknifing is a resampling technique that does not require multivariate normality and that tends to work well with small samples; as is the case with nonparametric techniques in general.

The direct effect of diabetes on mortality is positive (0.68) and almost statistically significant at the P < 0.05 level (confidence of 94 percent), which is noteworthy because the sample size here is so small – only 10 data points, 5 quintiles from the Health Professionals sample and 5 from the Nurses Health sample. The moderating effect is negative (-0.11), but not statistically significant (confidence of 61 percent). In the moderating effect graphs (shown side-by-side), this negative moderation is indicated by a slightly less steep inclination of the regression line for the graph on the right, which refers to high red meat intake. A less steep inclination means a less strong relationship between diabetes and mortality – among the folks who ate the most red meat.

Not too surprisingly, at least to me, the results above suggest that red meat per se may well be protective. Although we should consider a least two other possibilities. One is that red meat intake is a marker for consumption of some other things, possibly present in animal foods, that are protective - e.g., choline and vitamin K2. The other possibility is that red meat is protective in part by displacing other less healthy foods. Perhaps what we are seeing here is a combination of these.

Whatever the reason may be, red meat consumption seems to actually lessen the effect of diabetes on mortality in this sample. That is, according to this data, the more red meat is consumed, the fewer people die from diabetes. The protective effect might have been stronger if the participants had eaten more red meat, or more animal foods containing the protective factors; recall that the threshold for protection in the China Study II data was consumption of 221 g or more of animal food daily (). Having said that, it is also important to note that, if you eat excess calories to the point of becoming obese, from red meat or any other sources, your risk of developing diabetes will go up – as the earlier HCE graph relating food intake and diabetes implies.

Please keep in mind that this post is the result of a quick analysis of secondary data reported in a journal article, and its conclusions may be wrong, even though I did my best not to make any mistake (e.g., mistyping data from the article). The authors likely spent months, if not more, in their study; and have the support of one of the premier research universities in the world. Still, this post raises serious questions. I say this respectfully, as the authors did seem to try their best to control for all possible confounders.

I should also say that the moderating effect I uncovered is admittedly a fairly weak effect on this small sample and not statistically significant. But its magnitude is apparently greater than the reported effects of red meat on mortality, which are not only minute but may well be statistical artifacts. The Cox proportional hazards analysis employed in the study, which is commonly used in epidemiology, is nothing more than a sophisticated ANCOVA; it is a semi-parametric version of a special case of the broader analysis method automated by WarpPLS.

Finally, I could not control for confounders because, given the small sample, inclusion of confounders (e.g., smoking) leads to massive collinearity. WarpPLS calculates collinearity estimates automatically, and is particularly thorough at doing that (calculating them at multiple levels), so there is no way to ignore them. Collinearity can severely distort results, as pointed out in a YouTube video on WarpPLS (). Collinearity can even lead to changes in the signs of coefficients of association, in the context of multivariate analyses - e.g., a positive association appears to be negative. The authors have the original data – a much, much larger sample - which makes it much easier to deal with collinearity.

Moderating effects analyses () – we need more of that in epidemiological research eh?