Thanks for the generally excellent level of debate, marred by the inevitable personalisation of argument especially by those who have nothing better to contribute. May I be allowed to make a few comments.
The first case of (near fatal) exercise-associated hyponatremic encephalopathy (EAHC) happened in the 1981 56 mile Comrades Marathon in South Africa. Although I was involved in a research project in the Comrades medical tent on that day I did not personally see the patient. However she wrote to me a few weeks later to ask my advice. I told her that I had absolutely no idea what had caused her EAHC. Over the next 3 years I interviewed another 3 athletes who had developed exercise-associated hyponatremia (EAH). On the basis of that information, a series of calculations and 3 years of contemplation and reading the literature, I concluded that the condition occurred in athletes who ingested too much fluid during exercise. This was described in a paper published in 1985. In an editorial that accompanied the reprinting of that, by then, classic paper 20 years later, the author wrote that: “Tim Noakes was right 20 years ago and the passage of two decades has done nothing to diminish the accuracy of his conclusions”.
To evaluate our 1985 hypothesis we next completed a prospective, controlled, in-hospital study of 8 athletes as they recovered from either EAH or EAHC developed during the 1988 Comrades marathon. This study published in 1991 proved our 1985 conclusion since it confirmed that all these athletes were over-hydrated by between 2 and 6 litres (4-12lbs). Furthermore we also established that sodium depletion played no role in these cases since their sodium deficits at the end of the race was not different from those that developed in a control group of ultra-marathon runners.
What normally happens in medicine is that such evidence is pretty quickly absorbed and become the mainstream practice. But in this case, this did not happen. Instead I discovered that I became the target of a subtle disinformation program that apparently still continues today, judging by some comments on this blog. I found that I was no longer welcome at certain conferences or athletic events, funded by certain organisations. So I was cast as an evangelist, a religious zealot, someone who ignored all the published evidence that did not agree with his particular “religion”, and an iconoclastic egoist who was more interested in fame than in being correct.
Interestingly at the very time that I was being so typecast, the advice to endurance athletes became that they “should drink as much as tolerable” in order to prevent “dehydration”, heat stroke and an impaired performance. So instead of warning athletes of the dangers of overdrinking, conditions were developed which encouraged overdrinking. Whether or not this was the intended outcome, this was indeed the result as so clearly described by Devashish Paul. (Of course, when athletes like Devashish developed the condition it is natural that they should be blamed – as has occurred in this thread - and not those who gave them such dangerous advice). But it did not take a genius to predict what would be the outcome of this advice to “drink as much as tolerable”. And so predictably people died as a result of this advice. At present, an absolute minimum of 11 avoidable deaths, the majority in marathon runners and army personnel in the US, have occurred; the most recent at the 2007 London Marathon. In contrast in those scientifically-backward countries like South Africa and New Zealand where my opinion and that of my co-researcher Dr Speedy have credence, there have been no deaths from this condition and EAH and EAHC has essentially disappeared. With this background it is perhaps appropriate to correct some errors on some submission on this thread.
Philbert makes that error of labelling me an evangelist which is dismissive and unnecessary. The information I have presented since 1985 is based on hard evidence and is now known to be true. My understanding is that evangelists wish to force a personal belief on others, whether or not that belief is “true”. I studied EAH and EAHC for 10 years before we published the definitive evidence that the condition is due to overdrinking without evidence for sodium deficiency. Only thereafter did I become rather more vociferous in my opinion especially when what I had predicted would happen – avoidable deaths – began to happen. As a doctor my first responsibility is to do not harm. If I know that unnecessary harm is being done as a result of ignorance, I have an ethical responsibility to do something about it. If the price of that activism is to be labelled an evangelist, then perhaps that is a small cost.
Philbert also claims that there were many nephrologists saying the same sort of thing before “Noakes really got any steam behind him”. Again this is dismissive besides being untrue. There is no evidence in the published literature that “many nephrologists” were “saying this sort of thing” at the time of our first publication in 1985. How could they have since the condition was unknown at the time? And if the mechanisms were already so well understood by so many, why is it that so many avoidable deaths occurred in the US between 1993 and 2002, fully 17 years after our first publication? There is a saying that science goes through three phases: First they say that what you say is nonsense. Then they say that what you say is correct but it is irrelevant. Then they say that what you say is true but we have always known it. I appreciate Philbert’s support that we are now in the third phase of the truth of EAH and EAHC but he should be more circumspect in his descriptions of others, particularly if he is not in command of all the facts.
Like many others, I have knocked heads with Dr Coggan frequently over the past 20 years but never on the question of fluids and exercise which, in my understanding, is not within his area of expertise. My review today of his publication list on PubMed reveals that of the 59 listed papers he has published between 1984 and 2007, not one is on fluid balance during exercise. Thus I am surprised that he considers himself to be such an expert on the topic. But I am most relieved that in those 23 years he has not lost his venomous tongue, nor his capacity to use insults as his main weapon of argument. So he claims that I (not he) have not “conducted a single experimental study to support his (ie my) claims”. To combat my abject ignorance he advised that I should do more than just “skim through a few papers and/or chat with a few graduate students to understand the real story here”. To overcome their ignorance, visitors to this blog are also advised that: “you have to dig into the data and base your conclusions on what it actually shows (vs what a self-described iconoclast such as Noakes claims it shows)”.
In my defence, I would suggest that readers should access PubMed to see for themselves whether or not I have done any laboratory studies of fluids and exercise or whether my ideas of the etiology of EAH and EAHC are based solely on a fantasy driven by the egocentric need for a personal aggrandisement so that I can be “iconoclasatic”. (Actually it was a prominent member of the Gatorade Sports Science Institute who first labelled me as iconoclastic, not myself).
Not only has Dr Coggan never undertaken any studies of this topic, but he enjoys the rare privilege of the laboratory exercise scientist – absolute immunity from responsibility for any outcomes resulting from his advice. However in my position as a medical doctor and medical director of a number of ultramarathon and Ironman triathlon races over the past 30 years, I do not enjoy such absence of responsibility. Rather I am accountable for any adverse outcomes that result from the drinking advice that I give athletes in these races and for any treatments that they might receive, based on those opinions. So I am glad to report that the Ironman Triathlon races at which I was the medical director had the lowest reported incidence of post-race medical admissions of any such race on record and a negligible incidence of EAH and EAHC.
But Dr Coggan, who really understands, claims that: “Noakes is, to be blunt, someone who would apparently be just as happy to be known as being right. That is, IMO he is overly willing to ignore data that contradicts his unusual points of view (plural, because this is but one of many issues on which Noakes has adopted a position that is contrary to the evidence… as mentioned before he himself says that he’s an iconoclast”.
Later his insulting diatribe continues: “No, I think that Noakes is a true believer in his own religion, i.e. he’s not tailoring his message to try to achieve some altruistic goal”.
Surprising then that when we apply this incorrect, unscientific, egotistical knowledge purely for the purpose of self aggrandisement and without respect for what is really “true”, we deliver results that no other Ironman race has yet recorded and, in addition, we have an essentially negligible incidence of EAH and EAHC. Perhaps this is the kind of untrue “religion” that others should be adopting rather urgently.
Probably Dr Coggan is not aware that in November 2006, the Runner’s World (USA) magazine voted our work on EAH as one of the 40 most important “people or events” of the past 40 years in running. Which is not bad for work originating outside the United States of America. Such recognition suggests that at least some people consider that this work is rather more than that of an egotistical iconoclast who “just wants to be known”, whether or not he is right.
A great deal of the discussion is based on the concept that the body defends its weight so that if the weight is measured, then the correct drinking guidelines can be arrived at. In fact the body defends its osmolality through the thirst mechanism, and not the body weight. Thus the presence of thirst indicates that the brain considers that the osmolality has changed sufficiently to require correction. We have shown that the extent to which thirst develops is under genetic control so that some drink avariciously during exercise whereas others drink hardly at all. In an upcoming debate with the gentlemanly Dr Michael Sawka to be published in Medicine and Science in Sports and Exercise, I present the argument that the reason why exercise performance is impaired in persons who drink less than their thirst dictates during exercise is not because they are “dehydrated” but rather because they are thirsty.
According to this logic and supported by all the published evidence (including 2 studies of our own of which Dr Coggan appears ignorant – see also my recent article in the Journal of Sports Sciences), exercise performance is maximizes in those who drink enough to avoid thirst during exercise regardless of how “dehydrated” they become. Thus some will be thirsty when they are 2% dehydrated and others will not be thirsty even if they lose 6-10% body weight (as our data on Ironman triathletes seems to show). Interestingly in our as yet unpublished study we show that simply telling people they will not be drinking during exercise impairs their performance right from the start of exercise (that is in anticipation) and before they have become "dehydrated". This shows that the way in which not drinking affects performance is a little more complex than currently understood.
Finally there is now good evidence that humans evolved as long distance runners on the African savannah and that our ability to sweat (and become dehydrated) allowed us to outrun faster antelope whose inability to sweat (and to become dehydrated) prevented them from maintaining low body temperatures during very prolonged (4-6 hours) exercise in extreme dry heat (between 40-46 degrees Centigrade; 104-115 degrees Farenheit) when both had limited access to water. The most effective hunters would be those who developed the least thirst despite high levels of dehydration since they would have been the most likely to continue running for so long and therefore most likely to kill their quarry.
This evolutionary model predicts that the best endurance athletes will therefore be those best able to run without becoming thirsty even though they lose large amounts of weight. The low drinking rates of most of the world’s best endurance athletes in marathon, ultramarathon and Ironman triathlon races provides anecdotal support for this surprising hypothesis.
To follow a 4 hour hunt with minimal fluid replacement by the !kung San (Bushmen) in the Kalahari desert at 46 degrees Centigrade, readers might wish to view The Great Dance – a hunter’s story (http://www.rapidblue.com
That is my story. I will not respond further but in future scientific publications on this topic. So you are welcome to say what you wish.