Case Proven: Exercise Associated Hyponatraemia is Due to Overdrinking. So Why Did it Take 20 Years Before the Original Evidence was Accepted?
“History is replete with examples of correct ideas that were not accepted until subsequent generations confirmed their validity. Usually there is a logical reason for this delayed acceptance; often the fault lies with the researchers themselves.
So, are we who first concluded that EAH and EAHE are caused by overdrinking during exercise equally at fault? Here the evidence appears to be the following.
The original papers of Noakes et al (1985) and Frizzell et al (1986) were merely case reports and hence little more than anecdotes. That they both independently drew the same conclusions should, however, have been given more credence. In the pre‐scientific era of medical research they would certainly have achieved a greater impact.
But the paper of Irving et al (1991) unequivocally proved that fluid overload was present in all eight cases of EAHE in ultramarathon runners. Had these studies been completed in the 1950s and published in the Journal of Clinical Investigation, it is likely that they would have been accepted as “classical” and sufficient proof. But they were not, so the question remains: could we have done more?
The clear criticism is that we did not complete a study of the magnitude and impact of that of Almond et al (2005) published in the New England Journal of Medicine with an accompanying editorial. This made all the difference, even though the study did not come to any materially different conclusions from those that we had reached from our studies of runners in Durban, South Africa, and Ironman triathletes in Auckland, New Zealand. But Auckland is not Boston, and the Comrades marathon is not the Boston marathon. For the reality is that the influence of science is not independent of where that science is practised.
But in reality it would have been impossible to undertake a similar study in either New Zealand or South Africa as our preventive actions had ensured that the condition had essentially disappeared from our ultradistance events in New Zealand (Speedy et al., 2000) and South Africa (Noakes et al., 2004; Sharwood et al., 2002; Sharwood et al., 2004) and has yet to be reported in a 42 km marathon runner in either South Africa or New Zealand (Reid et al., 2004).
And finally there is the issue of timing. An editorial similar to that ultimately published in the British Medical Journal (Noakes, 2003) was submitted to the New England Journal of Medicine about two years earlier, after the death of Dr Kelly Barrett in the 1998 Chicago marathon. But it antedated the death of Dr Cynthia Lucero at the 2002 Boston marathon and hence was too early, too improbable, and advanced by scientists who were geographically too distant from the perceived centre of global medical science.
Perhaps one defence open to us is that we failed to secure our argument because it conflicted with the prevalent message that was being driven by the sports drink industry. Their unsubtle message has become what Dr Cade, the inventor of the industry,(Cade et al., 1972; Cade et al., 1971; Cade et al., 1992) preached in 1972: that sports drinks are a medicine that must be ingested during exercise in order to prevent heat illness and optimise performance (by preventing or alleviating fatigue) and that the more that is ingested the better. What we have learned is that, in the face of such a message and pitted against the power of modern marketing,(Taylor & Giles, 2005; Nature, 2005) an opposite scientific message may not be heard. In this case, only the death of Dr Cynthia Lucero in very public circumstances produced the tipping point that allowed the concealed truth to be exposed.”
Source: Noakes, T.D. & Speedy, D.B. (2006) Case Proven: Exercise Associated Hyponatraemia is Due to Overdrinking. So Why Did it Take 20 Years Before the Original Evidence was Accepted? British Journal of Sports Medicine. 40(7), pp.567-572.