MEDICUS MARCH 2016

Q & A

Q. Following the 2015 EAH Consensus Guidelines, what measures have been taken to disseminate the information? IR: The guidelines themselves were co-published and made open access

participation marathons. Those most at risk are slow, small and following a fixed fluid intake regime. All these factors combine to lead to excessive fluid intake, which is the primary aetiologic factor in EAH. Q. How does the body react to aggressive fluid intake? IR: Normally, and with only short periods of excessive fluid intake, we simply excrete the excess as urine. However, if high intake is prolonged, this protective mechanism can be overcome. Q. What are the risks associated with the condition? IR: What seems like a surprisingly small change in the serum sodium acutely can cause symptoms. Symptoms start at about a 7 per cent relative change, this being enough to cause early fluid shifts in the brain. The patients develop increasing cerebral, and sometimes pulmonary oedema. Usually symptoms start at a sodium level around 130mmol/L. At 125 mmol/L, altered mental state is usually obvious and deaths from seizures and progressive cerebral oedema have occurred below this level. Q. Besides excessive fluid intake, are there other contributing factors to the development of EAH? IR: Exercise promotes the secretion of anti-diuretic hormone (ADH) which will cause water but not sodium retention in the urine. This inappropriate secretion of ADH is the necessary second factor (after excess fluid consumption) in the development of EAH. Q. How difficult is it to develop universal guidelines for EAH prevention and why? IR: The hardest issues have been arguing against the prevailing sports culture where hydration to improve performance is aggressively promoted. This “if you don’t drink, you die” culture, didn’t exist until the mid-1980s (interestingly when EAH was first recognised – never having been reported before). Q. How can we prevent the occurrence of EAH? IR: By promoting a simple message of “drink to thirst”. If we all just listened to our bodies and drank when we felt thirsty, then we would not be a significant risk of either significant over or under hydration. Those three words “drink to thirst” are really the best summary of all of the research that we have done over the past two decades. Q. What about the relatively uncommon circumstances where our thirst sensation may not be adequate to prevent dehydration? IR: To be frank, I don’t think these exist. I think they are usually made up by proponents of aggressive hydration strategies to bolster their argument, often combined with advice to drink ahead of thirst to maintain performance. Mild dehydration (e.g. 2 per cent bodyweight) does not significantly alter athletic performance, and elite marathon runners are known to finish in near record times having lost 5-7 per cent of their bodyweight.

The hardest issues have been arguing against

the prevailing sports culture where hydration to improve performance is aggressively promoted

in both a major British and American sports medicine journal. We have realised that publishing in the scientific literature isn’t enough though, and that we need to get to the public and those with special interest, such as coaches and sports trainers. What we are talking about is a change in culture, one that involves confronting some firmly held views and strong vested interests.

To us, the science is settled. Evidence into action is the hard bit! ■

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