Full mechanism, in text

Drinking too much water can kill

1 · Drinking exceeds sweat loss

In an endurance race, a runner drinks plain water cup after cup on a schedule and takes in more than sweat removes, while the sweat also carries some sodium away.· Water accumulates
· Sodium is not replaced in step
· Plasma and the fluid between cells are diluted — this is where EAH starts

In the multivariate analysis of Almond 2005 (Boston Marathon), three things were independently associated with low sodium: weight gain during the race ( 4.2), finishing in more than 4 hours (odds ratio 7.4), and a that was too high or too low. Female sex, sports drink versus water, and use were not independently associated after adjustment.

Gaining weight instead of losing it is itself proof that more went in than came out.

2 · Paradoxical AVP keeps water in

Normally, once blood is diluted → antidiuretic hormone (AVP) should be switched off → the kidneys pass dilute urine and balance returns.But during endurance events, several kinds of signal can keep AVP raised even after the blood has become dilute:

· Exercise stress
· Nausea and vomiting
· Other stimuli unrelated to plasma concentration (non-osmotic)

→ AVP stays high when it should fall → the kidneys keep pulling water back into the blood → the surplus cannot be excreted

This is why EAH is more dangerous than simply drinking too much — the body's safety valve is stuck.

3 · Plasma Na+ collapses

Dilution plus a stuck AVP drives blood sodium down, to hyponatremia at or below 135 mmol/L, and symptoms escalate from headache and vomiting to seizures and coma.Dilution plus a stuck AVP drives blood sodium down, and plasma osmolality falls with it:

· Around 140 mmol/L: normal
· ≤ 135 mmol/L: hyponatremia (the definition Almond 2005 used)
· ≤ 120 mmol/L: critical hyponatremia

Symptoms escalate step by step: first headache, nausea and vomiting, then confusion and seizures, and in severe cases coma and stopped breathing.

Almond 2005 NEJM, Boston Marathon: at the 2002 race, 488 runners gave a usable blood sample at the finish; 13% had hyponatremia (≤ 135) and 0.6% critical hyponatremia (≤ 120). The paper opens by noting that hyponatremia had become an important cause of race-related death and life-threatening illness among marathon runners.

4 · Cerebral edema: water rushes in

Hypotonic plasma (low sodium) → the fluid outside is more dilute than brain cells → water rushes into brain cells down the osmotic gradient → brain tissue swells.But the skull is closed — the brain has no room to expand → intracranial pressure rises:

· Headache
· Nausea and vomiting (from raised intracranial pressure; and vomiting is itself one of the signals that push AVP up → a possible vicious circle)
· Confusion + seizures
· Coma → stopped breathing (brainstem compression)

Why it is hard to recognise on the course: early symptoms (headache + nausea) look almost identical to dehydration or heat illness — reflexively pushing more water = a fatal mistake.

First, check: body weight versus before the race + blood sodium. Heavier than before the race = EAH red flag. Stop drinking, do not add water, and get medical care immediately.

Treatment belongs in hospital: confusion or seizures mean an emergency, so call emergency services at once; in hospital fluids are restricted, and in severe cases doctors give hypertonic saline intravenously to bring sodium back up.

Full mechanism, in text

1 · Drinking exceeds sweat loss

2 · Paradoxical AVP keeps water in

3 · Plasma Na+ collapses

4 · Cerebral edema: water rushes in

Exercise-associated hyponatremia · cerebral edema

Full mechanism, in text

1 · Drinking exceeds sweat loss

2 · Paradoxical AVP keeps water in

3 · Plasma Na+ collapses

4 · Cerebral edema: water rushes in

Exercise-associated hyponatremia · cerebral edema