Hi Doc,
A friend of mine who, like me, is a man of a certain age (70), said LMNT has significantly reduced the frequency of night-time urination. Is there a mechanism that involves electrolytes that might be relevant?
Not that I can think of, unfortunately.
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Thank you very much.
Does sodium not regulate vasopressin and as a result water balance? Could that be the proposed mechanism
Plasma sodium concentrations impact vasopressin release, however this is not the same as routine dietary sodium intake – this can be a confusing concept, including for medical trainees.
In the vast majority of circumstances, when plasma sodium concentration is high (e.g. > 145 mEq/L), it reflects that the person is actually dehydrated, i.e., inadequate free water. This leads to an increase in vasopressin, which increases free water reabsorption in the distal nephron. This helps to “dilute” the plasma sodium concentration back down to normal, while producing more concentrated urine. This is why your urine turns dark when you haven’t drank enough water.
Regarding dietary sodium intake (or in this case, taking in additional sodium via a supplement): assuming healthy function of the heart, liver, and kidneys, the body will generally maintain “sodium balance” between dietary intake vs. urinary excretion. Increasing habitual sodium intake in this fashion would be expected to increase overall urine output, not decrease it, as the body acts to maintain sodium balance by excreting the additional sodium load.
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I cannot remember the exact paper (or text book) as it has been some years, but I recall sodium being promoted post exercise to increase water balance through increased thirst and retention.
Of course, this is just an article from Gatorade but…
“Sodium ingestion and maintenance of sodium concentration also stimulates renal mechanisms to reduce water loss in urine and conserve fluid.”
Is there any other possible way it promoted fluid retention?
https://www.gssiweb.org/sports-science-exchange/article/sse-122-sodium-ingestion-thirst-and-drinking-during-endurance-exercise#:~:text=.%2C%202007).-,SODIUM%20INGESTION%20IN%20ATHLETES,5%2D7%20mEq%2FL.
There seems to be a bit of older research on this and most if leaning on changes in osmolality
“The addition of sodium to a rehydration solution has been shown on numerous
occasions to have a positive effect on maintenance of rehydration throughout a recovery
period. Shirreffs and Maughan (1998) observed that participants were only in positive fluid
balance six hours after rehydration when a 100 mmol/L sodium solution was ingested
however they were essentially in fluid balance when a 50 mmol/L sodium solution was
ingested. As sodium is the main ion in the extracellular fluid, addition of sodium to a
rehydration solution maintains plasma osmolality and, therefore, plasma AVP concentrations
which leads to the avoidance of a diuresis seen following the ingestion of plain water”
Most of these are describing post-exercise rehydration situations, where exercise-induced hyponatremia (i.e., excessive dilution of plasma sodium by free water) leads to suppression of ADH as a way to excrete the excess free water and return plasma sodium concentrations (and thus osmolality) to normal.
Maintaining higher plasma sodium levels using a sodium-containing post-exercise rehydration solutions (compared with drinking plain water, which would only serve to dilute things further), this leads to less suppression of ADH and, as a result, less excretion of dilute urine during that immediate post-exercise period.
I do not know that simply consuming a sodium bolus before bed would be expected to have the same effect; as I mentioned above, across the 24-hour time period the net excretion of sodium will balance the sodium intake, such that people consuming very high sodium diets tend to produce more urine overall, in order to excrete their daily sodium load. In fact, when patients present with polyuria, the differential diagnosis includes osmotic diuresis due to excessive glucose in the urine (e.g., from diabetes mellitus), or from high solute intake (e.g., from dietary sodium, among other things). This is supported by findings of high sodium intake as a risk factor for nocturia, and trials of dietary sodium reduction showing benefit on reducing nocturia.
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