What is the primary outcome of excessive licorice consumption regarding urinary excretion?

Excessive licorice consumption primarily leads to increased potassium excretion in the urine. This phenomenon is primarily due to glycyrrhizin, a compound found in licorice, which can inhibit the enzyme 11-beta-hydroxysteroid dehydrogenase type 2. This inhibition leads to an increase in cortisol levels and mimics aldosterone's effects, which promotes the retention of sodium and water while enhancing the excretion of potassium. As a result, excessive intake can lead to hypokalemia (low potassium levels) due to the increased urinary loss of potassium.

While the other options present related physiological concepts, they do not encapsulate the primary outcome of licorice consumption. The excessive sodium retention from the aldosterone-like effects does not directly correlate with decreased sodium levels but rather increased sodium retention. Calcium retention is not directly influenced in this context and is less related to licorice consumption than potassium and sodium dynamics. Improved hydration is also not a primary outcome of excessive licorice intake, as the body may experience disturbances in electrolyte balance rather than enhanced hydration due to the effects on sodium and potassium levels. Thus, increased potassium excretion stands out as the primary outcome associated with excessive licorice consumption.