Gouty glycosuria is more common in males than females. The subjects are usually robust, middle-aged, and of full habit. Sugar is found intermittently in their urine in small amounts, but no acetone bodies. It is as a rule unaccompanied by thirst or wasting. It quickly responds to dietetic restrictions. As Gull long since observed, gouty glycosuria does not “discover itself,” but is “not uncommonly discovered.” This tersely sums up the clinical difference between this affection and true diabetes, albeit, as in all glycosurias, there is always the risk that carbohydrate excess, mental strain, or other adverse circumstances may aggravate the disorder and the case merge into one of true _diabetes_. Following the installation of glycosuria, the tendency to paroxysmal _articular_ outbreaks often ceases. The converse also has been observed, viz., that when, in sequence to dietetic restrictions, the sugar disappears, the articular pains may reappear. The fact that attacks of glycosuria may alternate with attacks of gout led to the assumption that a positive antagonism existed between the two disorders. Hence the phrase “the more sugar the less gout,” and _vice versâ_. This, however, with reservations, for a fugitive glycosuria has been seen during an acute articular paroxysm, and a classical outbreak in the toe has been known to supervene in the course of a well-established glycosuria. It is generally held that glycosuria is most commonly associated with _irregular_ forms of gout. But, in view of our ignorance of the intimate nature of even _regular_ gout, I should myself deprecate affixing the prefix “gouty” to any glycosuria other than one that has supervened in sequence to, or alternates with, gouty _arthritic_ seizures. Moreover, the glycosuria of gout is usually the alimentary glycosuria of fat elderly people, in whom the sugar excreted represents the unconsumed surplus of carbohydrate food. But fat elderly people are not necessarily “gouty,” neither is every so-called benign glycosuria inevitably linked on to a gouty diathesis. In fact, the relegation of glycosuria to the gouty category is but too often not a matter of diagnostic certainty, but rather an inference. Hence my plea that the prefix “gouty” would best be restricted to glycosurias occurring in individuals who suffer _regular_ attacks of gout, or those displaying those objective tokens pathognomonic of the disorder, _i.e._, _tophi_. Again, James Taylor has recently reminded us that, if nerve affections are relatively common in true _diabetes_, the same may be met with in _gouty glycosuria_, even when of temporary duration. Thus symptoms indicative of _peripheral neuritis_ may occur, _i.e._, lost knee jerks, paræsthesiæ, and paresis of the lower limbs. Now, as this authority pertinently observes, the subjects of _gouty glycosuria_ are frequently given to _alcohol_. Consequently the question whether or not the symptoms are due, not to sugar, but to _alcohol_, arises forthwith.