Now it has been customary to regard the _alimentary_ or other disturbances that precede an initial _articular_ attack as “gouty,” and likewise those that intervene between the gouty paroxysms in long-standing cases. In other words, in light of the subsequent _articular_ outburst, what was mysterious ceases to be a mystery. All the vague “acidities, flatulencies, megrims, and biliousnesses, of whatever occult kind,” are forthwith hailed as “gouty,” this merely upon the ground of the _sequence_ of clinical events, because the symptoms have disappeared from, _e.g._, the stomach to reveal themselves in the joint or joints, or _vice versâ_. Now my own view is that the antecedent hepatic or digestive disturbances that so frequently precede initial attacks of gout are in all probability, nay assuredly, _not_ gout. They should rather be regarded as the _cause_, the foundation, of the malady than its effect, a cause inoperative save in the presence of individuals victimised by inherent morbid tissue potentialities. For similar symptoms are but too common in the _non-gouty_. They are very common _antecedents_ of, _e.g._, _rheumatoid or atrophic arthritis_. Nevertheless we do not when the _arthritic_ disorder _subsequently_ manifests itself talk of the preceding digestive disturbances as “rheumatoid” dyspepsia. Then why this presumptive and retrospective diagnosis of similar prodromal phenomena as “gouty” dyspepsia? For there is pending the articular outbreak nothing distinctive in the digestive derangements, nothing that would enable us to diagnose them as “gouty.” They might, for aught we know, be significant of oncoming _rheumatoid arthritis_. Now in the case of the latter we regard the _prodromal_ digestive phenomena as probably indicative of some _infection_ located somewhere in the _alimentary tract_. It would be wiser, I think, to adopt the same attitude in regard to our “gouty” examples. Moreover, as we know, such dyspeptic symptoms recur from time to time throughout the life history of both rheumatoid and gouty arthritis. In the former disorder we regard them as indicative of _recurring infection_, followed as they so uniformly are by _exacerbations_ of the _joint_ trouble. Is it not time we adopted the same attitude towards the _gastric_ or _hepatic functional_ disorders that punctuate the course of _chronic gout_ with a periodicity that rivals that of the articular paroxysms? Unquestionably to my mind when we have regard to the extreme frequency with which _local foci of infection_, _e.g._, oral sepsis, etc., are found in gouty subjects, this would be the more rational attitude, the one more in conformity with modern medical thought.