How pregnant, too, with warning their findings! Processes that to our untutored minds seem simple are revealed as infinitely complex. Through what a maze must we thread our way if we would disentangle the intricacies of metabolism! Intricate enough, forsooth, in health, but how much more so in disease! For, as Sir Archibald Garrod eloquently phrases it, “it is becoming evident that special paths of metabolism exist, not only for proteins, fats, and carbohydrates as such, but that even the individual primary fractions of the protein molecule follow their several katabolic paths, and are dealt with in successive stages by series of enzymes until the final products of katabolism are formed. Any of these paths may be locked while others remain open.” It is with chastening reflections such as these that we may best approach our study of gout, that riddle of the ages upon which so many physicians from time immemorial have expended their dialectic skill. But, vast though the increase in our knowledge of the chemical structure of uric acid and its allies, uncertainty still dogs our steps, and, doubtful of the pathway to solution of the pathological mystery of gout, we must perforce approach the problem in a more strictly catholic attitude. _Uric acid_ has apparently failed us as the _causa causans_. Neither this substance nor its precursors can be held responsible for the fever, local inflammation and constitutional disturbances in gout, being, as they are, practically _non-toxic_. Albeit, though I hold this view, I do not for one moment suggest that _uric acid_ has nothing whatever to do with gout. The fact that _tophi_, its pathognomonic stigmata, are compounded of _biurate of soda_, would _per se_ stamp such an attitude as untenable. On the other hand, _uric acid_ must be viewed at its proper perspective as a _concomitant_ or _sequel_ of _gouty inflammation_, the essential cause of which must be sought elsewhere. “The old order changeth, giving place to new,” and happily with the advent of _bacteriology_ our views, or rather our hazards, as to the nature of joint diseases underwent profound modification. But, strange to say, though quick to apprehend the significance of infection, its causal relation to other joint disorders, we still seem unaccountably loth to discard our timeworn conception of “gouty” arthritis as of purely _metabolic_ origin. This to my mind is the more remarkable in that the onset, clinical phenomena, and course of acute gout, and no less the life history of the disorder as a whole, are emphatically indicative of the intrusion of an _infective element_ in its genesis.