It now devolves upon us to decide whether the phenomena of gout are best explicable as the outcome of _auto-intoxication_, or of _infection_ or _sub-infection_. The uric acid theory was in truth one of _auto-toxæmia_, the varied manifestations of gout being attributed to mechanical or toxic irritation by _uric acid_, the end-product of purin metabolism. But, as we hope to have shown conclusively, uric acid is _not toxic_, and _per se_ is apparently as innocuous as those other and intermediary products of metabolism which give rise to cystinuria and alkaptonuria. The question then arises, Is gout haply due to a retention of other metabolites? That outbreaks of gout follow fast on the heels of dietetic irregularities is proverbially true. But there is no certain evidence that the symptoms generally ascribed to auto-toxæmia are referable to substances derived from the foodstuffs under the action of the digestive juices. Toxic as are peptones and primary proteoses when they gain direct access to the tissues, the symptoms produced in no way resemble those affiliated to alimentary toxæmia, much less those of _gout_. Rather, according to Adami, do they approximate to those typical of _anaphylactic shock_. Normally, too, the mucous membrane proves an efficient barrier, these poisonous bodies during their passage through it being transmuted into harmless substances. Nor can we refer the symptoms of gout to a toxæmia secondary to _intestinal stasis_ or other causes. In other words, it cannot be attributed to assumed toxic action on the part of the intermediary and terminal products of protein disintegration. For seemingly these chemical outcasts of the economy become progressively less toxic on their downward path to effete matter. The diamines, too, produced by bacterial action on foodstuffs, are so minimal as to be negligible, while the toxicity of cholin and neurin is unestablished; and as for indol and skatol, they are with difficulty absorbed from the healthy colon. Experimental researches on carbohydrate and fatty disintegration have likewise proved sterile, while there is no evidence that the anaerobes present in the digestive tract produce ecto-toxins, or undergo lysis with release and absorption of their endo-toxins. In short, it is but too clear from the foregoing brief _résumé_ of recent experimental findings that, if _uric acid_ cannot be held responsible for the causation of _gout_, there is no evidence likewise that the disorder owes its genesis to any other of the as yet isolated _chemical_ products of gastro-intestinal digestive activities. Having dealt with this aspect of the question, we shall now pass on to consider whether the phenomena of gout can be more adequately explained on a basis of _infection_ or _sub-infection_.