My experience, like that of others, is, that it is not the quality, but the _quantity_ of the food that is responsible. Moreover, I believe that the _toxicity_ of the blood plasma thus produced exerts its evil effects _indirectly_, viz., by lowering the _vis resistantiæ_ of the individual to _microbic_ invasion. Nor have I any doubt that it is this same but too common tendency to gluttony on the part of the “gouty” which is in part responsible for the _cardio-vascular_, _hepatic_, and renal changes so frequently associated with gout in its later stages. Reverting to _alcohol_, there are many who regard it as _par excellence_ the predisposing cause of gout, and some even question whether gout would have evolved had alcohol been unknown to mankind. But the interesting point is, that _all_ forms of alcohol are not equally pernicious in this respect, and the difference in their potency in this direction is apparently little or at all referable to their _percentage content of alcohol_. Port, madeira, sherry, burgundy, strong ales, and stout are far more provocative of gout than distilled spirits. In England, where gout is prevalent, malt liquors are the common drink, whereas in Scotland, where the predilection is for whisky, the disorder is much more rare, and the same applies to Ireland. In the Burgundian province of France gout is common, but exceptional in the Rhenish district of Germany, where hock is largely consumed. The why and the wherefore of these vagaries is not as yet explicable; but of those forms of alcohol, most conducive to gout, neither their _acidity_, _sugar content_, etc., can be impeached as imparting to the alcohol its predisposing influence in this direction. Incidentally, to those who advocate the primary _renal_ origin of gout, one would propound the question, why is it that _distilled spirits_ are less provocative of gout than wines, seeing these particular liquors are so fruitful of _granular kidney_? Again, if alcohol be such a potent factor in gout, why is it so rarely met with in habitual drunkards, and how account for the comparative rarity in gouty subjects of _hepatic cirrhosis_, or for that matter of other disorders of alcoholic origin? Beset by these eccentricities of behaviour, Sir William Roberts was tempted to regard gout as “rather an incident of the legitimate dietetic use of alcoholic beverages.” The relationship of _alcohol_ to gout is as erratic as it is to _atrophic cirrhosis_. Thus an individual may drink hard through life, and escape cirrhosis; another luckless wight, though he be quite temperate, yet falls a prey thereto; still another, who may never have tasted alcohol, acquires cirrhosis; lastly, cirrhosis is occasionally met with in the lower animals, into whose diet alcohol does not enter.