Gout, with a section on ocular disease in the gouty

by Llewellyn J. Llewellyn

Yet again, J. H. Pratt, of Boston, writing in 1916, observes “the greatest confusion exists in the minds of many practitioners in America to-day regarding this disease (gout) and its diagnosis. In some parts of the country the diagnosis is frequently made in conditions that are not gout; in other sections there seems to be a skepticism in the minds of many practitioners regarding the existence of such a disease. In New England I have found that chronic gout, even when tophi occur, is often mistaken for rheumatism or arthritis deformans. Some physicians of large experience assert that they see gout frequently. Enquiry has shown that they mistake typical cases of arthritis deformans for gout, and the swellings about the joints and even Heberden’s nodes for ‘gouty’ deposits.”

Can it for one moment be denied that even to ourselves, living in England, the so-called “home of gout,” these trenchant criticisms are but too applicable. So long, then, as such confusion exists as to what does and what does not constitute gout, how can we, with any show of scientific precision, presume to discuss, much less lay down, dogmatic statements as to the geographical distribution and the race incidence of gout?

Food, Drink, and Occupation.—Gout, it has been well said, is the “Nemesis of high living,” for, unquestionably overeating is most fertile in evoking any latent tendency thereto. Attempts to throw all the blame on particular foodstuffs, e.g., red meats, etc., on the ground that these highly nitrogenous substances engender excessive formation of uric acid, have failed of their object. Even the much-maligned “purin bodies” have of late been largely absolved of blame, and the virtues of a “purin-free” diet, e.g., milk, are probably referable to the intestinal asepsis that such a regimen promotes.

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.

In like fashion, an habitually intemperate man may pass through life without incurring gout. Another, handicapped by his heritage, though he be strictly abstemious, yet falls a prey thereto. Even a total abstainer, when coming of gouty stock, may develop gout, haply through overeating.

To my mind, the only supposition deducible from these facts is that some individuals are born with a tendency to gout, and that this tendency may never assert itself as actual disease; that in others the dormant proclivity, under the influence of alcohol, forthwith becomes manifest; lastly, in some again, so nicely poised is the equilibrium of their nuclein metabolism, that the most venial alcoholic indulgence suffices to evoke an outbreak.

I incline, therefore, to the view that alcohol per se is not a cause of gout; in other words, alcohol will not, in the absence of a gouty heredity, produce gout. On the other hand, given an innate proclivity thereto, alcohol, especially certain forms of it, will almost infallibly evoke the disease; this often though the subject be conspicuously moderate in its use.