That exogenous factors, i.e., infections, bring to fruition these latent morbid tissue potentialities of the gouty, is my belief. Hence my contention that dietaries for the “gouty” should be such as promote gastro-intestinal asepsis. Albeit, infections are but the “seeds,” and who can doubt that the ideal diet for the “gouty” should also take cognisance of the “soil”—the pathological groundwork of gout?

The “soil” in gout is, I believe, one peculiarly favourable to microbic invasion, and here again recent studies of the cytology of the blood bid fair to yield us some criterion whereby the “degree of body resistance” to infections may be gauged.

But until the bio-chemist reveals to us the why and the wherefore of their peculiar tissue vulnerability our dieting of the “gouty” must perforce consist largely in diminishing the exogenous excitants of the malady. Ultimately, when researches now in progress have fructified, we may be able to influence the endogenous factors, may correct the functional defect of this or that viscus, stabilise the nuclein exchanges, and heighten the resistance of the tissues. In short, as Sir Archibald Garrod puts it, “we must consider the soil as well as the seed which falls upon it, and that he is the best exponent of the healing art who treats the individual patient rather than his disease.”

The Accessory Food Factors.”—“Due nourishment, not gluttonous delight,” is the true clue to the rational dietetic treatment of the “gouty.” But this question of “due nourishment,” how complex it grows in light of recent revelations. Thus, it is now generally agreed that to satisfy the animal needs for growth and the maintenance of nutrition something more than a due admixture of proteins, fats, carbohydrates, and inorganic salts is essential.

We must, of course, ensure that the caloric value of the food intake be adequate, and the supply of protein sufficient to maintain the nitrogen balance, also that the intake of protein suffice for the exigencies of tissue waste, not forgetting that for this is required a sufficient quota of the individual primary fractions of the protein molecule.

But this, we now know, is not all, for there are other and indispensable dietetic components. In the food we eat are substances of hitherto unguessed-at potency—the “vitamines,” or, as they are now more properly termed, “accessory factors of diet.”

Of these elusive bodies but three as yet have been isolated: fat-soluble A, water-soluble B, and water-soluble C. In infancy absence of the first-named “vitamine” leads to rickets. Lack of the second engenders scurvy, of the third beri-beri.

But, apart from these well-defined “deficiency diseases,” McCarrison has pointed out that the absence of these “accessory food factors” leads to grave functional derangements, especially of the organs of digestion and assimilation and those subserving endocrine functions, not to mention malnutrition of the nervous system and the induction of hyperadrenalinæmia and chronic inanition.

A heavy indictment, but, more pertinently to our subject, McCarrison inclines to think that bilious vomiting, cyclical acidosis, mucous disease, and other metabolic disorders met with in children are very probably due to deficiency of certain “accessory food factors.” In light of this it is interesting to recall that these same symptom complexes are by Comby and others regarded as manifestations of infantile gout.

More arresting still is McCarrison’s observation that all the clinical phenomena distinctive of “deficiency diseases” as a whole are apparently the result of nuclear starvation of all tissue cells. In short, these “accessory food factors” are essential to due nutrition of the nuclear substance. How interesting this in light of the generally accepted view that “gouty” individuals are victimised by some inherent defect or alteration of nuclein metabolism. Does not this seem to indicate that one of the clues to successful dieting of the “gouty” must be adaptation of the nuclein intake to the needs of the individual, in short that we must strive for the stable maintenance or conservation of nuclein metabolism?