Under the one term, rheumatism, are included a number of conditions which may be of entirely distinct pathogeny. Acute articular rheumatism will be considered among the infections, although it is not certain whether it is a specific disease or due to mitigated bacteria of various types. Some have considered it as a mitigated sepsis. It is also uncertain whether there is any real connexion between what is ordinarily called chronic rheumatism and acute articular rheumatism, either in the sense that the chrome form is a persistence of the latter or of its results or that acute articular infectious rheumatism requires for its lodgement, the metabolic state characteristic of so-called chrome rheumatism.

It is also in dispute whether arthritis deformans is a distinct disease, or whether the name is applied to two or three sub-types or superficially similar but really distinct diseases and, if so, whether any or all of these are essentially different from chronic rheumatism.

In typic gout, the presence of an excess of uric acid in the system, the deposit of uratic concrements in the joints, and the general relation of the exacerbations and remissions of the disease to period of retention and marked elimination, have been rather positively demonstrated.

Lithaemia, though the term is often misapplied, seems also to consist in an excessive introduction or endogenic formation of uric acid and its congeners, the purins generally. The general conception that it is a mild or atypic form of gout also seems to be correct. How far chronic rheumatism and lithaemia are identical, is disputed.

A very practical question is as to the truth of the older theory that uric acid etc., are nitrogenous waste that has failed of relatively complete oxidation into urea and of the more modern theory that the former are absolutely independent of true protein metabolism and due either to introduced free purins or nuclein compounds or to endogenic metabolism of similar compounds which are originally formed from purin foods or from protein.

The consideration of this entire problem is further confused by the occasional exacerbation of gout and chronic rheumatism by certain starchy and saccharine diets and by the claim made by some that lactic acid is the cause of the trouble.

It does not appear either on any single theory as to the nature of these diseases nor clinically, that there is, with regard to protein, a close analogue to either diabetes or obesity, in the sense that a distinct disease results from the impaired ability of the body to oxidize protein foods.

All things considered, it must be admitted that the dietetic management of the diseases here, as commonly, grouped together, rests on an empiric basis, none too firm, and not in all respects conforming to the most accepted theories.

However, typic gout and, to a less degree, chronic rheumatism and lithaemia are produced by overindulgence in eating and drinking, especially in regard to meaty foods and alcoholic liquors. It can scarcely be said that the classic victim of gout is of sedentary habits, until these are forced upon him by the disease or advancing years or both; chronic rheumatism occurs by preference in those who have led rather active, out-of-door lives, with exposure to cold and damp; lithaemia alone corresponds to the a priori conception of a sedentary, in-door life, with resultant insufficiency of oxidation.

It seems to be advisable, in all diseases of this nature, to reduce the protein ration nearly to the Chittenden minimum although, in the so-called "poor man's gout", we may find a ration inadequate in all respects and the same is true for many cases of arthritis deformans, and even for some of chronic rheumatism and lithaemia.

On the other hand, it is inexpedient to establish a diet excessively rich, absolutely or relatively, in starches, sugars and fats, since they probably tend ultimately to produce an excess of oxalates in the system.

The prejudice against red meats seems to be entirely without foundation.

Alkalies, including juicy fruits such as orange and lemon are usually considered to be indicated, especially in gout, chronic rheumatism and lithaemia but the urinary acidity should be tested, for it is by no means always high.

Water should usually be given rather freely, yet, as many cases in this group tend to develop interstitial or diffuse nephritis, there is no wisdom in advocating excessive quantities.

Glycosuria - which must not be confused with the slight reduction of copper solutions by uric acid and urates, salicyluric acid from medication, etc., - diabetes and obesity show some tendency to complicate gouty and lithaemic cases, and the diet should be regulated accordingly.

The toxicity of uric acid is not conspicuous although its presence in excess seems to indicate perverted metabolism and, very likely, the presence of some more toxic congener or congeners. The urinary elimination is not a reliable index to the amount in the system, either directly or by suggesting a reciprocal relation. A single estimation is of practically no value. However, if daily examinations show repeatedly a low elimination, followed by a sudden rise and then a fall, as is the case in gout in passing a crisis, we may safely diagnose retention followed by a discharge.

Although the relation of this group of diseases to uric acid is not entirely clear, it seems advisable to avoid the purin-contain-ing foods as much as possible (See Tables, Chapter XIV (Purin Bodies)), and also to avoid vegetables and fruits rich in oxalates, all foods that tend to produce fermentation and putrefaction, and to make the diet a simple one based largely on milk, eggs and cereals, including bread stuffs.