Diet
Truly in respect of diet the gouty have “suffered much of many physicians,” have been the butt, so to speak, of all the fads and frailties of medical opinion. Should that chemical outcast “uric acid” but appear in excess in the urine, it was, and still is for many, an infallible index, not only of gout, but of gout maintained and nurtured by improper feeding. The inference seemed obvious: the ideal diet for the gouty was a diet free from any uric acid-forming material. This achieved, the gouty “will be free from his leprosy, and henceforward, if he abide by the prescribed regime, all will be well with him.” But, as Sir James Goodhart, from whom we take this last passage, pertinently asks, “is this so?” The answer is, I fear, in the negative. For who has not met with gouty veterans who, having run the gamut of endless dietetic experiments, still remain “gouty,” though, mirabile dictu, still avid for fresh ventures?
For myself, I know of no stereotyped diet for the “gouty,” for in this respect every man is a law unto himself. “Get the acid out of your system,” is the watchword of many, and, I fear, often to the undoing of their victims. Bent on the annihilation of the disease, they overlook the individual. But, weary of futile chasing of uric acid out of the economy, most students of gout now agree that the aim of all dietetic measures should be to secure, as far as possible, gastro-intestinal asepsis. For, as experimental studies have shown, it is possible, by means of a judiciously selected and varied diet, to modify the character and even to inhibit the growth of the intestinal flora. The far-reaching nature of such an influence is clear when we reflect that all abnormal fermentative and putrefactive processes in the alimentary canal appear to be referable to the action of microbial agents.
Diet in Acute Paroxysms.—The initial outbreak of gout may occur at any age, and respect must be had to this as well as to other individual peculiarities. If the subject be young, say in the forties, and a free liver, he may at the onset experience distaste for food, if not actual nausea. If so, let him follow his bent, and confine himself to hot water, barley-water, or hot weak tea. Such a modified process of starvation is beneficial rather than harmful. Drinking freely of bland diluents promotes the elimination of toxic or waste materials, while the intake of hot water stimulates the hepatic cells and promotes the excretion of bile.
Milk, easy of digestion and rapid absorption by a febrile patient, is the ideal form of nourishment. Moreover, a milk diet constitutes the most effectual means of attaining a comparative degree of intestinal asepsis. From two and a half to three pints may be taken in the twenty-four hours. While some will find no difficulty in assimilating it, others soon experience nausea, vomiting, and even diarrhœa, from the passage of undigested curds. It is therefore advisable to begin with small amounts given at regular intervals. If ill digested, it may be diluted with some alkaline water, or three to five grains of citrate of soda added to each tumblerful.
To obviate monotony the intake may be varied by oatmeal or barley gruel, veal, mutton, chicken, or vegetable broth, but strong soups and animal extracts must be avoided. There is no objection, however, to bread and milk, tapioca, semolina, or sago puddings.
With the disappearance of fever and the decline of acute symptoms fish may be introduced into the dietary, with later on a little white meat or chicken. This may be safely done when local pain and tenderness decline, and alike the tension of the parts, as shown by pitting. Moreover, at this stage the appetite usually asserts itself. Still the return to regular diet must be made slowly and cautiously, if we wish to combat the very common tendency in these patients to functional gastro-intestinal and hepatic derangements. Lastly, in acute sthenic gout occurring in a robust subject there is no need whatever for alcohol in the febrile stage. Also, it may be added, the younger and the stronger the patient, the better will he thrive on a pure milk or a lacto-farinaceous diet, and the less urgent the necessity for relinquishing the same until all fear of a relapse has passed.
On the other hand, in acute asthenic gout in an elderly and perhaps somewhat debilitated subject one must more than ever have regard to the individual, especially if he be an old time sufferer, perhaps with multiple joint involvement. Such a man “has not so much the gout as the gout has him.” He has to be helped to support his burden. In short, the diet for the young and plethoric differs from that suitable for the old and asthenic.
Restriction of such to a milk diet is sometimes positively harmful. The mischief is, that, once begun, every attempt at a more varied diet immediately provokes a relapse.[60] As Sir Thomas Watson wisely observed: “They must be allowed a certain quantity of their accustomed good cheer, or they become an easier prey to the disease. In such cases you must ‘trim’ as well as you can between opposite dangers, between the Scylla of excess and the Charybdis of debility.” In short, you must maintain their vigour and their strength. For this a pure milk diet will not suffice. In addition thereto, pounded or minced chicken, a little fish, sole or whiting, may be given. When also, as often happens, they have been wont to take alcohol, two ounces of mature brandy or whisky, well diluted with Salutaris or other mineral water, may be allowed them every twenty-four hours.
Indeed, if the subject be old and broken down, it may be necessary to increase the amount of stimulant. In such cases to go on treating the disease, heedless of long-established habits, is bad policy. Wholly to withhold alcohol may well precipitate disaster. Homilies on abstinence or temperance are best postponed pending convalescence.
Moreover, these cases of acute gouty polyarthritis, whether in the middle-aged or old, very commonly run an afebrile course. If then, as not infrequently happens in these distressing cases, the patient’s progress is slow and unsatisfactory, there need be no hesitation in renouncing a strictly lacto-farinaceous regimen in favour of a more mixed diet: clear vegetable soups, well-made Julienne, mutton, veal, and chicken broths, lightly boiled fish of the digestible kinds, pounded and minced chicken, etc.
Even when in these cases pyrexia is present, it is rarely continuous, but is diversified by afebrile intervals. If then, while the paroxysm is in full flare, it be deemed advantageous to adopt a milk diet, it is all the more important that in the inter-paroxysmal stages we take full advantage of these periods of enhanced digestive capacity.
Diet in Chronic Gout.—Sydney Smith, writing to the Countess of Carlisle in his seventy-first year, humorously apostrophises his gout: “What a very singular disease it is! It seems as if the stomach fell down into the feet. The smallest deviation from right diet is immediately punished by limping and lameness, and the innocent ankle and blameless instep are tortured for the vices of the nobler organs.”
Precisely so, but what constitutes the “right” diet? We are told that this is good and that is bad for gout. Some would have us eschew red meat and cleave unto white; for others common salt is the devil that must be cast out. Some speak ill of all the fruits of the earth. Strawberries especially, they say, are the bane of gout, yet in these same Linnæus found salvation. For many, again, sugar is anathema, tea and coffee but uric acid solutions, and alcohol in all forms rank poison!
What a trial the gouty subject who, obsessed by his “acidity,” has passed through the furnace of many spas! “Everything I eat turns to acid” is his plaint. He has been all things by turns—a fruitarian, a vegetarian, no meat or all meat, etc. Such persons, in truth, are “uric acid” maniacs. But—forget it not—they are of our making, and often in their multitude of counsellors have found, not wisdom, but starvation! Well would it be if the evil done ceased with themselves, but unfortunately they seek converts to whatever cult they affect.
The Fallacy of Fixed Dietaries.—As Bacon in his “Regimen of Health” (1597) wisely observes: “Some physicians are so regular in proceeding according to art for the disease as they respect not sufficiently the condition of the patient.” The wisdom of this has, I fear, been overlooked by those who hold that the ideal diet for the “gouty” is one destitute of the precursors of uric acid. Its acceptance makes not for flexibility in dieting, but rigid, undiscriminating routine.
Apart from the violation of principle, the direct result is, that the victim runs amok among the carbohydrates, with as a frequent penalty an acute outbreak, this although uric acid is not a direct product of carbohydrate metabolism; nor, as far as is known, does the carbohydrate intake influence the rate of formation of uric acid. Thus do theory and practice come into conflict, and, as usual, the patient pays. How pernicious this obsession that uric acid is a morbid agent! Uric acid is not an etiological entity, and, as Walker Hall rightly observes, “it is high time that every practitioner made a point of fully educating the public in this respect.”
Any attempt to formulate a set dietary proves but a snare and a delusion. No regime is applicable to the “gouty” as a class, nor even to the individual “gouty” subject at all periods of his life history. His disease persists for an indefinite period, and, like most chronic maladies, undergoes variations. Pari passu his digestive capacity rises and wanes. The regime therefore must be adapted and readapted to his varying necessities. For it is the patient, and not the “gout,” dictates the diet. But only too commonly the disease is dieted, the victim ignored—hinc illæ lachrymæ!
Our dietetic ventures must obviously rest on a sounder basis. This we do know, viz., that functional disturbances of digestion generally precede a “gouty” paroxysm, and that their amelioration is followed by relief of symptoms. The aim of our dietetic measures then is the prevention of digestive disturbances, not the routine withdrawal or reduction of uric acid precursors.
The dietetic treatment of the “gouty” is that of the “dyspeptic,” with, if anything, an added discrimination, for an unknown factor intrudes—the “gouty diathesis”—which has also to be reckoned with, but of this later. Now “dyspeptics” cannot be dieted by rule of thumb. Whether they be “gouty” or “non-gouty” matters not. A careful study of the phenomena of digestion, if not essential in every case, is certainly called for in the more obstinate and obscure forms. In short, an attempt should be made to determine the special form of “indigestion.” Is the derangement of function a disorder of motility or secretion? Is it catarrhal or nervous in origin?
That such is the proper mode of procedure is undeniable. For are we not too prone to assume that the “dyspepsias” of the “gouty” are sui generis, all due to one cause, the materies morbi of gout, instead of being merely “excitants” of gout and due to a variety of digestive functional disabilities, and these of equally diverse origin?
Thorough Physical Examination a Necessary Prelude to Dieting.—When we recall that the “dyspepsias” of the “gouty” endure through long years, the suggestion that every effort should be made to localise and establish the exact nature of the underlying derangement seems almost superfluous. Yet how often is the question dealt with offhand, though, ideally speaking, I cannot help thinking that the primary outbreak of gout should be the signal for an exhaustive examination by all modern methods. The consequences of dyspepsia in the “non-gouty” are bad enough, but infinitely more so in the “gouty” subject. But it is the former group, not the latter, that has been the favoured object of study by experts, which is, I think, somewhat unfair.
There is need of a searching investigation, a more common invoking of the tests whereby the functional efficiency of the stomach may be gauged. We know that there may exist on the one hand hyperchlorhydria and on the other hypochlorhydria. But we need to know more as to disturbances in gastric motility, delay or hurry in digestion, not to mention abnormalities in shape, position, size, tone, pyloric end rhythm, etc. In view of the almost general admission that gastro-intestinal derangements are causally related to outbreaks of gouty arthritis, surely our remissness in this matter is somewhat surprising, the more so in light of the heroic procedures, viz., ileocolostomy and colectomy, advocated in rheumatoid arthritis, a condition by many deemed related to gout.
Leaving such aside, none will, I think, deny not only the value of test meals for free HCL variations and experimentation with all kinds of foodstuffs, but also of X-ray examination of the alimentary tract. How subversive of all preconceptions the revelations of radiography in gastric and intestinal conditions, of what infinite value in disentangling the ambiguous significance of purely subjective sensations! Thus, alterations in gastric tone, motility, and peristalsis may hark back to remote lesions in gall bladder or appendix, and these also account for variations in free HCL.
“Great eaters,” said Sydenham, “are liable to gout, and of these the costive more especially”—an observation the truth of which all will confirm. It may be taken as a maxim that nothing for the gouty is more prejudicial than constipation. Here it is obviously of importance that we know the site of delay, whether in the lower coils of the ileum, the colon, or merely the rectum, i.e., dyschezia. How else obtain this information, save through X-ray examination?
Any departure from normal in consistency, colour or content of the fæces should be noted so as to identify hepatic or pancreatic derangements. An analysis of the urine should always be undertaken, its reaction noted, the presence of albumen or casts ascertained. It is important, too, that we do not overlook glycosuria or oxaluria, or substances indicative of excessive intestinal putrefaction. All these bear far more pertinently on diet than estimates of uric acid.
The behaviour of the skin, whether inactive or not, must also be taken into consideration. Moreover, as the subjects of gout are usually middle-aged or old, it is highly important to note the general drift of metabolism, whether in the direction of obesity or undue leanness. Herewith we must take an inventory, as it were, of the subject’s general mode of living. What are his habits in respect of food and drink? Is his diet excessive or improper in quality? Are his meals taken at irregular times? Does he masticate his food properly?
In the matter of exercise, his occupation or pursuits require thought. Do they involve excessive exertion or favour a sedentary habit? For both these factors bear narrowly on his power or not of disposing of ingested material. Indeed, all the foregoing reflections stand in close relationship to the complex processes of digestion and metabolism, and the efficacy of our prescribed regime will depend on how far our suggested innovations meet the particular needs of the subject under review.
Need for Collaboration of Clinician and Bio-chemist.—Before we shall be able to lay down a diet for the “gouty” on truly scientific grounds much remains to be done. Our clinical examinations, in no way to be despised, must nevertheless be supplemented by the more subtle tests of the bio-chemist. Consider the complexity of the problem. We have to diet not only the “gouty,” but the “potentially” gouty.
They shade the one into the other. Even the man who has had gout has his periods of respite, of apparent unblemished health. If seen at such a juncture, he may display the relics of his gouty attacks, i.e., tophi. But can we say of him that he actually now has gout? He has crossed the Rubicon, disclosed his morbid trend, but meanwhile he has apparently recrossed to the vantage ground of normal metabolism. He stands again with those who are about to, but have not yet developed the disorder, i.e., the “potentially” gouty.
Who will deny that it is when a man is, so to speak, gravid with, but not yet delivered of, gout that dietetic measures will avail him most? But this, alas! carries with it as its postulate the diagnosis of latent gout. Now, Walker Hall suggests that “the nuclein metabolism of the gouty patient is run at high pressure or full capacity, instead of the usual normal quarter or at half-pressure capacity, in order to cope with the ordinary processes of assimilation, and that there is very little reserve energy.” Does not this seem to indicate that a fruitful sphere of research might be the invoking of “endurance” tests and other methods of determining the functional capacity or efficiency of the various viscera?
At present we content ourselves with blaming the stomach, the liver, the kidneys, etc., and often on very inadequate grounds. It would be a great step forward if we could determine betimes which particular viscus is functionally deficient. There are signs that this boon will not be long withheld, signs that not only can the functional efficiency of the stomach be tested, but also of the liver, kidneys, and even the spleen.
Thus Labbe and Daughin study the colloidal nitrogen in the urine, and find the ratio to the total nitrogen much augmented when the functional efficiency of the liver is depressed. Again, Bauer and Spiegel use the bilirubin content of the blood to the same end. They maintain that there is a bilirubin threshold, the assessment of which denotes the functional capacity of the liver. In health the blood content thereof is surprisingly uniform. But in passive congestion of the liver it rises very markedly, and the same after administration of cholagogues.
In like fashion the value of blood urea concentration is extolled by Kast and Wardell as a satisfactory index of the functional power of the kidney. The uric acid content of the blood is by Baumann, Hansmann, Davis, and Stevens regarded as a very delicate index of renal function, though unreliable in the presence of œdema, cardiac decompensation, or when the urine is highly concentrated in hot weather. These are but a few of the methods available, and in the same way Frey has devised tests for the functional efficiency of the spleen, while Barton invokes the administration of urea, chlorides, adrenalin, creatine, etc., to assess the functional capacity of the liver, kidney or spleen.
Such is the trend of modern medicine—to link up clinical with laboratory findings—and in gout perhaps more than in any other disease is this collaboration urgently called for. For who can doubt that gout is a malady of mixed intrinsic (endogenetic) and extrinsic (ectogenetic) origin?
We need to know more about the endogenous factor, the basal perversion of cell structure or function, that differentiates the tissues of the “gouty” from those of their fellows. For it is these inherent peculiarities—structural, physical, or chemical—that give to the disease its sui generis character. How then in the “living” subject shall these hidden morbid potentialities be identified? How save through the medium of function, the outward expression of metabolic activities, in other words by appraisement of the functional capacity of the various viscera? For gout primarily is a disorder of function, or, as Rendu phrased it, a primordial “vice of nutrition.” Hence our insistence on the invoking of the various laboratory methods for elucidating the functional powers, the efficiency or not of the liver, kidneys, etc.
This satisfactorily achieved, we may, through their reflected functional disability or disabilities, divine somewhat the nature of the innate tissue peculiarities of the “gouty,” may hope at long last to translate the misty “gouty diathesis” in terms of functional deficiency, deficiency of the working capacities of the stomach, liver, or kidneys, and perhaps find that the basal flaw in some lies in the liver, in others in the kidney, and thus the older clinicians be justified of their claims for “hepatic” or “renal” varieties of gout.
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?
Again, as before stated, one of the results attaching to deficiency of “vitamines” is functional derangement of the organs of digestion and assimilation. Such disturbances are prominent in gout, and that “errors of diet” play an important rôle in the genesis of the disorder can scarcely be denied. At the same time there is no proof as yet that the absence of some mysterious “accessory factor” makes for the development of the disorder.
Nevertheless reflection on these findings is, I think, wholly apposite. It should, at any rate, chasten those who affect extreme dietaries on insufficient grounds. They are not justified of results, for, with Sir Archibald Garrod, I venture to doubt “whether by dieting our ‘gouty’ patients we achieve nearly as much as we think we do.”
Such good, moreover, as we do compass, is, I think, exerted indirectly. Even in the inter-paroxysmal periods of the disorder, despite good or perhaps exuberant health, gout is there. Its morbid tissue potentialities are latent, though functionally inactive. To maintain this state of passivity is the aim of all dietetic measures, viz., to diminish or withdraw the dietetic factors that are provocative of gout.
The diet most void of offence is one the least calculated to excite digestive disturbance—one that makes more surely for gastro-intestinal asepsis. At this juncture it is interesting to note McCarrison’s observation that although the absence of certain “accessory food factors” is the essential etiological agent in the genesis of “deficiency diseases,” yet he holds that infections and parasitic agencies are often important causes in determining the onset of symptoms.
Similarly in the causation of gout, “errors of diet” are not the only agencies at work. They are in truth but contributory factors in that such indiscretions favour the incidence of catarrhal states. These again promote increased toxicity of the intestinal flora with sequential disturbance of general nuclein metabolism and associated specific local reactions in certain tissues.
I make no apology for this somewhat lengthy digression. In the sphere of dietetics, as elsewhere, “a little knowledge is a dangerous thing.” We need to walk more circumspectly in this matter of dieting; and to this end reflection on the disabilities that still beset us cannot fail to be salutary, and will form, I think, a fitting prelude to our suggested mode of procedure.