Etiology and Morbid Anatomy
To the antiquity of gout and no less its distinctive clinical facies, when of classic type, we owe not a little. Its salient phenomena have endured unchanged from the time of Hippocrates onward through the ages. So it is that, even allowing for the enhanced powers of discrimination of latter days, we are in no doubt that the gout of the ancients is the gout of to-day. How signal the advantage thus accruing, when we come to consider the conditions which engender or tend to engender the disease! For, quâ its broad etiological factors, we find ourselves in accord with the physicians of old, our experience a confirmation of their old-time findings.
Our forefathers, like ourselves, realised the innate complexity of the problem, that in the development of the disorder both heredity and environment played a rôle. In other words, that in the genesis of gout not only intrinsic but extrinsic agencies were concerned. Of the intrinsic influences the most important are age, sex, heredity, bodily conformation, and individual peculiarities.
Age.—Gout is slow in evolution, tardy of appearance, confined in the main to the middle and declining years of life. Said Sir Thomas Browne, “Leprosie awakes not sometimes before forty, the gout and stone often later.” Experience but confirms the dictum, for, as Cullen long since observed, it rarely declares itself under the age of five-and-thirty. This relative immunity of youth is not the least striking feature of the disorder; whence the Hippocratic aphorism, “Puer non laborat podagra, ante veneris usum.” Both Sydenham and Heberden were also doubtful of its occurrence before the age of puberty. Gairdner, however, records the incidence of fits of gout even in infants at the breast! and in one death therefrom. Garrod, too, met with two cases of classical type in girls, both of them under ten years of age. But Scudamore states that he never witnessed more than one example of a first attack before twenty, or any after sixty-six.
For myself, I have never seen a case under thirty-five years of age, and am sceptical as to the occurrence of infantile gout of regular type, believing with Scudamore that “the commonly asserted cases which represent the existence of the gout in very early youth are really examples of rheumatism.” Nor am I less but more inclined to cavil at the claims of Comby and others, as to the frequency in children of irregular manifestations. As Osler dryly observes, “The tendency in some families is to call every affection gouty. Even infantile complaints such as scald-head, naso-pharyngeal vegetations, and enuresis, are often regarded, without sufficient grounds, I believe, as evidences of the family ailment.”
To sum up, the majority of cases of gout ensue between thirty-five and fifty years of age. But, given a strong hereditary taint, it may break out in youths and young adults, or haply even in children. But such, in my experience, are phenomenally rare. Indeed, it may be said of gout that only exceptionally is it met with at either extreme of life; though Garrod records several examples in which the initial attack was postponed until nigh eighty years of age; while in one instance, a lady experienced her first classical attack of podagra in her ninety-first year.
Sex.—In the matter of liability to gout the sexes stand in marked contrast, the disorder being infinitely more common in males. Out of eighty cases submitted to the French Academy, seventy-eight were men and only two women; but according to other authorities, this is an under-estimate. Thus in James Lindsay’s series of cases of gout, 84·7 per cent. were males, 15·3 per cent. females, percentages which he notes “are in accordance with the observations of other writers.” J. Lambert, out of 125 examples of gout, noted that 102 were men, i.e., 81·6 per cent., twenty-three women, i.e., 18·4 per cent.
From my own experience, the figures submitted to the French Academy probably represent the ratio of incidence in males as opposed to females. This certainly, if regular, in opposition to “irregular,” types of gout be the criterion; for it must be admitted that regular gout does occur in women, though exceptionally rare either prior or subsequent to the climacteric.
As to the current opinion that the regular manifestations of gout in women are of asthenic as opposed to sthenic character, this has, I think, often proved a source of fallacy. At any rate, in many of these cases the assumed gouty inflammation resolves itself into one of inflamed bunion. Again, in but too many instances, women, showing Heberden’s nodes, are held to have gout or “rheumatic gout.” The latter term, as Pye-Smith observed, “is a bad name for osteoarthritis,” to which category Heberden’s nodes belong.
Judged by the one unequivocal diagnostic criterion, i.e., tophi, gout in women is extremely rare. If to this be added the further fact, viz., the rarity in their sex of classical attacks in the great toe, we see clearly that the diagnosis of gout in women is often a matter of assumption rather than of certitude.
Moreover, having regard to the fact that the diagnosis of gout in women is frequently based on so-called “masked and irregular manifestations,” I must admit that, to my mind, statistics, purporting to indicate the percentage incidence of gout in women and men, are not very convincing.
As to the why and wherefore of the relative immunity of women it may be due to the fact that their habits and mode of life are less calculated to evoke the disorder. There is also the further possibility that the catamenial discharges to a certain extent are protective against gout, for most authorities support Hippocrates’ aphorism, “Mulier podagra non laborat nisi ipsi menstrua defecerint.”
Heredity.—By the ancient physicians gout was held to be hereditary, and even to-day most will agree that “From father to son its seeds are transmitted, and bear fruit in exact proportion to the degree in which circumstances prove favourable to their growth.” Cullen, indeed, went further and held it purely hereditary; but, on the other hand, the belief, that it is often acquired is widely countenanced.
That gout is an hereditary disease is, I think, beyond question, and certainly, of all arthritic disorders, gout furnishes by far the greater number of instances in which parents and children are victimised by the same articular affection. Scudamore in 522 cases found that 332 could trace their disease to the father, mother, grandfather, grandmother, or aunt. But in the remaining 190 no evidence of the existence of gout in their forbears could be elicited. Out of eighty examples submitted to the French Academy an hereditary predisposition was established in thirty-four, and in the residue it appeared to have been acquired. Garrod found that 50 per cent. of his hospital examples of gout were hereditary, and of his private patients nearly 75 per cent. came of gouty stock. Again, Sir William Roberts found that “fully three-fourths of the cases of gout occurring among the easy classes, can be traced back distinctly to a gouty ancestry.” Luff’s estimate is even higher, inasmuch as analysis of a series of 300 examples disclosed a “definite family history of gout in 81·3 per cent.”
Nevertheless, Garrod’s experience, he tells us, convinced him that “in this country gout is frequently acquired even at a moderately early age, for in many most inveterate cases not the least hereditary influence could be discovered.” For myself, I find it difficult to appreciate the attitude of those who, like this observer, postulate innate or static morbid proclivities on the part of the “gouty,” and in the same breath, as it were, are equally insistent that it may be “acquired” de novo. Now, in the taking of family histories positive evidence is more valuable than negative. Surely, therefore, in the light of Garrod’s and Luff’s findings, it is obvious that heredity plays not merely an important, but an essential and indispensable rôle in the genesis of gout. To my mind, accordingly, the balance of evidence is more in favour of the same ancestral taint, though apparently undiscoverable, being present in the remaining 20 or 25 per cent., than that the disease in their instance was wholly and newly acquired.
Personally, I therefore question whether the alleged acquisition de novo of gout is not apparent rather than real. My own opinion is that the innate predisposition thereto is always inherited, and the predisposing factors, that we presume may originate gout, are in reality merely excitants or determining agents. In other words, the remote, the primary or essential cause of gout, is an inborn morbid tissue potentiality, and in the absence of this intrinsic warp the various contributory or exciting causes are impotent to evoke the disorder.
Apart from statistical proof of heredity, how else, save on the basis of an organic predisposition to the disease, can we explain the fact that of a large number of individuals, of slothful habit, and given to alcoholic and dietetic excesses, not one may get gout; while others who lead literally “a godly, sober, and righteous life,” become martyrs thereto. How escape then the conviction that in gout “breed is stronger than pasture”? for, apart from gluttony and indolence, gout is much more prone to arise in persons in whose pedigree it can be traced than in others.
It is not gout, but the predisposition thereto, that is inherited. This proclivity, moreover, may descend to the children of those who, in their own persons, have never suffered from the disease. In Luff’s series it was so in 27 per cent. of the cases, i.e., the disease was transmitted from grandparents to grandchildren without the fathers or mothers suffering from “active gout.” In other words, the morbid potentiality may lie latent until evoked. Thus, the females of “gouty” families, infinitely more often than not, escape overt gout, but hand on nevertheless their inborn liability thereto to their offspring. Looked at in this light, I see no difficulty in accepting the fact that gout may skip a generation. The son of a gouty parent, happily warned by the excesses of his father, may remain immune, while in turn his son, forgetful of his evil heritage, may bring it again to fruition.
The more one reflects on the essential cause of gout, the more inevitable seems the conclusion that gouty individuals, as Walker-Hall contends, “possess some inborn defect or alteration of nuclein metabolism.” And the vague phrases “constitutional” or “nutritional,” as applied by older writers to the disorder, are only explicable on the basis of inherited structural peculiarities, with their correlated perversions of tissue function.
That such constitute the pathological groundwork of gout, is, I think, further indicated by the fact that “gouty” inflammation, in virtue of its associated uratic deposition, is sui generis. No tissues, other than the gouty, react in this specific fashion. Does not this seem to indicate that the inborn tissue peculiarities dictate, so to speak, the character of the pathological reaction; this indifferently, whatever the nature of the so-called predisposing causes which, if our assumption be correct, are merely provocative of gout, in other words, do but evoke or make manifest what is already latent.
To sum up, on statistical, and more cogently, general clinical and pathological grounds, my own conclusions are that—
(1) Gout is always an hereditary disease.
(2) The factors currently regarded as predisposing agencies are in reality merely determining agents, not the cause of gout, but the occasion of its appearance.
(3) In the absence of an hereditary taint, these same are powerless to evoke the specific manifestations of true “gouty” inflammation as estimated by associated uratic deposition.
Bodily Conformation and Individual Temperament.—Of the hereditary character of gout no doubt remains, but as to the influence of physical build and temperament no such certainty prevails. Said Cullen, “Gout attacks especially men of robust and large bodies, men of large heads, of full and corpulent habit, and men whose skins are covered with a thicker rete mucosum, which gives a coarser surface.” Doubtless, in its more sthenic form, gout affects persons like Falstaff, of sanguine temperament and corpulent habit. But its milder or more asthenic manifestations occur often in men like Cassius, of lean and nervous type.[5]
Of objective stigmata, I know of none, save tophi, that can be truly regarded as pathognomonic of the outward semblance of the “gouty.” The skin of the face may be coarse, unctuous, and studded with ramifying venules. Such appearances, though not always, betray the tippler. Indeed, such stigmata as these are only of value as indicating the habits of the individual, favourable or not, to the development of gout.
Again, it has become a tradition with us that gout produces characteristic teeth. The mere fact that they are “ground down” so as to display the dentine in section is held as evidence of a “gouty” diathesis, or of lithæmia. The teeth of the gouty, it is true, often appear long and square-topped; but the gouty, no more than others, are immune from early recession of the gums. Again, we must recollect that there are several causes which may lead to the teeth being worn down more quickly than normally. Thus the formation of the jaw may be such that the upper and lower incisors meet edge to edge instead of overlapping. This so-called “edge to edge bite” subjects the incisors to marked attrition. Also we must recall that these effects may be aggravated by the nature of the diet. All of us are familiar with the fact that in old horses the teeth are ground down to the gums. The same also is observed in races condemned to live on coarsely prepared flour and hard vegetable food.
In conclusion, having regard to the marked frequency with which disorders leading to early recession of the gums are met with in the “gouty,” and the ease with which the early attrition of the teeth is explicable on tangible mechanical reasons, I am inclined to refer such changes to their combined agency, rather than to the nebulous “gouty” diathesis.
Again, despite Duckworth’s assertion that “the gouty throat is like no other,” I am convinced that it presents no specific appearances. Nor have I been able to satisfy myself that striated and fluted nails of, it is usually affirmed, exceptionally brittle nature, are distinctive of gout any more than the premature whitening of the hair so frequently accredited to the subjects of this diathesis.
One point, however, I would emphasise is, the frequency with which potentially gouty persons suffer from local syncopes and asphyxias of the hands. They are precisely similar to those met with in rheumatoid or atrophic arthritis, certain cases of which, as we shall see later, have another affinity with gout, viz., retardation in the output of exogenous purin.
Locality, Race, Climate, etc.—As to the geographical distribution of gout, the salient fact would appear to be the almost complete restriction of the disorder to the temperate zone. Among the natives of Africa gout, according to Livingstone, is unknown. Neither apparently is it to be met with in Turkey, China, Japan, Peru, and the Brazils. The indigenous peoples of India, and the East Indian Archipelago, also seem exempt, though the immunity does not extend to Europeans resident in these tropical climes.
It is significant that Duckworth, inquiring of practitioners from foreign parts as to their experience of gout, found that little or none was forthcoming “save where Europeans have formed part of the community.” This statement, to my mind, does but add cogency to my contention that gout is always hereditary.
If we restrict our purview to the British Isles and the Continent, we find that as a nation we have achieved the unenviable distinction of being facile princeps in point of the liability to and incidence of gout. The bulk of examples, too, are met with in England, the disorder being much less frequent in Scotland and Ireland. Moreover, in the two latter countries, the disorder is practically restricted to the upper classes. By contrast, in England it has extended to the lower orders also, in respect of which peculiarity we stand unique as compared with all other countries.
Reverting to the Continent, gout appears to be more common in France than in Germany, Austria, and Italy. Indeed, it is said to be endemic in Normandy, Burgundy, and the Rhone Valleys. In Holland, according to Duckworth, there is practically no gout, and the same is true of Russia, save in Petrograd and the Baltic Provinces.
In Belgium, also, gout is not common, and in Greece it is much less prevalent than in France or England.
In regard to the incidence of gout, its greater prevalence in temperate as opposed to tropical climes, and the disparities between different countries, it would be unsafe to assume that the variations are the outcome solely of climate. Thus the immunity of, e.g., strict Mohammedans is attributable in part to their sobriety and the less highly nitrogenous character of their food. But, if seduced into the ways of the “infidel,” their exemption, it is said, ceases. Europeans, of “gouty” heritage, may, if temperate, escape gout when resident in the tropics, otherwise they fall victims thereto just as surely as at home.
Gout, indeed, is more a matter of morals than climate. In the palmy days of the Roman Empire, when luxury and indolence were rampant, gout flourished, but declined following the installation of a republican form of government. In like fashion and for similar reasons, the inhabitants of modern Greece suffer infinitely less from the ravages of gout than of yore. In short, the climate of Italy and Greece has presumably endured unchanged, but the “habits” of their peoples have altered.
Formerly it was held that the incidence of gout in any country or district varied according as to whether the population drank wine and malt liquors, or distilled spirits. Where the taste for the latter predominated, the disease was relatively rare, whence the comparative immunity of Scotland, Russia, Poland, and Denmark. But what of the rarity of gout in the wine-producing country Spain? Nor for that matter have I ever seen it claimed that gout was especially prevalent in Portugal, the home of “port,” that bête noir of the “gouty.” In truth, dogmatism is here out of place, for though overeating and overdrinking are undeniably important factors in eliciting gout, they are not the sole factors.
In reviewing the statements made as to the geographical distribution and the race incidence of gout it is but too manifest that they are largely provisional; indeed, such information as we do possess as to its relative frequency in various countries, must be taken cum grano salis. Thus, who can doubt that the various affirmations must have been very largely influenced by the “personal equation,” that what one authority would define as gout would by another be deemed inadmissible to this category. Moreover, many of the original statements were made at a time when the differentiation of arthritic disorders, as we now know it, was but in its infancy. For obvious reasons, therefore, no researches in this sphere can ever be satisfactory, until the opinion of the profession at home and abroad be crystallised into some definite pronouncement, some precise definition, of the exact criteria by which the diagnosis of gout stands or falls.
In justification of these strictures, may I cite some opinions as to the frequency of gout in the United States. In 1890, Sir Dyce Duckworth affirmed that in America gout was “practically unknown.” But a few years later, we find Sir William Osier convinced that gout was often unrecognised in the United States. More pertinent still, only twenty years after Duckworth’s affirmation, Luff quoted the statistics of the Johns Hopkins Hospital, Baltimore, from which it appeared that during a period of fourteen years 0·26 per cent. of the total admissions thereto were examples of gout. This he contrasts with the number of cases of gout admitted to St. Bartholomew’s Hospital, London, during a similar period. Mirabile dictu, the percentage was only 0·37, but a third more than that of the Johns Hopkins Hospital!
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.
That alcohol will produce the disorder even more swiftly and surely if reinforced by overeating also, cannot, I think, be gainsaid. As to the modus operandi of alcohol in inducing gout, I believe that it acts indirectly, viz., by slowly sapping the protective mechanisms of the body, and so paving the way to infections.
Much stress has been laid on the fact that certain occupations conduce to gout; but, if we exclude plumbers, painters, or other workers in lead, no other callings in life can be held to entail a specific predisposition to its development, save in so far as they promote overeating, overdrinking, and inactivity.
It is well established that workers in lead are specially prone to develop gout. I take pride in noting that two of my predecessors at the Royal Mineral Water Hospital, Bath, William Falconer (1772) and Caleb Hillier Parry (1807), drew attention to the frequent occurrence of gout in those exposed to the action of lead; nevertheless the major part of our knowledge of lead as a predisposing cause of gout we owe to Sir Alfred Garrod (1854). This authority noted that at least one out of every four gouty patients that had come under his care at King’s College Hospital had at some time in their lives been the subjects of plumbism, and for the most part were plumbers or painters. Out of 136 undoubted examples of gout, Sir Dyce Duckworth noted that of these twenty-five males showed signs of lead poisoning, and were either plumbers, painters, compositors, or workers in lead mills. My colleague, James Lindsay, out of a total of 482 instances of males afflicted with gout, found that 108, or 22·4 per cent., were workers in lead.
In light of these findings the question naturally arose as to whether lead impregnation per se could produce gout. It was then elicited that the association of lead with gout was noticeably less frequent in Scotland and in the North of England than in London. On this interesting point Dr. T. Oliver observes, “We do not see in the north that intimate relationship between gout and saturnine poisoning. Workmen from the south develop it in the North of England. The natives of the north, though equally exposed, seldom become gouty even when the kidneys are affected.” Again, Osler tells us that in America lead-gout is comparatively rare, though chronic lead poisoning is frequently met with in that country in association with arterio-sclerosis and contracted kidneys. Again, Frerichs, out of 163 cases of plumbism in the Berlin Hospital, found not a single case of true gout.
Some remarkable instances illustrating the influence even of medicinal doses of lead in determining outbreaks of gout are on record. In a man aged 25-30, suffering from chronic diarrhœa, Sir Lauder Brunton prescribed lead and opium pills. In less than ten days he returned with gout in one of his joints, though he had never previously suffered from an attack. My colleague, Dr. Munro, tells me of an even more striking case. A lady under his care had used a hair wash, for many years, with apparently no ill effects. She recommended a friend of hers to try the same lotion, and within a few days she developed acute arthritic gout, though she had never previously experienced the disorder. Analysing the preparation, Dr. Munro found the clue in the contained lead.
As to proffered explanations of lead-gout some have sought it in the production by this poison of arterio-sclerosis and chronic nephritis. But this is scarcely satisfying when we contrast the frequency of chronic plumbism and associated arterio-sclerosis and contracted kidneys with the relative rarity of lead gout.
The balance of evidence would appear to be in favour of the view that lead per se cannot produce gout. For the incidence of lead-gout is scarcely appreciable, save in a population amongst whom from other causes gout is prevalent. In short, lead in the absence of an hereditary bias, is impotent to evoke gout.
As to its modus operandi, I think it exerts its effect through derangement of the intestinal secretions, and so favours the migration inwards into the system of pathogenic bacteria.
As for occupations other than those concerned with lead, it is certainly notorious that gout is extremely frequent in those that are rich in opportunities for overeating, overdrinking, and sluggish habits. This point has never been more clearly illustrated than by James Lindsay, whose analysis I take the liberty of transcribing.
Thus, out of 482 males the victims of gout, eighty-one were cabmen, coachmen, grooms, stablemen, and bus drivers; fifty-one were draymen, publicans, barmen, cellarmen, potmen, innkeepers, maltsters, coopers, storekeepers, brewers’ travellers, and brewers’ labourers; twenty-five butlers, men servants, ship’s stewards, and hotel servants; while forty-five were labourers, and of the residue, although all kinds of trades and occupations were represented, yet no other class reached ten in number.
Of these various stations and occupations, it cannot be held that, in themselves, these callings necessarily contain the “seeds of the gout.” The banefulness resides in the associated habits of living; for but too frequently repletion, intemperance, and indolence go hand in hand with these vocations. In other words, dietetic excesses, overloaded intestines, and too much alcohol, what more likely to impair the digestive functions, to increase the toxicity of the intestinal flora, and in turn to upset the equilibrium of general nuclein metabolism, with its associated specific local reaction in certain tissues?
Mental and Physical Over-exertion, etc.—Sydenham said of gout that it destroys “more wise men than fools,” and in a letter to Dr. Short, he complains, “I send you a short tract upon Gout and Dropsy instead of the thicker volume, which in my own mind I had determined on, viz., a history of such chronic diseases as my practice has most especially met with. By applying my mind, however, to its utmost, and by bringing all my powers of thought on the subject, I brought on a fit of gout, such as I had never before suffered from; so that the fact itself warned me to lay aside, even against my own will, such lucubrations, and to take care of myself; well satisfied with having, in some measure, dealt with these two diseases. Whenever I returned to my studies, gout returned to me.”
It is doubtful if, in the absence of an hereditary proclivity, intellectual strain would promote the development of gout. On the other hand, there is, I think, no doubt that immoderate mental exertion will indirectly precipitate an outbreak. I can well understand that the illustrious Sydenham, absorbed in his life study, forgot to take a normal amount of exercise. Perhaps, like the renowned Jenner, he would have said, “I never walk at all except from my house into my carriage. I hate walking, and if I could, I would get my servants to carry me to bed.” Nevertheless, I doubt not that Sydenham’s intellectual efforts necessarily entailed sedentary habits, which brought in their wake digestive and intestinal derangements, whence his occasional gouty outbreaks.
Gout, indeed, has taken its full toll of the “Intellectuals.” Thus Scudamore tells us that “The late Mr. Pitt and his father had gout at a very early period of life. The father was never a votary of Bacchus, and neither of Venus (as we are told), but both were ardent students.” Probably, in many instances, however, the evils of immoderate study are reinforced by more reprehensible excesses. The ancients insisted on sexual debauchery as favouring outbreaks of gout. Whence the Latin verse:
“Ut Venus enervat vires, sic copia vini,
Et tentat gressus, debilitatque pedes.”
Doubtless, in some instances of this supposed origin, a gonococcal arthritis was confused with gout. Doubtless sexual neurasthenia with diatetic excess favours the onset of gout. In the same way grief, anxiety, and other depressing emotions are provocative of gout in that they impair the digestive functions, lead to hepatic torpor, and sluggish bowels.