Attempts to “explain” the nature of scurvy continued. In particular, efforts were made to relate it to the absence of fresh fruit and vegetables in the diet, and by the middle of the nineteenth century there was a fair consensus that this was the main cause of the disease. Just as in the eighteenth century, when there had been attempts to accommodate scurvy within the then popular humoral theory of disease, so in the nineteenth century there were efforts to explain it by drawing on concepts borrowed from the embryonic nutritional science of the period. This explanation involved an interesting conceptual shift from the conviction that there were positive causes of scurvy (such as coldness or too much dietary salt) to the belief that it resulted from a dietary deficiency - albeit an undefined one.
Two writers were particularly vocal in developing this theme. One was George Budd, a pioneer thinker in the development of the concept that there were clearly definable “Disorders Resulting from Defective Nutriment” (to use the title of his series of articles in the London Medical Gazette in 1842 [Budd 1840, 1842]). The second was Robert Barnes, who in 1864 produced his less widely available On the Occurrence of Sea Scurvy in the Mercantile Navy.... Budd, in a frequently referenced article in Tweedie s Library of Medicine, stated quite unambiguously that scurvy was the result of a lack of a single essential dietary principle and of that alone; he furthermore described this antiscorbutic principle as a thermolabile one, present in fresh fruit and vegetables and with uncanny foresight prophesied that it would “be discovered by organic chemistry or the experiments of physiologists in the not too distant future” (Budd 1840: 77; Hughes 1973).
Twenty years later Barnes reaffirmed the essential dietary nature of scurvy in a 10,000-word official report. Basing his arguments on “experiments and facts” he stated, “There is no fact so well attested by the history of mankind as the dependence of scurvy upon the negation of fresh vegetable food. . . the abolition of scurvy is entirely a question of diet, and a very simple question of diet.” Barnes, basing his calculations on returns obtained from the Dreadnought (Naval) Hospital, attempted to arrive at a figure for the depletion period necessary for the emergence of scurvy and concluded that “symptoms such as. . . blotches like bruises, swelling of the gums, lassitude and emaciation. . . have generally been manifest in from 60 to 80 days.” He acknowledged, however, that there was a strong factor of individual variation (Barnes 1864: 330).
But what was the nature of this deficient element that was absent from scorbutigenic diets yet present in vegetables and fruits? E. A. Parkes, an eminent clinician, presented the problem in four simple sentences, logically and within the currently accepted framework of dietary knowledge in 1869:
The peculiar state of malnutrition we call scurvy is now known not to be the consequence of general starvation, though it is doubtless aided by this. Men have been fed with an amount of nitrogenous and fatty food sufficient not only to keep them in condition, but to cause them to gain weight, and yet have got scurvy. The starches also have been given in quite sufficient amount without preventing it. It seems, indeed clear that it is to the absence of some of the constituents of the fourth dietetic group, the salts, that we must look for the cause. (1869:492)
And the missing components in Parkes’s opinion were the salts of organic acids, such as citric, malic, and tartaric - compounds known to be of vegetable origin. Parkes’s advice, included in his army manual Practical Hygiene, was that, “In time of war every vegetable should be used which it is safe to use, and, when made into soups, almost all are tolerably pleasant to eat.... Good lemon juice should be issued daily (l oz.) and it should be seen that the men take it” (1869:494).
Parkes’s theory of the nature of scurvy was by no means the only one in the field during the nineteenth century. There were many others, and as late as 1908, J. M. Cowan, writing in the standard Oxford manual A System of Diet and Dietetics, while admitting “the undisputed fact that a plentiful diet of fresh vegetables cures the disease” went on to state, “The exact nature of the fault is, however, undetermined” (1908: 645). Cowan referred to a number of theories of scurvy then in vogue. These were a deficiency of potash salts; a deficiency of dietary bases (alkali); ptomaine poisoning; and a specific infection (Cowan 1908: 645). Cowan’s uncertainty about the cause of scurvy was echoed in 1911 by the Encyclopedia Bri-tannica, which stated,“... the modern tendency is to suspect an unknown micro-organism. . . even among the more chemical school of pathologists it is disputed whether the cause is the absence of certain constituents in the food or the presence of some actual poison...” (517).
Had Cowan been aware of it, these alternative theories had already been rendered redundant by an experiment reported the previous year from Oslo - in Carpenter’s opinion “the most important single paper in the whole history of this subject” (Carpenter 1986: 173). This was the classic study by A. Holst, in which he produced scurvy in guinea pigs by feeding them a grain diet - in an experiment originally designed to study the nature of beriberi.
Holst had fortuitously chosen one of the few species unable to produce vitamin C endogenously and had fed them a diet completely lacking in vitamin C. The guinea pigs died after a month on the diet, and it was noted that the tissues showed degenerative changes similar to those known to occur in human scurvy (Holst and Frohlich 1907). Until the characterization of the “antiscorbutic factor” and the development of chemical methods of assessing it in the 1930s, the prevention of scurvy in guinea pigs was the standard technique for measuring the antiscorbutic potency of a preparation.
The last quarter of the nineteenth century also witnessed a proliferation of interest, both in America and in Europe, in “infantile scurvy” - a form of avitaminosis C occurring in very young children and characterized primarily by defective bone development. It was later referred to as “Barlow’s disease,” after Thomas Barlow, a London physician, who described its true nature and distinguished it from rickets, with which it was frequently associated and often confused (Evans 1983).
It is interesting to note that the emergence of infantile scurvy, like that of “sailors’ scurvy” three centuries previously, was probably a consequence of developments in technology, namely, too great a dependence on processed foodstuffs from which the vitamin C had been destroyed and, in particular, evaporated and condensed milks, the use of which increased significantly during the second half of the nineteenth century (Carpenter 1986: 158-72). The subsequent introduction of orange juice supplements for babies ensured the sudden eradication of “Barlow’s disease,” although isolated reports from Germany, as late as the 1980s, described its occurrence in babies fed only on oat gruel.
World History
