R E Hughes. Cambridge World History of Food. Editor: Kenneth F Kiple & Kriemhild Conee Ornelas. Volume 1. Cambridge, UK: Cambridge University Press, 2000.
The human body requires an adequate supply of ascorbic acid (L-xyloascorbic acid or vitamin C) to enable it to function normally, and a lack of the vita-min results in the emergence of the condition known as scurvy (scorbutus or avitaminosis C). Unlike plants, and the majority of animals thus far studied, humans are unable to produce ascorbic acid endogenously and, thus, are dependent upon dietary sources—mainly fruit and vegetables—for a supply of the vita-min. In the absence of vitamin C, formation of collagen, an essential glycoprotein component of connective tissue, is impaired, which is believed to be the main underlying biochemical lesion in scurvy (Counsell and Hornig 1981; Englard and Seifter 1986).
The earliest signs of scurvy (fatigue and lassitude) may emerge in humans some 12 weeks after removal of dietary vitamin C, and the more overt traditional signs (hemorrhagic spots under the skin [petechiae], softening of the gums, and defective wound healing) after some 17 to 26 weeks of deprivation.
In 1753, James Lind concluded his pioneer study of scurvy with a chronological Bibliotheca Scorbutica, which imparted a mild historical flavor to his text (Stewart and Guthrie 1953). But more than a century was to pass before the first sustained efforts to produce a history of the disease emerged. One of these was J. Maré’s 200-page article in the Dictionnaire Encyclopédique des Sciences Médicales in 1880, and the second was August Hirsch’s 60-page article in his Handbook of Geographical and Historical Pathology (1883-6). Both of these pioneer works are now completely eclipsed by K. J. Carpenter’s comprehensive History of Scurvy and Vitamin C (1986), to which the reader is referred for a more extended treatment.
Simple logic dictates that scurvy became a clinical possibility when evolving hominoids (unlike most other animals) lost the ability to biosynthesize vitamin C from carbohydrate precursors. This loss would, presumably, only have occurred in an environment that provided early humans with an adequate intake of dietary vitamin C. By the same token, scurvy itself would not have emerged until a change in food consumption patterns or in the seasonal availability of the vitamin resulted in a deprivation of vitamin C.
The main dietary sources of vitamin C are fruit and vegetables, particularly when eaten raw, and to a much lesser extent, fresh meat (salting or drying meat results in a loss of its vitamin C content). Grains, nuts, eggs, and dairy products (with the exception of fresh milk, which contains small amounts) provide little or no vitamin C.
There can be little doubt that the unstable and fluctuating environmental conditions of primitive humans must have, from time to time, produced highly scorbutigenic situations, but the precise frequency of the disease in prehistoric and early historic times is obscure. Some commentators have claimed to discern descriptions of scurvy in the writings of early classical writers such as Pliny and Paulus Aeginita, but this must remain a matter of considerable conjecture.
There is some evidence that scurvy afflicted the armies of the Crusaders in the thirteenth century, and the writings of Jacques de Vitry (c. 1220) and Jean Sire de Joinville (1224-1319) have been quoted in this respect (Major 1978: 585-6). Indeed, de Joinville’s description of the “army sickness” reveals a situation at least as fearful as the depredations of the attacking Turks:
…our legs shrivelled up and became covered with black spots, and spots of the colour of earth, like an old boot: and in such of us as fell sick the gums became putrid with sores, and nor man recovered of that sickness, but all had to die.… The proud flesh in our men’s mouth grew to such excess that the barbour-surgeons were obliged to cut it off, to give them a chance of chewing their food or swallowing anything. It was piteous to hear through the camp the shrieks of the people who were being operated for proud flesh, for they shrieked like women in childbirth. (Major 1978: 586)
Scurvy as an Occupational Disease
Curiously enough, the change that most clearly and finally precipitated the emergence of scurvy as a recognizable disease was not so much dietary as technological. Scurvy first established itself as a discrete and clearly definable feature of early medicine because of those technological advances that enabled the building of ships capable of prolonged sea voyages.
By the end of the fifteenth century the ship had acquired the structure that was to characterize it for the next three centuries, and the newer naval technology meant that humans could now remain at sea for months at a time—long enough to deprive themselves of an adequate supply of the fresh fruit and vegetables that are the main dietary source of vitamin C. Consequently, it was during the early voyages of exploration in the fifteenth century that the first clear pictures of scurvy emerged. In this sense scurvy (or scorbutus as it was described in the Latin texts of the day) may truly be regarded as one of the earliest occupational diseases.
Perhaps the most widely quoted example of explorer’s scurvy is that described by Jacques Cartier, the Breton explorer, who during his discovery of the Saint Lawrence River in 1536 lost 25 of his crew to a “strange and cruell disease.” Certainly his description of their condition—the loss of strength and “their skins spotted with spots of blood of a purple colour … [and] their gummes so rotten, that all the flesh did fall off, even to the rootes of the teeth, which did also almost all fall out” is consistent with the petechiae and connective tissue defects now accepted as cardinal features of scurvy (Major 1978: 586).
But a similar condition prevailed among the crew of Vasco da Gama during his return voyage from Africa in 1498; and almost a hundred years later Richard Hawkins could assert that during his 20 years at sea he had witnessed some 10,000 cases of scurvy (Carpenter 1986: 1-26).
A century and a half after that, George Anson lost three-fourths of his men and officers, mostly to scurvy, in his 1740-4 voyage around the world. In fact, it has been estimated that during the critical period between 1600 (when long sea voyages had become more common) and 1800 (when the prophylactic effect of lemon juice rations had proved effective), scurvy was responsible for over 1 million deaths among seamen—almost certainly more than the sum total lost during the same period in naval battles, shipwrecks, and to diseases other than scurvy (Roddis 1951: 48, 72).
In the seventeenth century scurvy was considered primarily a scourge of sailors and soldiers. “In Navies and Camps, Scorbutick Feavers are very frequent, and arrive to a great height of malignity, sweeping them away like the Plague sometimes” wrote Everard Maynwaringe in 1664, adding “And I remember, in a hard and long voyage at sea, most of our people were very Scorbutick … who at our first setting out were sound and healthy (Maynwaringe 1679: 57).
Much was written about the possible causes of scurvy among sailors. Bad (i.e., cold and wet) air, poor diet, idleness, and a melancholy outlook were viewed as major predisposing causes. Overindulgence in salted meat was held to be a main dietary cause—particularly as this could explain the peculiar prevalence of the condition among sailors. And some commentators introduced their own specific dietary causes. Thomas Willis, for example, blamed sugar, whereas Maynwaringe accused tobacco, although neither explanation gained general acceptance.
“Land Scurvy”
George Budd, one of the more competent writers on scurvy in the early nineteenth century, wrote, “Scurvy has, unquestionably, existed in the north of Europe from the most remote antiquity. That we have no mention of it in the early history of the northern nations must be imputed to the extreme ignorance of the people, especially as regards medicine” (Budd 1840: 58).
It is the case that medieval medical texts and herbals contain no clearly identifiable references to scurvy, although the numerous remedies for loose or “wagging” teeth have sometimes been thought to indicate unrecognized scurvy (e.g., Henslow 1899: 112). Nor does scurvy appear to have been included among the main diseases responsible for hospitalization in medieval England (Clay 1909). Thus, as already suggested, the general consensus would appear to relate the recognition and acceptance of scurvy as a specific clinical lesion to its occurrence among sailors during the fifteenth and sixteenth centuries.
Certainly it was in the sixteenth century that sporadic references to scurvy began to appear in the medical texts and herbals. Thus, although there are no recognizable references to scurvy in the herbals of Leonhard Fuchs (1542), Hieronymus Bock (1552), and Pietro Andrea Mattioli (1565),William Turner’s Herbal (1568) comments on its appearance on the Continent. And Henry Lyte’s translation of R. Dodoens’ Cruÿdeboeck (1578) refers to:
Spooneworte [Cochlearia sp., scurvy grass] …a singular remedie against the disease of the mouth … called by the Hollanders and Frise-landers Scuerbuyck, against whiche evill it hath bene lately proved to be very good and is in great estimation and much used of the Hollanders and Friseans. (Dodoens 1578: 117-18)
Similarly, J. C. von Kraftheim’s Consiliorum et Epistolarum Medicinalium (1591: 285) gave dietary precepts to be followed in scurvy. But surprisingly, Philip Barrough’s comprehensive The Method of Physick (third edition, 1596) contained no reference to scurvy, nor did Felix Plater’s Observationum in Homines Affectibus Plerisque, Corpori & Animo … (1651). However, William Clowes, in his A Profitable and Necessary Booke of Observations … (1596) described treating two sailors who were “sicke at the sea of the Scorby.”
One of the earliest descriptions of scurvy in English can be found in Thomas Johnson’s version of J. Gerarde’s Herbal(1633) as part of the entry for scurvy grass (Cochlearia officinalis), the most favored of the antiscorbutic herbs (see following). It related scurvy to its supposed classical “precursors” and is worth quoting in some detail:
The juice of Spoonewort given to drinke in Ale or Beere … perfectly cureth the disease called ofHippocrates, Voluulus Hematites: of Pliny, Stomacace; of Marcellus, Oscedo and of the later writers, Scorbutum of the Hollanders and Frisians, Scuerbuyck: in English, the Scurvie … this filthy, lothsome, heavy, and dull disease, which is very troublesome and of long continuance. The gums are loosed, swolne, and exulcerate, the mouth greevously stinking; the thighes and legs are withall very often full of blew spots, not much unlike those that come of bruises; the face and the rest of the body is oftentimes of a pale colour: and the feet are swolne, as in a dropsie … a disease haunting the campes, which vexe them that are besieged and pinned up and it seemeth to come by eating of salt meates, which is increased and cherished with the cold vapors of the stone walls … Hippocrates has written: their gums (saith he) are infected, and their mouthes stinke that have great spleenes or milts and … can hardly be cured of this malladie, especially of the ulcers in the legs and blacke spots. The same is affirmed by Paulus Aegineta in this third booke, 49 chapter, where you may easily see the difference between this disease and the black jaunders, which many times are so confounded together that the difference or distinction is hard to be known but by the expert chirurgions who offentimes serving in the ships, as wel her Majesties as merchants, are greatly pestered with the curing thereof.… (Gerarde 1633: 402)
By the early seventeenth century references to cases of scurvy among land dwellers were beginning to appear; initially, it was believed that there were two forms of the disease, and references were made to “sea scurvy” and to “land scurvy.” This dichotomy continued until it was finally dispelled by Lind in 1753. Such an apparent sudden increase in the incidence of scurvy among land dwellers in Britain during the seventeenth century was commented on by a number of writers. Marchmont Nedham in his Medela Medicinae (1665) supported his claim that scurvy was on the increase in England by referring to the Bills of Mortality, which recorded an increase in the deaths from scurvy from 5 in 1630 to over 100 in 1656. Similarly, Gideon Harvey commented in 1675:
Many years it [scurvy] remained on that Coast [i.e., Holland] before we were sensible of it here in England: for there are many Physicians yet living who in the former part of their Practice had so much as heard of the Name of this Disease, whereas within the last 20 or 30 years past it’s grown very familiar among us. (Harvey 1675: 211)
There is confirmatory evidence that in Wales, too, scurvy was regarded as a new disease at the beginning of the seventeenth century. Sir Thomas Wiliems of Trefriw, a priest and practicing physician, compiled the manuscript for his projected Thesaurus Linguae Latinae et Cambrobritannicae during the period 1604-7; under the entry for the plant “Britanica” he refers to scurvy as “a new disease in our land, Wales” (“clevyt newydh yn ein gwlad ni Cymru”)(Hughes 1990).
William Vaughan (1575-1641), also writing from Wales, reflected the growing importance of scurvy in seventeenth-century medicine in his The Newlanders Cure (1630). He recommended the tops and leaves of turnips as antiscorbutics; more significant, perhaps, he used contemporary thought on scurvy to illustrate his anti-papist sentiments in his verses “Description of the Catholicke Scurvy ingendered by the Mystery of Iniquity …”:
..As doth the former scurvy beate
For want of Sunne and Motions heate
Upon the Spleene, the Breathe and Skinne
So doth that Old and Scurvy sinne
Withe Purple Spots go on to Stayne
Both Soule and Body, all for Gaine …
(Vaughan 1630: 112)
Whether these writings reflected a true increase in the incidence of scurvy among land dwellers, or merely indicated a greater awareness of its presence, is not known. According to John Floyer (better known for his introduction of a minute watch to measure pulse rate),”Scurvy was a new Name for an old Disease”—and there were others who regarded scurvy merely as an older disease that had changed its nature (Floyer 1722: 3; King 1970: 149).
Diet and Scurvy
A true increase in the incidence of scurvy would have required a fairly substantial change in the dietary pattern (or in the dietary availability of vitamin C), and there is little evidence that any such substantial and sudden change occurred in Britain at the time. Rather, such knowledge as is available would appear to suggest that the consumption of turnips, cabbage, and other vegetables by the “husbandman” sector of the population of Britain in the seventeenth century would have provided them with adequate amounts of the vitamin (Powicke 1926).
Yet with diets of the poorer classes of the day, one is less certain. And of earlier centuries little is known, although if one accepts the general view that the pre-sixteenth-century working-class diet was predominantly grain-based with supplements of salted and/or dried meat or fish but with very little fresh fruit and vegetables, then scurvy must have been of frequent occurrence (Prentice 1939: 118-36).
Of the fifteenth-century peasant diet, it has been written:
… it seems likely that the winter diet of salt bacon, bread and peas gave little protection against scurvy, so that by the end of the winter most of the poor country people must have been in at least a pre-scorbutic condition. (Drummond and Wilbraham 1964: 77)
However, the comparative absence of any clearly recognizable references to scorbutic afflictions among a population that during the winter period presumably subsisted on a scorbutigenic diet is somewhat puzzling.
It was not until the enthusiasm of the Dutch market gardeners spilled over into seventeenth-century Britain that a general, albeit small, reduction in the scorbutigenic potential of the British diet occurred. Yet this, for some unaccountable reason, would seem to be the period that witnessed an apparent increase in the incidence of scurvy. However, a much more significant change in the British diet was yet to occur. The end of the seventeenth century witnessed the introduction of the potato on a large scale—a crop that was subsequently to become, for a very substantial proportion of the population, the main dietary source of vitamin C and, hence, the prime protector against widespread scurvy.
Potatoes and Scurvy
In 1662 a Committee of the Royal Society considered a proposition “to plant Potatoes through all ye parts of England,” and in 1664 Forster pressed the case for widespread cultivation of the potato in his England’s Happiness Increased. It is not known to what extent Forster’s advice was acted upon, although Thomas Moffet claimed in 1665 that “pottato-roots are now so common and known amongst us, that even the Husbandman buys them to please his Wife” (Moffet 1746: 324). In 1691 Richard Baxter, the religious writer, in his last literary composition (The Poor Husband-man’s Advocate) suggested that all smallholders should plant a quarter of an acre of potatoes to provide themselves with “a half year’s wholesome food” (Powicke 1926).
Nevertheless, it is unlikely that these statements reflected any widespread use of the potato, and it is probable that until the end of the seventeenth century it remained primarily a horticultural curiosity cultivated by that sector of the populace least likely to suffer from dietary inadequacies, a situation reflected by the somewhat esoteric recipes for its use in the cookery books of the period (e.g., Salmon 1696: 263).
In the eighteenth century, however, potatoes were much more widely grown. According to The Complete Farmer (1777):
the culture of this plant has, within these last thirty years, been extended to almost every part of England. … It is esteemed, and now very generally used at the tables of persons of all ranks; and inestimable for the poor being a cheap and very wholesome food … in Ireland, particularly in the province of Munster, they are the principal, and almost the only food of the poor there for almost eight months in the year. (Society of Gentlemen 1777)
The importance of the potato in the social etiology of scurvy has not always been fully appreciated, although Carpenter has clearly underlined the significant role that it played in the history of scurvy, particularly in Britain and in Ireland. Its significance stems from two facts. First, although comparatively low in vitamin C (10 to 20 milligrams [mg] per 100 grams [g]), potatoes were eaten in such large amounts that they frequently accounted for a very high proportion of the vitamin, and for many they represented its sole source. In Ireland, during the nineteenth century, daily consumptions of up to 4.5 to 6.5 kilograms (kg) per person were recorded (Letheby 1870: 26; Salaman 1970: 331), which would have provided an estimated daily intake of about 400 to 600 milligrams of vitamin C—some 40 to 60 times the quantity required to prevent scurvy. In the 1840s, scurvy was, therefore, a natural consequence of the failure of the potato crop. As suggested earlier, unlike potatoes, cereal grains contain no vitamin C, and thus the maize imported to alleviate the famine had no effect at all against scurvy.
It is also important to note that potatoes can be stored for many months with very little loss of fluid (and consequently with a retention of ascorbic acid), thereby providing a source of the vitamin well into the winter when fresh sources are absent. Even today a substantial sector of the population of Britain obtains the bulk of its vitamin C from potatoes, particularly in the winter months.
By the same token, many of the outbreaks of scurvy in the nineteenth century (as in the Irish Famine of 1845-8 and in the Exeter hospital epidemic in 1846) were directly traceable to a reduced supply of potatoes (Carpenter 1986: 101; Shapter 1847: 945-8). In charting the history of scurvy, a role of paramount significance must be accorded to the potato; its establishment in Italy and Spain some centuries before it attained popularity in Britain was possibly a factor in determining the higher frequency of scurvy in northern Europe in the sixteenth and seventeenth centuries (Salaman 1970: 142-6). During the last three centuries the potato has doubtless protected millions of people from the ravages of the disease.
Early Writers and Theories
Many of the reports of scurvy in Europe in the sixteenth century emphasized its essential prevalence in the colder northeastern areas. “The Scurvy is properly said to be endemical in most of our Northern Countrys, that border upon the Baltick Sea, or adjacent to the German Ocean: As Denmark, Swedland, Norway, Ffrisland, Holland, England etc. But in High Germany, France, Spain and Italy, the Scurvy is accounted sporadical … but here and there one” (Maynwaringe 1679: 16). Such was the comparative rarity of scurvy in southern France that Lazarus Riverius, writing “from my study in Montpelier on the 8th of July 1653,” dismissed the condition, commenting, “The scurvy is usual in the North [of France?] but almost unknown in the South … (Riverius 1655: 357-61). The non sequitur that a cold and damp atmosphere conduced to scurvy prevailed in Europe until well into the eighteenth century.
A. S. Hess, however, in commenting on the apparent absence of references to scurvy in the classical medical writings, offered a truer explanation: “Greek, Roman and Arabic writers do not seem to have been acquainted with scurvy. This is as we should expect, for fruits and vegetables grew in such plenty in these southern countries that scurvy must have been a disorder of rare occurrence” (Hess 1920: 1). This (together with the comparatively early adoption of the potato in southwestern Europe) is presumably also the explanation of the differential distribution pattern of scurvy reported for Europe in the sixteenth and seventeenth centuries.
A parallel development to this apparent increase in scurvy (or the recognition of it) among land dwellers in parts of northern Europe in the seventeenth century was the appearance of the first medical texts devoted entirely to the condition. Unfortunately, however, it is impossible to determine whether the appearance of the texts resulted in an increased awareness of the condition, and hence an apparent increase in its incidence, or whether the texts were produced in response to a genuine increase in the frequency of the disease.
In any event, these medical texts first appeared on the Continent, and J. Ecthius’s De Scorbuto (1541) is usually regarded as the pioneer study; the ensuing two centuries saw a substantial proliferation of “scorbutic” texts—Lind in 1753 referred to some 40 of them in his Treatise; but few of these early compilations showed any great originality of thought or interpretation. Probably the two most influential were John Wier’s De Scorbuto published in Basel as a part of his Medicarum Observationum … in 1567 and Severinus Eugalenus’s De Morbo Scorbuto Liber … first published in 1604 and then again in much changed forms under the hands of subsequent editors up to 1658.
John Wier [Wierus]—better known perhaps for his De Praestigiis Daemonum (1563)(a treatise opposing the persecution of witches)—was probably the more scientific of the two. His treatise on scurvy was reprinted in its entirety by Daniel Sennert in 1624 as one of the six component works in his De Scorbuto (1624). In the prefatory remarks to an English translation that appeared in 1622, the translator indicated that he had translated Wierus rather than Ronsseus or Langius or Ecthius because of a tendency on their part to “wade into deep difficulties” and because they “paynteth out the signes, and poynteth to the cure, but affordeth not the pith and marrow of speciall medicines …” (Wier 1622: ii).
Wier’s De Scorbuto was also the basis of the Traetice of the Scorbut written in 1676 by Gwilym Pue [Puw], a Welsh Catholic recusant priest and physician. Pue’s treatise, incidentally, contained a case history of a supposedly scorbutic patient—probably Pue himself (Hughes In press). S. Eugalenus exerted a similar influence during a slightly later period, and he was freely quoted until well into the eighteenth century, but his work, even in the later ‘improved’ editions, was less well presented and much more anecdotal than that of Wier. Lind was highly critical of Eugalenus and of Willis, the English physician who uncritically represented Eugalenus in his Tractatus de Scorbuto (1667).
Despite the considerable attention that it attracted, very little, in reality, was known about scurvy in the seventeenth and eighteenth centuries. There was fairly general agreement about its main clinical features but little was known of its cure and still less of its cause. The traditional belief that it was essentially a disease of the spleen persisted until well into the eighteenth century. The situation was further complicated by a tendency to assume that there were different types of scurvy. As indicated earlier, it was believed that “sea scurvy” was a different condition from “land scurvy”; there were references too to “hot scurvy” and to “cold scurvy,” to “acid scurvy” and to “alkaline scurvy,” and the situation was further confused by the belief that these categories were not mutually exclusive.
Furthermore, there were probably different “grades” of scurvy, corresponding to different degrees of vitamin C deprivation. Scurvy, when it occurred among land dwellers, was presumably often a case of chronic partial vitamin C deficiency (hypovitaminosis C) rather than the “full” scurvy (avitaminosis C) that afflicted sailors after their much longer periods of complete deprivation of the vitamin. Hence the confusion between the clear-cut symptoms of complete deficiency among sailors and the chronic (and often seasonal) hypovitaminosis C that could befall land dwellers.
The “Antiscorbutic” Plants
The classical interpretation that diseases and ill health reflected a change in the humoral balance of the body was a powerful element in seventeenth- and eighteenth-century medical thought. Dietary and pharmacological treatments advocated for diseases were frequently devised primarily to counteract or correct the supposed deviant humoral patterns. Edward Strother, in introducing his influential An Essay on Sickness and Health in 1725, was quite categorical on this point: “It is therefore a standing Rule that our Meats and Drinks ought to consist, as nearly as can be, of Particles contrary to the Cause of the Disease reigning …” (1725: 30).
Correspondingly, eighteenth-century texts on diet and nutrition attached considerable importance to a categorization of foods in terms of their supposed humoral properties so that physicians could select appropriate foods to counteract specific diseases. “The best way of curing the Gout,” wrote W. Stephens (1732: 60) “is to hinder the Generation of this gouty Humour in the Body; this is to be effected no other way, that I know of, but by Diet.”
The same was to hold true in the case of scurvy. For “hot,” “alkaline,” “sea,” scurvy, cooling acidic foods, such as oranges and lemons, were advocated; “cold,” “acid,” “land,” scurvy, in contrast, could be treated by the “hot” antiscorbutic plants such as scurvy grass, brooklime, and the cresses. Thus there developed a tradition, reinforced by empirical observations, that “sea-scurvy” could be treated by oranges and lemons, whereas the methods of choice for scurvy among land dwellers centered on the antiscorbutic herbs. When John Woodall extolled the virtues of lemon juice as a cure for scurvy among sailors he carefully contrasted its value with that of the traditional anti-scorbutics “namely Scurvy-grasse, Horse reddish roots, Nasturtia Aquatica … and many other good meanes” whose virtues extended, however, “only to the Cure of those which live at home …” (Woodall 1639: 61).
Turner, in describing the virtues of brooklime in his Herbal of 1568, penned what must be one of the earliest references to scurvy in an English herbal: “… I have proved it my selfe by experience that brooklyme is very good for a decease that reigneth much in Freseland called the Scourbuch. I sod the herbe in butter milke, the cheese and butter taken away, and gave the patientes it so” (128). Clearly, this statement lends further support to the belief that scurvy was either comparatively rare or unrecognized in sixteenth-century Britain.
As it happens, the concentration of foliar ascorbic acid in the three antiscorbutic herbs (Cochlearia officinalis [scurvy grass], Veronica beccabunga [brooklime], and Nasturtium officinale [watercress])—and particularly in scurvy grass—is low when compared with other angiosperms. Although fresh preparations of the “antiscorbutics” would, in sufficient amounts, certainly have cured scurvy, it seems likely that their entry into, and retention by, sixteenth-century medical literature probably reflected a priori thoughts on the humoral nature of “land scurvy” more than any observed genuine therapeutic value.
James Cook provided his crew with a wide range of vegetables and fruit and scurvy grass collected whenever available, and this, no doubt, protected them from the disease. Had Cook, however, relied on fresh scurvy grass alone, a weekly supply of some 100 pounds of scurvy grass leaf would have been required for a ship with a complement of 100, to provide the Dietary Reference Value of vitamin C (40 mg daily) for the prevention of scurvy.
Nevertheless, the antiscorbutic triumvirate retained a position of importance in the herbals of the sixteenth, seventeenth, and eighteenth centuries, although, as has recently been shown, almost all of the original ascorbic acid would have been lost because of the form in which the preparations were ultimately administered—a finding that must cast considerable doubt on their overall effectiveness (Hughes 1990).
A Nosological Safety Net
The picture was further confused in the eighteenth century by a readiness of physicians to describe a whole range of unrelated conditions as “scurvy”; and the term became a convenient nosological safety net for the not inconsiderable number of diagnostic failures of the century. In the words of one physician: “It is yet a suficient Answer to Patients when they enquire into their ailments to give this Return to a troublesome Enquirer, that their Disease is the Scurvy, they rest satisfied that they are devoured with a Complication of bad Symptoms …” (Strother 1725: 150). At the end of the century the maverick Sir John Hill declared on the title page of his The Power of the Water Dock against the Scurvy (1777) that “If any one is ill, and knows not his Disease, Let him suspect the Scurvy.”1
With such confusion surrounding scurvy, one cannot with any certitude delineate the true importance of the ailment among land dwellers in the seventeenth and eighteenth centuries, and in the absence of details of dietary patterns (and particularly of the consumption of vegetables by the population in general), there must remain considerable doubts about its true incidence. About all that is clear is that the use of the term “scurvy” was almost certainly more common than the disease itself.2
Nevertheless, epidemics did occur; Hirsch lists some 30 such outbreaks during the eighteenth century in such diverse areas as Canada, Denmark, and Russia (1885: 521-3). Among the seafaring population, however, the picture was much more clearly delineated, and right through the seventeenth and eighteenth centuries scurvy was the most feared of all the hazards associated with long sea voyages, and with good cause. As we have already noted, it has been estimated that between 1600 and 1800 scurvy accounted for some million deaths at sea and that in almost every naval campaign of any length during this period scurvy played an important role (Roddis 1951: 72).
James Lind
The name of James Lind is deservedly associated with a substantial advance in the understanding of scurvy. A ship’s surgeon, he soon came face-to-face with the ravages of the disease among sailors. Others before him had successfully used empirically discovered remedies in the cure of scurvy, and their use of citrus fruits as the antiscorbutic remedy par excellence was well established (see, for example, Zulueta and Higueras 1981).This was presumably known to Lind, who himself quoted J. G. H. Kramer’s observation “… if you have oranges, lemons or citrons ‘ you will, without other assistance cure this dreadful disease” (Stewart and Guthrie 1953: 154).
John Woodall in his The Surgions Mate (1617) quite clearly drew attention to the prophylactic value of lemon juice—which had, in any case, already been successfully used by James Lancaster in his East Indian voyage at the beginning of the century. In 1696 William Cockburn underlined the importance of fresh fruit and vegetables to sailors in his Sea Disease, or Treatise of their Nature, Cause and Cure and in his Essay on Sickness and Health (1725). Edward Strother also had pointed out that “eating Lemons and Oranges” would cure scurvy in sailors.
But Lind’s achievement was that he subjected these empirically derived claims, and others, to the test of scientific experimentation in what has been claimed to be the first controlled clinical study in the history of medicine. Here is a description of it in Lind’s own words:
On the 20th of May, 1747, I took twelve patients in the scurvy, on board the Salisbury at sea. Their cases were as similar as I could have them. They all in general had putrid gums, the spots and lassitude, with weakness of the knees. They lay together in one place, being a proper appartment for the sick in the fore-hold; and had one diet common to all, viz. water-gruel sweetened with sugar in the morning; fresh mutton-broth often times for dinner; at other times puddings, boiled biscuit with sugar etc. and for supper, barley and raison, rice and currants, sago and wine, or the like. 0Two of these were ordered each a quart of cyder a day. Two others took twenty-five gutts [drops] of elixir vitriol three times a day, upon an empty stomach; using a garble strongly acidulated with it for their mouths. Two others took two spoonsfuls of vinegar three times a day upon an empty stomach having their gruels and other food well acidulated with it, as also the gargle for the mouth. Two of the worst patients, with the ten-dons in the L arm rigid (a symptom none of the rest had) were put under a course of sea water. Of this they drank half a pint every day, and sometimes more or less as it operated, by way of gentle physic. Two others had each two oranges and one lemon given them each day. These they [ate] with greediness at different times, upon an empty stomach. They continued but six days under this course, having consumed the quantity that could be spared. The two remaining patients took the bigness of a nutmeg three times a day, of an electuary recommended by an hospital-surgeon, made of garlic, mustard seed, rad. raphan., Balsam of Peru, and gum myrrh; using for common drink, barley water well acidulated with tamarinds; by a decoction of which with the addition of cremor tartar, they were gently purged three or four times during the course.
The consequence was that the most sudden and visible good effects were perceived from the use of the oranges and lemons; one of those who had taken them, being at the end of six days fit for duty. The spots were not indeed at that time quite off his body, nor his gums sound; but without any other medicine, than a gargarism of elixir vitriol he became quite healthy before we came into Plymouth which was on the 16th of June. The other was the best recovered of any in his condition; and being now deemed pretty well, was appointed nurse to the rest of the sick. Next to the oranges, I thought the cyder had the best effects.… (Stewart and Guthrie 1953: 145-7)
Lind’s note on the partial efficacy of cider has been quoted in support of the thesis that cider, as prepared traditionally in the eighteenth century, would have contained significant amounts of vitamin C and that it could have played a significant role in the prevention of scurvy (French 1982: 59-66). Although this may have been the case, such evidence as is available would suggest that in general, very little of the original vitamin C would survive a fermentation procedure (Hughes 1975, 1990).
Lind’s book A Treatise of the Scurvy appeared in 1753; a second edition was published in 1757 and a third and “updated” version in 1772 (a bicentenary reprint of the first edition was published in 1953 [Stewart and Guthrie 1953]). A French translation appeared in 1756 with subsequent reprints, and an Italian translation was published in 1766.
Not all of Lind’s conclusions, however, were characterized by the same degree of scientific acumen that he displayed in his famous “scurvy trial,” and it is clear that he claimed “antiscorbutic” properties for preparations that modern analysis would suggest are quite devoid of vitamin C (Hughes 1975). Nevertheless, his experimental demonstration that oranges and lemons could cure scurvy, his critical assessment of the literature of scurvy, his demonstration that the distinction between “land scurvy” and “sea scurvy” was a spurious one, and his advocacy of the use of various prophylactic foods by ships’ crews must place him among the most significant figures in the history of nutrition.
Unfortunately, although subsequent commentators advocated the official adoption of lemon juice by the naval authorities as a prophylactic measure, they met with little success for many decades (Carpenter 1986: 73, 87). The purchase of vegetables by ship captains was sanctioned but the practice soon lapsed, and scurvy among sailors continued unabated. Indeed, when the Channel Fleet returned to port in 1780 after a cruise of only six weeks, there were 2,400 cases of scurvy present (Lloyd 1981: 12).
But in 1795, largely as a result of the advocacy of Gilbert Blane, himself a prominent and influential naval surgeon (actually “physician to the fleet”), the official issue of lemon juice to naval personnel in Britain was sanctioned (the practice was not, however, officially extended to the merchant service until 1844).Within two years, cases of scurvy in naval hospitals were rare occurrences, and there were clinicians who complained that they had never seen a true case of scurvy—a situation that would have been unthinkable a few years previously. J. Turnbull’s almost monotonously successful treatment of the few scorbutic sailors arriving at Liverpool in 1848, merely providing them each with two lemons daily, was, perhaps, the final elegant vindication of Lind’s pioneer study (Turnbull 1848).
Limes and Scurvy
A minor setback in keeping scurvy at a distance occurred in the 1850s when, for economic reasons, the British Admiralty contracts were changed so that the West Indian lime (Citrus aurantiifolia) was substituted for the lemon (Citrus limon). The superficial similarity between the two fruits had already led to the use of the terms “lime juicer” and “limey” by Americans in referring to British ships and sailors. Furthermore, the terms “lemon juice” and “lime juice” were used carelessly and often without distinction in referring to the two species. In fact, at the beginning of the century the lime was sometimes referred to as the “sour lemon” (Green 1824: 316).
An unfortunate consequence of this change was the reported failure of stored lime juice to offer protection against scurvy—as in the ill-fated “Nares” expedition to the Arctic in 1875. The apparent failure of lime to prevent scurvy led to the rejection by some observers of the thesis that lack of fresh fruit and vegetables was the only cause of scurvy. A. H. Smith, in a comprehensive article stimulated by outbreaks of scurvy among troops issued lime juice during the First World War, concluded that lime juice (as contrasted with lemon juice) as an antiscorbutic agent was “worthless” (Smith 1919).
The reason for this apparent lack of antiscorbutic potency on the part of lime juice preparations is still incompletely understood. It is true that lime juice has a lower vitamin C content than lemon juice, but it is still high enough to be regarded as a moderately good source of the vitamin. It is possible that the vitamin C molecule is much less stable in lime juice than in lemon juice—a belief that was apparently confirmed by Harriette Chick in 1918 using the guinea pig as an assay system. This observation would suggest that the protective and stabilizing factors present in lemon juice (high acidity, tannins, anthocyanins, etc.) are less potent in lime juice preparations. However, in a recent study, Carpenter found no essential difference between the rate of loss of ascorbic acid in lime and lemon juices (Carpenter 1991, personal communication).Whatever the true explanation, the apparent discrepant protective capacities of the two forms was an important feature in the history of scurvy, introducing a puzzling diversionary element into an otherwise fairly smooth development.
Scurvy in the Nineteenth Century
In general, the importance of scurvy diminished during the nineteenth century. It no longer posed a problem to mariners (the greater rapidity of sea vessels was a contributory factor in this respect), and it no longer occupied a position of importance in the medical texts. The eighteenth-century tendency to use the term “scorbutic” indiscriminately with reference to almost any unidentifiable or challenging condition seemed also to be dying. And an increase in the intake of vegetables (and to a lesser extent, fruit) reduced the possibility of scurvy occurring among the general population.
Nevertheless, sporadic outbreaks of scurvy occurred from time to time, and a number of these led to detailed reports in the medical press—some of them substantial ones, such as that by J. O. Curran in 1847 of cases of scurvy following the potato famine in Ireland (Curran 1847) and that of R. Christison describing a similar outbreak in Scotland in 1846 (Christison 1847).
Scurvy outbreaks occurred most frequently in “closed” communities subjected to the same (inadequate) dietary pattern—hospitals, prisons, and work-houses. The numerous reports presented to Parliament in the nineteenth century on conditions in the prisons and workhouses provide useful information on the adequacy of the diets in these institutions (Johnston 1985). The availability of potatoes—and to a lesser extent, vegetables—was of paramount importance in this respect; fruit was almost totally absent from the normal prison and workhouse diet. Thus, the outbreaks of scurvy among convicts at Millbank in 1822 and in Pentonville in 1847 were a direct result of a lack of vegetables.
W. Baly, in 1843, in a simple type of controlled experiment, was able to show that outbreaks of scurvy at Pentonville Prison could be eliminated by including adequate amounts of potatoes in the diet (Baly 1843). In 1851, R. Boyd described two cases of scurvy (a female aged 38 and a male aged 59) in the Somerset County Pauper Lunatic Asylum resulting from “a continued diet of one meal of bread and cheese daily for three months.” Of particular significance to Boyd was the observation that this occurred “despite a plentiful allowance of cider (nearly 3 pints daily), which is supposed to be antiscorbutic” (Boyd 1851: 520; see also French 1982).
In the second half of the century potatoes were a regular feature of such institutional diets and outbreaks of scurvy diminished, although some cases still occurred among sailors despite the official adoption of lemon juice as a prophylactic. “It is very rare for London physicians to see cases of scurvy such as they are presented at our seaports,” wrote P. Black in 1876 (12), confirming Boyd’s earlier statement that “Scurvy is now seldom seen in ordinary hospital practice in this country except in the [naval] hospital ship Dreadnought ” (Boyd 1851: 520). Nevertheless, there were still isolated epidemics in communities deprived of fresh food supplies for long periods—as among British soldiers in the Crimean War and among some of the persons on Arctic expeditions.
“Explaining” Scurvy in the Nineteenth Century
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. …d lemon juice should be issued daily (l oz.) and it should be seen that the men take it” (1869: 494).
Parkes… 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 Britannica, 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.
Experimental Scurvy in Humans
Following the identification of ascorbic acid as the “antiscorbutic factor,” human volunteers attempted to induce scurvy in themselves by subsisting on a vita-min C-free diet. J. Menshing, in Germany, ate a virtually vitamin C-free diet for 100 days; his blood vitamin C fell to zero but there were no discernible signs of scurvy. H. Rietschel and H. Schick repeated the experiment, extending the period of deprivation to 160 days but again without the appearance of any overt signs of scurvy (Rietschel and Mensching 1939). J. H. Crandon, in the United States, deprived himself of vitamin C and noted the appearance of the first recognizable signs of scurvy after some 5 months (Crandon, Lund, and Dill 1940).
However, the first controlled study designed to produce scurvy in humans was undertaken at Sheffield in England during the latter stages of the Second World War and published in 1953 (eight years after the conclusion of the work) as Medical Research Council Special Report (Medical Research Council 1953).Twenty young volunteers (aged 21 to 34) took part in the experiment; anecdotal reports indicate that they were conscientious objectors to military service, although, understandably perhaps, this information was not included in the official report of the study.
All participants were placed on a vitamin C-free diet. Ten received no supplements; seven were given 10 mg ascorbic acid daily; and three received 70 mg ascorbic acid daily. The general picture to emerge was that the classical signs of scurvy (hyperkeratotic follicles, gum lesions, impaired wound healing—in that order) were experienced by those in the deficient group but not by either of the supplemented groups. The hair follicle changes occurred after 17 weeks of deprivation and the gum changes after 26 weeks—somewhat later than the corresponding period calculated by Barnes in 1864. The difference presumably reflected differences in the subjects’ vitamin C status at the beginning of the deprivation period. Furthermore, a supplement of 10 mg ascorbic acid was sufficient to restore the scorbutic subjects to normal health.
The report recommended that “in order to arrive at a figure for a daily allowance which covers individual variations and includes a safety margin, it is suggested that the minimum protective dose of 10 mg be trebled” (Medical Research Council 1953: 145). For 40 years the United Kingdom Recommended Daily Allowance for vitamin C remained at 30 mg, and the experimental evidence for this amount was the single “Sheffield Study” of 1944—a study that, in terms of sex and age alone, it may be argued, was based on a completely unrepresentative population group.
A similar investigation, but with fewer participants, was reported from the United States in 1969. The subjects in this instance were prisoners who “bought” remission periods by subjecting themselves to scurvy. The signs of deficiency appeared somewhat earlier than in the “Sheffield Study”—skin lesions in 8 to 13 weeks and gum changes in 11 to 19 weeks (Hodges et al. 1971). Both the Sheffield and the U.S. projects included wide-ranging physiological and pathological examinations, and further projects of this nature are unlikely to add very much to our clinical knowledge of the condition.
There remain, of course, peripheral problems that are of some academic interest but of little practical significance, such as the identification of further species unable to synthesize ascorbic acid and, therefore, susceptible to scurvy—and the mirror image of this, the search for a mutant form of guinea pigs resistant to scurvy. One of the more interesting current problems centers on the apparent refractiveness of the elderly to scurvy; it has been shown that persons over 80 years of age may have extremely low blood levels of ascorbic acid without the emergence of any of the expected clinical features (Hughes 1981: 60).
Scurvy Today
Our current knowledge of the vitamin C requirement of the body allows us, in a perverse way, to assess the validity of some historical claims of dietary interest. L. Cornaro, who reputedly attained a century of life by prudent living, recommended for the poorer and older members of the community a diet of bread, panada, and eggs. A diet so structured, however, would be almost completely lacking in vitamin C and almost certain to produce scurvy in a matter of months (Cornaro 1768: 98). Similarly, the numerous accounts of survival for considerable periods on diets, which simple inspection indicates to be completely vitamin C-free (such as that of John Ferguson, who in the eighteenth century lived, allegedly for 18 years, only on water, whey, and barley water [Umfreville 1743]), must now be regarded as largely apocryphal.
The life, and untimely death, of William Stark was more in keeping with what we now know of scurvy and vitamin C. Stark, perhaps the best known of all dietary masochists, achieved historical immortality by experimenting on his own body. He may be regarded as the founder of the now firmly rooted “Death by Diet” brigade. A 29-year-old unmarried physician living in London, he decided to test whether very simple diets would support health. From July 1769 to February 1770 he subsisted on diets such as meat, bread, and water; or bread and cheese; or honey and bread; or sugar and water. This highly scorbutigenic regime was relieved only by a small amount of fruit on one occasion in December 1769. Stark died on February 23, 1770, almost certainly from scurvy, judging by the entries in his detailed diary of the study. It is interesting to note, despite his general lassitude and fatigue, entries such as “had strong desires,” “Venus semel,” and “Venus bias,” which appeared at least weekly in his diary up to within a fortnight of his death, suggesting little impairment of the procreative capacity even in severe scurvy (Smyth 1788; Drummond and Wilbraham 1935).
Scurvy is today a rare condition—so rare that individual cases usually merit a short note in the medical press. Persons on a mixed, balanced diet would normally be expected to daily ingest more than the amount of ascorbic acid required to protect them against the disease. Thus, in the United Kingdom the mean ascorbic acid intake is some 60 mg daily 50 percent above the current U.K. Reference Daily Intake of 40 mg. The only persons likely to fall into a scurvy-risk category are those who, for economic or dietary reasons, subsist on a diet deficient in fruit, vegetables, and fresh meat—such as a diet based primarily on nuts and grain and dairy products or the proverbial American scorbutigenic diet of doughnuts and black coffee.
Indeed, even the ingestion of large amounts of fresh meat (particularly liver) will provide sufficient amounts of vitamin C to prevent scurvy in the comparative absence of fruit and vegetables. This explains why Eskimos (the name of which, apparently, means “raw flesh eaters”) remain scurvy-free even though their intake of plant sources is minimal. A turn-of-the-century account underlines this fact:
In 1893, at Kharborova, a Samoyad settlement on the Yugor Straits … six Russian priests, whose religion forbade them to eat reindeer or other such meats, but allowed salted fish, were left in a hut by a wealthy mine-owner to pass the winter. … A small Russian peasant boy was left to wait on them. The priests lived almost exclusively on tea, bread and salted fish; the boy lived upon similar food, except that instead of the salted fish he ate fresh reindeer meat. None of them had any vegetables. In the following May, when the Samoyads and peasant traders returned, they found that all the six priests had died of scurvy, whereas the little boy, who had lived upon fresh meat and had not eaten salted fish was alive and well, and had buried all his late masters in the snow. … (Jackson and Harley 1900: 252-3)
Recently reported cases of scurvy include that of a 9-year-old American girl who consumed nothing but tuna sandwiches and iced tea (without lemon) (Ellis, Vanderveen, and Rasmussen 1984), and that of a 24-year-old British male whose main form of sustenance was peanut butter sandwiches (Pozniak and Tomson 1983).
Epidemics of scurvy have been equally rare in the twentieth century. They occurred on a limited scale among soldiers in World War I (Smith 1919) and, particularly, among Indian personnel fighting in Iraq, where some 11,000 cases were reported (Willcox 1920). J. D. Comrie stated that he had personally examined 600 cases of scurvy in 1919 in North Russia (Comrie 1920).
Even today, however, we have the occasional reminder that the history of scurvy is not as completely closed a book as modern science would perhaps lead us to believe. Recently it has been reported that scurvy remains a serious public-health problem for Ethiopian refugees in Sudan and Somalia, where the incidence of scurvy in six camps ranged from 14 percent to 44 percent. It was found that the standard relief food (mainly cereals, legumes, and oil) distributed to the refugees was almost completely deficient in vitamin C (Desenclos et al. 1989).
The condition sometimes described as “chronic scurvy” or hypovitaminosis C (in which a person subsists on a suboptimal intake of vitamin C but without the emergence of the clinical features of overt scurvy) may affect substantial sectors of a population and, in particular, the institutionalized elderly; but its clinical significance, if any, is a matter of continuing dispute that need not concern us here.