The newest theory, and the one at present most widely accepted, is the vitamine (accessory factor) theory. It was evident to Lind in the seventeenth century that scurvy could be prevented and cured by means of fruits or vegetables, a fact which became increasingly clear to succeeding generations. Until the latter part of the nineteenth century, however, this miraculous virtue of plants stimulated little inquiry and no research. As far back as 1841 Budd realized that “the explanation depended on the study of organic chemistry, and the experiments of physiologists,” but until recently it was not perceived that the solution of the problem involved the introduction of a new chemical factor. This view suddenly took shape after Eijkman in 1897 showed the nature of polyneuritis in fowl, and Hopkins in 1906, going a step farther, demonstrated the necessity of one or more unidentified food factors for the normal nutrition of the rat. The work which established this novel theory on a scientific basis in relation to scurvy was the classic investigation of Holst and Froelich, referred to so frequently in connection with experimental scurvy. These investigators showed that the mere drying of vegetables was sufficient to deprive them of their antiscorbutic power, although from a chemical standpoint they seemed unaltered; that high degrees of heat had generally the same effect; that under certain conditions these foods withstood prolonged heating, demonstrating that the antiscorbutic factor was not a ferment; that acids and alkalies played no essential rôle in the etiology; that fats, proteins and carbohydrates were not significant factors; that as little as 1.0 g. of cabbage suffices to afford protection to a guinea-pig. In other words, by a process of exclusion they showed that it is a disorder due to the lack of an unidentified food factor.
Subsequent studies, carried out within the past few years, have served only to strengthen this viewpoint. For example, an “artificial orange juice” composed of the various salts, citric acid, and sucrose in the proportions in which they are found in the natural juice, failed, in the experience of Hess and Unger, to protect or to cure guinea-pigs—demonstrating that this preparation did not contain the essential factor. In the same way, Harden and Zilva were able to protect animals from scurvy with a preparation of lemon juice which had been almost entirely deprived of its salts. It is needless to multiply these examples. It is sufficient to state that there has been no investigation during the last years of intensive study of scurvy, which has tended to weaken the vitamine hypothesis. It may be stated, therefore, that experiments have demonstrated that scurvy is due essentially to the lack of a specific vitamine. It is unwise to proceed farther and place it in the group of so-called “deficiency diseases,” including beriberi, pellagra, etc., unless the reservation is made that these several diseases may present marked differences. It is quite possible that one may be what might be termed a simple deficiency disease, whereas another may have important additional etiologic factors. At any rate, unless it is realized that there has been no proof that all are due to similar deficiencies, we may, by stamping them all alike and by grouping them together, be misled into taking their close relationship for granted. In regard to scurvy, there may well be other etiologic factors, but they are of a secondary character. Bacterial invasion has been referred to in this connection, and it is possible that toxins are absorbed from the intestine after nutrition has been disturbed. Diarrhœa and digestive disturbances may play a rôle. Whether the total intake of food or the correlation of its constituents—protein, carbohydrate, fat and salts—affects the action of the vitamine, is one which has not been well studied clinically or experimentally. In regard to beriberi, it is claimed that there is a direct ratio between the quantity of carbohydrate ingested and the amount of vitamine required. No such interrelationship exists in regard to scurvy. This was evident a few years ago (1917) when some infants receiving pasteurized milk, prepared with the addition of 3 per cent. flour, did not tend to develop scurvy more readily than others receiving simple pasteurized milk. A consideration of the antiscorbutic vitamine will be postponed for a subsequent chapter.
Etiology.—In considering infantile scurvy we are concerned almost entirely with the artificially-fed baby. It is true that in the literature we meet with scattered reports of scurvy in breast-fed babies and that these cases seem to constitute a noteworthy group; in point of fact, they are comparatively few. The collective investigation of the American Pediatric Society includes ten infants who had been given breast milk exclusively, and Concetti adds another ten in his compilation of 682 cases.[7] In spite of their paucity these cases require separate consideration because they represent an important aspect from an etiologic standpoint. How are we to explain the fact that human milk may lead to rather than protect against this disorder? On investigating more closely it is found that these cases differ in several important respects from the group which has been artificially fed. They are of a different age; instead of being in the second half year of life they are generally but a few months old. Furthermore, the signs are not the same. The hemorrhages involve the upper extremities fully as frequently as the lower extremities, and often appear at unusual sites—for example, on the scalp or as large subcutaneous effusions at various parts of the body. In many instances it has been noted that the nursing mothers were suffering from some debilitating disease such as tuberculosis or syphilis, or had an insufficient supply of milk, or that there had been some other unusual factor, as Freund has shown in an article devoted to this particular aspect. It is not necessary, however, to fall back on these attendant circumstances to exclude from consideration many of the cases. For example, Crandall’s case of “scurvy in an infant of six weeks” should be invalidated, not because, as Freund suggests, the mother had rheumatism and insufficient milk, but because of the age of the infant, and the course of the disease; first one arm was involved, then the other, then hemorrhages appeared on the skin, and finally it was cured by giving a teaspoonful of fresh cream before each nursing. Had the baby really suffered from scurvy it could not have been cured by this means. Southgate’s case must also be rejected, not because the mother was tuberculous but in view of the symptoms—the arms and legs were pseudoparetic, “the legs, feet and hands were double their normal size,” and moderately large hemorrhages were present on the back and chest. It seems hardly necessary to discuss in detail the score of cases which comprise this group, as, in general, the same criticism applies to all. Some evidently were congenital syphilis, still more must be regarded as sepsis, and others as unknown toxic conditions. Apart from these cases the question must be considered whether scurvy can occur in a breast-fed infant. Personally, we have never met with a case of this kind, and, as Finkelstein aptly remarks, there has been “no necropsy of a breast-fed case or conclusive X-ray picture.” It seems possible only if an infant, for a period of months, has obtained a scanty supply of milk, or when the milk has been exceedingly deficient in the antiscorbutic vitamine. Even under such conditions it does not seem possible for scurvy to become manifest in six weeks (Crandall’s case), or in four weeks, as in a case reported by the American Pediatric Society, unless we believe that the infant suffered also from a certain degree of intrapartum or congenital scurvy. In view of the fact that an infant requires about one pint of milk to furnish it with an adequate daily quota of the antiscorbutic factor, it is theoretically possible, under extreme conditions, for it to become scorbutic, in spite of being nursed at the breast. Such an occurrence must be regarded as exceedingly rare, far more so than the current statistics illustrate, for considerably less than a pint of milk a day will prevent the appearance of manifest scurvy for a period of several months. Some of the reported cases may have been latent scurvy, rendered acute by a complicating bacterial infection.
It might be expected that by ascertaining the occurrence of infantile scurvy in countries where it is endemic, we could learn under what conditions and how frequently breast-fed babies develop this disorder. Approaching the question from this angle, it is found that the available data is meagre and not entirely convincing. Peculiarly enough infantile scurvy has rarely been reported from Russia, where scurvy is, in many sections, endemic. For example, although Tschudakoff, who personally examined over 10,000 persons, in connection with the great scurvy epidemic in Russia (1898–99) found 11.11 per cent. of the people suffering from this disease, he did not meet with a single case under the age of five years. Fuerst writes that Filatow, the celebrated Russian children’s specialist, declared that he knew of no instance of Barlow’s disease described in the Russian literature.[8] Shortly after the recent war scurvy broke out among the wet-nurses in an infant asylum in Vienna. A very few of the infants nursed by these women developed the disorder, far fewer than might have been expected (personal communication). Hopkins recently wrote a communication to the effect that in the island of Aruba, in the Dutch West Indies, they had been unable to grow any crops in 1912, 1913, 1914, that 3000 cases of scurvy had developed there during the year 1915, and that in 1917 it was again being noted. In answer to a personal inquiry regarding the occurrence of scurvy among the infants of Aruba, he wrote that “infantile scurvy is very rare,” although “most all of the babies are breast-fed for about a year.”[9]
On the other hand, descriptions of the coincidence of scurvy in mother and nursling are even more fragmentary; in fact, we have been able to find but two reports of this kind. The one most frequently cited is that of Cheadle, which consists merely of the following bald statement: “With the exception of one or two doubtful cases, of which the details of breast-feeding and diet are imperfectly given, the only instances of scurvy arising in sucklings are those when the nursing mother has been suffering from scurvy at the time.” The other report has been gleaned from a recent editorial in the British Medical Journal, which refers to the above mentioned outbreak of scurvy in Vienna, affecting in some cases both mothers and breast-fed infants.
It is difficult to pass judgment on this question in view of the paucity of data. In the near future, probably, when we learn in detail about the epidemics of scurvy which occurred during and immediately following the war, we shall be in a better position to weigh its pros and cons. In view of the above data it does not seem that nursing infants readily develop scurvy, even though their mothers do not obtain a full quota of antiscorbutic vitamine in their food. This appears to be the clinical result, whatever its interpretation may be. It cannot be explained on the assumption that human milk contains a particularly large quota of this factor. In a test carried out to elucidate this question it was found that eight ounces a day of breast milk was insufficient to alleviate the symptoms in a case of scurvy, and that twelve ounces barely sufficed. This milk was from a woman who was on a liberal diet containing an adequate supply of vegetables. It had been previously demonstrated that sixteen ounces of cow’s milk is sufficient to cure infantile scurvy, so that it is evident that human and cow’s milk do not differ essentially in this respect. There are, however, other factors to be considered—for example, the incomparable freshness of the milk suckled from the breast, which may endow it with additional potency, or the possibility that the lack of vitamine may be compensated for by the large quantity of milk consumed. It also may not be entirely immaterial whether the vitamine is supplied in one dose, as, for example a daily feeding of orange or tomato juice, or whether this factor is furnished to the infant in frequent small quantities in the mother’s milk throughout the day. In this connection we cannot help contrasting the relation of beriberi to breast feeding. As is well known, infants which develop beriberi are almost always nursed and not bottle-fed, and show signs of this disorder, although the mothers are in apparent health, and give no clinical evidence of disease.
Turning to a consideration of the artificially-fed infant, there exists a somewhat similar situation in regard to the occurrence of scurvy on a diet of raw cow’s milk. In almost all reports of this kind the quantitative viewpoint is entirely disregarded, and little or nothing is stated to indicate how much milk the infant consumed. And yet this factor is of essential importance in interpreting the cause of the nutritional failure. It is clear, for example, that if a baby receives but eight ounces daily of raw milk—one-half the requisite amount—it may well develop scurvy, notwithstanding the fact that the milk has not been heated. In addition to the quantity, there are other factors which play a greater or less rôle in the relation of raw milk to the etiology of scurvy. It is no doubt of consequence whether the fodder of the cows was rich or very poor in the antiscorbutic factor, and, accordingly, whether the baby received what may be termed an “antiscorbutic-rich” or an “antiscorbutic-poor” milk. Furthermore, the age of the milk must be borne in mind, for we have found that even raw milk loses some of its potency on becoming stale.[10]
One of the mooted questions relative to the etiology of scurvy is the rôle of heated milk, and more particularly of pasteurized milk. In view of the vogue which pasteurization has acquired in the large municipalities, especially in the United States, this aspect has assumed increasing importance, and deserves detailed investigation. Pasteurization has achieved so much in limiting the infectious diseases, especially the diarrhœal disorders of infancy, that it has come to be looked upon as heresy to deprecate its virtues in any regard.
It has become increasingly evident that in the course of pasteurization milk loses an important measure of antiscorbutic vitamine. The term pasteurization, when employed in this connection, is not meant to be synonymous merely with the heating of milk to 140° to 165° F., but embraces the entire commercial process—the heating, handling, subsequent cooling, aging and all other factors involved. There can be no doubt that milk which has undergone this elaborate treatment has suffered in its antiscorbutic property. In 1914 Hess and Fish reported mild cases of scurvy occurring among infants who had received milk heated to a temperature of 165° F. for thirty minutes. This degree of heat is claimed by many physicians and hygienists, including the National Commission on Milk Standards, not to destroy its chemical constituents. Nevertheless typical cases of scurvy supervened after this diet had been followed for a period of six to nine months. Subsequent experience, published by Hess in 1917, with milk heated to only 145° F., served to confirm the previous observations. That these cases were true scurvy was proved by the fact that a cure resulted when raw milk was substituted. A similar experience in Berlin reported by Neumann and others was convincing, but was not heeded in this country. In 1901 one of the largest dairies in that city established a pasteurizing plant where all milk was raised to a temperature of about 60° C. After an interval of some months infantile scurvy began to be reported from various sources throughout the city. Neumann depicts the situation as follows: “Whereas, Heubner, Cassel and myself had seen only thirty-two cases of scurvy from 1896 to 1900, the number of cases suddenly rose from the year 1901, so that the same observers—not to mention a great many others—treated eighty-three cases in 1901 and 1902.” At a spirited meeting held by the Berlin Medical Society in 1903 to discuss this subject, Heubner was able to report 65 cases. An investigation was made, and the pasteurization discontinued. The result was almost immediate, the cases decreasing just as suddenly as they had increased. These reports and others demonstrate that unless additional antiscorbutic food is given, a diet of pasteurized milk will lead to the development of scurvy. As the antiscorbutic vitamine is not entirely destroyed by pasteurization, the severity of the disorder will be in inverse ratio to the amount of milk which is consumed.
It has been our experience that milk pasteurized in the home or institution did not lead to scurvy to the same extent as that which was commercially pasteurized. Babies fed on home-pasteurized milk did not develop manifest scurvy. The difference in the two processes consists mainly in the amount of handling during the process of heating and the subsequent aging which the milk undergoes. An interval of forty-eight hours usually elapses between commercial pasteurization and the delivery of the milk to the consumer. In New York city most of the better-grade milk is pasteurized at the farm, so that it is subjected to a longer period of aging than the poorer grade, which is not pasteurized until it reaches the city. Although our results indicated the effect of freshness or staleness on milk which had been heated, they showed also that other factors must be involved, for home-pasteurized milk which is forty-eight hours old is superior to the commercial product of the same age. This difference we believe is due to the handling which the milk undergoes, to the mechanical processes involved in commercial pasteurization.