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In 1917 Baumann and Howard published the only metabolism study which has been carried out on guinea-pigs suffering from scurvy, and they are of the opinion that this disorder has a profound effect on the mineral metabolism of this animal. The calcium was excreted in notably large amount; potassium was also lost, and to a greater extent than sodium; the only element which was consistently retained during the active stage as well as during the period of recovery, was magnesium. This study was followed shortly by one from the same laboratory, by Howard and Ingvaldsen, carried out on a monkey suffering from scurvy. It was inconclusive, not conforming to the experiments on the guinea-pigs; the authors state that the "changes in the mineral excretion of the monkey during the scorbutic period were not sufficiently significant to admit of easy interpretation." "The marked loss of the various mineral substances encountered in experiments with man and guinea-pig was not observed in the present series." It should be remembered, however, that the diets of the guinea-pigs and the monkeys were quite different, the former consisting mainly of oats, and the latter of condensed milk. It is quite possible that the basic diet may play a r?le in the metabolism of this disease, although, as stated elsewhere, its effect cannot be noted clinically. Special attention should be paid to this factor in metabolic studies, in view of the widely-held opinion that the carbohydrates exert a potent influence in the development of beriberi.

The investigations of the nitrogen metabolism in man and in animals have been most unsatisfactory. The two on human beings--an infant and an adult--were negative; that on guinea-pig scurvy cannot be utilized on account of the restricted diet of oats, which contained insufficient nitrogen, whereas the one on the monkey showed some loss of nitrogen, which led the authors to suggest an increased nitrogenous catabolism in scurvy. This comprises the total data on this subject.

Summarizing the results of these few metabolic studies, it may be stated that they harmonize on one point only--the positive balance of calcium during the active stage of the disease. The investigation of Baumann and Howard on adult scurvy, of Lust and Klocman and of Moll on infantile scurvy, and of Howard and Ingvaldsen on the monkey, are all in agreement in this important conclusion.

RELATION OF SCURVY TO OTHER DISEASES

In the foregoing there has been frequent reference to the close relationship between scurvy and the incidence of the infectious diseases--to the fact that a scorbutic condition increases the susceptibility to infection. This is indeed one of the most characteristic, as well as one of the most important phenomena associated with scurvy and other disorders resulting from vitamine deficiency. Mention has been made of the special susceptibility to the diphtheria bacillus, and to the organisms leading to coryza and the respiratory diseases, but no doubt this applies also to invasion by other bacteria. We wish, however, to confine ourselves to the nutritional disorders, first in their relationship one to the other, and second, as a group of deficiency diseases, due to a lack of vitamines of various kinds. As is well known, in addition to scurvy, this group generally includes beriberi, a disease attributed to a lack of the water-soluble vitamine, and xerophthalmia, an eye condition which recently has been brought about in rats by placing them on a diet free from fat-soluble vitamine. These, however, form only the nucleus of the disorders which commonly are included in this category. Schaumann, the first to formulate this classification, illustrated his conception of the interrelationship by depicting the various members as spokes of a wheel surrounding a central hub. He included scurvy, rickets, osteomalacia, typical beriberi, ship-beriberi, pellagra and mehlnaerschaden. Funk made a similar classification of disorders which he termed the "avitaminosen." There is a tendency to enlarge rather than to decrease the membership of this class, and recently war or hunger edema, infantile atrophy and diarrhoea, sprue, coeliac disease, leprosy and others have been proposed as suitable candidates. At the present time it is impossible to determine which and how many of this motley company should be associated with scurvy. Some, possibly, are the result of a lack of vitamine, but for the present it will be well to bear in mind that three vitamines only have stood the test of experiment, and only these three therefore can be definitely connected in a causal relationship with pathologic conditions. In addition to this consideration of the interrelationship of the "deficiency diseases," the kinship of allied disorders--more particularly of rickets--must be discussed.

In considering the vitamines in connection with diseases of the nervous system, mention may be made of "central neuritis" and the "peripheral neuritis" which has been reported from the West Indies. This bears only a partial resemblance to beriberi, as there is no edema, nor dyspnoea, and its course is more chronic. Judging from the report of Edwards from Jamaica, the cases more closely resemble pellagra, terminating after many years. A degeneration of the cells of the spinal cord was found and "in some isolated patches of the cerebellum and in the roots of the optic and auditory nerves." The disease occurs among the poor classes whose diet is inadequate chiefly in nitrogen.

There is no adequate reason for placing in this group "coeliac disease," a nutritional disorder of children recently described by Still, and suggested by McCarrison as belonging to the category of the vitamine deficiency diseases. A case of this kind has come to our attention which resembled pellagra in many respects. It showed the bright red, denuded tongue, the intestinal symptoms, the occasional edema, marked loss in weight, and evanescent erythema--all symptoms of markedly disturbed nutrition but not distinctive of a lack of vitamines.

The relation between scurvy and rickets is a subject which was discussed by Glisson. With the renewed interest in infantile scurvy which followed Barlow's work toward the end of the last century, children's specialists ranged themselves into opposing camps on the question of the interrelationship and interdependency of these two diseases. Some accepted Barlow's dictum that infantile scurvy is an absolutely distinct and separate entity; others, for example, Hirschsprung, declared that the so-called scurvy was merely a form of rickets; whereas a third group considered it a combination of rickets and scurvy. This last viewpoint was actively maintained by Cheadle on the clinical side, and later by Schoedel and Nauwerk on the pathologic side--the latter declaring that rickets is "an inseparable component of infantile scurvy," and that the entire disease should be regarded merely as "an episode in the course of rickets." Even Barlow, in a paper published in 1894, wrote: "Rhachitic changes already present may act as a physiological determinant of the sites in which scurvy becomes manifest" and "rickets as a basis plus inadequate food gives the simplest explanation of the typical case" .

We had an exceptional opportunity to test this thesis in 1914, in an institution where scurvy broke out among infants who were on a diet of pasteurized milk. All these infants were receiving cod liver oil daily, as prophylactic treatment against rickets. Many infants have been seen since that time, who in spite of receiving cod liver oil developed scurvy, and others in whom large doses of this oil failed to mitigate the scurvy, although it prevented rickets. The same failure has been encountered in the treatment of scurvy in guinea-pigs. This experience has been without exception, both from a prophylactic and a curative standpoint.

Confusion between the two diseases has resulted from the fact that the majority of infants in the Temperate Zone have some degree of rickets. Thus the two diseases have been found very frequently associated in pathologic examination of the bones, leading some to infer that they are in some way interdependent. They have been also confused clinically, as mentioned in another connection, owing to the fact that beading of the ribs--the rhachitic rosary--has been mistakenly regarded as a pathognomonic sign of rickets, whereas it is also a sign common to scurvy. It is important to bear in mind that from the pathologic viewpoint scurvy and rickets present strikingly dissimilar pictures--the former is characterized by an almost complete cessation of activity of bone-forming elements, whereas the latter is distinguished by a hyperplastic condition leading to a marked overgrowth of cartilage and of abnormal bone. Viewed from the pathologic, etiologic and clinical standpoint, we believe that there is no basis for assuming an interrelationship between the two disorders, and that scurvy will develop as readily and as rapidly where rickets is absent as where it is present.

The only evidence in favor of a true interrelationship is furnished by a necropsy report of Hart and Lessing on one of five monkeys fed on a scorbutic diet. This animal died of disseminated tuberculosis, and the bones showed "the classic picture of severe rickets." This occurrence cannot be explained, although illness and lack of exercise no doubt played a r?le. Until similar cases are reported, the incident must be regarded merely as interesting and suggestive.

It is premature to discuss the relationship of these two disorders from the vitamine standpoint. In 1910 Schaumann suggested that rickets was due to a lack of a specific food factor, and somewhat later Funk included it among the "avitaminosen." Recently Mellanby, as the result of experiments on dogs, has affirmed that the fault lies in a lack of the fat-soluble or a closely-related vitamine. Investigations of the near future will probably decide the merits of this contention; our experience is that rickets develops in infants even where the diet contains adequate fat-soluble vitamine. If rickets is proved to be a disorder depending on a vitamine, it belongs, naturally, in the same group as scurvy. This would indicate relationship, but not interrelationship. Just as the mere fact that a lack of vitamines leads to scurvy and to beriberi does not signify, in theory or in practice, the existence of pathogenetic interrelationship. However, as stated, this is a subject which does not as yet rest on a secure foundation.

One cannot survey the various diseases of the bones--scurvy, rickets, osteoporosis, osteogenesis imperfecta, osteomalacia, etc.,--without realizing that this group is at present in a state of great confusion and will have to be rearranged and winnowed. The differentiation between some of these diseases is not in every instance clear morphologically--for instance, early cases of scurvy and osteoporosis--so that it is difficult to consider them satisfactorily from the standpoint of pathogenesis. Clinical differentiation is still more difficult and uncertain. It seems probable that new entities will be established, as has happened in the past. It is not so long since rickets included almost all the bone diseases of infants. Gradually congenital syphilis, scurvy, and achondroplasia were segregated as distinct diseases. Probably a similar separation of other pathologic conditions, now so entangled as to be indistinguishable, will be evolved.

From what has been stated, it must be evident that this subject not only is in a state of flux but that it is in a state of great confusion. This applies not only to the relationship of vitamines to these disorders, but to their identification and demarcation pathologically as well as clinically. During the past few years we have begun to regard these diseases from a new viewpoint, which no doubt will be helpful, but it is probable that they will not be sharply defined and their relationships determined until it is possible to bring about each disease definitely and regularly in an experimental animal. Until this time we should proceed slowly, and not bring about "confusion worse confounded" by yielding to the vogue, and grouping together heterogeneous and little-understood clinical conditions under the caption of deficiency diseases. There is a growing danger of attributing every unexplained nutritional disorder to the new, overworked, but ill-defined vitamines--of their sharing with the secretions of the endocrine glands the fate of becoming the dumping-ground for every unidentified disorder.

Extract from "Treatise on Scurvy," by James Lind, London, 1772.

It is then, when cold, to be corked up in a bottle for use. Two dozen good oranges, weighing five pounds four ounces, will yield one pound nine ounces and a half of pure juice; and when evaporated, there will remain about five ounces of rob, or extract; which in bulk will be equal to less than three ounces of water. So that thus the acid, and the virtues of twelve dozen lemons or oranges, may be put into a quart bottle, and preserved for several years.

I have now some extract of lemons which was made four years ago.

Those who intend this extract for making punch may infuse some of the fresh peel of the oranges or lemons into the spirit before it is used.

But for this purpose I find it is sufficient to add a very small quantity of the outer peel to the extract a little before it is taken off the fire, and there will be all that is requisite to make it entirely equal to the freshest fruit.

I am inclined to believe by the description given by Cartier of the ameda tree, with a decoction of the bark and leaves of which his men were so speedily recovered, that it was the large swampy American spruce tree.

BIBLIOGRAPHY

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CHICK, H., and SKELTON, R. F.: The Relative Content of Antiscorbutic Principle in Limes and Lemons, Lancet, London, 1918, II, 735.

CHICK, H., and RHODES, M.: An Investigation of the Antiscorbutic Value of the Raw Juices of Root Vegetables, Lancet, London, 1918, II, 774.

COMBY, J.: Twelve New Cases of Infantile Scurvy, Arch. de M?d. des Enfants, 1917, XX, 337.

COPLANS, M.: On the Etiology of Scurvy, Lancet, London, 1904, I, 1714.

COUTTS, F. J. H.: Upon an Inquiry as to Dried Milks, etc. Report to the Local Govt. Board, 1918, New Series No. 116, 31.

CURRAN, J. O.: Observations on Scurvy, etc., The Dublin Quart. Jour. Med. Sciences, 1847, IV, 107.

CZERNY A., and KELLER, A.: Handbuch des Kindes Ernaerung, etc., Leipzig, 1907, II, 93.

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