By W.J. McCormick, MD
Summary: In the nineteenth century, deadly infectious diseases such as tuberculosis, pneumonia, typhoid, and scarlet fever ran rampant in America and Europe. Then modern medicine came along in the 1900s and put an end to these epidemics through measures such as drug therapy, sanitation, and immunization. At least that’s how the conventional story goes. But does medicine really deserve credit for eradicating these infectious illnesses? In this fascinating article from 1947, Dr. W.J. McCormick points out a startling fact: the rate of each disease mentioned began steadily decreasing around the late 1800s—well before the advent of modern medicine. Moreover, the decline did not speed up as medical practices became standard in the early twentieth century, as one would expect if the “triumph of medicine” story were true. Given the facts, Dr. McCormick says, it appears some factor other than medicine was primarily responsible for bringing the great infectious diseases of the nineteenth century under control. That factor, he says, was the “anti-infection” nutrient, vitamin C. Thanks to revolutionary advances in food production, citrus fruits and other vitamin-C–packed foods became widely available for the first time in the late 1800s, steeling individuals against infection and spurring one of the great public health successes in history—a success wrongly credited to the medical and pharmaceutical fields, the author concludes. From The Medical Record, 1947. Lee Foundation for Nutritional Research reprint 5A.[The following is a transcription of the original Archives document. To view or download the original document, click here.]
The Changing Incidence and Mortality of Infectious Disease in Relation to Changed Trends in Nutrition
During the past century, there has been a general downward trend in the incidence and mortality rates of infectious diseases—notably tuberculosis, pneumonia, diphtheria, scarlet fever, whooping cough, rheumatic fever, typhoid fever, and erysipelas; there has been a similar decline in puerperal and infant deaths. During the same time, there has been a marked shift in the age incidence of a number of infectious diseases from infant to older-age groups and a marked general reduction in the case-fatality rates.
The usual explanation offered for this changed trend in disease has been the forward march of medicine in prophylaxis, therapy, and public-health protective measures. But from a study of the literature, it is evident that epidemiologists generally recognize that these changes in incidence and mortality have been neither synchronous with nor proportionate to such measures.
Considering each disease separately, evidence regarding the changed trend will be given, and in the discussion following an attempt will be made to track down the unidentified prophylactic factor, which the author believes to be nutritional, and fit it into the picture of each disease.
Tuberculosis—formerly known as the Great White Plague, consumption, or phthisis—was responsible for the deaths of one-fifth of all mankind in western Europe at the beginning of the nineteenth century. In London the rate was even higher—30 percent. The yearly death rate from this disease in western Europe at that time has been estimated at 1,000 per 100,000 [of the] population. From 1812 to 1840, the death rate from tuberculosis in the American cities of Boston, Philadelphia, and New York was about 400 per 100,000, while in Budapest in 1874 the rate was double this amount.
During the past century, there has been a consistently steady reduction in mortality from tuberculosis, until at present the rate in England is 69, in Canada 45.8, and in the United States 41.3 per 100,000. The orderly rate of this reduction may be seen by reference to Table 1, from Pringle,1 which shows a decline in death rate from tuberculosis in the city of Ipswich, England, during the past 100 years (1841 to 1940) from 399 to 69 per 100,000. These figures, indicating an almost even decline throughout the century, are closely parallel to the figures for a corresponding period in Massachusetts, in which a reduction of mortality from 444 to 36 per 100,000 occurred between 1859 and 1939. At the middle of this period, the rate had declined to 254, and previous and subsequent to this date the decline followed an almost even grade.[Table 1:] Yearly Average Tuberculosis Death Rates per 100,000 in City of Ipswich, England, in Ten-Year Periods, 1840–1940. (See original for data.)
A noticeable feature of the mortality trend of this disease has been a shift in the age incidence. Forty years ago, the peak for males fell in the third decade of life. It now falls in the 50-to-60-year age group. The rate for the under-5-year group has also shown a disproportionately greater reduction. The under-1-year mortality rate for tuberculosis dropped from 1,000 to 645 per 100,000 living between 1868 and 1900. In this same age group, from 1900 to 1932, the rate fell to 39. Apparently tuberculosis is increasingly becoming a disease of older age groups.
During and following the First World War and the recent Second World War, there was a sharp rise in the incidence of and mortality from tuberculosis in Europe, particularly in the countries most involved. According to Time (April 14, 1947), tuberculosis—on the rise for the first time in a century—is now Europe’s No. 1 killer.
Germany, which formerly had one of the world’s lowest TB [tuberculosis] death rates, now has one of the highest. In Berlin alone 150 deaths and 400 new cases are reported weekly. The U.S. occupation zone has 117,983 TB cases. In Poland the monthly TB death rate is estimated at 18,000, mostly children. In Greece there are 150,000 severe cases, [for] only 5,000 TB hospital beds. Romania, with a population of 16,500,000, has 600,000 TB cases. Yugoslavia has an estimated 157,000 cases.
At the beginning of the present century, pneumonia stood ahead of tuberculosis as a cause of death. At that time the famous Osler referred to this disease as “the old peoples’ friend,” because it took so many of the aged at a time when life became burdensome. During the last half century, there has been a steady decline in mortality from this disease—with the exception of the upsurge from 1918 to 1920 as a result of the postwar influenza pandemic. Since 1900 the yearly death rates for pneumonia in the United States, per 100,000 at five-year intervals, were as follows: 1900—202.2; 1905—169.3; 1910—155.9; 1920—207.3 (influenza pandemic); 1925—121.7; 1930—102.5; 1935—104.2; 1940—70.3; 1944—48.6. A closely similar decline in mortality from this disease has occurred in Canada.
Prior to the present century, diphtheria—also known also as malignant angina, membranous croup, angina suffocans, garotilla, etc.—was the major scourge of infancy and childhood. Following the Napoleonic wars, intensive epidemics occurred in England, France, and other European countries. The virulence of these outbreaks was so great that frequently whole families were wiped out. In one French family of seventeen, there were thirteen deaths in one epidemic. The case-fatality rates in these early times were very heavy. In 39 epidemics from 1557 to 1805, an average rate of 80 percent has been reported (Ozanam). From 1805 to 1830, the case-fatality rate has been estimated at 25 percent (Academie Royale de Medicine). At present the case-fatality rate in Ontario is approximately 10 percent.
The modern trend of this disease is shown by reference to the mortality records of the city of Toronto, which go back to 1885. The average yearly deaths per 100,000 for consecutive ten-year periods (1886 to 1945, inclusive) were as follows: 132.0, 66.0, 34.5, 19.7, 8.2, 0.3. The diphtheria death rates for the United States follow a closely similar trend, the figures being as follows: 1900—40.3; 1910—21.1; 1920—15.3; 1930—4.9; 1940—1.1; 1944—0.9. These figures clearly show a consistently steady reduction in mortality that began over sixty years ago.
Recently, however, there has been a wartime increase in the incidence of diphtheria in both Europe and America. In Halifax, Nova Scotia, in 1940, there was an epidemic of considerable intensity involving both the civilian and military population of the city. There were 891 cases in all—588 civilians and 303 in the armed forces. An unusual feature of this outbreak was the high proportion of adults affected, 69.2 percent of the cases being over fifteen years of age. In Ottawa, Ontario, in the fifteen months prior to November 1946, there were 204 cases of diphtheria and 32 deaths, including a number of nonresidents who were treated in the city, thus indicating a case-fatality rate of 16 percent.
A similar wartime increase in diphtheria has been noted in the United States. According to Health News, August 19, 1946, “the increase in diphtheria morbidity and mortality in upstate New York that began in 1945 has continued in 1946, with 231 cases and 21 deaths being reported this year—the highest since 1934.” Baltimore also has had a steady increase in diphtheria since 1941, reaching epidemic proportions in 1944, with 142 cases and 9 deaths.
Recent reports from Europe also indicate that the wartime and postwar incidence of diphtheria has assumed almost pestilential proportions, being very virulent with a high case-fatality rate. In 1943 about 630,000 cases were reported in European countries in which records were available. Including countries in which records were not available, it may reasonably be assumed that there were fully 1,000,000 cases in that year, with about 50,000 deaths. In the years 1944 and 1945, with European conditions even more chaotic, it has been estimated that the toll of 1943 has been maintained.[Graph, with title:] Diphtheria—Case Rates per 100,000 in Toronto, Canada, and New York City, 1900–1940. (See original for data.)
The mortality rates for scarlet fever have been on a steady decline since before the beginning of the present century. The trend of this disease is shown by the average yearly death rates per 100,000 in the cities of Toronto and Montreal for consecutive five-year periods from 1890 to 1945, which are respectively as follows: 36.6 and 66.0; 18.8 and 15.4; 24.7 and 35.8; 12.8 and 11.6; 17.9 and 22.2; 4.4 and 8.4; 5.7 and 12.8; 1.9 and 6.8; 1.5 and 3.6; 2.2 and 2.5; 0.5 and 0.4. The mortality decline for this disease in the United States has been very similar, the rates per 100,000 being as follows: 1900—9.6, 1910—11.4, 1920—4.6, 1930—1.9, 1940—0.5, 1944—0.3.
The case-fatality rate for this disease has also declined greatly in this same period. In the city of Toronto prior to 1900, the case-fatality rate varied from 10 percent to 20 percent. This rate has gradually declined until during the last ten years it has varied from 0.25 percent to 1 percent. A similar decline has occurred in the province of Ontario as a whole.
The mortality rates for whooping cough have also shown a gradual decline since before the turn of the century. The average annual death rates per 100,000 for consecutive five-year periods from 1895 to 1945 in the city of Montreal were as follows: 32.4, 30.6, 19.6, 21.2, 20.4, 14.7, 12.3, 8.8, 6.8, and 4.2. The rates in other large cities throughout Canada and the United States have shown a similar trend.
The declining mortality from this disease in the United States and Canada is well shown by the statistics of the Metropolitan Life Insurance Company (Table 2), in which the average yearly death rates per 100,000 for consecutive five-year periods from 1910 to 1945 are as follows: 6.7, 4.8, 4.6, 3.5, 3.4, 2.5, 1.7.[Table 2:] Five-Year Averages of Annual Death Rates from Infectious Diseases—White Children Ages 1 to 14 Years, Metropolitan Life Insurance Co., Industrial Department, 1911–1945. (See original for data.)
The average yearly death rates for rheumatic fever in the city of New York for consecutive five-year periods from 1900 to 1945 are as follows: 8.2, 9.1, 6.2, 4.3, 3.8, 4.6, 3.6, 2.1, 1.3.
The mortality rates from typhoid and paratyphoid fever have also steadily declined since before the turn of the century. The modern trend of this disease is shown by the average yearly death rates per 100,000, for consecutive ten-year periods from 1885 to 1945 in the cities of Toronto, Montreal, and New York, which are respectively as follows (Table 3):
54.4, 32.3, 22.1; 19.8, 28.7, 17.7
19.2, 29.9, 11.0; 2.8, 12.0, 2.9
0.7, 11.1, 1.1; 0.1, 1.3, 0.2
The case-fatality rate of this disease has also markedly declined, from about 20 percent prior to 1900 to about 5 percent at the present time.
The mortality rates for erysipelas have steadily declined since 1880. The average yearly death rates per 100,000 for this disease for consecutive five-year periods from 1880 to 1945 in the city of Montreal are as follows: 12.0, 9.6, 6.3, 6.5, 5.2, 5.2, 5.0, 4.1, 3.1, 4.2, 3.5, 1.6, 0.5. A similar decline for this disease has been recorded in other large cities of Canada and the United States.
Maternal deaths have been on the decline in Canada since 1921, beyond which time the records are incomplete. The death rates for puerperal disease in all nine provinces of Canada in this 25-year period indicate an average decline from a rate of approximately 5.3 in 1921 to 2.3 in 1945 (Table 4). A very similar trend has been in evidence in the United States.[Table 4:] Five-Year Averages of Annual Maternal Death Rates, Puerperal Causes, in Canada by Provinces, per 1000 Live Births. (See original for data.)
Infant mortality—[age] under one year—has shown a steady reduction in Canada and United States since the beginning of the century. The death rates [of those] under one year per thousand living births in the city of Montreal, based on the yearly average of consecutive five-year periods from 1900 to 1945, are as follows: 274.7, 268.6, 220.2, 183.0, 160.6, 126.8, 105.9, 83.0, 64.5, 61.2 (1945 alone). The infant death rates in other large American cities show a very similar trend.
From a cursory examination of the above data, it is quite obvious that there [was and] has been a general decline in mortality from practically all the common infectious diseases both before and since the beginning of the present century. There are doubtless a number of factors that may have contributed to this regression—better nutrition and hygiene, particularly in the younger age groups, improved medical therapy, artificial immunization, and public-health measures such as quarantine, pasteurization of milk, chlorination, and filtration of municipal water supplies, etc.
Regarding tuberculosis: the advent of sanitarium treatment, [resulting in] the segregation of a considerable number of active cases, and the more-recent mass X-ray surveys for the early detection of otherwise unrecognized cases have saved and will save many fatalities from this disease. The fact remains, however, that this disease was definitely on the decline in both Europe and America long before any of these control measures were instituted, indeed even long before Koch’s discovery of the specific etiological organism in 1882.
Furthermore, the rate of mortality decline was practically as rapid before as since the adoption of these controls. Commenting on this orderly decline, Ross2 says: “While the control measures that have been applied have possibly accentuated the decline in young adults and influenced, through public-health education, all age groups, it seems reasonable to attribute the general decline to other factors—more general in character and of which but little is really known.”
In support of this statement, Ross compares the tuberculosis mortality figures of Mexico City with those of Ontario, showing that the decline in the former has been more rapid than in the latter in spite of the fact that “Mexico City had no sanatoria, no diagnostic clinics, no antituberculosis movement.”
On this same subject, McKinnon3 says: “Quite obviously, then, all the factors mentioned are not adequate in themselves to explain the recorded decline. Some other factor or factors must have been operating during this period, and it is necessary to cast farther afield in search of them.”
Regarding the general decline in tuberculosis mortality, Davis4 says: “Is it that we are effecting more cures? Yes, we are effecting more apparently arrested cases…Do you think that alone accounts for the drop in the death rate? Without hesitating the answer is no—the figures are nowhere near commensurate. Can it be due to our methods of diagnosis? To some extent—yes. Does this account alone for the drop in the death rate? Again the answer is no. Can it be that we have developed more resistance to the disease? Yes, it could be…”
In the epidemiological history of diphtheria, we have a picture somewhat similar to that of tuberculosis. The decline in mortality was well underway long before the end of the last century, and it had continued on an almost even grade until, during the last decade, it approached the vanishing point.
At the beginning of the century, antitoxin came into general use, and later (1930) artificial immunization by toxoid was adopted by the health departments of many of our large urban centers. By reference to the accompanying charts of the case rates of diphtheria in New York City and Toronto, Canada, the general decline in incidence is shown [along] with an apparent accentuation of same following the following the introduction of toxoid immunization in these cities, which began in New York in 1925 and in Toronto in 1930. [However,] these graphs show one marked upsurge in New York shortly following the adoption of toxoiding that corresponds in timing with a similar upward fluctuation in Toronto before toxoiding was begun.
In fact the deviations from the calculated baseline of incidence in both cities show a striking parallel all through the 40-year period. From 1930 to 1940, the decline was apparently more free from upward fluctuations in both cities, which has been cited as evidence of the effect of immunization. But from present indications, when the graph is completed to date, a disturbing upward fluctuation will be noted within the last few years.
In a number of centers in the United States and Canada, serious outbreaks of diphtheria have recently been reported, to say nothing of the major upsurge in Europe. In the United States as a whole, there was approximately a 30 percent increase in incidence in 1945. In upstate New York, Baltimore, Halifax, Nova Scotia, and Ottawa, Ontario, outbreaks of epidemic proportion have been reported. A disquieting feature of these outbreaks has been the development of a considerable number of cases in supposedly immunized subjects [as well as] the marked invasion of adult age groups.
In the Halifax epidemic,5 66 of the cases admitted to hospitals had previously received one or more doses of toxoid or antitoxin or were Schick negative [i.e., tested negative for diphtheria]. Fifteen cases developed in persons supposedly immune by Schick test. Of these, 9 cases developed in less than three months from the time the test was made, while the remaining 6 had been negative a year or more previously. Five cases had received antitoxin within two months previously.
In the Ottawa epidemic,6 of 99 cases under fifteen years of age, 36 were found to have previously received three doses of toxoid. One of 25 cases in adults had been toxoided in the army.
In the Baltimore outbreak of 1944,7 63 percent of all cases had a record or history of prior toxoid inoculation. Of the fatal and malignant (“bull-neck”) cases, 77.8 percent—and 61.8 percent of the remaining milder cases—had previously been toxoided. Since the number of the preschool and school-age children of Baltimore who had been toxoided was estimated at 75 percent, the ratio of incidence in the toxoided and nontoxoided groups was about even, with the malignant cases showing a selectivity for the toxoided group. Commenting on these findings, the authors of the report say, “This may be a reflection of the increasing amount of inoculation being done in Baltimore, but it is by no means certain that this is the only factor involved.”
Thus it would appear that, with the exception of the recent postwar increase in Europe and America, the decline in diphtheria mortality has generally followed a rather even course during the past sixty years or more, with up and down fluctuations prior and subsequent to the adoption of artificial immunization. The protective efficacy of the latter seems to be adversely reflected in the reports of the Halifax, Ottawa, and Baltimore epidemics of the last few years. The present trend in this, as in other infectious diseases, seems to be toward a shift in age incidence from the younger to older age groups.
Regarding pneumonia, it will be seen by the statistical data previously presented that the decreased mortality has followed a fairly even grade—with the exception of the 1920 upsurge, which was incidental to the postwar influenza pandemic. The decline was almost as rapid prior to as following the introduction of chemotherapy, which has been the only factor likely to have materially influenced the epidemiology of this disease.
Regarding typhoid fever, this enteric infectious disease, which has generally been thought to be propagated by pollution of drinking water or milk, has been on a steady decline in mortality since 1885. No one can question the favorable influence of water chlorination and milk pasteurization on the incidence of this disease, but, strange to say, the decline in mortality and case-fatality rates had begun long before the adoption of either of these control measures. This would seem to indicate, as with the diseases previously discussed, the operation of some major unidentified prophylactic factor.
Regarding the other infectious diseases listed—scarlet fever, whooping cough, rheumatic fever, and erysipelas—these, as shown in the previous statistical data, have all exhibited a steady decline in mortality and case-fatality rates since before the turn of the century, although no specific control measures have been generally applicable. In recent years, however, artificial immunization for scarlet fever and whooping cough has been given a limited trial.
Regarding maternal and infant mortality (under one year): these, as previously indicated, have also shown a steady decline in keeping with that of the infectious diseases although no specific control measures have been applicable, thus indicating the possible influence of the same unidentified prophylactic factor.
The Author’s Hypothesis
From the foregoing it is clearly apparent that some unidentified major prophylactic factor or factors, general in application, must have been operating in bringing about such a uniformity in reduced mortality from so many infectious diseases in the same period of time. The fact that the decline has followed practically the same pattern in diseases such as scarlet fever, rheumatic fever, whooping cough, measles, erysipelas, diarrhea, enteritis, and even appendicitis (Table 2)—in which no specific control measures have been applicable, as in tuberculosis and diphtheria—points significantly to the overall nature of the prophylaxis.
The most logical explanation would seem to be that resistance to infection in general has been increased gradually throughout the past century, particularly in the younger age groups, and that the major factor in producing this result is most likely to have been some changed trend in nutrition. On this basis, artificial control measures, which have been applied mostly within the last two decades, have played a minor or supplemental role.
The major change in nutrition in this period has been brought about by the tremendous increase in the production, distribution, and consumption of citrus and other vitamin-C–containing fruits in North America and most of Europe, made possible by the gradual development of better transportation throughout the century—steamships, railways, and motor highways.
Prior to 100 years ago, ocean transport by sailing ships and lack of refrigeration made practically impossible the import by the United Kingdom of citrus and other fresh fruits from Mediterranean ports or North Africa. With the advent of steamships and railways, imports of these fruits to England and other northern European countries from Spain, Algiers and the Middle East gradually increased.
The citrus fruit industry began in America in 1886, at which time the annual U.S. production amounted to nearly 3,361,000 bushels. The production has gradually increased (more rapidly in the last two decades), until in 1944 the total amounted to 278,369,600 bushels. The production of canned citrus juices began in U.S.A. in 1929, in which year the total pack was 6,150,000 lb. By 1945 the annual output had reached a total of 1,738,170,000 lb.
The production of canned tomato juice began in U.S.A. in 1930, in which year the total pack was 6,930,000 lb. By 1945 the annual output of this juice—second only to citrus in vitamin-C content—had reached a total of 924,000,000 lb.
The production and consumption of fresh and canned tomatoes, in ever increasing quantity, has now become general throughout the Americas and most of Europe. One hundred years ago the tomato, or love apple as it was then called, was thought to be unfit for food and the cause of cancer. Then it was grown for ornamental purposes only.
Today the use of these fruits and juices has become routine as an essential part of modern nutrition, and, significantly, the decline in mortality rates of the infectious diseases dealt with in this treatise has been closely proportionate to the increased use of these fruits and juices. Significant also may be the fact that the inception of the citrus and tomato juice canning industry (1929–1930), which has greatly increased the consumption of these fruits, closely coincided with an apparent acceleration in the mortality decline of most of these diseases.
This nutritional revolution has, perhaps, been applied more intensively in infancy and childhood than in the older age brackets. Fifty years ago, infants, when not breast-fed, were fed artificially on modified cow’s milk, condensed milk, or proprietary foods in powder form, which frequently was conducive to malnutrition. Even breast-feeding at that time—owing to impoverished maternal diets—often had to be abandoned.
Pediatricians at that time sanctioned the use of orange juice in small quantity—0.5 to 1 oz after the age of ten months. Many mothers, however, hesitated to use fruit juices of any kind in the feeding of infants and young children because of the then popular fear of its producing “colic.”
Infant feeding today presents a greatly different picture. The infant of one month now gets its full ounce or more of orange juice daily, which is gradually increased until at six months fully four ounces or more is given—in addition to supplemental feedings of homogenized fruits and vegetables, wheat-germ-enriched cereal foods, etc. If orange juice should disagree, vitamin C in tablet form is substituted.
The author believes that the major factor in the protective influence of this dietary revolution with regard to the prevention of infectious diseases has been the greatly increased intake of vitamin C, which has been referred to by nutritionists as the “antitoxic” or “anti-infection” vitamin. The anti-infectious properties of this vitamin are [a result of] its effect on the reticuloendothelial system in building up and maintaining stability and invulnerability of the submucosal and subcutaneous connective tissues.
The proliferation of fibroblasts and collagen fibrils depends on a normal plasma concentration of vitamin C, thus maintaining the stability of the intercellular cement substance, which in turn is essential to optimal resistance to infectious invasion. By reason of its chemical action as a reducing agent—and sometimes as an oxidizing agent—vitamin C is also a specific antagonist of chemical and bacterial toxins. An optimal intake of this vitamin is therefore a means of building up natural immunity or resistance against all infectious diseases as well as counteracting their toxic manifestations.
The following references to the literature pertaining to the anti-infectious action of vitamin C are submitted to show the prophylactic and therapeutic effect of this vitamin in the diseases under discussion.
Regarding [Scurvy and] Tuberculosis
Richard Morton, one of the earliest writers on this disease, states in his famous Phthisiologia (1689) that “scurvy is wont to occasion a consumption of the lungs.” Many investigators have studied the effect of vitamin C in this disease because of its favorable effect on fibroblastic connective tissue formation—so essential to the healing of the exudative or ulcerative lesions.
Harris8 finds that the excretion of vitamin C is decreased in tuberculosis; that deficiency of vitamin C reduces the resistance of guinea pigs to tuberculosis infection; and that similar effects have been observed in man. Birkhang9 found that C hypervitaminosis, induced by daily administration of ascorbic acid, produced an increase in body weight and reduction in the tuberculosis lesions of guinea pigs. Microscopic examination revealed less caseonecrotic lesions and more collagenous tissue in and around the tubercular centers than was observed in the controls.
Bauer and Vorwek10 report vitamin C deficiencies of from 1000 to 4000 mg in tuberculosis cases. They state that there appears to be a certain parallelism between the activity of tuberculosis and the extent of vitamin C deficiency. Albrecht11 found that daily subcutaneous injections of vitamin C in tubercular patients increased appetite, improved general health and blood picture, and frequently decreased the temperature. He also found it to be of value in pneumothorax therapy.
Pilz12 finds that vitamin C favourably influences the process of recovery in tuberculosis. It increases vitality, eliminates night sweats, improves appetite, and, combined with calcium, raises blood values. A daily dose of 300 mg is given until deficiency is made up, and thereafter [a dose is given that is] sufficient to maintain normal levels. Nicita13 reports that tubercular patients show a diminished vitamin C urinary content that is proportional to the severity of the disease. He advocates the administration of large amounts of this vitamin to counteract toxemia. Boissevain and Spillane14 found that vitamin C, in concentration of 0.001 percent, inhibits the growth of human tubercle bacilli in artificial media.
Radford, de Savitsch, and Sweany15 report the effect of vitamin C on 111 far-advanced and fibroid tubercular cases. The patients were divided into three groups: the first received 500 cc of orange juice daily, and the second received 250 cc of synthetic vitamin C. The third group, used as controls, was given imitation orange juice. No other therapy was employed except routine rest. In three months a greater percentage of the treated patients showed a more favorable response than the controls in red-blood-cell count, lymphocytes, monocyte-lymphocyte ratio, neutrophil-lymphocyte ratio, hemoglobin, and albumin-globulin. At six months the treated groups still showed greater improvement in blood cells and hemoglobin. At nine months the greater amelioration of the treated groups with respect to blood-cell counts, sedimentation rates, and blood fibrogen was still maintained.
Hasselbach16 found a close relationship between fever and vitamin C intake and cites clinical cases to show that vitamin C reduces toxic manifestations, including fever. McConkey17 reports that of 437 pulmonary cases admitted to a New York state hospital for tuberculosis in 1926 and 1927, 47 developed intestinal tuberculosis, whereas of 399 admitted in 1928 and 1929 who received a prophylactic treatment consisting of 3 oz of citrus or tomato juice and 1/2 oz of cod-liver oil with each meal, only three developed intestinal tuberculosis. Furthermore, of 913 other patients admitted during 1930 to 1938 who received the same prophylactic treatment, only nine developed intestinal tuberculosis.
Borsalino18 reports a study of the capillary resistance of 140 tubercular patients. He found that administration of vitamin C rapidly increased capillary resistance and stopped hemoptysis, which reappeared when the treatment was discontinued. Moore et al.,19 in a recent survey of nutrition among the northern Manitoba Indians, report a very high mortality rate from tuberculosis and pneumonia among the Indians of Canada (761 and 383, respectively, per 100,000). In the tribes covered by their study, the death rate for tuberculosis in 1942 was 1400 per 100,000. (The comparable figure for the white population of Manitoba was 27.)
In their analysis of the daily per-capita food intake, the researchers found vitamin C to be in greatest deficiency—less than 1/71 of the recommended allowance. In conclusion they say: “It is not unlikely that many characteristics, such as shiftlessness, indolence, improvidence, and inertia—so long regarded as inherent or hereditary traits in the Indian race—may at the root be really the manifestations of malnutrition. Furthermore, it is probable that the Indians’ great susceptibility to many diseases, paramount amongst which is tuberculosis, may be attributable among other causes to their high degree of malnutrition arising from lack of proper foods.”
Regarding Vitamin C in Pneumonia
In 1936 Gander and Niederberger20 found that vitamin C favourably influenced the course of pneumonia. When the vitamin C status was brought up to normal saturation level early in the disease—preferably the first day of illness—the temperature dropped abruptly to normal and the pain subsided. The pulse remained in good tone, and remarkable improvement in general condition was noted. The researchers were led to the clinical study by the observation that the seasonal incidence of the peaks of vitamin C deficiency (December and April) corresponded with the periods of highest mortality from pneumonia. Furthermore, they correlated the age incidence of the disease with the degree of vitamin C deficiency usually found at different ages—the greatest deficiency occurring in age groups above fifty years, in which pneumonia also has its highest incidence.
In the same year, Hochwald21 independently reported similar results, his findings indicating that massive doses of vitamin C—500 mg every 90 minutes until the temperature drops to normal—exerted a curative effect in croupous pneumonia, as shown by improvement in general condition: lessened prostration and dyspnea, earlier return to normal temperature, quicker disappearance of local findings, and normalization in white-blood-cell picture.
More recently, Slotkin and Fletcher22 have reported on the prophylactic and therapeutic value of vitamin C in postoperative pneumonia. They summarize their findings as follows: “Pulmonary complications in old, debilitated patients requiring prostatic surgery is a common cause of death. The pulmonary lesions most noted are bronchopneumonia, lung abscess, and purulent bronchitis. Most of these cases are so-called ‘wet chests,’ due to capillary secretions. Ascorbic acid, which increases the tonicity of these capillaries, has been of great value in alleviating these patients and restoring prompt pulmonary action by disappearance of this infiltration…It is a valuable adjunct in tiding these aged patients over their critical postoperative period.”
Slotkin further reports23 that since publication of his original paper on this subject, “ascorbic acid has been used routinely by the general surgeons in all surgical procedures in the hospital (Millard Fillmore, Buffalo) as a prophylaxis against pneumonia, with complete disappearance of this complication [resulting].” In this connection it may be of interest to note that bronchopneumonia is often the terminal cause of death in frank scurvy and that the “rusty-brown” sputum of pneumonia may in reality be a sign of the hemorrhagic status of a subclinical scorbutic background.
Regarding Vitamin C in Diphtheria
In the early history of this disease, when it was known as malignant angina or gangrenous sore throat, many observers reported the frequent concurrence of “gangrenous gingivitis.” Some physicians at that time regarded this complication as an extension of the disease from the throat. Others regarded this severe form of gingivitis as evidence of a scorbutic background. Boerhaave, a Dutch physician of international repute in the early 18th century, held strongly to this viewpoint.
The quite frequent occurrence of epistaxis and the profuse bleeding from the denuded fauces upon removal of the false membrane so characteristic of diphtheria are very suggestive of the hemorrhagic status of scurvy. One thing is certain: scurvy was at that time very prevalent in central and northern Europe, where the available supply of fresh fruits was much less than in countries bordering on the Mediterranean. The basic concurrence of this condition may have determined the very high case-fatality rate (80 percent) at that time.
The close relationship between the vitamin C status and the degree of diphtheritic intoxication is shown by Ravina,24 who observes that guinea pigs have greater resistance to diphtheria toxin after injections of vitamin C than controls not so treated. In 25 benign, 10 severe, and 4 malignant cases of the disease, a marked deficiency of vitamin C was found in 28 percent of the subjects under fifteen years of age and in 52 percent of those over fifteen years of age. For effective therapy he recommends large daily doses of the vitamin—150 mg for children under three years of age and 500 mg for adolescents and adults.
In Russia, Bagasheva25 uses a combined therapy for diphtheria consisting of antiserum, hypertonic dextrose, nicotinic acid, and vitamin C.
Regarding Vitamin C in Rheumatic Fever
Abasy, Hill, and Harris26 found a striking difference in the excretion of vitamin C in 107 active rheumatic fever cases compared with controls. They concluded that large amounts of this vitamin are indicated both therapeutically and prophylactically. Roff and Glazebrook27 reported the occurrence among naval trainees of a gingivostomatitis—commonly associated with rheumatic fever—that was shown to be due to vitamin C deficiency.
Glazebrook and Thomson28 studied the effects of hemolytic streptococcus infection in potentially scorbutic and control groups in 1500 youths in a naval training school. Of these, 335 were given liberal daily supplements of ascorbic acid, the remainder being used as controls. There developed 16 cases of rheumatic fever and 17 cases of pneumonia among the controls and no case of either disease among the youths who received the extra vitamin C. These authors felt that there was a close relationship between the cases of pneumonia and rheumatic fever. They noted the occurrence of a low-grade basal lung consolidation that was characterized on the one hand by its tendency to progress into rheumatism and on the other hand by its disappearance when treated with vitamin C.
Rinehart29 studied the effect of vitamin P—a plant pigment found in the peeling of lemons and oranges—in conjunction with vitamin C in the treatment of rheumatic fever. It had been found that vitamin P had a favorable influence on purpuric and hemorrhagic conditions resulting from vascular permeability in infections, notably rheumatic. All his cases showed a slowing of the sedimentation rate, which was paralleled by marked clinical improvement. He concludes, “If nutritional deficiency of vitamin C and P prove to be conditioning factors that prepare the soil for rheumatic fever, [then] the prophylactic implications are clear.”
Regarding Vitamin C in Whooping Cough
In 1936 Otani30 and in 1937 Ormerod et al.31,32 reported very favorable results in the vitamin C therapy of this disease. The former reported on the intravenous vitamin C treatment of 81 cases of whooping cough in hospital clinics and concluded that vitamin C has a definite antagonistic action on the toxin of the Bordet-Gengou bacillus. The latter reported on the oral vitamin C therapy of 29 cases—500 mg the first day, then a daily average of 200 mg thereafter. They concluded that “this treatment markedly decreases the intensity, number, and duration of the characteristic symptoms.”
Regarding Nutritional Deficiency as the Major Etiological Factor in Maternal and Infant Mortality
The epochal work of Ebbs et al.33–35 has furnished indubitable evidence of the lifesaving effect of improved maternal nutrition on both mother and child. The researchers studied the effect of supplemental feeding of 90 women on poor diets and with low income in the last half of pregnancy, as compared with 120 controls, unsupplemented, on equally poor diets as well as another group of 170 women with higher incomes who were advised regarding proper diet.
The supplemental foods supplied in these studies consisted of milk, eggs, cheese, oranges, tomatoes, wheat germ, and vitamin D. The women on the supplemented and good diets enjoyed better health and had fewer complications throughout the puerperium—and the health of their infants was much better—than those on the unsupplemented poor diet. The incidence of miscarriages, prematures, stillbirths, and deaths before six months was significantly higher in the poor-diet group. In a subsequent study by Burke et al.36 in which 216 maternal cases were observed, very similar findings were recorded.
It is the author’s belief that the gradually increased use of citrus fruits and juices in maternal and infant feeding during the past half century has been the major factor in reducing the maternal and infant death rates. The increased intake of vitamin C would, for the physiological reasons previously stated, tend to minimize puerperal infection, decrease the incidence and severity of pre- and post-partum hemorrhage (the bête noire of obstetrics), and by increasing the tensile strength of connective tissues, prevent cervical and perineal lacerations, thus still further lessening the danger of maternal infection. In the infant this dietary revolution would, for the same reasons, tend to reduce the incidence of neonatal pneumonia, diarrhea and enteritis (now taking such a heavy toll in war-ravaged Europe), and other infectious diseases of early infancy.
Regarding Vitamin C and Resistance to Infection in General
Jusatz39 finds that vitamin C has a stimulating effect on the production of antibodies. He claims that it increases the agglutinin, hemolysin, and precipitin titers and the opsonic index of experimental animals treated with vaccines or toxoids. Madison and Manwaring,40 confirming these findings, were able to bring about a ten-to-thirty-fold increase in precipitin titer via optimal intake of vitamin C. During the recent war, it was found that German children receiving a supplement of 50 mg of vitamin C daily were less susceptible to infection than controls.41 More recently, Nungster and Ames, of the University of Michigan, reported to the American Society of Bacteriologists (1947 convention) that vitamin C greatly increases the phagocytic action of white blood cells against infectious bacteria.
The author’s hypothesis that increased vitamin C intake associated with the increased consumption of citrus fruits, tomatoes, etcetera [is] the major heretofore unidentified factor in bringing about the general reduction in mortality of infectious diseases would also account for the shift in the age incidence of tuberculosis, diphtheria, poliomyelitis, and other diseases from the under-five-years to older age groups. This is explained by the fact that the infant in the nursery is given the full benefit of this nutritional reform, whereas after this age perverse dietary habits are gradually acquired through lack of parental guidance and inadequacy of public-health education. The increased use of candy, carbonated beverages, tea, coffee, tobacco, and alcohol by our juvenile and older age groups tends gradually to displace the more wholesome nutritional habits of early childhood.
After all, we should recognize that natural resistance to disease is developed by fundamental improvement in nutrition and hygiene. Such resistance gives protection against all diseases. Artificial immunization, on the other hand, is dependent on the conversion of a portion of this latent general resistance to a specific resistance, such as in toxoiding for diphtheria.The injection of an attenuated virus or bacterial toxin elicits a reaction of the organism to that specific morbific agent only and draws upon our reserves of natural immunity to meet this conversion demand.
If repeated demands exceed the supply, we are left physically bankrupt. In other words, we cannot strike back with more than we have, and we cannot get out of anything more than we put into it. Thus the fundamental prerequisite for successful artificial immunization is an ample reserve of natural immunity. In our search for shortcuts in the prevention and cure of disease, we are prone to overlook this basic truth. In the modern use of chemotherapy, we are already beginning to find flies in the ointment. The specific benefit of the sulfonamides is sometimes obtained at the expense of toxic damage to some vital uninvolved part of the human mechanism. (In a previous paper,37 the author has shown that vitamin C deficiency is conducive to sulfonamide sensitivity.)
We are now beginning to find that even the more benign penicillin has its drawbacks in stepping up the virulence of certain organisms. The author is inclined to believe that the principle of trying to eradicate disease by concentrating our attack against the associated microorganisms is fundamentally unsound. If we wish to eliminate a desert or swamp, we do not proceed to cut down the sagebrush and cactus of the former or the lush characteristic verdure of the latter. Instead, we change the condition of the soil. By irrigation we make the desert blossom like a rose, and by drainage we eliminate the swamp.
Dr. Alexis Carrel38 has said: “Microbes and viruses are to be found everywhere—in the air, in water, in our food…Nevertheless, in many people they remain inoffensive. Among human beings some are subject to diseases and others are immune. Such a state of resistance is due to the individual constitution of the tissues and the humors, which oppose the penetration of pathogenic agents or destroy them when they have invaded our body. This is natural immunity.
“But natural immunity does not exclusively derive from our ancestral constitution. It may come also from our mode of life and alimentation…Some diets increase the susceptibility of mice to experimental typhoid fever. The frequency of pneumonia may also be modified by food. The mice belonging to one of the strains kept in the mousery of the Rockefeller Institute died of pneumonia in the proportion of 52 percent while subjected to the standard diet. Several groups of these animals were given different [more nutritious] diets. The mortality from pneumonia fell to 32 percent, 14 percent, and even to zero, according to the food.
“We should ascertain whether natural resistance to infections could be conferred on man by definite conditions of life. Injections of specific vaccine or serum for each disease, repeated medical examinations of the whole population, and construction of gigantic hospitals are expensive and not very effective means of preventing diseases and of developing a nation’s health. Good health should be natural.”
A great English physician, Dr. Leonard Williams, has said: “The discovery of the vitamins has entirely altered our conception of the causes and origins of disease. Until lately disease was regarded as a sin of commission by some unseen and subtle agency. The vitamins are teaching us to regard it—in some degree at any rate—as a sin of omission on the part of civilized or hypercivilized man. By our habit of riveting our attention on microbes and their toxins, we have sadly neglected the side of the question that concerns itself with our own bodily defenses.”
Charcot has said: “Disease is from of old, and nothing about it has changed. It is we who change, as we learn to recognize what was formerly imperceptible.”
Statistical data are presented to show the marked decline in mortality and case fatality of many infectious diseases within the past century.
The uniformity of this decline in so many diseases and over such a lengthy period of time suggests the operation of some major overall factor improving natural resistance, compared with which our artificial control measures have played a minor or supplemental role. The existence of such a factor has been recognized by epidemiologists but not yet identified.
The author advances the hypothesis that some major change in the trend of nutrition offers the most likely explanation and singles out the greatly increased consumption of citrus and other fruits rich in vitamin C as the unidentified factor. Correlated statistical data show a close parallel—in both time and extent—between the development of this nutritional trend and the mortality decline in infectious diseases.
The physiological action of vitamin C is discussed in relation to its “anti-infection” role, and the literature relative to the prophylactic and therapeutic use of this vitamin in infectious diseases is reviewed.
By W.J. McCormick, MD, 16 Gothic Ave., Toronto, Canada. Reprinted from The Medical Record, September 1947, Medical Journal and Record Publishing Company, Inc., by the Lee Foundation for Nutritional Research.
1. Pringle, A.M.N. “Tuberculosis Throughout the Century.” Med. Off., Apr. 10, 1943.
2. Ross, Mary A. “Tuberculosis Mortality in Ontario.” Can. Pub. Health Jour., 25: 73, 1934.
3. McKinnon, N.E. “Mortality Reductions in Ontario, 1900–1942.” Can. Jour. Pub. Health, 36: 423, 1945.
4. Davis, Paul V. “Tuberculosis Epidemiology.” Dis. of Chest, p. 21, September 1939.
5. Morton, A.R. “The Diphtheria Epidemic in Halifax.” Can. Med. Assoc. Jour., 45: 171, 1941.
6. Lomer, T.A. Personal communication to the author, December 16, 1946.
7. Eller, C.H., and Frobisher, Martin, Jr. “An Outbreak of Diphtheria in Baltimore in 1944.” Am. Jour. Hyg., 42: 179, 1945.
8. Harris, L.J. “Nutrition and Its Effect on Infectious Disease.” Lancet, 1: 811, 1937.
9. Birkhang, K.E. “Tuberculosis in Animals Treated with Ascorbic Acid.” J.A.M.A., 112: 2376, 1939.
10. Bauer, G., and Vorwerk, W. “Beitrag Zum Vitamin C-Defizit Bei Lungentuberkuloesen.” Beitr. Z. Tuberk, 91: 262, 1938.
11. Albrecht, E. “Vitamin C Als Adjuvans in der Therapie der Lungentuberkulose.” Med. Klin., 34: 972, 1938.
12. Pilz, I. “Vitamin C: Ein Wichtiges Adjuvans in der Behandlung der Lungentuberkulose,” Med. Klin., 34: 227, 1938.
13. Nicita, A. “Recerche Sulla Eliminzione Della Vitamina C nei Tuberculotici” Riv. Di Patal. e Clin. d. Tuberc., 12: 41, 1938.
14. Boissevain, C.H., and Spillane, J.D. “A Note on the Effect of Synthetic Ascorbic Acid on the Growth of the Tubercle Bacillus.” Am. Rev. Tuberc., 35: 661, 1937
15. Radford, M., de Savitsch, E.C., and Sweany, H.C. “Blood Changes Following Continuous Administration of Vitamin C and Orange Juice to Tuberculous Patients.” Am. Rev. Tuberc., 35: 784, 1937.
16. Hasselbach, F. “Vitamin C und Waermeregulation.” Schweitz. Med. Wschr., 67: 877, 1937.
17. McConkey, Mack. “Cod Liver Oil and Tomato Juice in Prophylaxis of Intestinal Tuberculosis.” Am. Rev. Tuberc., 43: 425, 1941.
18. Borsalino, G. “La Fragilite Capillare Nella Tuberculose Polmonare e le Sue Modificazione par Azione Della Vitamin C,” Gior. Di Clin. Med., 18: 273, 1937.
19. Moore, P.E., Kruse, H.D., Tisdall, F.F., and Corrigan, R.S.C., Can. Med. Assn. Jour., 54: 223, 1946.
20. Gander, J., and Niederberger, W. “Vitamin C in der Behandlung der Pneumonie.” Munchen Med. Wchnschr., 51: 2074, 1936.
21. Hochwald, A. “Beobachtungen uber Askorbinsaure-Wirkung bei der Kruppen Pneumonie.” Wien. Arch. f. Inn. Med., 29: 353, 1936.
22. Slotkin, G.E., and Fletcher, R.S. “Ascorbic Acid in Pulmonary Complications Following Prostatic Surgery: A Preliminary Report.” Jour. Urol., 52: Nov. 6, 1944.
23. Slotkin, G.E., Personal communication to the author, December 2, 1946.
24. Ravina, A. “The Vitamin C Therapy of Diphtheritic Intoxication.” Presse Med., 53, 8, 1945.
25. Bagasheva, A.M. “Combined Therapy of Diphtheria with Antiserum, Hypertonic Solution of Dextrose, Nicotinic, and Ascorbic Acid.” Soviet Med., 8: 7, 1944.
26. Abasy, M.A., Hill, N.J., and Harris, L.J. “Vitamin C and Juvenile Rheumatism.” Lancet, 2: 1413, 1936.
27. Roff, F.S., and Glazebrook, A.J. “The Therapeutic Application of Vitamin C in Peridental Disease.” Jour. Roy. Nav. Med. Serv., 25: 340, 1939.
28. Glazebrook, A.J., and Thompson, S. “The Administration of Vitamin C in a Large Institution and Its Effect on General Health and Resistance to Infection.” Jour. Hyg., 42: 1, 1942.
29. Rinehart, J.F. “The Treatment of Rheumatic Fever with Crude Hesperidin (Vitamin C).” Paper read before California Heart Association, Los Angeles, May 6, 1944.
30. Otani, T. “Vitamin C Therapy of Whooping Cough.” Klin. Wchnschr., 15: 1884, 1936.
31. Ormerod, M.J., and Unkauf, B.M. “Ascorbic Acid Treatment of Whooping Cough.” Can. Med. Assn. Jour., 37, 134, 1937.
32. Ormerod, M.J., Unkauf, B.M., and White, F.D. “A Further Report on the Ascorbic Acid Treatment of Whooping Cough.” Can. Med. Assn. Jour., 37: 268, 1937.
33. Ebbs, J.H., Tisdall, F.F., and Scott, W.A. “The Influence of Prenatal Diet on the Mother and Child.” Jour. Nutrit., 22: 515, 1941.
34. Ebbs, J.H., Scott, W.A., Tisdall, F.F., Moyle, W.J., and Bell, M. “Nutrition in Pregnancy.” Can. Med. Assn. Jour., 46: 1, 1942.
35. Ebbs, J.H., Brown, A., Tisdall, F.F., Moyle, W.J., and Bell, M. “The Influence of Improved Prenatal Nutrition on the Infant.” Can. Med. Assn. Jour., 46: 6, 1942.
36. Burke, S.B., Beal, V.A., Kirkwood, S.B., and Stuart, H.C. “The Influence of Nutrition During Pregnancy upon the Condition of the Infant at Birth.” Jour. Nutrit., 26: 569, 1943.
37. McCormick, W.J. “Sulfonamide Sensitivity and C-Avitaminosis.” Can. Med. Assn. Jour., 52: 68, 1945.
38. Carrel, Alexis. Man, The Unknown, New York and London, Harper Bros., 1935, p. 207.
39. Jusatz, J.H. “Uber den Influss von Vitamin C auf Immunitatsvorgange.” Ztschr. f. Vitaminforsch., 9: 75, 1939.
40. Madison, R.R., and Manwaring, M.H. “Ascorbic-Acid Stimulation of Specific Antibody Production.” Proc. Soc. Exper. Biol. Med., 37: 402, 1937.
41. Summary of Certain Public Health Measures Adopted in Germany During the Present War.” Bull. War Med., 2: 5, 1941.
Reprint No. 5a
Lee Foundation for Nutritional Research
Milwaukee 3, Wisconsin
Printed in U.S.A.
Note: Lee Foundation for Nutritional Research is a nonprofit, public-service institution, chartered to investigate and disseminate nutritional information. The attached publication is not literature or labeling for any product, nor shall it be employed as such by anyone. In accordance with the right of freedom of the press guaranteed to the Foundation by the First Amendment of the U.S. Constitution, the attached publication is issued and distributed for informational purposes.