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Transcript
The Potentialities and Limitations of Epidemiology John Cassel, M.B.B.Ch., M.P.H. To gain some understanding of the contributions that may legitimately be expected from epidemiology, it is first of all necessary to define what is meant by epidemiology and briefly trace the development of this scientific discipline. To a newcomer to this field the term "epidemiology" would seem most logically to be concerned with a study of epidemics, and epidemics are usually thought of as outbreaks of infectious diseases. Consequently, epidemiology is frequently considered as a science restricted to a study of outbreaks of infectious diseases. Historically this would have been an adequate formulation as at the time of the development of this discipline infectious disease epidemics were the most important and terrifying of the health problems afflicting mankind. These diseases therefore commanded practically all the attention and interest of all the health disciplines including epidemiology. Today however, as I hope to indicate, this would be inadequate as a definition. The origin of the science of epidemiology can be traced to the Hippocratic era in the Golden Age of Greece. Hippocrates was one of the first physicians to recognize that disease outbreaks were not happenstance occurrences, attacking unfortunate individuals at random. Different populations were subject to different types of diseases, and these occurred at different seasons. Furthermore within any population various subgroups existed with different degrees of susceptibility to these diseases. Some diseases for example, attacked children primarily, others adults, some were most prevalent among the poor or among those who lived in a certain sector of the city. * Presented at Public Health Seminar, Princeton, New Jersey, March 6, 1962 2 From these beginnings two cardinal principles evolved which characterize and are central to the science of epidemiology. These are, firstly that the unit of study of epidemiology is the group rather than the individual. By this we mean that the epidemiologic method is not the most appropriate technique for discovering why any particular person became ill when he did. More appropriately epidemiology can provide answers as to the reasons people with a certain set of characteristics are more or less likely to become ill than other people without these characteristics. The second point central to epidemiology is that its major contributions have been in the identification of those reasons for illness in aspects of the environment or way of life of the group under study. As mentioned previously the diseases of most concern to the Hippocratic physicians, and indeed to physicians for the next 25 centuries were the infectious diseases. Furthermore for this same period the aspect of the way of life of people of most concern to epidemiology was the relation of man to his physical environment. Thus for example in Hippocratic times the occurrence of disease was explained in terms of the strength and direction of the prevailing winds, the amount of rainfall and sunlight, the height above sea level or the nature of the soil. It is most important to recognize further than the particular aspects of the physical environment that were selected for examination as explanations of disease mere determined by the existing theories concerning the causation of disease. This relationship between the variables selected for study and prevailing theories of disease causation is equally true today and requires to be fully understood to appreciate the potential contribution of modern epidemiology. In the Hippocratic times of which we are speaking for example disease was thought to be due to a disturbance of the balance of the four humors,_ blood, phlegm, black bile and yellow bile, which existed in the body. The 3 proportions of these humors was in turn determined by the distribution of various attributes of living matter. These were categorized as being wet or dry, hot or cold. The amounts of wetness or dryness, heat or cold were themselves determined by the proportions of what were considered to be the four elements making up the environment. These elements were earth, water, fire and air. Thus according to these concepts the explanation for the occurrence of disease should be sought in those aspects of the environment which might influence the exposure of people to these four elements. It was therefore perfectly logical, given this theoretical framework, to search for an explanation for disease in the strength of the winds or amount of humidity for example. This concept of disease remained almost unchanged for more than a thousand years. The next major theory about cause of disease occurred in the middle ages when the idea of miasmas was introduced. Miasmas were foul odors, or gases. According to this new theory it was thought that many diseases, in addition to being produced by exposure to different proportions of the elements, as defined by Hippocrates, could be caused by exposure to these miasmas. Many of our modern terms for disease in fact, are still derived from this theory. For example, the word malaria means "mal" - bad, "aria" - air, as originally it was thought that malaria, or the fever of malaria, was caused by exposure to foul smelling air or gases. As the idea of miasmas as a cause of disease became more accepted the variables in the physical environment examined to explain the occurrence of disease changed. Thus many diseases were thought to be due to living in low marshy places or in areas of the city where excreta was thrown indiscriminately into the street. As you might expect, many people living in those circumstances did have high disease rates, but the reasons for the occurrence of such diseases given by the physicians of that day would be very different from those given today. Thus once again the variables invoked as causes of disease were determined by the existing theories. 4 The next major advance in our ideas about causation occurred with the discovery of micro-organisms at the turn of the last century. The classical findings of Pasteur and Koch ushered in a new and very important era in medicine which led to far reaching results. On the one hand these discoveries have led to the tremendous improvements in our ability to treat many diseases and to a marked change in the factors in the environment studied to explain disease. Under the influence of the new micro-organismal theory epidemiological enquiries were now directed towards those aspects in the environment which might be envisioned as "breeding places" for bacteria. Thus attention was (and still is) focused on exposure to contaminated water or food or polluted air for example. Simultaneously however, these discoveries have tended to blind medical thought insofar as ideas about causation of disease are concerned. The new findings were so exciting that for many decades it was thought that knowledge about these micro-organisms and how man came into contact with them was all that needed to be known to understand the cause of disease. This view is still widely prevalent in medical thinking, but gradually the realization has been developing that the presence of a micro-organism is at best only a partial cause and sometimes not even the most important part of a cause of a disease, even an infectious This point of view can perhaps be best illustrated by some examples. About the turn of the century the specific micro-organism responsible for the disease cholera was identified and it was found that people who had this disease excreted large amounts of the cholera bacillus in their stools. Despite this it has never been possible to produce cholera in human volunteers by feeding them cholera bacilli no matter how large a dose that is given. At the most a transient diarrhea occurs but usually there are no symptoms at all. Apparently other things besides the cholera bacillus have to be present before cholera can be produced and these other things are sometimes more important for our understanding of the disease than is the bacillus. In fact, even with our extensive knowledge of the cholera bacillus today we cannot explain why 5 cholera becomes transformed periodically from a minor pestilence of some oriental bazaar to a raging epidemic, and it is unlikely that further study of the bacillus alone will provide us with the answers. As a second example we might think about tuberculosis. The cause of tuberculosis is said to be the tubercle bacillus. In a certain sense that is a useful formulation, but in another sense it is not very useful. It is rather like saying, "the cause of automobile accidents is the automobile". This is undoubtedly true, but the automobile does ether things than cause automobile accidents, and accidents can be caused by things other than the automobile. Intensive study of the tubercle bacillus does not tell us why it is that of a hundred people exposed to the bacillus in the United States only about three will develop tuberculosis. Why do the other 97 not develop the disease even though they had been just as exposed to the tubercle bacillus? How do they differ, these 97 from the three who do get it? Why is it that in other countries, of a hundred people exposed to the tubercle bacillus, ten or 20 or 30 will get the disease tuberculosis? Why is it that in more and more people who are developing the disease tuberculosis today, we cannot find the tubercle bacillus? We find some other bacillus which we call "atypical" tubercle bacilli, but it seems to be the same disease. Thus to consider the tubercle bacillus as "the cause" of tuberculosis is useful up to a point, but beyond that point it is net very useful. To understand the limitations of the microbiological model of the cause of disease it is necessary to realize that the science of bacteriology and from it most of the science of medicine has developed in a very peculair fashion, outside the main stream of development of other sciences. Specifically this is the only science which classified the object is its study, bacteria, as good or bad. No physicists classifies his atoms as good or bad, nor do chemists classify their elements as good or bad. But we as physicians classify bacteria as "good", that 6 is bacteria that do no harm or are beneficial, or "bad", that is pathogenic. One of the most eminent microbiologists in this country, a man called Rene DuBos of the Rockefeller Institute has advanced a rather ingenious theory to explain why this is so. He suggests that in nature man occupies the pinnacle of the pecking order, that is he can eat anything on this earth and not be eaten by any other animal. In this he is different from all other animals who can eat some and be eaten by others. The one living species over which we have no control however are the microorganisms. In DuBos" view this lack of control has been responsible for microbiology developing this pattern of classifying bacteria as good or bad. Whether this explanation is adequate or not it becomes necessary to consider the question, what makes a microbe good or bad? The particular bacillus that sours the French peasant's milk and makes very delicious cheese is a good bacillus, without which he could not make his cheese. That same bacillus sours your milk here in the refrigerator and therefore is a bad bacillus, an evidence of unsanitary habits. A hundred years ago tulip growers concentrated on a mottled red and white variety of tulip which was the most prized type. This mottling occurred when a particular virus lived in association with the tulip. A number of years later mottled tulips were no longer the fashion and people demanded solid colors- reds, whites, yellows, and so on. Suddenly then this virus which previously had been eagerly sought after became a "bad" virus, and tulips were sprayed to get rid of it. The virus had not changed, but our ideas of what was good or bad had. Or consider the virus which "causes" poliomyelitis. A hundred years ago it was neither good nor bad. People were exposed to the virus but poliomyelitis occurred very infrequently and paralysis was very rare indeed. In the course of a hundred years the virus as far as we know has not changed, but suddenly polio has become a major crippling disease of young adults and children. We have changed, not the virus. The same may be said of infectious hepatitis. Man has probably been exposed to the virus for many centuries but only in the last ten to fifteen years have we started seeing major epidemics 7 of this disease. We will not be able to explain these phenomena by only studying the virus concerned. The development of the germ theory of disease had a further unfortunate consequence for epidemiology. Believing that the answers to the causation of disease had been found, epidemiological investigations became more restricted in their scope. Prior to this time the questions for which epidemiology had sought answers were concerned with identifying the factors in the way of life of people which increased their risk of developing disease. Subsequent to the discovery of bacteria most studies have become concerned only with the identification of the means and vehicle of infection in a specific outbreak in an attempt to control that outbreak. Thus epidemiology changed its emphasis from a research or investigative science to an applied technology. As such it performed some very useful functions and doubtlessly was responsible for saving many lives, but it ceased, for a number of decades at least, to add to our knowledge concerning factors responsible for disease. Unfortunately it is this infectious disease "epidemic fighting" function of epidemiology which has become the prevailing concept of the discipline and which, in my opinion, is one of the least important of its potential contributions. Over the past twenty to thirty years there has been a resurgence of interest, in the contributions epidemiology, as an investigative science, can make to understanding disease process. Through such understanding it is hoped rational_ leads for intervention can be developed. This re-awakening of interest has occurred simultaneously with a growing realization of the limited utility of the rigid micro-organismal model of disease causation. In addition to the factors mentioned previously which tend to cast some doubts on the usefulness of this model, two further developments in the field of health have occurred which make a more sophisticated theory imperative. The first of these developments has been the dramatic increase in the non infectious chronic diseases as major causes of death and disability in modern industrialized 8 society. This change in the nature of our major health problems had only occurred over the last 40-50 years. During this period the diseases which for thousands of years have been the cripplers and killers of mankind have decreased to their lowest point in human history, but have been replaced by a set of new diseases. Coronary heart disease, lung cancer, diabetes, arthritis and mental disorders for example may have occurred before, but never to the extent that we are seeing them today. The micro-organismal model of causation gives us very little help in suggesting the factors we need search for to explain these modern "plagues." The second development is that it is becoming increasingly clear that we cannot explain the occurrence of disease solely in terms of man's relationship to his physical environment. A very important factor is man's relationship to other people, that is his relationship to his human environment. Here also the theory which only postulates that exposure to a micro-organism is the cause of disease is of very little use in determining what social or cultural factors, that is human environmental factors, need to be studied to understand disease occurrence. How then does this micro-organismal theory need to be modified to make it more useful for our purposes, that is for the prevention and treatment of disease? First of all it is necessary to recognize that inherent in the micro-organismal theory of disease is the idea that there is a single cause whether this be a micro-organism or some other agent for each disease, that each disease has its cause and each cause has its disease. This concept of a single cause we no longer find at all useful in any disease. The lack of utility of any single cause theory can be easily illustrated by considering a disease like cancer of the breast. This is a useful disease to study in terms of "cause" because we can produce it very easily in certain experimental animals - mice. It has been found that strains of mice extremely susceptible to breast cancer can be bred. Breast cancer occurs very infrequently under normal circumstances in mice, but by selective breeding a strain can be bred in which 60 to 70, 9 sometimes as high as 80, per cent of the offspring will develop breast cancer. Thus it is possible to postulate a genetic factor, something passed down through the genes as a "cause" of breast cancer. Ii., has also been found that if these genetically susceptible mice are taken from their mother's breast at birth, and allowed to suckle from a mother who is from a non-susceptible strain, such mice will not develop breast cancer. The explanation for this is that the susceptible mothers excrete a virus in their breast milk which has to be present for the breast cancer to develop in their offspring. So a virus is implicated in the cause of breast cancer. Baby mice who are born from non susceptible mothers however and are allowed to suckle from susceptible mothers (that is are fed on the milk containing this virus) do not develop breast cancer. Furthermore not all mice born of susceptible mothers and suckled by these mothers from birth develop breast cancer. This only develops in female offspring, not in the males. If female sex hormone (estrogen) is injected into such male offspring shortly after birth however, they too will develop breast cancer. Thus a third factor - a hormonal factor may also be thought of as a "cause" of breast cancer. Finally, mice in which all three factors are present, that is they have been bred and suckled by genetically susceptible mothers and are themselves female, who are then placed on a restricted caloric intake rarely develop breast cancer. Now in terms of a single cause theory, what is "the cause" of breast cancer in mice? Is it caused by genetic transmission or by a virus or by a particular hormone or by dietary factors? Obviously no single factor is the cause; all four factors have to be present for breast cancer to develop and any attempt to say the cause of breast cancer in mice is genetic or is viral for example, is obviously not very useful. Thus we have to change our thinking from a single causal theory to a multi-causal theory recognizing that many factors can cause any particular disease, and that what may be causal under certain circumstances may not he causal under others. 10 Even the acceptance of a multi-causal theory however is not sufficient for our purposes in trying to understand the causes of any disease. We have to pose the further question - for what purpose do we want to understand causes? Are we concerned with the causes responsible for the onset of the disease, that is the causes responsible for making a person sick or are we concerned with the causes responsible for recovery from this disease. These factors, those responsible for the onset of disease and those causing recovery may be, and frequently are, very different. An elementary illustration may make this clearer. We have many theories about the causes of onset of coronary heart disease. These include the amount of fat in the diet, the amount of exercise taken, the amount of cigarettes smoked, the level of blood pressure, genetic factors and so on. Whatever the particular causes, let us consider two men each of whom has a heart attack as a result of the same causes and let us assume that each has the same amount of damage to his heart by virtue of this attack. Despite this we know from clinical experience that one of these men may be an invalid in bed for the rest of his life and the other man can be someone like ex-president Eisenhower, completely capable of undertaking the strenuous task of directing a country. Thus even though they may have had identical conditions leading to the onset of their disease, there are very different conditions determining their recovery. In other words although it is true that water quenches fire, the cause of fire is not necessarily lack of water. There is one further aspect of "cause" that must be taken into consideration for fuller understanding of disease process. For both types of causes, those responsible for onset and those responsible for recovery from disease, we should be concerned with questions of "how" and questions of "why". How does a person develop diabetes for example, would be answered by "some disturbance in insulin metabolism". Our knowledge of the relationship between this disturbed insulin metabolism and the disease we call diabetes however does not tell us why this patient at this point in time developed this disorder. If, in addition or our 11 knowledge about the relationship of insulin metabolism to diabetes, we knew for example that immigrants to a new country develop the diabetes rates of that country to the same extent as they absorb some of the customs of the new country, and if we knew what these customs were, we would be getting some clues that could help us answer these why questions. These customs might include changed dietary habits, exercise habits and the amount and types of emotional strain. These causal factors would tell us something about why or under what circumstances people develop diabetes and thus increase our knowledge about what needs to be changed to prevent new cases occurring. It is in the identification of this category of causes that epidemiology, in our opinion, has its major contribution to make. Perhaps the relevance and importance of these points can be made more clear by an illustration. To do this I would like to present, very briefly, some data from a modern epidemiological study of a disease which has traditionally been explained on the basis of one cause. I think it will become evident how much more can be learned about this disease if the questions are posed and the results interpreted within this broader theoretical framework. The disease I have selected is tuberculosis and the "cause" of tuberculosis, using the more traditional model of causation, would of course be the tubercle bacillus. Knowledge of the role the tubercle bacillus plays in tuberculosis has obviously been very helpful in telling something about how people get sick - they get sick because of the tubercle bacillus, but it tells us very little about how they recover and it tells us nothing at all about why they get sick. As indicated above, the vast majority of people who are exposed to the tubercle bacillus do not develop tuberculosis. To determine why some people who are exposed to the tubercle bacillus develop tuberculosis, it is helpful to seek answers to a prior question, how do people who get tuberculosis differ from those who do not get tuberculosis? 12 One relatively recent study in Seattle, Washington has given some clues to that question. This study started by dividing the city of Seattle into four economic areas. Area 1 was the poorest, with the worst housing and most overcrowding. Area 2 was a little better but it also was poor and had overcrowding. Area 3 was about average for Seattle with somewhat higher property evaluations and Area 4 was the richest, most well to do area of the city. Having divided Seattle into these four areas, the investigators examined the distribution of tuberculosis by area. As might be expected the rates were highest in area 1 (the poorest area) and lowest in area 4 (the richest area) and this was true for both males and females. Examining the distribution by race, they found the same relationship for whites but for non-whites the pattern was almost reversed. The highest rates for non-whites occurred in the richest area both for males and females. The non-whites living in this area were not domestic servants but professional people - doctors, lawyers, business executives and so on. The lowest rates for non-whites occurred in area 2, which in addition to being one of the poorer areas was that part of the city in which non-whites lived in compact neighborhood groups, having many opportunities for inter personal contact and development of friendships. The highest rates for non-whites thus occurred in the area where they were a distinct minority living without opportunity for warm personal contacts with other people. Conversly for whites the rates were highest in those areas in which there were a high proportion of non-white neighborhoods and where the whites had little opportunity for social interaction. The next characteristic examined was residential and job mobility. In contrast to non-tuberculous people those who developed tuberculosis had been characterized by being very highly mobile. They had moved from home to home about five times more frequently than does the average person in the United States and they had had very frequent job changes. The third characteristic 13 was marital status. Fewer of the tuberculous had been married and far more of them had been divorced, or widowed than is true for the population as a whole. Finally, the fourth distinguishing characteristic was that a large proportion of the tuberculous were living alone in one room. To summarize then, we find that the characteristics of the tuberculosis at this point in time are that they are strangers in the neighborhood in which they live, they have had multiple residential and job changes, their marriages are frequently broken (if they have ever been married) and they are living alone. People with these characteristics have been referred to by sociologists as "marginal men". They do not belong, they have few friends, few neighbors that they know well, no kin, and very little contact with fellow human beings. In an effort to determine whether the findings of this study in Seattle had been observed elsewhere, I attempted to review as much of the recent tuberculosis literature as possible. No study was found that had specifically addressed itself to that question but one study did provide corroborative evidence although this was accidental. This was a study done in Britain in which the investigators addressed themselves to the question of the relationship between overcrowding in a home and chance of developing tuberculosis. The authors selected some 14,000 or 15,000 families living in a city and used the living arrangements (less than one person per room, one person per room; or more than one person per room) as an index of crowding. All family members were then x-rayed to find out if the people who were living in houses with more than one person per room had more tuberculosis than the ones who were not crowded. Before analysing the data all lodgers in these homes were eliminated as the authors felt that these would weight the one person per room category. The families were also categorized by social class as it is known that tuberculosis occurs much more frequently in the lower social classes. Their findings indicated increased tuberculosis rates in family members as social class declined but no relationship between tuberculosis and overdrowding in any social class. Fortunately they 14 included, as an appendix, their findings on the lodgers in these families. Despite the fact that the lodgers were living under the same general conditions as the family members, their rates were almost twice as high, particularly in the low social classes. The major difference between lodgers and family members of course is that the lodgers are more likely to be people without families, or kin, living alone, often single, and are lonely people. If the findings of these studies are accepted they pose a number of further questions. How is it possible that these factors can increase the chances of getting tuberculosis? Obviously not all people who are isolated develop tuberculosis even when they are exposed to the bacillus, and therefore what are the differences between isolated people who develop the disease and isolated people who do not develop the disease? What else needs to happen? A further study sheds some light on these questions. In this second study a group of people employed in a TB hospital were all investigated. A group of these employees who had developed tuberculosis was selected and for each person who had developed tuberculosis an employee was found who had not developed tuberculosis but who was in other respects as similar to the employee with tuberculosis as possible. Thus each tuberculosis employee was matched with a non-tuberculosis employee of the same race, age, sex, date of employment, type of work, result of the tuberculin test at the beginning of employment, appearance of the first x-ray, presence or absence of any other significant disease, marital status, income and history of alcoholism. In other words, the two groups were as far as possible identical except that one group had developed tuberculosis and one had not, although both had had exposure to the tubercle bacillus as a result of working in a T.B. Hospital. In each group the number of situations which were likely to produce stress over the previous ten years was measured. These stress factors included economic factors like financial 15 worry and loss of job and social and personal factors like marital stress, social withdrawal, personal crises and so on. It was found that the actual number of such stressful situations did not differ in the two groups, but the distribution of these stresses over time did differ very markedly. In the first group, that is those who did not develop tuberculosis, the stressful situations were distributed randomly, some years being relatively free of such situations and some years having multiple stress situations. In the tuberculous group however, the stressful situations mounted in a crescendo like fashion, each year being worse than the previous one. These situations reached a peak about 1 to 2 years before tuberculosis was diagnosed. Thus it appears that people exposed to mounting life stress who are deprived of help and support from society who have no friends, or kin, that is no one interested in them, have to handle these threats unaided. One of the consequences is the disease we call tuberculosis. A further question that would follow from such a formulation might be why tuberculosis? There is evidence to show that tuberculosis is not the only deleterious consequence of such a set of circumstances. People who develop schizophrenia and who commit suicide for example have very similar characteristics to those who develop tuberculosis. In order to develop tuberculosis some additional factors must therefore be present. Some of these factors have been tentatively identified in yet another study from Seattle. In this study a group of tuberculosis patients in a hospital were investigated to determine the relationship between their hormone balance and their recovery from tuberculosis. The hormones being measured are produced by the adrenal gland and called the 17-keto-steroids. It was found that there were wide fluctuations in the levels of this hormone in different patients and that there was a close relationship between the emotional state of the patient and the level of his hormone. Those patients who had very low levels of hormone tended to be apathetic, depressed, withdrawn, and feel hopeless. The closer the hormone level came to the normal for 16 their age and sex the more the patients tended to be calm, contented and well-adjusted to their situation. The patients who had very high levels tended to show the classical signs of anxiety, restlessness, aggressiveness, hostility, fearfulness and a refusal to stay in bed. Under adequate therapy those patients whose levels were nearest normal tended to recover fastest. Those patients whose level was lowest tended to die and those patients whose levels were highest tended neither to recover nor die, but become chronic. If the emotional state of the patient was changed, the hormone level would also change as would the response to tuberculosis. Thus if an apathetic, withdrawn patient was made more calm and contented his level of hormone tended to rise and his chance of recovery from tuberculosis improved. Thus it is now possible to reformulate our concept of the causes of tuberculosis. Exposure to mounting life stresses in people deprived of emotional support from society will lead to their being overwhelmed with a resulting increase in depression and apathy. Such emotional states may lead to an alteration in hormone balance which increases susceptibility to the tubercle bacillus. If any of these factors are missing, tuberculosis is unlikely to occur. For example those people having similar mounting life stresses who are well integrated in society, who can get support from a wife or a husband, or from neighbors or from kin, are not likely to become so depressed and apathetic and withdrawn and thus would not have the alteration in their hormone level. Exposure to the tubercle bacillus would therefore not be followed by tuberculosis. This illustration was deliberately selected fcr a disease of traditional concern to epidemiology, namely an infectious disease. The reason for this selection was to indicate, as dramatically as possible, that if modern epidemiology has a contribution to make in increasing our understanding of such diseases where so much is already known, it has an even greater potential contribution in the study of conditions for which little at present is known. Thus not only can all 17 "diseases" in the traditional sense be studied by epidemiological methods, non-infectious chronic diseases as well as infectious, but many other states of health are amenable to such investigation- For example epidemiological studies have been conducted on accidents, industrial absenteeism, fetal survival and growth and maturation. In addition there is growing realization that various psychological factors including behavior development, emotional state and intelligence can be studied in a similar fashion Finally it is our belief that increased understanding of the various manifestations of social maladjustment, including for example delinquency, chronic dependency and criminality can also be gained through epidemiological investigation. For all such conditions the major contribution of epidemiology will be in its ability to elucidate the role of environmental factors, particular factors in the human environment in the causal chain. The most important single factor which up to the present has limited the intelligent application of epidemiological techniques to such problems has been our inability to develop an adequate conceptual scheme indicating the relevant social and cultural processes. Whatever the present limitations of the bacteriological theory of causation, it did, for a time, provide a useful model which led to an intelligent selection of relevant variables in the environment in studying disease. To proceed further and gain understanding of the health role of social and cultural processes we need a. new model which takes into account the modern view of causation and which will indicate the types of social and cultural variables we need to study. To provide such a model requires the closest collaboration of the social and the health sciences and is a task that is at present of central concern to our department of Epidemiology. If the opportunity presents itself, I should very much like to discuss our thinking in this regard with you during the group meetings and obtain your reactions. These views that I have presented on epidemiology can be summarized very 18 briefly. According to our view epidemiology is one of the sciences concerned with the study of the processes which determine or influence the health of people (our definition of health incidentally is very broad and includes social as well as physical and mental health). People live in groups and it is with their health in relation to their behavior in social groups that epidemiology is primarily concerned. Before concluding, I should like, in a few words, to outline the basic strategy or method of epidemiological enquiry. Up to this point, I have been concerned solely with the theoretical basis upon which epidemiology is, or at least should be; founded. Without such a basis it is our opinion that epidemiological investigation is sterile. The theoretical formulations should not be confused however with the methods and techniques by which such investigations are carried out. These methods, while requiring considerable skill for their execution can be simply stated. Essentially epidemiology is an observational science and its methods are similar to those of all observational sciences. The essential element of the method is comparison, and in the case of epidemiology this is in essence a comparison between the characteristics of groups with the condition being studied and the characteristics of groups without the condition. From a knowledge of the similarities and differences between such groups, hypotheses as to the causal processes can be derived. To carry out such studies, data is thus required concerning the state of health or condition being studied, the nature of the group in which the condition is being studied and the habitat or environment of that group. The groups selected for study may vary in size from a single family unit to a total nation. They may also differ in kind, but whether it is an informal relatively intimate group or a formal organized group, the same general principles will apply. Special indices such as incidence and prevalence rates have been developed to quantify these data and describe their distribution, taking into account the differing 19 numbers of people at risk in varying groups and differing lengths of time for which they are observed. Various statistical procedures are required to determine the strength of any associations found to exist between group or habitat characteristics and the state of health being studied. Formal rules have been developed as to the generalizations possible depending on the nature of the sample and the way in which the data were collected. All these factors bear the same relationship to epidemiology that laboratory techniques bear, for example, to bacteriology. They are essential tools without which scientific epidemiological investigation is impossible. A knowledge of these tools however without any grasp of the basic theory leads to pedestrian studies of very limited usefulness. It is my hope that if social workers decide to apply epidemiological methods to a study of their problems, they will address themselves not only to the scientific techniques required, but to the even more challenging area of the development of meaningful conceptual models which can be made operational and tested. It is in this latter area that I see great opportunities for fruitful collaboration between the existing disciplines-of social work and epidemiology.