Download John Cassel, The potentialities and limitations of epidemiology

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
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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
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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.
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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
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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
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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
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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
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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,
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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.
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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
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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?
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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
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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
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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
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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
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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
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"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
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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
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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.