 Epi- is the study of the distribution and determinants of health/disease in populations.

It is the basic science of public health—which means the end goals of epi are found in its application to
control health problems.
 Epidemiologists seek to figure out why a disease develops in some people but not in others.
Underlying premise: disease and ill health are not randomly distributed in human populations, but each
of us has certain characteristics that predispose us to, or protect us from, disease, these characteristics may be
genetic or environmental.
 The basic goal of epidemiology is to identify the causes of disease.
 It is very difficult to PROVE causality with the scientific methods that we apply, so instead…we
usually talk about the factors that are associated with disease—putative risk factors. Risk factors
are factors that increase a person’s risk for disease.
 Major epidemiologic studies that changed public health: 1940s, Flouride Community Intervention Trials, 1949,
Framingham Heart Study, 1954, Salk Vaccine Trial, 1964, Cigarettes and lung cancer.
 Well known risk factors that increase a women’s risk of breast cancer: living in North America, having a
high socioeconomic status, never marrying and being Jewish.
 These are not direct causes—these factors serve to identify more proximate causes. (Never married women are
at increased risk of breast cancer because they are more likely to be childless. Childlessness is associated with less differentiated breast
tissue is more susceptible to carcinogens). Association.
 Proximal—more specific—more close, more narrowed down.
 Proximate—event which is closest to, or immediate responsible for causing.
 Distal cause—usually associated with risk factors
 Early “Causal Theory” for Infectious Diseases—Germ theory: one cause, one disease: Organism is ALWAYS
found with the disease. Organism is NOT BOUND with any other disease. Organism, isolated from one who has the disease and cultured
through several generations, produces the disease.
 Web of causation—disease occurrence can be explained by a complex web of many interconnected
factors, including both host and environmental determinants as well as “agent” (Incorporates notion of
multiple causes of disease).
 Causal pies—sufficient cause, one whole pie, complete causal mechanism that inevitably produces
disease…requires all piece to contribute to disease.
 Component cause—each factor in a sufficient, each piece of the pie.
 Necessary cause—causal component that is a member of every sufficient cause—shows up in every
sufficient cause—a component cause is a member of every sufficient cause.
 Necessary and Sufficient—without this, a disease never develops, and with it, a disease always
develops.
 Necessary and Insufficient—there is a causal component that shows up in every causal pie
“sufficient” can get the disease without completing the causal pie—may be the only reason.
 Unnecessary and Sufficient—causal component does not show up in every sufficient pie, but when
it’s there it makes up the pie and disease occurs.
 Unnecessary and Insufficient—causal component does not show up in every sufficient pie, and when
it’s there is does not cause disease—ineffective complement.
 “Blocking the action of a single component cause stops completion of a sufficient cause—and prevents
disease.”
 How to find a cause—develop a hypothesis, test hypothesis by making comparisons, determine if
association exists and make causal inferences.
 Determine if associations are true: consider alternative explanations—random error, bias,
confounding
 Random error the probability that the observed results are due to chance. (A 2-fold increase in deaths due to car
accidents in people living in rural areas is due to the “luck of the draw.”)
 Bias—a systematic error in the ways the study subjects were selected or the data were gathered. (Sick
people who took Vioxx (and subsequently developed poorer health) might be more willing to participate than people in good health who
took Vioxx).
 Confounding—a distortion in the results that arises from comparing dissimilar groups. (The association
between prenatal infection and schizophrenia in offspring may not be due to an infecting virus causing psychosis, but to use of medications
to treat infection).
 The larger the association, the more likely the exposure is causing the disease.
 Strong associations are more likely to be causal because they are unlikely to be entirely to biased and
confounding.
 Weak associations may be causal but it is harder to rule out bias and confounders.
 Association is observed repeatedly in different persons, places, times and circumstances.
 Replicating the associations, in different samples and with different study designs and different
investigators gives evidence of causation.
 Koch postulates (The microorganism will occur in every case of disease and can explain the pathology and clinical changes associated
with the disease). Causal specificity—one to one relationship between cause and disease) The microorganism must be shown to be distinct
from any others that might be found with the disease and is not found with any other disease. If microorganism is isolated and repeatedly
grown in culture, it will induce a new case of disease in a susceptible animal.
 Measures of Disease Occurrence—number of people affected by diseases, size of the population from
which cases arise, length of time that the population is followed.
 Types of calculation—proportion, division of 2 related numbers; numerator is a subset of denominator—
rate, division of two numbers; time is always in numerator—ratio, division of 2 unrelated numbers.
 Incidence—cumulative incidence: proportion of a candidate population that becomes diseased over a
specified period of time.
o Average risk of getting a disease over a certain period (risk=probability of getting a disease)
o # new cases/population at risk in a given time
 Incidence—incidence rate: occurrence of new cases of disease that arise during person-time of
observations
o # new cases/person-time at risk
 Point prevalence—current prevalence
 Period prevalence—prevalence is prevalence in a one-year period
 Cumulative incidence—proportion, 0-1, new cases (research on causes, prevention, & tx of disease)
 Incidence rate—true rate, 1/time, 0-infinity, new cases (research on causes, prevention & tx of disease)
 Prevalence—proportion, 0-1, existing cases, resource planning
 Measures of disease frequency: crude-mortality rate, cause specific mortality rate, age specific mortality rate, years of potential
life lost, live birth rate, infant mortality rate, case fatality rate, survival rate.
 Odds- P/1-P …#new cases/#without disease
 We need the data because they tell us something about the burden of disease—help us project over tome,
prevalence, incidence, disease-specific mortality—they tell us something about the distribution of
disease (comparisons)
 Comparisons are crucial…how do we compare? Make sure we are comparing two things that are similar (same time
periods, adjusted/crude, etc.)--Difference between two risks or rates (excess risk)—proportionate increase in risk or rate (ratio measures)
 Hill’s Causal Criteria—Strength of Association (mentioned before)
o Consistency—Associations observed repeatedly by different people in different geographic
areas, circumstances and times are more likely to be causal. (Associations between cell phone use and brain
cancer were found in European studies, but not replicated in the US. Why Not?)
o Specificity—one cause for each disease—single exposure—should cause disease
o Temporarily—exposure precedes disease…this is the most important criterion (Prospective studies do
a good job establishing the correct temporal relationship between an exposure and a disease). A prospective cohort study of
smokers & non-smokers starts with two groups when they are healthy and follows them to determine the occurrence of
subsequent lung cancer.
o Biological Gradient—Dose response—the higher the exposure, the higher the risk of disease.
o Plausibility—there should be an existing biological or social model to explain the association.
(Cigarettes contain many carcinogenic substances).
o Coherence—The cause-effect interpretation should not seriously conflict with generally know
facts of the natural history and biology of the disease. (Suicide and antidepressants: rise in rates of suicide in
adolescents, behavioral changes in lab animals associated with drugs that affect serotonin levels).
o Experiment—RCT, also includes examination of cessation of exposure.
o Analogy—similarities between the observed association and any other associations. (Maternal rubella
and birth defects, so can accept another possibility that another viral disease during pregnancy can have negative implications for
offspring.)