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Lecture 1a:
Cohort studies: longitudinal follow up studies [exposure occurs BEFORE outcome = exposure à outcome]
• Well define group of individuals who share a common characteristic or experience (e.g. born same year, went to same event)
• Used to find multiple outcomes from a single exposure
• Participants classified according to exposure status and followed up over time [participants are always free of disease initially]
Prospective Vs Retrospective cohort studies:
Case-control study: slide 25
• Examines multiple exposures related to a SINGLE outcome
• Participants selected based on OUTCOME STATUS [except the control subjects don’t have any outcome]
• Participant selection: 1st step= the case definition should be clearly defined to make sure that all cases are based on the same diagnostic criteria [the
criteria specified should include:
1. Person: patient characteristics (age, sex, race, occupation, exclusion criteria)
2. Place
3. Time (period associated with illness onset)
4. Clinical features
Ø Control group: random sample from the general population that gives rise to the cases è recruiting >1 control per case may improve the statistical
power of the study [more than 4 controls per case is not considered to be more efficient]
Lecture 2b:
- When smth fulfils the criteria of a potential confounder what do we do to test if indeed it confounds the exposure-disease relationship
à Calculate crude estimate à stratify and calculate the crude estimate in each strata = pooled risk ratio aka adjusted estimate
è IF the adjusted estimate differs from the crude by 10 % or more then we consider it a confounder
Example:
- Even after the above techniques we can still have some ‘residual confounding’. What are the causes?
Ø Unmeasured confounding (i.e. not all parameters are taken into consideration)
Ø Some confounding categories are too broad
Ø Missclassification in measure of confounder
- What is overadjustment?
- Summary:
- What is bias?
Any systematic error in a study that results in an incorrect estimate of the association between exposure and risk of the disease
2 categories of bias:
1. Information bias
2. Selection bias
Example:
- What is the population attributable risk?
Ø Is the risk in the population that would be eliminated if the exposure were eliminated [PAR= Risk in population – risk in nonexposed]
We change the ‘exposed’ component with the population
Ø If we don’t know the risk in the population à PAR = AR X Proportion of exposed
Example:
- What is the number needed to harm (NNH)? (Aka number needed to treat in order to harm)
= The number of individuals who must be treated so that one of them presents an adverse reaction accountable to treatment
è It should be high as this indicated lesser likelihood of harm relative to the comparator
Example:
- What do we mean by the term efficacy?
à Efficacy is what is measured in trials è can it work?
- What is effectiveness?
à Whether the treatment achieves its goals in real life è does it work in the real world?
When the 95 % CI doesn’t include 0 à we can say that this is statistically significant
SOS:
Lecture 3b: Part II Statistical testing of hypothesis
2. Presence of control group: allow for the study of the effectiveness of the intervention beyond any placebo effects
- In the absence of a control / placebo group à we call it active control (old/conventional treatment) or if we
want to compare doses the control/active group will be the ones receiving the lowest dose
Crossover design: removes patient variation à we can investigate the participants response to either active
intervention AND the control intervention i.e a specific type of RCT where you assess 2 or more interventions. In this
design, all participants receive all the interventions, but the order in which they get the interventions is randomisedè
more study power (precise and efficient results)
- If the wash out period is not adequately performed = carry over effects
- In cross over designs participant drop out increases because participants are followed up over a longer period
of time
When can we NOT use cross over RCTs?
Ø When the treatment cures or totally alleviates the symptom
Ø Treatment persists or has long term effects (leading to carry over effects)
Ø Disease / symptoms have slow or delayed response to treatment
Ø When the outcome is a self-limiting condition
Cluster randomization trials: instead or randomizing individuals we randomize clusters like hospitals, schools,
worksites etc. à used in public health and general practice research (not so much in investigating medical
Lecture 4b: treatments)
Ø Non-randomized trials: only difference with RCT: 2 groups are not created from the sample using
randomization
Ø Non-controlled: only intervention arm (no control group)
3 types of RCTs: [RCTs mainly test therapeutic interventions]
1. Superiority trial: we want to show that the intervention is superior than the standard or control group)
2. Equivalence: shows that 2 treatments are not too different in efficacy
3. Non-inferiority: when we are looking for new treatments that have the same efficacy but demonstrate better quality in other aspects à to show non
inferiority margin: we look at the upper limit of the 95 % CI
In order to prove superiority etc. we need to a have a margin of clinical significance à i.e. the threshold for which the study can claim
superiority/equivalence/non-inferiority
• In order to have statistical significance the 2 confidence intervals should NOT overlap
Hawthorne effect: aka observer bias à when study participants change their normal behavior because they know they are being observed
[minimized by observing participants discretely]
Lecture 4c:
What helps us formulate a good clinical Q?
PICO: Population/Population Intervention Comparator and Outcome
P: patient problem à most important characteristic of the patient
(primary problem, disease, or coexisting condition) sometimes gender,
race and age are also relevant
Systematic reviw: you are systematically reviewinbg and summarizing evidence around a topic à have pre-defined inclusion and exclusion criteria, asses the
quality of included studies, presents the findings etc in a more sophisticated way
Ì Systematic reviews highlight consistency
Strengths of systematic reviews:
How to conduct a
systematic review
Week 5:
- What information does a population pyramid give us?
à The count or percentage of a population by age and sex
à Can also be used to display other data such as disease or a health characteristic by age and sex
Migration People migrate for a range of ‘push’ (natural disasters, war, poverty) and ‘pull’ factors (education and economic prospects
Globalization
Epidemiology of major chronic conditions I: cardiometabolic and cerebrovascular conditions:
SUMMARY:
HIV & AIDS:
Week 8:
Lecture 8a: Infectious disease transmission I
- What characteristics helps us determine the nature of an infection?
Infectivity Ability of an agent to establish an infection in the host, given that the host is exposed to the agent
à refers to the proportion of exposed persons who become infected
Pathogenicity The ability to cause disease in an infected host
à refers to the proportion of infected individuals who develop clinically apparent disease
Virulence Measures the severity of the disease, which can vary from low to high
à Case fatality ratio or Proportion of severe cases out of all cases
Infective dose Amount required to cause infection in susceptible individuals
Reservoir The natural habitat of the agent (humans, animals, environmental sources)
- Human reservoir: variola virus
Source of The person or object from which the host acquires the agent
infection
- What is a carrier?
A person with inapparent infection but who is able to transmit the pathogen to others
- What is cocooning?
à immunizing people who are likely to come into contact with a susceptible person so that the susceptible person is unlikely to be exposed to the
pathogen e.g., adults that will come in contact with newborns < 2 months are advised to take the pertussis vaccine
Lecture 8b: Infectious disease transmission II
- What is public health surveillance?
Public Health Surveillance is the ongoing, systematic collection, analysis, and interpretation of health-related data
Goal: provide information to be used for public health action
- What are the 4 types of surveillance?
- Step 5:
Ø Time: epidemic curves (describe start, peak, end and
Outliers [shape of distribution can give info on the
Nature of disease & mode of transmission]
Ø Place: residence, possible exposure, maps/areas
of risk
Ø Person: distribution of cases by age, sex, exposures
- Step 6: Develop + test hypothesis on pathogen, mode of transmission, source of outbreak, period of interest
à Analytical epidemiology: case control investigations or retrospective cohort investigations
• Case control: compares people with illness with a sample of people without the illness à cannot directly calculate attack rates
• Cohort study: includes all individuals in a confined setting and compare those who were exposed with those not exposed à can calculate attack rate
- Step 8: verify the hypothesis with additional tests Step 9: communicate results Step 10: implement control
measures
Lecture 8c: Infection control
- Where do infections occur?
Ø Health care associated infections (HAI): occurs in a patient in a healthcare facility that is not present or incubating at the time of admission à includes
infections that only become apparent after discharge & occupational infections of staff
Risk factors:
o Very young people (premature babies and very sick children) o Hand washing techniques (inadequate hand washing by
and Very old people (the frail and the elderly) hospital staff, visitors, and patients)
o Present comorbidities o Antibiotics (resistant bacteria)
o Immunocompromised o procedures/Equipment (urinary catheters, central/peripheral
o Length of stay in a healthcare facility Surgery and Wounds venous catheters, respiratory devices)
o High-risk patient care areas (ICU, NICU)
- Notification of infectious diseases: Registered medical practitioners have a statutory duty to notify the ‘proper officer’ at their local council or local
health protection team (HPT) of suspected cases of certain infectious diseases. [ κατάλογος υποχρεωτικά δηλουμένων λοιμωδών νοσημάτων]
Week 9: Epidemiological paradigms: Adult life risk factors, Early Life programming, Life course epidemiology
Adult life risk factors approach Ø Chronic disease is the result of adult behaviors and risk factors
Account for almost 50% of burden of disease
• Smoking
• Poor diet
• Exercise
• alcohol consumption)
Limitations:
- Approach fails to explain many of the geographical and social differentials in chronic disease
- Emphasized an individuals lifestyle as a cause and solution of health problems but ignores broader
determinants of health
Early life programming Early life = duration of pregnancy and first 3 years of life
Ø Fetal origins of adult disease hypothesis: period of gestation has significant impacts on developmental health
• See examples:14- and wellbeing outcomes for an individual ranging from infancy to adulthood
• Stimulus/insult at sensitive period of developmentà permanent effects on structure, physiology +
metabolism è predispose to chronic diseases
Ø Barker hypothesis: intrauterine growth retardation, low birth weight and premature birth have a causal
relationship to the orrigins of HTN, CAD and non-insulin dependent diabetes à early life exposure influence
diseases that occur later in life
Ø Thrifty phenotype hypothesis: in settings in which fetal environment does not match the adult environment à
catch up growth and disconnection between foetal programming à adult environment can predispose adult to
metabolic disease, including obesity and T2D
Potential mechanisms: how can an exposure in utero or postnatal increase risk for a chronic disease in midlife
- Structural changes in organs. – hormonal changes - epigenetic modifications
!! Intergenerational transmission of programmed effects à these effects may be transmitted non-gnomically to
subsequent generations (mechanisms unknown)
Limitations:
- Potential confounders: people whose growth was impaired in untero may continue to be exposed to an
adverse environment in childhood or adulthood
- Later adverse env. May increase the rates of specific chronic disease and not the effects of programming
Life Course epidemiology Ø Long term effects on later health of physical or social exposures that occur during gestation, childhood,
See examples:18 adolescence, young adulthood and later adult life à integrates both biological and social risk processes in all life-
course stages
Ø Critical period model: sees the time window of exposure as key à looking at a particular period of time where
an exposure would lead to [permanent devastating developmental changes while in another period it wouldn’t
have the same severity e.g., fetal alcohol syndrome
o Fetal origins of adult disease hypothesis: one example of critical period model
Ø Accumulation of risk model: adverse exposure early in life increases risk has an additive effect with adverse
influences in later life à focuses mostly on accumulation of exposure throughout life-course
A. Uncoorelated: exposures that have an independent effect on disease risk irrespective of later exposures
B. Coorelated: when exposures are ‘clustered’ or ‘chains of risks’
1. Risk clusteringà accumulation of exposures related to the # of other exposes (often connected to
socioeconomic factors)
2. Chain of risk à sequence of linked exposures that raise disease risk because one negative exposure à
leads to another etc
Week 10.1: Primary prevention
Types of prevention:
PRIMARY SECONDARY TERTIARY
è eliminates the causes of disease or increases resistance to è Interrupts disease process before it Limits the physical &social consequences of
disease à keeps the disease process from being established becomes symptomatic symptomatic disease
- Efforts of primary prevention directed at:
A. Whole population: ‘the population strategy’ è aims to reduce average risk à by shifting the
population to the left
✅ don’t have to identify high risk population
B. People at high risk: ‘the high-risk individual strategy’ èaims to protect susceptible ppl as a result
of a particular exposure
✅ efficient for ppl at greatest risk of a specific disease
❌ requires screening programs to identify high risk (time and costly)
*Sometimes the 2 strategies are combined
- Primary prevention can be implemented via:
I. Health promotion: activities and interventions directed at individuals, families, communities or whole pop à enables them to take greater
control over their health
o Medical or preventive: aim to reduce morbidity and mortality, involves health professionals
o Behavioral change: encourage ppl to adopt healthy behaviors
o Educational: gives knowledge and information, and skills so ppl can make informed choices about their health behaviour
o Empowerment: helps ppl identify their concerns and gain skills and confidence to act upon them
o Social changes: aim is to change the physical, social and economic environment to promote health
- What are the most common theoretical models of behavioral change?
1. Health belief model: before seeking preventive measures, people must believe
§ Severity: disease is serious if acquired
§ Susceptibility: I or my children are at risk of disease
§ Perceived benefit: this measure will prevent the disease
§ Perceived barriers: there are no serious risks or barriers involved in obtaining the preventive measure
è this is used to promote screening
2. Transtheoretical model: ppl don’t change their behaviour dramatically in 1 moment à change is a process and patients have different
counselling and informational needs depending on where they are in this process
3. Theory of planned behavior: explores how ppl form intentions for behaviour change
These intentions are influenced by a person’s attitude and beliefs, the presumed attitudes and beliefs of other important individuals (subjective norms),
and perceived behavioural control
II. Specific protection:
o Diseases: e.g., vaccines, antimicrobial prophylaxis
o Deficiency states: fluoride to prevent dental caries,
o Injuries & toxic exposures: helmets and goggles or other protective equipment
Week 10.2: Secondary disease prevention
- What is secondary prevention?
Interrupts disease process before it becomes symptomatic à aims to reduce the impact of disease or injury that has already occurred by detecting
and treating disease or injury ASAP or slow its progression
Examples:
• regular exams and screening tests to detect disease in its earliest stages (e.g., mammograms to detect breast cancer)
• daily, low-dose aspirins and/or diet and exercise programs to prevent further heart attacks or strokes
- How is early detection of disease achieved in secondary prevention?
I. Screening: occurs in community setting and applied to a population
II. Case finding: occurs in a clinical setting and applied to an individual
àTargeting resources at individuals or groups at high risk of a particular disease à actively searching systematically for at risk people rather
than waiting for them to present with signs or symptoms of active disease
Ø Periodic health examination: Annual checkups: medical Hx, physical exam, FBC, urinalysis, CXR, ECG
Ø Lifetime health monitoring: the idea of modifying the periodic examination to focus only on the conditions that would be most likely to be found
in a person of a given age, gender and family Hx
Ø Health protection packages: Gender and age-appropriate immunisations, screening, and counselling à Performed when patients attend for unrelated
symptoms rather than for a specific preventive purpose
Exceptions requiring specific preventive visits: Pregnant women Babies, infants, children Elderly
- What are health risk assessments?
à Use questionnaires or computer programmes to elicit and evaluate information concerning individuals in a clinical or occupational medical practiceè
these computer algorithms calculate a persons risk age è serve to raise awareness
Data collected include: weight, height, BP, Cholesterol level, previous and present conditions, family Hx, social Hx
Ø Negative predictive value: From all ppl who tested neg on the screening how many are unaffected
When we increase cut off: When we decrease cut off:
decrease the false positives increase the false positives
(specificity increases), (specificity decreases),
increase false negatives decrease false negatives
(decreases sensitivity) (increases sensitivity)
See example: 29-30
Week 12: Predicting and modifying health- related behavior in population groups II: targeting wider determinants
Social epidemiology: branch of epidemiology that studies the social distribution and social determinants of states of health
- What socio-structural factors affect health?
• Social class
• Gender Race/ethnicity