Association refers to a relationship between two or more variables, which can be positive or negative. Causation implies that one variable leads to or causes another dependent variable. It is important to distinguish between association and causation to determine if a risk factor truly causes a disease. Several criteria must be evaluated to judge causality, including temporal relationship, strength of association, dose-response effect, consistency of findings, biological plausibility, and consideration of alternative explanations. Modern diseases often have multiple interacting factors (multifactorial causation) that contribute to development of disease. Rothman's component cause model represents diseases as having multiple sufficient causes, each composed of several necessary component causes.
Concept of Association, Causation and Correlation
Association - Spurious, Indirect & Direct
Multi-factorial causation
Guidelines for Judging causality
Additional Criteria for Judging causality
A principal aim of epidemiology is to assess the cause of disease. However, since most epidemiological studies are by nature observational rather than experimental, a number of possible explanations for an observed association need to be considered before we can infer a cause-effect relationship exists.
Concept of Association, Causation and Correlation
Association - Spurious, Indirect & Direct
Multi-factorial causation
Guidelines for Judging causality
Additional Criteria for Judging causality
A principal aim of epidemiology is to assess the cause of disease. However, since most epidemiological studies are by nature observational rather than experimental, a number of possible explanations for an observed association need to be considered before we can infer a cause-effect relationship exists.
this presentation takes you through the concept of association observed between variables in a study and how could it become a causative association in step-wise manner.Exemplify using Bradford hill criteria. slides after references are extra slides not covered in the presentation.
Lecture for Post and Undergraduate.
From the past two decades Non Communicable diseases are increasing in both developing and developed countries due to which developing are experiencing double burden of diseases.
CM 1.3 Agent Host and environmemtal factors ,epidemiological triad ,multi fac...Anjali Singh
This lecture is for the First Year Students -Agent Host and environmental factors(CM3.1) -Causation of disease has given various concepts- ranging from older theories to modern theories
Older theories started from 10,000 years ago back till the early 19th century which was based on supernatural theory, bad air, living things generation form non-living things
These theories were followed by the germ theory of disease given in 1960 by Louis Pasteur when he demonstrated the presence of bacteria in the air and disapproved of the spontaneous generation of disease
1873 advanced germ theory was established
1877 Robert Koch showed that anthrax is caused by bacteria
After that gonococcus, typhoid cholera, TB, and diphtheria bacterium were discovered and finally, medicine shed the dogma of magic and superstition and wore the robe of scientific knowledge
this presentation takes you through the concept of association observed between variables in a study and how could it become a causative association in step-wise manner.Exemplify using Bradford hill criteria. slides after references are extra slides not covered in the presentation.
Lecture for Post and Undergraduate.
From the past two decades Non Communicable diseases are increasing in both developing and developed countries due to which developing are experiencing double burden of diseases.
CM 1.3 Agent Host and environmemtal factors ,epidemiological triad ,multi fac...Anjali Singh
This lecture is for the First Year Students -Agent Host and environmental factors(CM3.1) -Causation of disease has given various concepts- ranging from older theories to modern theories
Older theories started from 10,000 years ago back till the early 19th century which was based on supernatural theory, bad air, living things generation form non-living things
These theories were followed by the germ theory of disease given in 1960 by Louis Pasteur when he demonstrated the presence of bacteria in the air and disapproved of the spontaneous generation of disease
1873 advanced germ theory was established
1877 Robert Koch showed that anthrax is caused by bacteria
After that gonococcus, typhoid cholera, TB, and diphtheria bacterium were discovered and finally, medicine shed the dogma of magic and superstition and wore the robe of scientific knowledge
Causation. A number of models of disease causation have been proposed. Among the simplest of these is the epidemiologic triad or triangle, the traditional model for infectious disease. The triad consists of an external agent, a susceptible host, and an environment that brings the host and agent together.
The Presentation explains basic models of disease causation, to understand the etiology or causes of disease & altered production and helps to understand the applicability of causal criteria applied to epidemiological studies.
Models of Causal RelationshipsDrawing upon the concepts presente.docxroushhsiu
Models of Causal Relationships
Drawing upon the concepts presented earlier in the chapter, this section introduces models of disease causation. Relationships between suspected disease-causing factors and outcomes fall into two general categories: not statistically associated and statistically associated.15 Among statistical associations are non-causal and causal associations. Possible types of associations are formatted in Figure 9–2.
We have already considered the role of statistical significance in evaluating an association and noted that evaluation of statistical significance is used to rule out the operation of chance in producing an observed association; a nonstatistically associated (independent) relationship is shown in box A of the diagram (left side).
FIGURE 9–2 Map of possible associations between disease-causing factors and outcomes.
Source: Data from B MacMahon and TF Pugh, Epidemiology Principles and Methods. Boston, MA: Little, Brown and Company; 1970.
As shown in Figure 9–2, a statistical association may be either noncausal or causal. What is meant by a noncausal (secondary) association? Suppose factor C is related to disease outcome A. The association may be due to the operation of a third factor B that is related to both C and A. Thus, the association between C and A is secondary to the association of C with B and C with A. For example, periodontal disease (C) is associated with chronic obstructive pulmonary disease (A).16 One possible explanation for this association is the secondary association
of smoking (B) with both periodontal disease (C) and chronic obstructive pulmonary disease (A). This model suggests that the increased risk of chronic obstructive pulmonary disease associated with periodontal disease is related to the role that smoking may play as a cofactor in both conditions. Here is a map of a secondary association: C ← B → A.1
With respect to causal associations, the relationship between factor and outcome may be indirect or direct. An indirect causal association involves the operation of an intervening variable, which is a variable that falls in the chain of association between C and A. An illustration of an indirect association is the postulated relationship between low education levels (C) and obesity (A) among men.17 Men who have lower education levels tend to be more obese than those who have higher education levels. It is plausible that the relationship between C and A operates through the intervening variable of lack of leisure time physical activity (B). An indirect association involves an intervening variable in the association between C and A. This relationship may be formatted as follows: C → B → A.1 Note that the arrow between C and B has been reversed in contrast with an indirect noncausal association.
Multiple Causality
The foregoing section provided models of causality that employ more than one factor. As stated earlier in this chapter, the measure risk difference implies multivariate causality ...
Title: Sense of Smell
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the primary categories of smells and the concept of odor blindness.
Explain the structure and location of the olfactory membrane and mucosa, including the types and roles of cells involved in olfaction.
Describe the pathway and mechanisms of olfactory signal transmission from the olfactory receptors to the brain.
Illustrate the biochemical cascade triggered by odorant binding to olfactory receptors, including the role of G-proteins and second messengers in generating an action potential.
Identify different types of olfactory disorders such as anosmia, hyposmia, hyperosmia, and dysosmia, including their potential causes.
Key Topics:
Olfactory Genes:
3% of the human genome accounts for olfactory genes.
400 genes for odorant receptors.
Olfactory Membrane:
Located in the superior part of the nasal cavity.
Medially: Folds downward along the superior septum.
Laterally: Folds over the superior turbinate and upper surface of the middle turbinate.
Total surface area: 5-10 square centimeters.
Olfactory Mucosa:
Olfactory Cells: Bipolar nerve cells derived from the CNS (100 million), with 4-25 olfactory cilia per cell.
Sustentacular Cells: Produce mucus and maintain ionic and molecular environment.
Basal Cells: Replace worn-out olfactory cells with an average lifespan of 1-2 months.
Bowman’s Gland: Secretes mucus.
Stimulation of Olfactory Cells:
Odorant dissolves in mucus and attaches to receptors on olfactory cilia.
Involves a cascade effect through G-proteins and second messengers, leading to depolarization and action potential generation in the olfactory nerve.
Quality of a Good Odorant:
Small (3-20 Carbon atoms), volatile, water-soluble, and lipid-soluble.
Facilitated by odorant-binding proteins in mucus.
Membrane Potential and Action Potential:
Resting membrane potential: -55mV.
Action potential frequency in the olfactory nerve increases with odorant strength.
Adaptation Towards the Sense of Smell:
Rapid adaptation within the first second, with further slow adaptation.
Psychological adaptation greater than receptor adaptation, involving feedback inhibition from the central nervous system.
Primary Sensations of Smell:
Camphoraceous, Musky, Floral, Pepperminty, Ethereal, Pungent, Putrid.
Odor Detection Threshold:
Examples: Hydrogen sulfide (0.0005 ppm), Methyl-mercaptan (0.002 ppm).
Some toxic substances are odorless at lethal concentrations.
Characteristics of Smell:
Odor blindness for single substances due to lack of appropriate receptor protein.
Behavioral and emotional influences of smell.
Transmission of Olfactory Signals:
From olfactory cells to glomeruli in the olfactory bulb, involving lateral inhibition.
Primitive, less old, and new olfactory systems with different path
These lecture slides, by Dr Sidra Arshad, offer a quick overview of physiological basis of a normal electrocardiogram.
Learning objectives:
1. Define an electrocardiogram (ECG) and electrocardiography
2. Describe how dipoles generated by the heart produce the waveforms of the ECG
3. Describe the components of a normal electrocardiogram of a typical bipolar leads (limb II)
4. Differentiate between intervals and segments
5. Enlist some common indications for obtaining an ECG
Study Resources:
1. Chapter 11, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 9, Human Physiology - From Cells to Systems, Lauralee Sherwood, 9th edition
3. Chapter 29, Ganong’s Review of Medical Physiology, 26th edition
4. Electrocardiogram, StatPearls - https://www.ncbi.nlm.nih.gov/books/NBK549803/
5. ECG in Medical Practice by ABM Abdullah, 4th edition
6. ECG Basics, http://www.nataliescasebook.com/tag/e-c-g-basics
Prix Galien International 2024 Forum ProgramLevi Shapiro
June 20, 2024, Prix Galien International and Jerusalem Ethics Forum in ROME. Detailed agenda including panels:
- ADVANCES IN CARDIOLOGY: A NEW PARADIGM IS COMING
- WOMEN’S HEALTH: FERTILITY PRESERVATION
- WHAT’S NEW IN THE TREATMENT OF INFECTIOUS,
ONCOLOGICAL AND INFLAMMATORY SKIN DISEASES?
- ARTIFICIAL INTELLIGENCE AND ETHICS
- GENE THERAPY
- BEYOND BORDERS: GLOBAL INITIATIVES FOR DEMOCRATIZING LIFE SCIENCE TECHNOLOGIES AND PROMOTING ACCESS TO HEALTHCARE
- ETHICAL CHALLENGES IN LIFE SCIENCES
- Prix Galien International Awards Ceremony
New Directions in Targeted Therapeutic Approaches for Older Adults With Mantl...i3 Health
i3 Health is pleased to make the speaker slides from this activity available for use as a non-accredited self-study or teaching resource.
This slide deck presented by Dr. Kami Maddocks, Professor-Clinical in the Division of Hematology and
Associate Division Director for Ambulatory Operations
The Ohio State University Comprehensive Cancer Center, will provide insight into new directions in targeted therapeutic approaches for older adults with mantle cell lymphoma.
STATEMENT OF NEED
Mantle cell lymphoma (MCL) is a rare, aggressive B-cell non-Hodgkin lymphoma (NHL) accounting for 5% to 7% of all lymphomas. Its prognosis ranges from indolent disease that does not require treatment for years to very aggressive disease, which is associated with poor survival (Silkenstedt et al, 2021). Typically, MCL is diagnosed at advanced stage and in older patients who cannot tolerate intensive therapy (NCCN, 2022). Although recent advances have slightly increased remission rates, recurrence and relapse remain very common, leading to a median overall survival between 3 and 6 years (LLS, 2021). Though there are several effective options, progress is still needed towards establishing an accepted frontline approach for MCL (Castellino et al, 2022). Treatment selection and management of MCL are complicated by the heterogeneity of prognosis, advanced age and comorbidities of patients, and lack of an established standard approach for treatment, making it vital that clinicians be familiar with the latest research and advances in this area. In this activity chaired by Michael Wang, MD, Professor in the Department of Lymphoma & Myeloma at MD Anderson Cancer Center, expert faculty will discuss prognostic factors informing treatment, the promising results of recent trials in new therapeutic approaches, and the implications of treatment resistance in therapeutic selection for MCL.
Target Audience
Hematology/oncology fellows, attending faculty, and other health care professionals involved in the treatment of patients with mantle cell lymphoma (MCL).
Learning Objectives
1.) Identify clinical and biological prognostic factors that can guide treatment decision making for older adults with MCL
2.) Evaluate emerging data on targeted therapeutic approaches for treatment-naive and relapsed/refractory MCL and their applicability to older adults
3.) Assess mechanisms of resistance to targeted therapies for MCL and their implications for treatment selection
ARTIFICIAL INTELLIGENCE IN HEALTHCARE.pdfAnujkumaranit
Artificial intelligence (AI) refers to the simulation of human intelligence processes by machines, especially computer systems. It encompasses tasks such as learning, reasoning, problem-solving, perception, and language understanding. AI technologies are revolutionizing various fields, from healthcare to finance, by enabling machines to perform tasks that typically require human intelligence.
Lung Cancer: Artificial Intelligence, Synergetics, Complex System Analysis, S...Oleg Kshivets
RESULTS: Overall life span (LS) was 2252.1±1742.5 days and cumulative 5-year survival (5YS) reached 73.2%, 10 years – 64.8%, 20 years – 42.5%. 513 LCP lived more than 5 years (LS=3124.6±1525.6 days), 148 LCP – more than 10 years (LS=5054.4±1504.1 days).199 LCP died because of LC (LS=562.7±374.5 days). 5YS of LCP after bi/lobectomies was significantly superior in comparison with LCP after pneumonectomies (78.1% vs.63.7%, P=0.00001 by log-rank test). AT significantly improved 5YS (66.3% vs. 34.8%) (P=0.00000 by log-rank test) only for LCP with N1-2. Cox modeling displayed that 5YS of LCP significantly depended on: phase transition (PT) early-invasive LC in terms of synergetics, PT N0—N12, cell ratio factors (ratio between cancer cells- CC and blood cells subpopulations), G1-3, histology, glucose, AT, blood cell circuit, prothrombin index, heparin tolerance, recalcification time (P=0.000-0.038). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and PT early-invasive LC (rank=1), PT N0—N12 (rank=2), thrombocytes/CC (3), erythrocytes/CC (4), eosinophils/CC (5), healthy cells/CC (6), lymphocytes/CC (7), segmented neutrophils/CC (8), stick neutrophils/CC (9), monocytes/CC (10); leucocytes/CC (11). Correct prediction of 5YS was 100% by neural networks computing (area under ROC curve=1.0; error=0.0).
CONCLUSIONS: 5YS of LCP after radical procedures significantly depended on: 1) PT early-invasive cancer; 2) PT N0--N12; 3) cell ratio factors; 4) blood cell circuit; 5) biochemical factors; 6) hemostasis system; 7) AT; 8) LC characteristics; 9) LC cell dynamics; 10) surgery type: lobectomy/pneumonectomy; 11) anthropometric data. Optimal diagnosis and treatment strategies for LC are: 1) screening and early detection of LC; 2) availability of experienced thoracic surgeons because of complexity of radical procedures; 3) aggressive en block surgery and adequate lymph node dissection for completeness; 4) precise prediction; 5) adjuvant chemoimmunoradiotherapy for LCP with unfavorable prognosis.
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Ve...kevinkariuki227
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
Report Back from SGO 2024: What’s the Latest in Cervical Cancer?bkling
Are you curious about what’s new in cervical cancer research or unsure what the findings mean? Join Dr. Emily Ko, a gynecologic oncologist at Penn Medicine, to learn about the latest updates from the Society of Gynecologic Oncology (SGO) 2024 Annual Meeting on Women’s Cancer. Dr. Ko will discuss what the research presented at the conference means for you and answer your questions about the new developments.
- Video recording of this lecture in English language: https://youtu.be/lK81BzxMqdo
- Video recording of this lecture in Arabic language: https://youtu.be/Ve4P0COk9OI
- Link to download the book free: https://nephrotube.blogspot.com/p/nephrotube-nephrology-books.html
- Link to NephroTube website: www.NephroTube.com
- Link to NephroTube social media accounts: https://nephrotube.blogspot.com/p/join-nephrotube-on-social-media.html
Anti ulcer drugs and their Advance pharmacology ||
Anti-ulcer drugs are medications used to prevent and treat ulcers in the stomach and upper part of the small intestine (duodenal ulcers). These ulcers are often caused by an imbalance between stomach acid and the mucosal lining, which protects the stomach lining.
||Scope: Overview of various classes of anti-ulcer drugs, their mechanisms of action, indications, side effects, and clinical considerations.
Ozempic: Preoperative Management of Patients on GLP-1 Receptor Agonists Saeid Safari
Preoperative Management of Patients on GLP-1 Receptor Agonists like Ozempic and Semiglutide
ASA GUIDELINE
NYSORA Guideline
2 Case Reports of Gastric Ultrasound
2. Why is Association & Causation
important?
To decide if a factor A causes disease B or not!
Is the link true or only facile?
Is it true or by chance?
If we know the cause(s) we can cure/treat
/prevent/minimize the illness. (in a patient or the
society)
2
3. Association & Causation
Association
Relation between two or more
variables
Generally found in snapshot
(cross-sectional) studies
Relationships can be positive or
negative
Correlation! (factors moving
together– like poverty and under
nutrition)
Causation
A variable (s) lead to another
variable that is dependent/
outcome/ event/disease
So it suggests Etiology of
disease
We need analytical studies to
find out/prove cause(s)
3
4. Associatio
n
Defined as occurrence of two variables more often than would be
expected by chance.
An association is present if probability of occurrence of a variable
depends upon one or more variable.
4
6. TYPES OF ASSOCIATION
1. SPURIOUS ASSOCIATION
2. INDIRECT ASSOCIATION
3. DIRECT (Causal) ASSOCIATION
A. One-to-One Causal association
B. Multi-Factorial Causation 6
8. Positive:Occurrence of higher value of a predictor variable
is associated with occurrence of higher value of another
dependent variable.
Negative: Occurrence of higher value of a predictor variable
is associated with lower value of another dependent variable.
Ex - Female literacy and IMR
8
9. Causal: Independent variable mustcause change in dependent
variable.
Ex – salt intake and hypertension
Non-causal: Non-directional association between two variables.
Ex – alcohol use and smoking
9
10. Spurious Association
Spurious (not true) association
•Not real, only apparent
Example1: A study in UK of 5174 births at home and 11156 births at
hospitals showed perinatal mortality rates of 5.4/1000 in home
birth and 27.8/1000 in hospital births. (but this is spurious)
Exapmle2: Fire and Fire Brigade may be found together in a
snapshot--but Fire brigade is not the cause of FIRE.
10
11. SPURIOUS ASSOCIATION
Some observed associations b/n a suspected factor and disease
may not be real
This Fallacy of presumption arises when two variables are
improperly compared (due to Bias).
PMR
Home Deliveries (5174)
Perinatal
Mortality
Rate
Hosp Deliveries (11,156)
27.8 / 1000
5.4 / 1000
11
12. INDIRECT ASSOCIATION
It is a statistical association between a characteristic of
interest and a disease due to the presence of another
factor i.e. common factor (confounding variable)
12
13. E- Goitre
Altitude
Iodine Deficiency
(Confounding Factor)
Yudkin & Roddy’s wrong hypothesis on Sucrose and CHD association
(Smoking is the Confounder).
Jacob Yerushalamy identified the association b/n Smoking and Low
birth weight babies is due to Confounding.
13
16. DIRECT ASSOCIATION
A. One-to-One Causal Relationship
This model suggests that two factors (A & B) exhibit one
to one relationship, if – Change in A is followed by Change in B.
Cause (A) Effect (B)
16
17. DIRECT ASSOCIATION
A. One-to-One Causal Relationship
This model suggests that two factors (A & B) exhibit one
to one relationship, if – Change in A is followed by Change in B.
Cause (A) Effect (B)
Paramyxo Virus Measles
17
18. KOCH’S POSTULATES (Germ Theory of Disease)
Hemolytic Streptococci
1. Necessary, and
2. Sufficient.
But this model does not fit well for many diseases, like in
Tuberculosis, tubercle bacilli is clearly a necessary factor, but its
presence may or may not be sufficient to produce the d/s.
A Single Factor may produce several Outcomes.
Erysipelas
Scarlett Fever
Tonsillitis
18
19. B. Multifactorial Causation
In Several Modern Diseases, more than one factor is
implicated in the Web of Causation.
Eg: Both Asbestos exposure and Smoking cause Lung
Cancer independently.
As our Knowledge on disease increases, we may discover a
common biochemical event, which can be altered by each of these
factors
19
20. Multiple factor leads to the disease.
Common in non-communicable diseases
Alternative causal factors each acting independently.
Ex: In lung cancer more than one factor (e.g. air pollution, smoking,
heredity) can produce the disease independently.
Either the causes are acting
Independently OR Cumulatively
20
21. Smoking
Air pollution Reaction at cellular level Lung cancer
Air pollution Reaction at cellular level Lung cancer
+
Exposure to asbestos
Independently
Exposure to asbestos
Cumulatively
Smoking
+
21
23. General Models of Causation
The most widely applied models are:
– The epidemiological triad (triangle),
– The web
– The wheel and
– The sufficient cause and component causes models
(Rothman’s component causes model)
23
27. Rothman’s Component Causes and
Causal Pies Model
• Rothman's model has emphasised that the causes of disease comprise
a collection of factors.
• These factors represent pieces of a pie, the whole pie (combinations of factors)
are the sufficient causes for a disease.
• It shows that a disease may have more than one sufficient cause, with each
sufficient cause being composed of several factors
27
28. • The factors represented by the pieces of the pie in this model are called
component causes.
• Each single component cause is rarely a sufficient cause by itself, But may
be necessary cause.
• Control of the disease could be achieved by removing one of the components in
each "pie" and if there were a factor common to all "pies“ (necessary cause) the
disease would be eliminated by removing that
alone.
A
U B
C
N 28
29. A
U B
C
N
Known components (causes) – A,
B,
C
Unknown component (cause) -
U
N – Necessary cause
Known components causes
+
Unknown component cause = Sufficient cause
+
Necessary cause 29
31. If a relationship is causal, four types of causal relationships are possible:
(1) Necessary And Sufficient
(2) Necessary, But Not Sufficient
(3) Sufficient, But Not Necessary
(4) Neither Sufficient Nor
Necessary
31
32. A factor is both necessary and sufficient for producing the disease.
Without that factor, the disease never develops and in the presence of
that factor, the disease always develops
Types of causal relationships I:
Each factor is both necessary and sufficient
FACTORA DISEASE
32
Necessary and Sufficient
33. Necessary, But Not Sufficient
Each factor is necessary, but not, in itself, sufficient to cause the disease .
Thus, multiple factors are required, often in a specific sequence.
Ex: Carcinogenesis is considered to be a multistage process involving both initiation
and promotion. A promoter must act after an initiator has acted. Action of an initiator
or a promoter alone will not produce a cancer.
33
36. Sufficient But Not Necessary
The factor alone can produce the disease, but so can other factors that are
acting alone
Either radiation or benzene exposure can each produce leukemia without
the presence of the other.
Even in this situation, however, cancer does not develop in everyone who
has experienced radiation or benzene exposure, so although both factors
are not needed, other cofactors probably are. Thus, the criterion of sufficient
is rarely met by a single factor.
36
38. A factor by itself, is neither sufficient nor necessary to produce disease
This is a more complex model, which probably most accurately represents
the causal relationships that operate in most chronic diseases.
Types of causal relationships: IV.
Each factor is neither sufficient nor necessary
38
Neither Sufficient Nor Necessary
39. – Temporal association
– Strength of association
– Specificity of association
– Consistency of association
– Biological plausibility
– Coherence of association
39
Additional criteria for judging causality
40. Temporal association
The causal attribute must precede the disease or unfavorable
outcome.
Exposureto the factor must have occurred before the disease
developed.
Length of interval between exposure and disease very important.
Its more obvious in acute disease than in chronic disease.
40
41. Temporal relationship (Relationship with
time)
• Cause must precede the effect.
o Drinking contaminated water -occurrence of diarrhea.
o However in many chronic cases, because of insidious onset and ignorance of
precise induction period, it become hard to establish a temporal sequence as
which comes first -the suspected agent or disease.
41
42. Strength Of The
Association
Relationship between cause and outcome could be strong or
weak.
With increasing level of exposure to the risk factor an increase in
incidence of the disease is found.
• Strength of association can be estimated by relative risk.
• Relative risks/Odds ratio greater than 2 can be considered strong
• Larger the relative risk, greater the likelihood of a causal association.
42
43. Dose-Response
Relationship
( The Biological gradient )
As the dose of exposure increases, the risk of disease also increases
If a dose-response relationship is present, it is strong evidence for a causal
relationship.
However, the absence of a dose-response relationship does not
necessarily rule out a causal relationship.
In some cases in which a threshold may exist, no disease may develop up to a
certain level of exposure (a threshold); above this level, disease may develop
43
44. The causal relationship of cigarette smoking and lung cancer
has been based on three points.
Relative risk
Dose-response relationship
Decrease in risk on cessation of smoking
44
45. Biologic Plausibility Of The
Association
The association must be consistent with the other knowledge (viz
mechanism of action, evidence from animal experiments etc).
Sometimes the lack of plausibility may simply be due to the lack of
sufficient knowledge about the pathogenesis of a disease, so the criterion of
biological plausibility should not be applied rigidly.
It is difficult to demonstrate where the confounder itself exhibits a
biological gradient in relation to the outcome. 45
46. e.g. – cigarette smoking and lung cancer hypothesis is biologically
plausible.
Food intake and cancer are interrelated is an old one.
Positive association of intestine, rectum, and breast cancer is
biologically logical.
46
47. Consistency Of The
Association
Consistency is the occurrence of the association at some other time
and place repeatedly.
Repeated observation of an association in different populations
under different circumstances.
Example: consistent association between lung cancer and cigarette
smoking – 50 retrospective study and almost 9 prospective studies.
47
48. Specificity Of The
Association
Specific exposure is associated with only one disease.
Specificity implies a one to one relationship between the cause and
effect.
It’s the most difficult to occur for 2 reasons:
Single cause or factor can give rise to more than 1 disease
Most diseases are due to multiple factors.
Ex: Smoking is associated with many diseases.
• Not everyone who smokes develops cancer
• Not every one who develop cancer has smoke 48
49. Coherence of the association
Based on available evidence or should be coherence with known facts that
are thought to be relevant.
i.e. historic evidence of rising consumption of tobacco in form of cigarette
and rising incidence of lung cancer are coherent.
49
50. Deriving causal inferences: example
Assessment of the Evidence Suggesting Helicobacter pylori Ulcers as
a Causative Agent of Duodenal
1. Temporal relationship.
• Helicobacter pylori is clearly linked to chronic gastritis. About 11% of
chronic gastritis patients will go on to have duodenal ulcers over a 10- year
period.
2. Strength of the relationship.
• Helicobacter pylori is found in at least 90% of patients with duodenal ulcer.
50
51. 3. Dose-response relationship.
• Density of Helicobacter pylori per square millimeter of gastric mucosa is
higher in patients with duodenal ulcer than in patients without duodenal ulcer
4. Replication of the findings.(consistency)
• Many of the observations regarding Helicobacter pylori have been
replicated repeatedly
5. Consideration of alternate explanations.
• Data suggest that smoking can increase the risk of duodenal ulcer in
Helicobacter pylori-infected patients but is not a risk factor in patients in
whom Helicobacter pylori has been eradicated
51
52. 6. Biologic plausibility.
• Helicobacter pylori also induces mediators of inflammation.
• Helicobacter pylori-infected mucosa is weakened and is susceptible to the
damaging effects of acid.
7. Cessation of exposure.
• Eradication of Helicobacter pylori heals duodenal ulcers at the same rate as
histamine receptor antagonists.
52
8. Specificity of the association.
Prevalence of Helicobacter pylori in patients with duodenal ulcers is 90% to
100%.
53. References
Park’s Text book of Preventive & Social Medicine. 25th ed.
Community medicine with Recent advances by A.H.Suryakantha
Textbook of Community Medicine by Sunder Lal, Adarsh,
Pankaj. 6th ed