Here are some ways to protect against random error in epidemiological studies:
- Increase sample size. Larger sample sizes reduce the impact of random variation between samples and populations.
- Use random selection. Randomly selecting subjects from the target population helps ensure the sample is representative.
- Use random assignment. Randomly assigning exposures helps distribute potential confounding factors evenly between exposure groups.
- Replicate findings. Conducting multiple studies on the same question helps determine if findings are consistent or due to chance. Inconsistent findings may indicate random error.
- Consider direction and magnitude of effects. Large or dose-response effects are less likely due to chance alone.
- Use appropriate statistical tests. Tests like chi-
This document discusses various epidemiological study designs. It begins by defining descriptive studies, which involve systematically collecting and presenting data to describe a situation, and analytical studies, which attempt to establish causes or risk factors by comparing exposed and unexposed groups. The main types of descriptive studies covered are cross-sectional (examining a population at a single point in time), longitudinal (following a population over time), and ecological (examining population-level associations between exposures and outcomes). Advantages and disadvantages of each design are provided.
Statistics is the study of collecting, organizing, summarizing, and interpreting data. Medical statistics applies statistical methods to medical data and research. Biostatistics specifically applies statistical methods to biological data. Statistics is essential for medical research, updating medical knowledge, data management, describing research findings, and evaluating health programs. It allows comparison of populations, risks, treatments, and more.
The document discusses nursing as a profession and the criteria required for an occupation to be considered a profession. It outlines three main approaches to defining a profession - process, power, and trait approaches. The trait approach, as defined by Flexner, Bixler, and Pavalko, identifies key characteristics including a specialized body of knowledge, evidence-based practice, high intellectual functioning, individual responsibility, and public service. The document argues that nursing meets many of the trait-based criteria and is evolving into a fully recognized profession through the development of nursing science, research, and strong professional organizations.
Today’s presentation focuses on Jean Watson's Theory of Human Caring. During this presentation we will analyze the theoretical framework, review the critical components of the Theory of Caring, and discuss how the theory is utilized in nursing practice. This presentation will also detail application of Watson’s Theory of Caring into the peri-operative environment by instituting a “sacred space” and explain the process of implementing the sacred space. Enjoy!
This document discusses quantitative research methods and statistical inference. It covers topics like probability distributions, sampling distributions, estimation, hypothesis testing, and different statistical tests. Key points include:
- Probability distributions describe random variables and their associated probabilities. The normal distribution is important and described by its mean and standard deviation.
- Sampling distributions allow making inferences about populations based on samples. The sampling distribution of the mean approximates a normal distribution as the sample size increases.
- Statistical inference involves estimation and hypothesis testing. Estimation provides a value for an unknown population parameter based on a sample statistic. Hypothesis testing compares a null hypothesis to an alternative hypothesis based on a test statistic and can result in type 1 or type 2 errors.
Introduction to Epidemiology
1. Define epidemiology
2. Describe the history of epidemiology
3. Describe aims and components of
epidemiology
4. Discuss on the uses of epidemiology
Betty Neumann developed the Neuman Systems Model, which views clients holistically and focuses on stressors that can disturb a client's usual stability. The model uses primary, secondary, and tertiary prevention interventions to help clients retain, attain, or maintain optimal wellness. Neumann was influenced by general systems theory and saw people as complex systems composed of interrelated biological, psychological, socio-cultural, developmental, and spiritual variables that can be impacted by internal and external environmental stressors. Nursing aims to help the client system maintain stability through interventions that reduce the impact of stressors at different levels of reaction.
The document defines key epidemiological measures used to describe disease occurrence and impact, including prevalence, incidence, rates, and ratios. It provides examples of how to calculate and interpret these measures. The document concludes that prevalence describes the current disease burden, while incidence provides information on the risk of developing disease over time and is thus better suited for etiological studies.
This document discusses various epidemiological study designs. It begins by defining descriptive studies, which involve systematically collecting and presenting data to describe a situation, and analytical studies, which attempt to establish causes or risk factors by comparing exposed and unexposed groups. The main types of descriptive studies covered are cross-sectional (examining a population at a single point in time), longitudinal (following a population over time), and ecological (examining population-level associations between exposures and outcomes). Advantages and disadvantages of each design are provided.
Statistics is the study of collecting, organizing, summarizing, and interpreting data. Medical statistics applies statistical methods to medical data and research. Biostatistics specifically applies statistical methods to biological data. Statistics is essential for medical research, updating medical knowledge, data management, describing research findings, and evaluating health programs. It allows comparison of populations, risks, treatments, and more.
The document discusses nursing as a profession and the criteria required for an occupation to be considered a profession. It outlines three main approaches to defining a profession - process, power, and trait approaches. The trait approach, as defined by Flexner, Bixler, and Pavalko, identifies key characteristics including a specialized body of knowledge, evidence-based practice, high intellectual functioning, individual responsibility, and public service. The document argues that nursing meets many of the trait-based criteria and is evolving into a fully recognized profession through the development of nursing science, research, and strong professional organizations.
Today’s presentation focuses on Jean Watson's Theory of Human Caring. During this presentation we will analyze the theoretical framework, review the critical components of the Theory of Caring, and discuss how the theory is utilized in nursing practice. This presentation will also detail application of Watson’s Theory of Caring into the peri-operative environment by instituting a “sacred space” and explain the process of implementing the sacred space. Enjoy!
This document discusses quantitative research methods and statistical inference. It covers topics like probability distributions, sampling distributions, estimation, hypothesis testing, and different statistical tests. Key points include:
- Probability distributions describe random variables and their associated probabilities. The normal distribution is important and described by its mean and standard deviation.
- Sampling distributions allow making inferences about populations based on samples. The sampling distribution of the mean approximates a normal distribution as the sample size increases.
- Statistical inference involves estimation and hypothesis testing. Estimation provides a value for an unknown population parameter based on a sample statistic. Hypothesis testing compares a null hypothesis to an alternative hypothesis based on a test statistic and can result in type 1 or type 2 errors.
Introduction to Epidemiology
1. Define epidemiology
2. Describe the history of epidemiology
3. Describe aims and components of
epidemiology
4. Discuss on the uses of epidemiology
Betty Neumann developed the Neuman Systems Model, which views clients holistically and focuses on stressors that can disturb a client's usual stability. The model uses primary, secondary, and tertiary prevention interventions to help clients retain, attain, or maintain optimal wellness. Neumann was influenced by general systems theory and saw people as complex systems composed of interrelated biological, psychological, socio-cultural, developmental, and spiritual variables that can be impacted by internal and external environmental stressors. Nursing aims to help the client system maintain stability through interventions that reduce the impact of stressors at different levels of reaction.
The document defines key epidemiological measures used to describe disease occurrence and impact, including prevalence, incidence, rates, and ratios. It provides examples of how to calculate and interpret these measures. The document concludes that prevalence describes the current disease burden, while incidence provides information on the risk of developing disease over time and is thus better suited for etiological studies.
The document discusses boundaries in the nurse-client relationship. It acknowledges the power imbalance that exists, with nurses having more power, and clients being vulnerable. It defines personal relationships like friendships and romantic relationships as different from professional nurse-client relationships. It provides examples of situations that could challenge boundaries, such as gifts, self-disclosure, and dual roles. It emphasizes that nurses are responsible for maintaining professional boundaries regardless of client behavior.
The document provides an overview of Joanne Duffy's Quality Caring Model. It discusses Duffy's background, education, and career achievements. It then outlines the key concepts of the revised Quality Caring Model, including that humans exist in relationships, relationship-centered professional encounters, feeling cared for, and self-caring. The assumptions and propositions of the model are presented. The caring factors and relationships are explained, including with self, patients/families, healthcare team, and communities. The application and critique of the Quality Caring Model are also summarized.
This document discusses selection bias, which occurs when there are systematic differences in the characteristics of those selected for a study compared to the overall population from which they were selected. It provides examples of selection bias in case-control and cohort studies. Selection bias can be introduced when the probability of being included in the study depends on both the exposure and outcome of interest. This distorts the association observed in the study sample compared to the true association in the population. Differential participation or loss to follow up based on exposure and outcome status are common causes of selection bias.
The Government of Karnataka has notified a recruitment notification for the posts of Assistant Professors in Government First Grade Colleges in Karnataka. The Karnataka Examinations Authority will conduct a competitive examination for eligible candidates as per the Karnataka Education Department Services (Collegiate Education Department) (Recruitment) (Special) Rules, 2014. Vacancies exist for various subjects including Kannada, English, Hindi, History, Economics, Commerce, Physics, Chemistry and others. The pay scale is 15600-39100 with an Academic Grade Pay of 6000. The total number of vacancies is 1298 across general and backlog categories. Candidates must apply and appear for the competitive examination to be considered for these positions.
1. Myra Estrin Levine was an influential nursing theorist born in 1920 in Chicago. She had a varied nursing career and helped establish nursing as an applied science.
2. Levine developed the Conservation Model of Nursing, which focuses on maintaining wholeness and integrity through the conservation of energy, structural integrity, personal integrity, and social integrity.
3. The goal of nursing according to Levine is to promote adaptation through the conservation principles in order to achieve and maintain the patient's wholeness. Nursing interventions are aimed at testing hypotheses based on the conservation principles.
This document discusses causation in epidemiology. It defines causation as an event, condition, or characteristic that plays an important role in producing a disease. A cause can be sufficient, meaning it inevitably produces the disease, or necessary, meaning the disease cannot develop without it. Most diseases have multiple contributing factors rather than a single cause. Guidelines for determining a causal relationship include considering the temporal relationship between cause and effect, consistency of association, strength of association, and whether removing the potential cause reduces disease risk. Correctly establishing causation is important for disease prevention and control.
This document discusses criteria for determining causal association. It defines association and different types of association, including spurious, indirect, and direct causal association. Bradford Hill's criteria for making causal inferences are described, including strength of association, dose-response relationship, consistency of findings, biological plausibility, specificity of association, and temporal relationship. Examples for each criterion are provided, such as the relationship between smoking and lung cancer. The document concludes with a summary of association types and causal association criteria.
Jean Watson developed the Theory of Human Caring, which focuses on caring as central to nursing. The theory has major concepts of human health, environment/society, and nursing. Its major elements are carative factors, transpersonal caring relationships, and caring occasions. Watson's theory views caring as healthogenic and can be demonstrated through interpersonal relationships. It promotes health and growth while accepting people for who they are and who they may become.
This document discusses causal relationships in epidemiology. It defines causation as an event or condition that plays an important role in the occurrence of an outcome. There are different types of associations, including spurious, indirect, and direct associations. Direct associations can be one-to-one or multifactorial. Guidelines for assessing causality include temporality, strength of association, dose-response relationship, and consistency of findings. Causal inference involves applying these guidelines and ruling out alternative explanations like bias or chance to determine if an observed association is likely causal.
This document discusses sample size determination and calculation. It defines sample size as the subset of a population chosen for a study to make inferences about the total population. The key factors in determining sample size are the desired level of accuracy, allowing for appropriate analysis, and validity of significance tests. The document provides formulas and methods for calculating sample size for different study designs and populations, including using formulas, readymade tables, nomograms, and computer software. Accurately determining sample size is essential for research.
This document discusses the concepts of association and causation in epidemiology. It defines correlation as a measure of association between two variables, while causation requires one variable to be a suspected cause of the other. There are three types of association - spurious, indirect, and direct. Direct association can be either a one-to-one causal relationship or multifactorial causation from multiple independent factors. Six guidelines for judging causal relationships are temporal association, consistency, specificity, strength, coherence, and biological plausibility.
1. Establishing causality from observed associations is challenging due to problems like multiple causation, latent periods, confounding, and bias.
2. Criteria for judging causal inference include the strength and consistency of associations, temporality, dose-response relationships, plausible biological mechanisms, consideration of alternatives, and cessation of exposure.
3. Rothman's causality model proposes that diseases can have multiple sufficient causal pathways, where elimination of even one component can be useful for prevention.
Information bias can occur from flawed measurement of study variables, resulting in misclassification of subjects. There are two types of misclassification: non-differential, where the degree of misclassification is unrelated to exposure/outcome status, and differential, where the degree depends on status. Non-differential misclassification typically biases results towards the null, while differential can bias in either direction. Specific biases include recall bias, interviewer bias, observer bias, and respondent bias. Proper evaluation of measurement error and its direction is important to understand potential biases.
This document discusses network meta-analysis (NMA), which synthesizes both direct and indirect evidence from randomized controlled trials (RCTs) that compare multiple interventions. NMA allows for comparisons between interventions that have not been directly compared in RCTs. It provides treatment relative rankings and effect estimates. Assumptions of NMA include similarity of trials, homogeneity within comparisons, and consistency between direct and indirect evidence. Tests for heterogeneity and inconsistency help evaluate if these assumptions are valid. Software like Addis, WinBUGS, NetMetaXL, and RevMan can be used to conduct NMA.
This document discusses the concepts of association and causation in epidemiology. It defines association as the occurrence of two variables more often than expected by chance. Causation requires that one factor leads to a change in another factor. Several types of associations are described, including direct, indirect, spurious and causal relationships. Guidelines for determining if an association is likely causal include temporal relationship, strength of association, dose-response relationship, replication of findings, biological plausibility and consideration of alternative explanations. Models of causation like the epidemiological triad, web of causation and Rothman's component causes model are also summarized.
This document provides an overview of concepts related to causation in epidemiology. It discusses the difference between association and causation, outlines various types of causal relationships, and describes criteria for evaluating evidence of a causal relationship. Specifically, it explains that determining causation is a two-step process involving first establishing an association and then evaluating it against criteria like strength of association, consistency, and biological plausibility to determine if the relationship is likely causal.
The document discusses the concept of the exposome and causal relationships between exposures and disease. It defines the exposome as comprising all environmental exposures from conception to death, including processes inside and outside the body. Most disease is caused by multiple environmental and genetic factors interacting. Identifying causal relationships requires considering guidelines like temporal relationship and exposure-response. A new paradigm of systematically studying the full exposome may help uncover currently unknown disease causes, and this approach could also be relevant for workplace exposures.
CONCEPT OF DISEASE CAUSATION AND NATURE HISTORY OF DISEASE.pptxPRATIKAWALE5
This document discusses concepts related to disease causation and epidemiology. It defines disease and outlines historical concepts of disease causation from supernatural to germ theories. It emphasizes that disease results from interactions between an agent, host, and environment. Modern models recognize multiple interrelated factors. The natural history of disease progresses from pre-pathogenesis through pathogenesis phases. Disease manifestations vary in a spectrum from positive health to death. Unrecognized cases represent an iceberg of hidden disease burden in a community.
1. Epidemiology is the study of disease distribution, patterns, and determinants in populations. It analyzes who is affected, when and where diseases occur, and potential reasons.
2. A key challenge is distinguishing causation from mere association between factors and diseases. Causation requires strong evidence like consistency across different studies and populations. Association means a relationship exists but does not prove one factor causes the other.
3. Several types of causal relationships are possible, like necessary but not sufficient, where a factor is required for a disease but other factors also contribute. Most chronic diseases likely involve multiple interacting factors that are neither solely sufficient nor necessary.
The document discusses the etiology, or causes, of diseases in three categories: genetic, congenital, and acquired. It describes controllable and uncontrollable risk factors for disease causation. The natural history of a disease refers to its progression from exposure to causal agents to recovery or death. An iceberg phenomenon metaphor emphasizes that most disease cases remain undiscovered. Different theories of disease causation are described, including the germ theory, epidemiological triad, multifactorial causation theory, web of causation, and spectrum of disease.
Introduction to Epidemiology
History of Epidemiology.
Definition of Epidemiology and its components.
Epidemiological Basic concepts.
Aims of Epidemiology.
Ten Uses of Epidemiology.
Scope or The Areas of Application .
Types of Epidemiological Studies.
The document discusses boundaries in the nurse-client relationship. It acknowledges the power imbalance that exists, with nurses having more power, and clients being vulnerable. It defines personal relationships like friendships and romantic relationships as different from professional nurse-client relationships. It provides examples of situations that could challenge boundaries, such as gifts, self-disclosure, and dual roles. It emphasizes that nurses are responsible for maintaining professional boundaries regardless of client behavior.
The document provides an overview of Joanne Duffy's Quality Caring Model. It discusses Duffy's background, education, and career achievements. It then outlines the key concepts of the revised Quality Caring Model, including that humans exist in relationships, relationship-centered professional encounters, feeling cared for, and self-caring. The assumptions and propositions of the model are presented. The caring factors and relationships are explained, including with self, patients/families, healthcare team, and communities. The application and critique of the Quality Caring Model are also summarized.
This document discusses selection bias, which occurs when there are systematic differences in the characteristics of those selected for a study compared to the overall population from which they were selected. It provides examples of selection bias in case-control and cohort studies. Selection bias can be introduced when the probability of being included in the study depends on both the exposure and outcome of interest. This distorts the association observed in the study sample compared to the true association in the population. Differential participation or loss to follow up based on exposure and outcome status are common causes of selection bias.
The Government of Karnataka has notified a recruitment notification for the posts of Assistant Professors in Government First Grade Colleges in Karnataka. The Karnataka Examinations Authority will conduct a competitive examination for eligible candidates as per the Karnataka Education Department Services (Collegiate Education Department) (Recruitment) (Special) Rules, 2014. Vacancies exist for various subjects including Kannada, English, Hindi, History, Economics, Commerce, Physics, Chemistry and others. The pay scale is 15600-39100 with an Academic Grade Pay of 6000. The total number of vacancies is 1298 across general and backlog categories. Candidates must apply and appear for the competitive examination to be considered for these positions.
1. Myra Estrin Levine was an influential nursing theorist born in 1920 in Chicago. She had a varied nursing career and helped establish nursing as an applied science.
2. Levine developed the Conservation Model of Nursing, which focuses on maintaining wholeness and integrity through the conservation of energy, structural integrity, personal integrity, and social integrity.
3. The goal of nursing according to Levine is to promote adaptation through the conservation principles in order to achieve and maintain the patient's wholeness. Nursing interventions are aimed at testing hypotheses based on the conservation principles.
This document discusses causation in epidemiology. It defines causation as an event, condition, or characteristic that plays an important role in producing a disease. A cause can be sufficient, meaning it inevitably produces the disease, or necessary, meaning the disease cannot develop without it. Most diseases have multiple contributing factors rather than a single cause. Guidelines for determining a causal relationship include considering the temporal relationship between cause and effect, consistency of association, strength of association, and whether removing the potential cause reduces disease risk. Correctly establishing causation is important for disease prevention and control.
This document discusses criteria for determining causal association. It defines association and different types of association, including spurious, indirect, and direct causal association. Bradford Hill's criteria for making causal inferences are described, including strength of association, dose-response relationship, consistency of findings, biological plausibility, specificity of association, and temporal relationship. Examples for each criterion are provided, such as the relationship between smoking and lung cancer. The document concludes with a summary of association types and causal association criteria.
Jean Watson developed the Theory of Human Caring, which focuses on caring as central to nursing. The theory has major concepts of human health, environment/society, and nursing. Its major elements are carative factors, transpersonal caring relationships, and caring occasions. Watson's theory views caring as healthogenic and can be demonstrated through interpersonal relationships. It promotes health and growth while accepting people for who they are and who they may become.
This document discusses causal relationships in epidemiology. It defines causation as an event or condition that plays an important role in the occurrence of an outcome. There are different types of associations, including spurious, indirect, and direct associations. Direct associations can be one-to-one or multifactorial. Guidelines for assessing causality include temporality, strength of association, dose-response relationship, and consistency of findings. Causal inference involves applying these guidelines and ruling out alternative explanations like bias or chance to determine if an observed association is likely causal.
This document discusses sample size determination and calculation. It defines sample size as the subset of a population chosen for a study to make inferences about the total population. The key factors in determining sample size are the desired level of accuracy, allowing for appropriate analysis, and validity of significance tests. The document provides formulas and methods for calculating sample size for different study designs and populations, including using formulas, readymade tables, nomograms, and computer software. Accurately determining sample size is essential for research.
This document discusses the concepts of association and causation in epidemiology. It defines correlation as a measure of association between two variables, while causation requires one variable to be a suspected cause of the other. There are three types of association - spurious, indirect, and direct. Direct association can be either a one-to-one causal relationship or multifactorial causation from multiple independent factors. Six guidelines for judging causal relationships are temporal association, consistency, specificity, strength, coherence, and biological plausibility.
1. Establishing causality from observed associations is challenging due to problems like multiple causation, latent periods, confounding, and bias.
2. Criteria for judging causal inference include the strength and consistency of associations, temporality, dose-response relationships, plausible biological mechanisms, consideration of alternatives, and cessation of exposure.
3. Rothman's causality model proposes that diseases can have multiple sufficient causal pathways, where elimination of even one component can be useful for prevention.
Information bias can occur from flawed measurement of study variables, resulting in misclassification of subjects. There are two types of misclassification: non-differential, where the degree of misclassification is unrelated to exposure/outcome status, and differential, where the degree depends on status. Non-differential misclassification typically biases results towards the null, while differential can bias in either direction. Specific biases include recall bias, interviewer bias, observer bias, and respondent bias. Proper evaluation of measurement error and its direction is important to understand potential biases.
This document discusses network meta-analysis (NMA), which synthesizes both direct and indirect evidence from randomized controlled trials (RCTs) that compare multiple interventions. NMA allows for comparisons between interventions that have not been directly compared in RCTs. It provides treatment relative rankings and effect estimates. Assumptions of NMA include similarity of trials, homogeneity within comparisons, and consistency between direct and indirect evidence. Tests for heterogeneity and inconsistency help evaluate if these assumptions are valid. Software like Addis, WinBUGS, NetMetaXL, and RevMan can be used to conduct NMA.
This document discusses the concepts of association and causation in epidemiology. It defines association as the occurrence of two variables more often than expected by chance. Causation requires that one factor leads to a change in another factor. Several types of associations are described, including direct, indirect, spurious and causal relationships. Guidelines for determining if an association is likely causal include temporal relationship, strength of association, dose-response relationship, replication of findings, biological plausibility and consideration of alternative explanations. Models of causation like the epidemiological triad, web of causation and Rothman's component causes model are also summarized.
This document provides an overview of concepts related to causation in epidemiology. It discusses the difference between association and causation, outlines various types of causal relationships, and describes criteria for evaluating evidence of a causal relationship. Specifically, it explains that determining causation is a two-step process involving first establishing an association and then evaluating it against criteria like strength of association, consistency, and biological plausibility to determine if the relationship is likely causal.
The document discusses the concept of the exposome and causal relationships between exposures and disease. It defines the exposome as comprising all environmental exposures from conception to death, including processes inside and outside the body. Most disease is caused by multiple environmental and genetic factors interacting. Identifying causal relationships requires considering guidelines like temporal relationship and exposure-response. A new paradigm of systematically studying the full exposome may help uncover currently unknown disease causes, and this approach could also be relevant for workplace exposures.
CONCEPT OF DISEASE CAUSATION AND NATURE HISTORY OF DISEASE.pptxPRATIKAWALE5
This document discusses concepts related to disease causation and epidemiology. It defines disease and outlines historical concepts of disease causation from supernatural to germ theories. It emphasizes that disease results from interactions between an agent, host, and environment. Modern models recognize multiple interrelated factors. The natural history of disease progresses from pre-pathogenesis through pathogenesis phases. Disease manifestations vary in a spectrum from positive health to death. Unrecognized cases represent an iceberg of hidden disease burden in a community.
1. Epidemiology is the study of disease distribution, patterns, and determinants in populations. It analyzes who is affected, when and where diseases occur, and potential reasons.
2. A key challenge is distinguishing causation from mere association between factors and diseases. Causation requires strong evidence like consistency across different studies and populations. Association means a relationship exists but does not prove one factor causes the other.
3. Several types of causal relationships are possible, like necessary but not sufficient, where a factor is required for a disease but other factors also contribute. Most chronic diseases likely involve multiple interacting factors that are neither solely sufficient nor necessary.
The document discusses the etiology, or causes, of diseases in three categories: genetic, congenital, and acquired. It describes controllable and uncontrollable risk factors for disease causation. The natural history of a disease refers to its progression from exposure to causal agents to recovery or death. An iceberg phenomenon metaphor emphasizes that most disease cases remain undiscovered. Different theories of disease causation are described, including the germ theory, epidemiological triad, multifactorial causation theory, web of causation, and spectrum of disease.
Introduction to Epidemiology
History of Epidemiology.
Definition of Epidemiology and its components.
Epidemiological Basic concepts.
Aims of Epidemiology.
Ten Uses of Epidemiology.
Scope or The Areas of Application .
Types of Epidemiological Studies.
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.
This document discusses various theories of disease causation including the germ theory, epidemiological triad, multifactorial causation theory, and web of causation. It also covers the Devers epidemiological model and describes the spectrum and iceberg models of disease. Factors that influence health are categorized as human biology, lifestyle, environment, and the health system. The role of nurses in disease prevention includes participation in diagnosis, treatment, notification, identification of infection sources, and providing health education.
The document discusses various theories of disease causation including the germ theory, epidemiological triad, multifactorial causation theory, and web of causation. It also covers the Devers epidemiological model and describes the spectrum and iceberg models of disease. Nurses can play an important role in disease prevention through activities like early diagnosis, treatment, notification of diseases, identifying infection sources, and providing health education.
ARTÍCULO_Epidemiology the foundation of public health (Inglés) autor Roger De...Hilda Santos Padrón
Epidemiology is the basic science of public health as it describes the relationship between health, disease, and other factors in human populations. It uses study designs and methods to generate information to develop effective public health programs for disease prevention and health promotion. Unlike other medical fields, epidemiology is a philosophy and methodology that can be applied broadly. Successful application requires creative use of strategies and methods to answer specific health questions. Epidemiology describes disease patterns in terms of time, place, and person to understand causative agents and risk factors in order to suggest interventions.
This document discusses concepts related to disease causation and epidemiology. It defines key terms like association, correlation, causation, and describes methods for establishing causal relationships like Koch's postulates, Hill's criteria, and Evan's postulates. Various types of causal relationships and pathways are explained, as well as the difference between necessary and sufficient causes. Historical conceptual frameworks for analyzing disease causation are also outlined.
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.
The document discusses causality in health sciences from an epistemological perspective. It argues that causal claims require both probabilistic and mechanistic evidence, and that neither monistic nor pluralistic accounts fully capture the dual aspect of causal epistemology. The document proposes an "epistemic" account of causality, where causal beliefs are determined by the total evidence available to an agent. It also argues that epidemiology establishes "variational causal claims" through comparative studies of how disease risk varies with changes in exposure, rather than measuring regularity or invariance.
The document discusses different theories of disease causation:
1. The miasma theory attributed disease to polluted air. This led to a focus on sanitation and public health measures.
2. Germ theory identified specific microbes as the cause of different diseases, shifting focus to identifying and destroying disease agents.
3. The epidemiological triangle recognized diseases result from interactions between an agent, host factors, and the environment. This informed prevention through modifying exposure and susceptibility.
This document discusses causal relationships in epidemiology. It defines key terms like association, correlation and causation. It explains different types of associations like spurious, indirect and direct associations. It also discusses guidelines for assessing causality, including temporal sequence, dose-response relationship, consistency of findings, plausibility and coherence. The goal of epidemiology is to identify causal relationships between diseases and suspected factors through observational studies and making causal inferences.
John Snow is considered the father of epidemiology for his work investigating a cholera outbreak in London in 1854. Through mapping the locations of cholera cases and the water sources people used, Snow was able to determine that the source of the outbreak was the Broad Street water pump. Removing the pump handle stopped the outbreak. Snow's use of statistical mapping methods to identify the source of transmission pioneered epidemiological investigation techniques that are still used today.
This honors thesis examines the potential for acetaminophen to potentiate the effects of oxidant air pollutants and contribute to the onset of asthma. Using a mouse model, the study found that low, non-toxic doses of acetaminophen greatly increased the reflex irritant response to environmental tobacco smoke, likely by increasing oxidative stress in the airways. This is notable because acetaminophen usage has risen along with asthma rates in recent decades. The results suggest acetaminophen's metabolite NAPQI may potentiate the effects of oxidant pollutants, representing a possible new link between acetaminophen and asthma development.
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The document discusses various microbiology techniques for culturing microbes including inoculation, isolation, incubation, inspection, and identification. It describes how to produce pure cultures through methods like streak plating and describes different types of culture media including solid, liquid, enriched, selective, and differential media. The goals are to transfer microbes to produce isolated colonies, grow them under proper conditions, observe characteristics, and identify organisms through comparing data.
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Compliance, motivation, and health behaviors stanbridge
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2. On completion of your studies you should understand:
The purpose of studying cause and effect in
epidemiology is to generate knowledge to prevent
and control disease.
That cause and effect understanding is difficult to
achieve in epidemiology because of the long
natural history of diseases and because of ethical
restraints on human experimentation.
How causal thinking in epidemiology fits in with
other domains of knowledge, both scientific and
non-scientific.
The potential contributions of various study
designs for making contributions to causal
knowledge.
3. Cause and effect
Cause and effect understanding is the
highest form of achievement of scientific
knowledge.
Causal knowledge permits rational plans
and actions to break the links between
the factors causing disease, and disease
itself.
Causal knowledge can help predict the
outcome of an intervention and help treat
disease.
Quote Hippocrates "To know the causes
of a disease and to understand the use of
the various methods by which the disease
may be prevented amounts to the same
thing as being able to cure the disease".
4. Epidemiological contributions
to cause and effect A philosophy of health and disease.
Models which illustrate that philosophy.
Frameworks for interpreting and applying the
evidence.
Study designs to produce evidence.
Evidence for cause and effect in the
relationships of numerous factors and diseases.
Development of the reasoning of other
disciplines including philosophy and
microbiology, in reaching judgement.
5. A cause?
The first and difficult question is, what
is a cause?
A cause is something which has an
effect.
In epidemiology a cause can be
considered to be something that alters
the frequency of disease, health status
or associated factors in a population.
Pragmatic definition.
Philosophers have grappled with the
nature of causality for thousands of
years.
6. Epidemiological strategy and
reasoning: the example of Semelweis
Diseases form patterns, which are ever changing.
Clues to the causes of disease are inherent within these pattern.
Semelweis (1818-1865) observed that the mortality from childbed fever
(now known as puerperal fever) was lower in women attending clinic 2 run
by midwives than it was in those attending clinic 1 run by doctors.
Do these observations spark off any ideas of causation in your mind?
7. Births, deaths, and mortality rates (%) for all
patients at the two clinics 1841-1846
First clinic Second clinic
Births Deaths Rate Births Deaths Rate
20042 1989 9.92 17791 691 3.38
8. Semmelweis’ inspiration
In 1847, his colleague and friend Professor
Kolletschka died following a fingerprick with a
knife used to conduct an autopsy.
Kolletschka’s autopsy showed inflammation to be
widespread, with peritonitis, and meningitis.
“Day and night I was haunted by the image of
Kolletschka’s disease and was forced to recognise,
ever more decisively that the disease from which
Kolletschka died was identical to that from which
so many maternity patients died.”
Semelweis' inspired idea was that particles had
been transferred from the scalpel to the vascular
system of his friend and that the same particles
were killing maternity patients.
9. Semmelweis’ action
If so, something stronger than ordinary soap was
needed for handwashing
He introduced chlorina liquida, and then for reasons
of economy, chlorinated lime.
The maternal mortality rate plummeted.
Semelweis’s discovery was resented in Vienna.
.
10. Deep knowledge derives from the explanation of
disease patterns, rather than in their description.
Inspiration is needed, and may come from unexpected
sources, as here from Kolletschka’s autopsy.
Action cannot always await understanding the
mechanism.
Epidemiological data to show that laying an infant on
its front (prone position) to sleep raises the risk of
'cot death' or sudden infant death syndrome.
A campaign to persuade parents to lay their infants on
their backs has halved the incidence of cot death.
Epidemiologists are reliant on other sciences,
laboratory or social, to be equal partners, in pursuit
of the mechanisms.
11. Epidemiological principles and
models of cause and effect
Most important of the cause and effect ideas
underpinned by epidemiology is that disease is virtually
always a result of the interplay of the environment, the
genetic and physical makeup of the individual, and the
agent of disease.
Diseases attributed to single causes are invariably so by
definition.
The fact that “tuberculosis” is “caused” by the tubercle
bacillus is a matter of definition.
The causes of tuberculosis, from an epidemiological or
public-health perspective, are many, including
malnutrition and overcrowding.
This idea is captured by several well known disease
causation models, such as the line, triangle, the wheel,
and the web.
12. Clues
Stable in incidence
Clusters in families
Clues
Incidence varies rapidly
over time or between
genetically similar
populations
Is the disease predominantly
genetic or environmental?
Genetic
Environmental
14. Host:
Inhalation of infective
organism, age, smoking,
male sex,
cardio-respiratory disease
Environment:
Presence of cooling towers
and complex hot water
systems; aerosols created
but not contained,
meteorological conditions
take aerosol to humans
Agent:
Virulent
Legionella
organisms, e.g.
pneumophila
serotype
15. Control smoking
and causes of
immunodeficiency
Avoid wet type cooling
towers, look for a better
design and location,
separate towers from
population and enhance
tower hygiene
Minimise growth of
organisms and factors
which enhance
pathogenicity, e.g. algae
18. Models of cause and effect
Agent factors, arguably, receive less attention
than they deserve.
Characterising the virulence of organisms is difficult.
In other diseases conceptualising the cause as an agent
is not easy.
The concept of the disease agent has been applied to
infections but it works well with many non-infectious
agents, for example, cigarettes, motor cars, and
alcohol.
The interaction of the host, agent and environment is
rarely understood.
The effect of cigarette smoking is substantially greater
in poor people than in rich people.
19. Models: the wheel
The wheel of causation.
Emphasises the unity of the interacting factors.
Emphasises the fact that the division of the
environment into components is somewhat
arbitrary.
Model is applied to phenylketonuria, the
archetypal genetic disorder.
Phenylketonuria is an autosomal single gene
disease .
An enzyme required to metabolise the dietary
amino-acid phenylalanine and turn it into tyrosine,
is deficient.
20. The wheel: phenylketonuria
Brain damage is the outcome.
The cause of this disease could be said
to be a gene.
The cause of the disease could be
considered as a combination of a gene.
Exposure to a chemical and biological
environment which provides a diet
containing a high amount of
phenylalanine.
A social environment unable to
protect the child from the
consequences, of a gene disorder.
21. Models: the spider’s web
For many disorders our understanding of
the causes is highly complex.
Either the causes are truly complex, or equally likely,
our understanding is too rudimentary to permit
clarity.
These disorders are referred to as multifactorial or
polyfactorial disorders.
Mechanisms of causation are not apparent.
Portrayed by the metaphor of the spider’s web.
This modelindicates the potential for the disease to
influence the causes and not just the other way
around, so-called, reverse causality.
It also poses a fundamental question: Where is the
spider that spun the web?
22.
23.
24. Rothman’s component causes model
Rothman's interacting component causes model has
emphasised that the causes of disease comprise a
constellation of factors.
It has broadened the sufficient cause concept to be a
minimal set of conditions which together inevitably
produce the disease.
The concept is shown in figure 11
Three combinations of factors (ABC, BED, ACE) are
shown here as sufficient causes of the disease.
Each of the constituents of the causal "pie" are
necessary.
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" the disease would
be eliminated by removing that alone.
25. Figure 11
A B
C
A E
D
A E
C
Each of the three components of the
interacting constellations of causes
(ABC, ADE, ACE) are in themselves
sufficient and each is necessary
26. Application of guidelines/criteria
to associations
An association rarely reflects a causal relationship but
it may.
These six criteria are a distillation of, or at least,
echo the ten Alfred Evans' postulates in Last's
Dictionary of Epidemiology (4th edition) and the nine
Bradford Hill criteria.
27. Strength and dose response
Does exposure to the cause change
disease incidence?
If not there is no epidemiological basis for a
conclusion on cause and effect.
Failure to demonstrate this does not, however,
disprove a causal role.
The usual measure of the increase in incidence is the
relative risk and the technical name for this criterion
is the strength of the association.
Dose-response
Does the disease incidence vary with the level of
exposure? If yes, the case for causality is advanced.
The dose-response relation is also measured using the
relative risk.
28. Specificity
Is the effect of the supposed cause specific to
relevant diseases, and, are diseases caused by a
limited number of supposed causes?
Imagine a factor which was linked to all health
effects
Why would that be so?
Non-specificity is characteristic of spurious
associations eg underestimating the size of the
denominator.
While specificity is not a critically important
criterion epidemiologists should take advantage of
the reasoning power it offers.
29. Consistency
Is the evidence within and between studies consistent?
Consistency is linked to generalisability of findings.
Spurious associations are often local.
30. Experiment
Does changing exposure to the supposed cause
change disease incidence?
Often there have been natural experiments.
Deliberate experimentation will be necessary.
Human experiments or trials are sometimes
impossible on ethical grounds.
Causal understanding can be greatly advanced
by laboratory and experimental observations.
31. Biological plausibility
Is there a biological mechanism by which
the supposed cause can induce the
effect?
For truly novel advances, however, the
biological plausibility may not be
apparent.
Biologically plausible that laying an infant
on its back to sleep may lead to its
inhaling vomitus.
Overturned by the biologically implausible
observation that laying a child on its back
halves the risk of cot death.
Nonetheless, biological plausibility
remains relevant to establishing causality.
32. The pyramid of associations
1 Causal and mechanisms
understood
2 Causal
3 Non-causal
4 Confounded
5 Spurious / artefact
6 Chance
33. Interpretation of data, study design
and causal criteria
Causal knowledge is born in the imagination and
understanding of the disease process of the
investigator.
Same data can be interpreted in quite different
ways.
The paradigm within which epidemiologists work
will determine the nature of the causal links they
see and emphasise.
Researchers to make explicit in their writings their
guiding research philosophy.
No epidemiological design confirms causality and
no design is incapable of adding important
evidence.
34. Summary
Cause and effect understanding is the highest
form of scientific knowledge.
Epidemiological and other forms of causal
thinking shows similarity.
An association between disease and the
postulated causal factors lies at the core of
epidemiology.
Demonstrating causality is difficult because of
the complexity and long natural history of
many human diseases and because of ethical
restraints on human experimentation.
35. Summary
All judgements of cause and effect are tentative.
Be alert for error, the play of chance and bias.
Causal models broaden causal perspectives.
Apply criteria for causality as an aid to thinking.
Look for corroboration of causality from other
scientific frameworks.
37. BIAS
Systematic, non-random deviation of results and inferences from the truth,
or processes leading to such deviation. Any trend in the collection, analysis,
interpretation, publication or review of data that can lead to conclusions
which are systematically different from the truth. (Dictionary of
Epidemiology, 3rd ed.)
38. MORE ON BIAS
Note that in bias, the focus is on an artifact of some
part of the research process (assembling subjects,
collecting data, analyzing data) that produces a
spurious result. Bias can produce either a type 1 or a
type 2 error, but we usually focus on type 1 errors
due to bias.
39. MORE ON BIAS
Bias can be either conscious or unconscious. In epidemiology,
the word bias does not imply, as in common usage, prejudice or
deliberate deviation from the truth.
40. CONFOUNDING
A problem resulting from the fact that one
feature of study subjects has not been
separated from a second feature, and has thus
been confounded with it, producing a spurious
result. The spuriousness arises from the
effect of the first feature being mistakenly
attributed to the second feature. Confounding
can produce either a type 1 or a type 2 error,
but we usually focus on type 1 errors.
41. THE DIFFERENCE BETWEEN BIAS
AND CONFOUNDING
Bias creates an association that is not true, but confounding
describes an association that is true, but potentially misleading.
42. EXAMPLES OF RANDOM ERROR, BIAS,
MISCLASSIFICATION AND
CONFOUNDING IN THE SAME STUDY:
STUDY: In a cohort study, babies of women who bottle feed and women
who breast feed are compared, and it is found that the incidence of
gastroenteritis, as recorded in medical records, is lower in the babies
who are breast-fed.
43. EXAMPLE OF RANDOM
ERROR
By chance, there are more episodes of gastroenteritis in the bottle-fed
group in the study sample, producing a type 1 error. (When in truth
breast feeding is not protective against gastroenteritis).
Or, also by chance, no difference in risk was found, producing a type 2
error (When in truth breast feeding is protective against gastroenteritis).
44. EXAMPLE OF BIAS
The medical records of bottle-fed babies only are less complete (perhaps
bottle fed babies go to the doctor less) than those of breast fed babies,
and thus record fewer episodes of gastro-enteritis in them only.
This is called ias because the observation itself is in error.
45. EXAMPLE OF CONFOUNDING
The mothers of breast-fed babies are of higher social class, and the babies
thus have better hygiene, less crowding and perhaps other factors that
protect against gastroenteritis. Crowding and hygiene are truly protective
against gastroenteritis, but we mistakenly attribute their effects to breast
feeding. This is called confounding. because the observation is correct,
but its explanation is wrong.
46. PROTECTION AGAINST RANDOM
ERROR AND RANDOM
MISCLASSIFICATION
Random error can work to falsely produce an association (type 1 error)
or falsely not produce an association (type 2 error).
We protect ourselves against random misclassification producing a type
2 error by choosing the most precise and accurate measures of
exposure and outcome.
47. PROTECTION AGAINST TYPE 1
ERRORS
We protect our study against random type 1 errors by establishing
that the result must be unlikely to have occurred by chance (e.g. p
< .05). P-values are established entirely to protect against
type 1 errors due to chance, and do not guarantee protection
against type 1 errors due to bias or confounding. This is the
reason we say statistics demonstrate association but not
causation.
48. PROTECTION AGAINST TYPE 2
ERRORS
We protect our study against random type 2
errors by
providing adequate sample size, and
hypothesizing large differences.
The larger the sample size, the easier it will
be to detect a true difference, and the largest
differences will be the easiest to detect.
(Imagine how hard it would be to detect a 1%
increase in the risk of gastroenteritis with
bottle-feeding).
49. KEY PRINCIPLE IN BIAS AND
CONFOUNDING
The factor that creates the bias, or the confounding
variable, must be associated with both the
independent and dependent variables (i.e. with the
exposure and the disease). Association of the bias or
confounder with just one of the two variables is not
enough to produce a spurious result.
50. In the example just given:
The BIAS, namely incomplete chart recording, has to be associated with
feeding type (the independent variable) and also with recording of
gastroenteritis (the dependent variable) to produce the false result.
The CONFOUNDING VARIABLE (or CONFOUNDER) better hygiene, has to
be associated with feeding type and also with gastroenteritis to produce
the spurious result.
51. Were the bias or the confounder associated with just the independent
variable or just the dependent variable, they would not produce bias or
confounding.
This gives a useful rule:
If you can show that a potential confounder is NOT associated with
either one of the two variables under study (exposure or outcome),
confounding can be ruled out.
54. Learning objectives
Critically review the concept of causality in relation to disease.
Know Hill’s Criteria for Causality and why such criteria are needed
Offer coherent arguments of nature versus nurture on health and
disease.
56. Thinking about causality
What does the term “cause” imply?
“That which produces an effect” (Chambers 20th C)
Causality is the relation of cause and effect.
In health care, we usually talk of cause and effect as etiological factor (cause)
and disease or pathological process (effect), e.g:
Strep. Pneumoniea causes pneumonia and meningitis.
Arterial occlusion causes tissue necrosis
57. Is that what we mean?
However, what we really mean is:
infection with Strep. Pneumoniea, under a limited range of conditions, can lead
to the development of pneumonia and meningitis.
Arterial occlusion leads to tissue necrosis.
Is this splitting hairs? No, because it reflects our thinking about disease:
what it is, its causes, and, most importantly, what strategies are used to
tackle it.
58. Different levels of causality
Very few things have single, isolated causes. Instead they reflect
chains or nets, temporal sequences of events.
Proximal causes: close factors
Distal causes: distant factors
Predisposing factors
Genetic
Environmental
Lifestyle
59. Distinguishing cause and determinants
from chance associations
Many factors influence the development of disease in addition to
the direct cause.
Investigation of cause is complex;
nature of affected (and unaffected individuals)
nature of their exposure
60. Koch's Postulates
• 1. The specific organism should be shown to be
present in all cases of animals suffering from a
specific disease but should not be found in
healthy animals.
• 2. The specific microorganism should be isolated
from the diseased animal and grown in pure
culture on artificial laboratory media.
• 3. This freshly isolated microorganism, when
inoculated into a healthy laboratory animal, should
cause the same disease seen in the original
animal.
• 4. The microorganism should be reisolated in pure
culture from the experimental infection.
61. Hill’s criteria
Strength of association
Temporal relationship
Distribution of the disease
Gradient
Consistency
Specificity
Biological plausability
Experimental models
Preventive trials
62. Risk
Risk is the likelihood of an event occurring. In health care events, we
usually consider a negative consequence arising from exposure to a hazard.
Types of risk
Absolute: incidence of disease in any population
Relative: ratio of the incidence rate in the group exposed to the hazard to the
incidence rate in the non-exposed group
Attributable: Difference in incidence rates between exposed and non-exposed
groups.
63. Errors in thinking about causality
The following reflect common mistakes in thinking about causes of
disease
Genes cause disease
Disease is due to "Lifestyle”
Environment accounts for most variation in disease rates
Why are they problematic?
What do you think?
64. Problematic thinking: “disease-gene”
All disease is a product of gene-environment interaction.
Genes specify protein structures -ONLY
Only when genes come into contact with an environment is their
advantage or disadvantage apparent: environment could be
cellular or geographic.
Lifestyle, (includes ageing, nutrition, infection, toxin exposure)
65. Do genes cause disease?
It all depends…on who…you ask
Differentiate
gene
a. genetic material instructing proteins that confer
relative advantage or disadvantage (inherited
polymorphisms): “normal”.
b. germ-line mutations: instructing proteins that
confer relative advantage or disadvantage
(sporadic/random polymorphisms) in germ cells -
inheritable
c. somatic mutation: instructing proteins that confer
relative advantage or disadvantage (sporadic or
random) limited to one cell.
66. What proportion of cancer is due to “cancer-
causing genes”?
Can you see what is wrong with this question?
Only ~10% of cancers are believed to be related to specific “cancer causing”
genes, e.g. BRCA1;
Of these, most are “interactive”, accounted for by e.g. Ca prostate (~40% of
risk due to heritable factors; Ca Br. 27%; colorectal, 35%).
Very few, rare cancers, e.g. retinoblastoma
68. Comparison of US Federal expenditure to
allocation of mortality according to
epidemiological modelEpidemiological
model
Federal health
expenditure
1974-1976 (%)
Allocation of
mortality (%)
• System of
medical care
organization
90.2 11
• Lifestyle 1.3 43
• Environment 1.6 19
• Human biology 6.9 27
69. Interactions
Genes do not “cause” diseases. It is wrong to claim they do. Genes instruct
the manufacture of proteins, which may or may not advantage or disadvantage
the organism under certain conditions.
Similarly, no single disease can be attributed to environment. Even poisoning is
influenced by phenotypical detoxification, which is genetically modulated.
Lifestyle is even more complex that either genes or environment.
How to use a systematic approach which checks for error, chance and bias before reaching judgements on cause and effect.
That epidemiological approaches to and criteria for causality are not a checklist and therefore conclusions must be carefully judged and tentative.
The need to synthesise data from epidemiological studies and other disciplines before reaching conclusions
Epidemiology is best conducted as a multidisciplinary endeavour.
The model broadens the causal thinking within the gene/host envelope
& emphasis the broader cause
& provides a basis for prevention and control
There is no single cause
Causes of disease are interacting
Disentangling is high possible
Causality may be two way
This lecture is to prompt you to think about some of the issues in understanding how diseases might emerge.
There is much publicity, and even wild speculation about the benefits that will be derived from the “cracking” of the genetic code. However, the history of medicine is the history of claims of future benefit (see Porter’s article in the web-link).
This lecture looks at some issues, tries to prompt you to think and hopefully, it may open up a creative view that might just lead to identifying a new way forward for some aspect of health care.
As retrieved from: R. Fielding
Dept. Community Medicine,
HKU
http://www.commed.hku.hk/
In this lecture we will critically review the concept of causality in relation to disease. This involves an understanding of how we think about disease, as well as a background in the development of tools we now use to explore the relationship between disease causes and their effects. Finally, we need to consider the relative contributions of nature, as genetic processes, and nurture, as environmental influence, to develop a realistic model of how disease develops.
We use the word “cause” far too loosely. Few things in medicine have clear causes, though disease determinants, risk factors and precursors can and have been readily identified.
Loose language both reflects and leads to loose thinking. When we say a virus “causes” a disease, is that really the case?
For example, do the viruses associated with common Colds cause the colds? For causality to be confirmed, certain criteria must be met.
The effect should not occur in the absence of the putative cause;
The greater the “dose” of the cause, the greater should be the magnitude of the effect;
In the case of disease, the mechanisms should be biologically plausible;
Does the virus model of colds fit these criteria?
The cold viruses are almost always present, but cold symptoms are not;
Increasing the viral load increases symptoms. No symptoms in the absence of viruses.
Viruses are plausible biological agents.
So, viruses seem to be necessary, but they are only part of the picture. And that is the problem because it is all too often assumed that they are the whole picture. And that is wrong.
It is very rare that only one thing causes one effect so consistently that it is clearly known. It has long been understood that certain compounds or plants have physiological effects if ingested. This is where almost all of our active medicines come from.
However, let’s consider bugs some more:
Strep. Pneumoniea can lead to pneumonia, but not always. Many other factors will influence this. If the immune system is active and sharp, the body can protect itself from many microbes. But knock out t-lymphocytes, as in AIDS for example, and all kinds of things that were previously not “causes” become highly effective at producing disease. So, is the cause of these AIDS-related diseases, like fungal pneumonia, the fungal agent (proximal cause) or the human immune deficiency virus (pre-disposing factor)? Or is it the damage to the skin that enabled the virus to gain entry to the body? Or is it the emotional resistance to using condoms which enables the virus to cross from one person to another? Or the opportunity for unprotected sexual intercourse with more than one person (distal cause)?
When we look at things this way, we see chains or “nets” of cause and effect, with nodes where several factors converge and an effect emerges, or is suppressed, much like constructive and destructive interference between waveforms. (As an illustration of how our thinking influences how we see the world, in the causal network, diseases can be due to the suppression of “good” effects as well as the occurrence of “bad” effects. This implication isn’t apparent from the simple cause-effect model.)
How we think about causes will determine what we do to try to fix or prevent a disease. Indeed, we can go further and ask what exactly is a disease?
Generally, diseases are physiological abnormalities, determined on the basis of a change in form, function or feeling, or on the basis of a physiological measure falling outside of some pre-determined range of values (normal range).
Three main classes or dimensions of cause are popularly grouped under the following headings:
Genetic: all and any heritable factors associated with a disease Environment: all and any non-heritable factors, particularly those related to physical and/or internal physiological environment.
Lifestyle: the exposure history of a person or activities, habits, and locations that constitute their sequence of lived environments and acts. This is dependent upon a person’s location, acts, and interactions.
These three groups constitute the majority of popular “explanations” for why disease occurs where and when it does. This disease is due to “faulty genes”, that disease is due to “environmental influences”, another disease is due to “lifestyle factors”, and so on. However, “explanations are not causes, but everywhere they are treated as if they were”. (quote, source unknown).
However, there are some clearer and more specific criteria for determining if a agent is causally connected to an effect we label a disease.
Carefully controlled experiments that test equally rigourously derived hypotheses should be used to examine the effects of each postulated cause. In a laboratory situation it is possible to eliminate, or adjust for the effects of factors that are either not of interest, such as diet or family interaction, or which are considered to confound the impact of some putative cause. The effect of the causal agent can then be assessed by exposing half of the group of subjects to it and preventing exposure in the other half - the control group while both groups are kept in standard conditions. Such a design allows us to be confident that the consequent development of the effects of exposure only in those exposed, are due to the causal agent and not something else.
However, in most situations, these kinds of rigourously controlled experiments are impractical on large numbers of people who live their day-to-day lives in the real world. More important, they are often unethical. So we must adopt other methods.
Different types of evidence (which ultimately underpin the EBP standards of evidence) that can be used to determine the extent that a cause and effect are linked are found in two main sets of guidelines developed to address these questions:
Koch’s Postulates and Hill’s Criteria. Both are very similar, with Hill’s Criteria being derived largely from the earlier work of Koch.
The principles were developed by Koch, the microbiologist who identified the tuberculosis bacillus. At the time they were proposed (late 19th Century), most disease was believed to arise from infectious agents or other, almost completely unknown processes. Koch’s Postulates are still used today to demonstrate causal association between an infectious agent and the development of a disease.
Find a person with the disease, identify the microorganism, culture it, inoculate another animal with the cultured microorganism, and if it develops the same disease as the original person, you have isolated the infectious agent. These principles are in use today over 100 years after Koch proposed them. They work. For infections. For simple uni-causal conditions. However, they do not work for example, to help us identify the cause of lung cancer.
So how do we identify causes of diseases that are not a result of infectious, living organisms that can be cultured in a Petri dish, such as diabetes or lung cancer? For these kinds of diseases a different, but related set of decision tools are needed.
To distinguish cause from simple association several factors need to be considered. Hill’s Criteria outline these.
Strength of association: the stronger the association between a putative cause and effect, the more likely there is to be a connection between the two.
Timing: The cause should precede the effect. Never the other way around.
Distribution: The spatial distribution of the disease should approximate to the spatial distribution of the causal agent.
Gradient: The response should correlate with the dose; more dose=more effect.
Consistency: The cause-effect relationship needs to be duplicated in different studies in different places.
Specificity: People not exposed to the cause should not develop the effect.
Biological plausibility: the biological activity of the suspected cause should be consistent with its effects.
Experimental models: animal or other experimental models should demonstrate the effect under experimental conditions.
Preventive trials: removal of the suspected cause should lead to removal of the effect.
The above concepts of risk are very important in health care because they represents the strength of the cause-effect relationship for a disease (or associated protective factor, e.g. exercise in Type II diabetes).
Absolute Risk is not very useful because there are always variations in exposure to hazards within a population or group. Absolute Risk is an average that cannot show the differences in disease incidence due to differences in exposure.
Relative Risk is sometimes expressed as a percentage measure of proportionate increase or decrease (in the case of a protective agent) in disease rates in an exposed group. It is a more useful measure than Absolute Risk.
Attributable Risk represents the risk arising from exposure to a particular hazard (or protective factor), I.e. is the risk attributable to the given hazard.
Why are the above erroneous?
Because they over-simplify the true picture. They fail to consider that all our biological status is an interaction between the phenotype and the physical environment. Lifestyle is a way of saying “different environments” and no more. However, it’s a useful phrase because when people talk about environmental factors, they usually refer to things external to the body, such as solar radiation, air pollution, smoking and so forth. Lifestyle incorporates these and includes other things found to be important, such as activity level, diet and behaviour, which are more “interactive” aspects between phenotype and environment.
To take a specific, evolutionary perspective, genes encode information to make proteins. That’s all. Nothing more. Now, a specific protein may provide some advantage to an organism such as a cell, in terms of efficiency of metabolism, or absorption or excretion, or it may not. It might provide a disadvantage to that cell. Whether a protein is advantageous, neutral or disadvantageous is solely dependent on the interaction the cell has with its immediate surroundings, other proteins, and so forth. In environments that confer advantage, the cell is more likely to survive and reproduce, and hence the numbers of cells carrying that particular gene will also increase - the frequency of the gene will increase in the population. If the environmental conditions change, there may be a selective disadvantage against cells carrying that gene, so the gene frequency will decline with each cell that fails to reproduce. Useful genes are usually “conserved”, that is, they may not be expressed, or only be partly expressed under conditions where there is no advantage. Disadvantageous genes under one type of environment may prove to advantageous in a different environment. A gene that alters the structure of the red blood cell membrane so that malarial parasites are less likely to successfully develop will do two things: it makes it more difficult for the cells to function normally, but it doesn’t kill you. Malaria, on the other hand, can kill you, so it is to the organism’s advantage to be a little weaker, but alive to reproduce, than to be strong, perfect and dead before reaching puberty.
So it is the interaction of a specific phenotype with the range of selection pressures presented by environment and lifestyle that leads to the development of specific advantageous and disadvantageous outcomes. The disadvantageous ones we now call disease, but we have simply tended to ignore the advantageous ones, so far.
A key point here to remember is that, from a population perspective, gene frequencies only change over generational time, taking hundreds, if not thousands of years to increase or decline.
Follow the web-links, there are three, to see three different views of this question.
We can think of different levels of cause.
Normal variations in the human genome, some of which provide advantage and some disadvantage, such as height, eye colour and proportion. Taller people are more successful in life, they are more likely to get better jobs, earn more money and so are advantaged. Their offspring are more likely to get a good start and hence survive, ensuring that trait is maintained. The opposite will also be the case, namely that there are normal variants which are disadvantageous in the present environment of C21st Urban humankind. If there was a sudden change, such as the earth being struck by a large lump of space debris, these disadvantageous genes might come in very useful, ensuring that, while different individuals lived or died, the species as a whole would continue. This variation is the vital genetic flexibility of our species.
This includes inherited genes that confer strong disadvantage, such as that for Huntington’s chorea. These tend to be very rare, but because they are only expressed after reproduction, carriers are not selected against by failure of reproduction.
Germ line mutations. New changes or polymorphisms in the germ line, (which are heritable). The ones drawn to the attention of the medical profession are usually those that disadvantage the child or adult. Few parents take their child to a doctor because the child is too intelligent for school, or taller than their peers, or better at sports, or can play the piano at 3 years of age.
Somatic mutations. New changes to the somatic line (non-inheritable). This includes errors of DNA copying when cells divide, and is implicated as the basis of ageing and some if not most cancer.
There are a great many problems associated with attributing cause to diseases. Cancer is considered the “jewel in the crown” of medical cures. S/he who can cure cancer will undoubtedly win the Nobel Prize and be as famous as Jenner and Pasteur. However, it is seriously problematic from the point of view of cause.
At a recent guest lecture to HKU, the Chairman of the Imperial Cancer Research Fund, the oldest and wealthiest in the UK, the director, Sir Walter Bodmer, showed a slide indicating the only around 10% of cancers were due to heritable factors, which he considered at great length. He failed to discuss the other 90% of the most common diseases called cancer. With the exceptions of very rare cancers, such as retinoblastoma, most cancers arise only in the presence of certain environmental factors which have impacted over a lifetime. The longer a person lives and their environment determines their exposure. Their body’s ability to detoxify their environment is partly genotypically determined, but also depends on factors life income (poor can’t afford adequate nutrition, such as fresh fruits, vegetables, clean air), diet, and behaviour (toxin load, from smoking, alcohol use etc.)
“True” genetic cancers are very rare for a very good reason. They are selected against.
This table outlines some interesting data. The first column on the left gives the proportion of deaths attributable to the six top causes of mortality in the USA in 1973, listed in the second column (Heart dis. =all heart disease; CVD, cerebro-vascular disease; pneumon = pneumonia; Respiratory= all other respiratory diseases). The third to sixth columns list the proportional contribution to the disease estimated to arise from each of the four columns of: 1. medical care (how much medical care does to prevent mortality from the particular diseases in column two), 2. lifestyle, 3. environmental and 4.biological contributions. These proportions are derived from epidemiological studies which
What can you conclude about the predominant sources of cause or prevention of these conditions?
If we look at the fourth most important cause of death in the USA in 1973, accidents, we see that about 85% of the variance in accident rates arises from life style and environmental factors, with biology being largely irrelevant as a contributor (2%) and subsequent medical care accounting for little more than one sixth (13%) of the variation in mortality from accidents. Other causes, like cancer,have a larger estimated contribution from biology, but less from treatment.
Compare this table with the previous one. This table details the expenditure in the USA in 1974-6 on the four different areas or components listed in the previous table (medical care, lifestyle, environment and biology). The right hand column lists the total estimated contribution to overall mortality from each of the four areas. The middle column gives the proportion of government expenditure allocated to each of these four areas in 1974-1976.
While these data are getting dated now, the pattern of spending remains fairly unchanged. They do indicate one thing quite clearly when you consider this table with the data in the previous table. Can you say what this is?
A study of 44,788 pairs of twins in Swedish, Danish and Finnish twin registries (NEJM July 2000) estimated that heritable factors accounted for 42% of risk for prostate cancer, 35% for colorectal cancer and 27% for breast cancer. At present, current genes identified account for much lower proportions of risk in these diseases. So there remain major gaps in knowledge of the genetics of cancer, but still the majority of risk variation is accountable by other, non-heritable factors. Few diseases are caused purely by genes. Genes are only information carriers. External factors can and do disrupt every level from the genes themselves to their final phenotype. At the other end of the spectrum, injuries sustained in a road traffic accident (RTA) have a genetic component, but you wouldn’t want to look for a gene predisposing to RTAs. To do so would be considered silly.
Lifestyle is the term used to describe the range of exposures a person receives over their life. These exposures may be in the form of toxins, they may be in the form of microbiological agents, they may be in the form of a pattern of behaviour, dictated by a culture or family which modulates exposure to other toxins, such as tobacco or hazards such as work. Lifestyle is the interaction between heritable and non-heritable influences on a person. Genes exist because they serve some purpose. Polymorphisms are conserved because they provide some advantages under certain environmental conditions; for example it may be a “tolerable” side effect of some other advantageous feature, such as HLA typology, and important immune feature, or may confer some advantage in times of dietary stress. An example is that thalassemias and sickle-cell disease provide some benefit in areas of high malarial prevalence, though are disadvantageous at other times and places. Type 2 Diabetes “genes” are likely to be advantageous when nourishment is scarce, not when plentiful.
Finally, the uterine environment seems to “set” the embryo’s metabolism for what to expect after birth. In lean times, a poorly nourished mother may produce a baby whose metabolism is set to be efficient with energy extraction and storage. Fifty years later, if food has been plentiful, a person’s risk of heart disease, and probably their weight, is much increased. Similar uterine effects have been proposed for other disease, such as breast cancer. This model is called Barker’s Hypothesis.