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PubMed1999

Annotation: the development of antisocial behavior: an integrative causal model.

In this paper we have described an integrative causal model of the development of antisocial behavior in children and adolescents. The present model primarily integrates several previous models, but offers some new testable hypotheses. We believe that stable individual differences in propensity to antisocial behavior reflect variations in a number of dimensions of predisposing temperament and cognitive ability, each with its own genetic and environmental influences. The dimensions of predisposing temperament include oppositionality, harm avoidance, and callousness. Genetic influences are predicted to have only indirect effects on antisocial behavior via their influence on predisposition and on the youth's social environment. Environmental influences are expected to be important contributors to antisocial propensity, but these environmental influences reflect, in part, the genetic influences on the dimensions of predisposition (i.e. genotype-environment covariance). We also hypothesize that the levels of influence of the factors that determine individual differences in antisocial propensity change with development, such that genetic influences are of greater magnitude in early childhood and social influences contribute more strongly during later childhood and adolescence (both through independent effects and genotype-environment covariance). However, low levels of heritable predisposing child characteristics may protect against peer influences at all ages.

Adolescent↗

PubMed1999

[Causal research epistemology and epidemiology of complex systems].

Epidemiology now meets with the crisis of its most fundamental paradigm. The biomedical paradigm of the search for individual-level disease risk factors opposes the public-health paradigm of the search for contextual-level disease risk factors. The public-health paradigm exacerbates the causal research of disease risk factors in that it must now count on a hierarchy of scales of observation. This underlines the need to take into account nonlinear relationships among scales and variables as well as the dynamic aspect of the phenomena. It is concluded that the complex conceptualization required by the public-health paradigm will entail epidemiologists to develop new theories and to familiarize themselves with approaches more akin to those used in the study of complex systems.

Causality↗

PubMed2000

Infants' association of linguistic labels with causal actions.

Six experiments examined infants' ability to associate nonsense words with 2 causal actions: pushing and pulling. Although Experiment 1 found that 14-month-olds failed to form word-action associations, 18-month-olds in Experiment 2 provided reliable evidence of doing so. Additional experiments explored why 14-month-olds may not have formed such an association. Experiment 3 examined 14-month-olds' ability to discriminate a change in either the action or the label when the other element was held constant. Infants discriminated the change in label but not the change in action. When the language labels were replaced with music (Experiments 4-6), 14-month-old infants responded in terms of and discriminated between pushing and pulling. These results, in comparison with those from Experiments 1 and 3, suggest that for 14 month-olds, attempting to associate labels with actions may interfere with their discrimination of similar actions.

Age Factors↗

PubMed2000

[Application of the causal theory of action through analysis of therapeutic non-observance].

This paper presents an analysis of an aspect of non-observance in the treatment of type 1 diabetes mellitus, the absence of adaptation of insulin dosage in spite of hyperglycemia. The adaptation of insulin dosage by the patient is described as an intentional action, performed as a habit. The problem is analysed through the causal theory of action and the concept of akrasia. These considerations may be useful to understand other aspects of therapeutic non-observance.

Attitude to Health↗

PubMed1997

[Causality and epidemiology].

In examining the issue of causality within epidemiology, the text begins with a brief historical overview that reclaims the different meanings which the West's main philosophers have lent to this concept. It next delves into the historical roots of epidemiology as a scientific discipline and the transformations the concept of cause has undergone within this realm. With these presuppositions in place, the text goes on to analyze the 20th century development of epidemiology and the crisis it currently faces in terms of paradigm. Three alternatives are explored as ways out of this crisis: social epidemiology, Popperian criticism, and the contributions of molecular biology. Lastly, the text discusses the need for a new epidemiological theory grounded on the theory of complexity.

Causality↗

PubMed2003

Quantifying biases in causal models: classical confounding vs collider-stratification bias.

It has long been known that stratifying on variables affected by the study exposure can create selection bias. More recently it has been shown that stratifying on a variable that precedes exposure and disease can induce confounding, even if there is no confounding in the unstratified (crude) estimate. This paper examines the relative magnitudes of these biases under some simple causal models in which the stratification variable is graphically depicted as a collider (a variable directly affected by two or more other variables in the graph). The results suggest that bias from stratifying on variables affected by exposure and disease may often be comparable in size with bias from classical confounding (bias from failing to stratify on a common cause of exposure and disease), whereas other biases from collider stratification may tend to be much smaller.

Bias↗

PubMed2003

Causality and collateral estoppel: process and content of recent SSRI litigation.

In Tobin v. SmithKline Beecham Pharmaceuticals a jury in the U.S. District Court for the District of Wyoming found that the medication Paxil "can cause some individuals to commit homicide and/or suicide," and that it was a legal cause of the deaths in this case. A motion was recently put before the United States District Court for the District of Utah to adopt the findings of the Tobin case--via the application of collateral estoppel--to a case involving an individual's suicide while prescribed Paxil. This article summarizes these two cases, as reflected in court documents, and comments on limitations of common causality assertions.

Causality↗

PubMedDate not supplied

[Regression methods and causal inference: structural equations models].

The estimate of correlations among observed outcomes is crucial in biomedical research, especially when the aim of the study is to infer, from the magnitude of these correlations, the causal influence of certain, sometimes latent, factors. In such situations, a typical regression approach, known as "structural equation models" (SEM), which was introduced in the 1970s, becomes significant. These models allow hypotheses to be formulated quite clearly, thanks to some explicit and rigorous graphical representations, on which the "path analysis" is based. SEM, which were initially used in economics, have in the past decade been applied in a wide variety of fields, especially in genetic epidemiology. It's in this field that SEM are extraordinarily effective, representing a simple yet powerful means of estimating the contribution of genes and the environment to the phenotypic expression of a given disease. To this end, data on twins are particularly useful, and in this case the correlation between the outcomes describes the extent of similarity of the twin phenotypes. From this standpoint, SEM undoubtedly constitute one of the most promising statistical tools for family studies and quantitative genetic research. The method can be easily extended to traditional epidemiology, and some interesting applications have already been developed in occupational and social epidemiology. In this paper, we describe in detail the SEM approach and discuss the use of these models in genetic epidemiology, using twin studies as an example. We also discuss the application of SEM in fields other than genetic research.

Causality↗

PubMed2006

Periodontitis and cardiovascular disease: a review of shared risk factors and new findings supporting a causality hypothesis.

Periodontitis is a common chronic disease worldwide. It is a major cause of tooth loss among adults and recently has been suggested to increase the risk for developing several systemic diseases, including cardiovascular disease. Populations are not equally affected by periodontal disease because there are several environmental and host factors modulating susceptibility. Cardiovascular disease shares many of the same susceptibility factors. The purpose of this report is to identify risk factors and indicators common to periodontitis and cardiovascular disease, and also to discuss their possible interrelationship in this association. Recent findings to support a causal association between the 2 conditions are also presented.

Cardiovascular Diseases↗

PubMed2005

The causal homogeneity of biological kinds.

The aim of this paper is to show that biological kinds can be causally homogeneous, although all biological causes are identical with configurations of physical causes. The paper considers two different strategies to establish that result: the first one relies on two different manners of classification (according to function and according to composition); the other one exploits the idea of biological classifications being rather coarse-grained, whereas physical classifications are fine-grained.

Animals↗

PubMed2005

Diderot, Cabanis and Lamarck on psycho-physical causality.

Modern physics was born in the 17th century and modern biology one century later. Immediately, scientifics and philosophers ask themselves what is the relationship between those two sciences and between properties of non-living and living matter. Among those scientifics and philosophers, some think that mental phenomena are of biological nature--they are materialists--so they encounter a second problem: what is the relationship between properties of non-thinking and thinking living matter? This paper examines the doctrine of three French philosophers of the (post-) Enlightenment on those subjects: Diderot, Cabanis and Lamarck, and, as their answer is in terms of causality and supervenience, I compare succinctly their doctrine with those of Searle and Kim.

Animals↗

PubMed1995

[Cardiac death and acute myocardial infarct after psychological or physical stress--causality questions and insurance law].

Often, it is the question to the medical expert, if there is a causality in the lawful sense from professional effort or psychical stress to acute coronary death or acute myocardial infarction. Following the German social law the connection has to be probably. Probability is well defined juridically opposite to possibility. The medical expert has to answer if the physical or psychical stress has caused the fatality or not more than manifested. Here are discussed arguments that the atheromatosis of the coronary vessels has much more importance than the manifestation of acute death or myocardial infarction caused by spasmus. There is no evidence for the existence of spastic genesis without any arteriosclerotic focus.

Causality↗

PubMed1997

[Severe bronchial stenosis with upstream bronchiectasis in an arc welder: causal relation or epiphenomenon?].

This case concerns an arc welder who presented suppurative bronchiectasis and episodes of purulent left side pleurisy in relation to cystic bronchiectasis of the left lower lobe and a very severe stenosis at the origin of the main left bronchus. The medicolegal problem was to assess the causal relationship between these lesions and occupational exposure. They do not come under the heading of table 44 of the General List and we made this the aim of discretionary award in front of a regional committee of compensation for occupational disease.

Bronchial Diseases↗

PubMed1996

[Environmental and indoor air exposure to asbestos fiber dust as a risk and causal factor of diffuse malignant pleural mesothelioma].

In an interdisciplinary, multicentre case control study of the causal factors of the diffuse malignant mesothelioma (DMM) standardised histories where taken from n = 324 Patients suffering from DMM, n = 315 hospital control patients (KK) and n = 182 population controls (PK). For 66 DMM, 149 KK and 107 PK a risk from asbestos fibre dust at the workplace was not detectable. For latter persons indoor and outdoor asbestos exposure outside of the workplace were investigated. The following factors were examined: neighbourhood exposure from companies using asbestos, living in big cities and nearby main traffic roads, building materials containing asbestos, electric storage heaters and household contacts. For using electric storage heaters a statistically significant increased odds ratio (OR) was observed for DMM as well in comparison with KK (OR = 2.42; 95%-CI: 1.01-5.72) and in comparison for PK (OR = 2.91; 95%-CI: 1.08-7.80). Only outside of Hamburg an increased OR compared to KK was observed for people living in the neighbourhood of asbestos factories (OR = 16.3; 95%-CI: 1.35-196.8) and also, but only in Hamburg, compared to PK living nearby main traffic roads. There is only a trend for a mesothelioma-risk for household-contacts based on a few cases. In one DMM-patient without an occupational asbestos exposure the lung dust fibre analysis yielded 2.912 FB and 1.459 x 10(3) crocydolithe fibres per gram dried lung tissue. As a child he lived in the immediate vicinity of the blue asbestos mine in Wittenoom, Australia. Therefore in special cases a para-occupational asbestos or a neighbourhood asbestos exposure can be demonstrated as a risk factor of diffuse malignant mesothelioma.

Adult↗

PubMed1998

[Roaming through methodology. IV. Causality].

If a factor A is often followed by an event B, it may erroneously be concluded that one causes the other. Actually B may have been brought about by a factor C (the true cause), A being only an epiphenomenon of C. If factors other than C (for example D or E) can cause the same effect B, none of those factors is a necessary cause. Causes often are multiple: a single causal factor is often not sufficient for a certain effect to ensue, whereas that effect can result from a number of factors acting together (simultaneously or consecutively).

Causality↗

PubMed1998

Bayesian modeling for linking causally related observations in chest X-ray reports.

Our natural language understanding system outputs a list of diseases, findings, and appliances found in a chest x-ray report. The system described in this paper links those diseases and findings that are causally related. Using Bayesian networks to model the conceptual and diagnostic information found in a chest x-ray we are able to infer more specific information about the findings that are linked to diseases.

Algorithms↗

PubMed1998

Posttraumatic stress disorder and drug disorders: testing causal pathways.

BACKGROUND: Although there is a high degree of comorbidity between posttraumatic stress disorder (PTSD) and drug use disorders, little is known about causal relationships between PTSD, exposure to traumatic events, and drug use disorders. METHODS: In a longitudinal study in southeast Michigan, 1007 adults aged 21 to 30 years were initially assessed in 1989 and were followed up 3 and 5 years later, in 1992 and 1994. Psychiatric disorders according to DSM-III-R criteria were measured by the National Institute of Mental Health Diagnostic Interview Schedule. To take into account temporal sequencing, the associations between PTSD, traumatic events, and drug use disorders were analyzed by using Cox proportional hazards models with time-dependent covariates. RESULTS: Posttraumatic stress disorder signaled an increased risk of drug abuse or dependence (hazards ratio, 4.5; 95% confidence interval, 2.6-7.6, adjusted for sex), whereas exposure to traumatic events in the absence of PTSD did not increase the risk of drug abuse or dependence. The risk for abuse or dependence was the highest for prescribed psychoactive drugs (hazards ratio, 13.0; 95% confidence interval, 5.3-32.0). There was no evidence that preexisting drug abuse or dependence increased the risk of subsequent exposure to traumatic events or the risk of PTSD after traumatic exposure. CONCLUSION: The results suggest that drug abuse or dependence in persons with PTSD might be the inadvertent result of efforts to medicate symptoms, although the possibility of shared vulnerability to PTSD and drug use disorders cannot be ruled out.

Adult↗

PubMed1997

Test of the health promotion model as a causal model of construction workers' use of hearing protection.

The health promotion model (HPM) was tested as a causal model of construction workers' use of hearing protection (N = 359). Theoretical and exploratory models fit well, with the theoretical model accounting for 36.3% of variance and the exploratory model accounting for 50.6% of variance in hearing protection use. Value of use (benefits of using hearing protection), barriers to use, and self-efficacy were significant predictors in both the theoretical and exploratory models, but perceived health status was a predictor only in the theoretical model. In the exploratory model, where modifying factors were allowed direct relationships with use of hearing protection, two modifying factors--noise exposure and interpersonal influences-modeling--were significant predictors. Results of this test of the HPM are consistent with the revised HPM (Pender, 1996). There were significant direct paths from modifying factors to behaviour. Use of hearing protection was best predicted by behavior-specific predictors, such as perceived barriers to use of hearing protection. Results support the use of the HPM to predict use of hearing protection.

Adult↗