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PubMed2005

On the use of discrete choice models for causal inference.

Methodology for causal inference based on propensity scores has been developed and popularized in the last two decades. However, the majority of the methodology has concentrated on binary treatments. Only recently have these methods been extended to settings with multi-valued treatments. We propose a number of discrete choice models for estimating the propensity scores. The models differ in terms of flexibility with respect to potential correlation between treatments, and, in turn, the accuracy of the estimated propensity scores. We present the effects of discrete choice models used on performance of the causal estimators through a Monte Carlo study. We also illustrate the use of discrete choice models to estimate the effect of antipsychotic drug use on the risk of diabetes in a cohort of adults with schizophrenia.

Adolescent↗

PubMed1993

Estimating the causal effect of smoking cessation in the presence of confounding factors using a rank preserving structural failure time model.

Estimating the causal effect of quitting smoking on time to death or first myocardial infarction requires that one control for the differences in risk factors between individuals who elect to quite at each time t versus those who elect to continue smoking at time t. In this paper we examine the limitations of standard time varying Cox proportional hazards models to yield tests and estimates of this effect. Implementing the method of G-estimation proposed by Robins, we perform an observational analysis of data from the Multiple Risk Factor Intervention Trial (MRFIT) and estimate the causal effect of cigarette cessation while controlling for such time varying confounders as angina. We reject the null hypothesis of no effect of quitting on time to failure, and estimate that by quitting smoking, an individual increases by 50 per cent his time to death or first myocardial infarction (MI).

Adult↗

PubMed2000

Causal knowledge of predators' behaviour in wild Diana monkeys.

Wild Diana monkeys, Cercopithecus diana, of Taï forest, Ivory Coast, are preyed upon by leopards, Panthera pardus, and chimpanzees, Pan troglodytes. These two predators differ in their main hunting tactic and Diana monkeys attempt to avoid predation with two distinct antipredator strategies: conspicuous alarm-calling behaviour to leopards and silent, cryptic behaviour to chimpanzees. However, the Diana monkeys' choice of the appropriate antipredator strategy is complicated by the fact that chimpanzees themselves also fall prey to leopards. Chimpanzees give loud and conspicuous alarm screams when they detect a leopard. When these chimpanzees' leopard alarm calls were played back to different groups of Diana monkeys, in about half of the cases recipients switched from a chimp-specific cryptic response to a leopard-specific conspicuous response, suggesting that some individuals assumed the presence of a leopard. Groups whose home range was in the core area of the resident chimpanzee community were more likely to respond this way than more peripheral groups, indicating between-group differences in semantic knowledge. In a follow-up experiment, the monkeys' understanding of the chimpanzee alarm calls was further assessed with a prime-probe technique. Monkeys were primed with chimpanzee alarm calls and then, 5 min later, tested with leopard growls to see whether they were able to anticipate the presence of a leopard. Results were consistent with the hypothesis that monkeys responding cryptically to chimpanzee alarm calls did so because they were not able to understand the calls' meaning. Data are discussed with respect to three possible cognitive mechanisms, associative learning, specialized learning programmes, and causal reasoning, that could have led to causal knowledge in some individuals but not others. Copyright 2000 The Association for the Study of Animal Behaviour.

Journal Article↗

PubMed1998

Gulf War veterans' illnesses: a case study in causal inference.

The objective of this study was to determine from the published epidemiological literature whether there is evidence for a causal association between service in the Gulf War and illness in U.S. veterans. Eleven published studies were analyzed using standardized epidemiologic criteria for assessing causality. A consistent association was found between deployment to the Gulf and self-reports of symptoms. No consistency was seen in physical findings or laboratory results. Strength of association varied with different study designs. Dose-response information is limited, because of lack of quantitative data on exposures. Biological plausibility varies for different risk factors. Specificity of association is not seen. Frequency of self-reported symptoms is increased in U.S. Gulf War veterans compared to other veterans of the same era, but specific causes of illnesses cannot be ascertained. Major gaps in data that impeded this analysis include (1) lack of objective data on specific environmental exposures (2) lack of baseline health assessments, and (3) lack of objective measures of post-deployment health status. In future deployment of U.S. troops, accurate exposure and health data will be needed if the causes of subsequent illnesses are to be accurately assessed.

Environmental Exposure↗

PubMed2001

Relationships between 80 human papillomavirus genotypes and different grades of cervical intraepithelial neoplasia: association and causality.

To clarify the causal relationship between human papillomavirus (HPV) and cervical intraepithelial neoplasia (CIN), we analyzed 386 unfixed biopsy specimens by blot hybridization at Tm -40 degrees C, targeting 38 skin and 42 genital HPVs. By the recognition of PstI, BanI, and MspI cleavage patterns, single genital, but no skin's HPVs were identified with more than 10 copies per cell in 354 CIN (88 CIN I, 94 CIN II, and 172 CIN III). HPVs 40, 42, 43, 54, 62, or 71 was found in 10 CIN I, while HPVs 18, 30, 39, 51, 56, 59, 66, 68, 69, or 82 was found in 35 CIN I, 20 CIN II, or 8 CIN III. On the other hand, HPVs 16, 31, 33, 35, 52, 58, or 67 was identified in 43 CIN I, 74 CIN II, or 164 CIN III. The results are strongly indicative that most genital HPVs have potency to induce CIN I; however, HPV 16 and its closely related types are able to efficiently induce CIN III. We discuss the definition of causal HPV for CIN with regard to viral prevalence and viral load.

Biopsy↗

PubMed1980

[Natural law, causality and induction: a contribution to theorectical biology].

According to the situation of recent biology it seems to be necessary to continue the theorectical foundation of this science, and especially a foundation beyond physics and metaphysics. The preconditions of such a project are given with the problems of causality, natural law and induction. The discussion of these subjects in modern philosophy of science did not bring useful results, for philosophy of science itself is orientated by physics. On the other hand even the history of these problems in biology shows that the acceptance of physical or philosophical viewpoints leads to invincible difficulties. Therefore, in this paper, I have tried to demonstrate the necessity of analyzing these basic problems in a new way. The conditions and circumstances of a biological phenomenon have a special kind of multidimensional relationship, so that they cannot be reduced to simple linear systems of cause and effect. The fact that biological systems have a lot of retroactive effects make the description of their causality much more complicated than it is in physics. So the natural law in biology is characterized by its relativity concerning the parameters which create the special dependence of a biological phenomenon's constituent parts.

Biology↗

PubMed1985

[Causal analytic studies on demonstration of neuroendocrine parameters in combined hypoglycemia test in depressive subgroups].

With the help of an analytical path structure model (causal analysis) the aim of the study was to elucidate further, in female patients with various depressive disorders, some correlations of causal interdependencies between changes both in basal secretion of anterior pituitary hormones and in their responses to the (combined) insulin tolerance test (ITT) with extraneous factors--such as age, deviation from ideal body weight (in percentage), severity of depression and score in the Newcastle Scale (NCS)--that may influence these abnormalities. In various depressive subgroups the strength of influence and the different importance of deviation from ideal body weight and basal growth hormone (GH) concentration (as exclusion criteria) for their neuroendocrine reactivity in the combined ITT was shown. The hypothesis that cortisol hypersecretion may be the primary disturbance and the other possible neuroendocrine changes such as blunted GH, cortisol and TSH responses to stimuli in some depressive patients all may be secondary to the (elevated) cortisol level could not be corroborated. The endogenous mono- and bipolar subtypes of major depressive disorders showed intimate connections between the various neuroendocrine functional systems and the above mentioned extraneous factors resulting in a narrowed variability and a stronger coupling in the reactivity of these hormonal functional systems, a condition which can be seen as analogous to experimental results at the psychophysiological level in these nuclear groups of depressed patients, whose psychopathological state is also characterized by similar limitations in their "degree of freedom" (Heimann).

Adult↗

PubMed1993

Causal attributions for illness among Turkish psychiatric out-patients and differences between diagnostic groups.

Causal attributions of 152 Turkish non-psychotic psychiatric out-patients for the development of their psychological problems were examined by using a 31-item attributions for psychological problems questionnaire (APP). The factor analysis of the responses to the APP yielded seven factors, which were: attributions to conflicts within the family of origin and with the present family, attributions to personal-characterological and behavioural attributes, work problems, interpersonal conflicts and bad luck. Examination of the causal attributions of patients from three DSM-III-R diagnostic groups revealed no significant differences between diagnostic groups. The highest attributional scores were for conflicts with the present family and personal-characterological attributes.

Adolescent↗

PubMed1985

Development of learning-disabled and normally achieving children's causal attributions.

The causal attributions of learning-disabled (LD) and normally achieving (NA) children in grades 3 through 8 were compared. Attributions were measured by two scales that asked children to attribute hypothetical academic failure situations to factors that were either within (e.g., insufficient effort) or beyond (e.g., insufficient ability, blaming others) their control. Consistent with a learned helplessness hypothesis. LD girls, regardless of age, were more likely than NA children to attribute their failures to factors beyond their control. In contrast, LD boys' explanations for their failures paralleled those of NA children. That is, with increasing age the LD boys were more likely to attribute their failures to insufficient effort. Explanations and implications of sex differences in developmental patterns of LD children's causal attributions are discussed.

Achievement↗

PubMed1995

Mental health officers' causal explanations of combat stress reaction.

This study examined causal attributions for combat stress reaction (CSR) among 117 Israel Defense Forces (IDF) mental health officers. The impact of case characteristics (the level of objective stress in the situation, reaction of others in the same situation, soldier's previous functioning, and type of symptomatology) and respondent characteristics (professional affiliation, therapeutic orientation) on these attributions was also examined. Results show that mental health officers view CSR primarily as a response to external circumstances; it is not generally seen as resulting from personality traits or intrapsychic processes. Findings also indicate that causal attributions were influenced at least to some degree by the clinicians' professional affiliation, their therapeutic orientation, and their knowledge of the casualty's prior functioning.

Adult↗

PubMed1993

Causal attributions in psychiatric patients.

An instrument for a systematic assessment of attributions that psychiatric patients have about their disorder is presented together with some preliminary results, for example on differences between sex and diagnostic groups. The comparison with a sample of (mostly untreated) students demonstrates that causal attributions in psychiatric patients should be assessed with specifically designed instruments. The presented scale may help to investigate longitudinally the course of causal attributions during treatment.

Adult↗

PubMed1990

[Partial causality in case of physician liability].

The specific theories about causality related to the different branches of law do have importance in the politics of rules. In civil law and physician liability law as well the theory of adequacy is valid. This theory selects only certain conditions as legally effective out of the abundance of all existing conditions. In physician liability law it typically happens, that indifferent chains of cause and effect coincide, what matters is to distinguish one from another and according to conditions to determine the partial causality which has to be attributes to the physician. The example of the untreated peri-lunar luxation and subsequent lunar necrosis illustrates the legally effective problematic nature of two causes.

Germany↗

PubMed1998

[Pain syndromes with causal participation of the sympathetic nervous system].

The efferent sympathetic nervous system is organized into subsystems that innervate and regulate via separate peripheral sympathic pathways the different autonomic target organs. This review discusses mechanisms through which this efferent system may be causally involved in the generation of pain. Clinical pain syndromes in which this may be the case are "complex regional pain syndromes" (CRPS) type I (previously reflex sympathetic dystrophy) and type II (recently causalgia). The "sympathetically maintained pain" (SMP) is a symptom (and not a clinical entity) that can principally also be present in other pain syndromes. An explanatory hypothesis, which may explain the clinical phenomenology of CRPS (different types of pain, swelling, autonomic, motor and trophic changes) and the mechanisms involved, is described and discussed. This hypothesis consists of different components that either have been tested and verified experimentally or which are still hypothetical. The hypothesis consists of changes in the primary afferent (nociceptive and non-nociceptive) neurones (sensitization, ectopic impulse generation) and of the neurones in the spinal cord (preferentially in the dorsal horn) which are secondary consequences of the changes in the primary afferent neurones ("central sensitization"). These changes are not specific for SMP. The centerpiece of the hypothesis is a positive feedback circuit that consists of the primary afferent neurones, spinal cord neurones, sympathic neurones and the pathologic sympathetic-afferent coupling. This coupling can occur directly via noradrenaline (or possibly another substance) at different sites of the afferent neurone (at the lesion site, remote from the lesion site in the periphery and in the spinal ganglion). The direct coupling requires that the afferent neurone expresses adrenoceptors. Indirect coupling can occur via the vascular bed or otherwise, e.g. by changes of the neurovascular transmission. The activity in the sympathetic neurones to the affected extremity can change. This change does not consist of a generalized increase of sympathetic activity but of a change of the reflexes (e.g., thermoregulatory and nociceptive reflexes). From this follows that the pathophysiologal processes operating in CRPS may occur at four levels of integration that interact with each other: effector organ, peripheral afferent and sympathetic neurone, spinal cord, supraspinal centres. Recent experimental investigations on rats show that the sympathetic nervous system is possibly also causally involved in the generation of inflammation and inflammatory pain. The mechanisms by which this occurs are different from those operating in SMP during CRPS.

Animals↗

PubMed2000

Pressure sores: epidemiology, medico-legal implications and forensic argumentation concerning causality.

The aim of the present investigation was to identify the frequency and grading of pressure sores in a large series of unselected consecutive deceased subjects before cremation and to discuss aspects of the forensic argumentation concerning causality. A total of 10,222 corpses were examined prospectively over a 1-year-period (1998) for the occurrence, localization and grading of pressure sores. Epidemiological aspects (e.g. age, sex, underlying and contributing causes of death, place of death etc.) were taken from the death certificate. The mean prevalence of pressure sores was 11.2% (87.1% isolated sores; predominant localization of advanced grades on the sacrum in 69.6%). There was a positive correlation between the prevalence of sores and advanced age resulting in a clear female predominance in the age group of 80 years and over because of differences in life expectancy. A significant correlation was found between the prevalence of pressure sores and certain underlying diseases, e.g. trauma, senile dementia, neurological diseases, apoplexy and marasmus. Pressure sores of all grades were more frequently found in the deceased when a senior citizen's or nursing home was given on the death certificate as the domicile in the last period of life. The forensic argumentation for the causal relationship of a pressure sore as the focus of fatal infectious complications or septicemia has to be based on the results of clinical expertises and forensic investigations (evaluation of the institutional documentation of the patient's course, autopsy findings, histology, immunohistochemistry). The vast majority of physicians seem to pay only little attention to the potentially fatal outcome of pressure sores and fatalities associated with this condition are clearly underreported. From the point of view of social medicine, the prevalence of pressure sores in a defined population can be seen as a parameter for the quality of nursing and medical care. In bringing these fatalities to light, the field of legal medicine contributes to a general quality control of standards of nursing and medical care.

Age Factors↗

PubMed2006

Comments on 'Is partial coherence a viable technique for identifying generators of neural oscillations?': Why the term 'Gersch Causality' is inappropriate: common neural structure inference pitfalls.

To aid prospective neural connectivity inference analysts and hoping to preclude misconception spread, we exploit the didatic value of some of the issues raised by Albo et al. (Biol Cybern 90: 318-326, 2004) who claim that signal-to-noise ratio (SNR) values can lead to mistakes in structural inference when using partial coherence in connection to Gersch's 1970 method for spotting signal sources (Gersch in Math Biosci 14: 177- 196, 1972). We show theoretically that Gersch's method is able only to spot which measurement of some common underlying factor has the least amount of additive noise and that this has nothing to do with any reasonable notion of 'causality' as suggested by Albo et al. (Biol Cybern 90: 318-326, 2004). We also show that despite the inherent structural ambiguity of the model used by Albo et al. (Biol Cybern 90: 318-326, 2004) to back their claim, its data can nonetheless furnish the correct time precedence hierarchy between the activities in its measured structures, both when simple (correlation) and more sophisticated methods are used (partial directed coherence) (Baccala and Sameshima in Biol Cybern 84:463-474, 2001a) in a true depiction of time series causality.

Animals↗

PubMed2001

The T911C (F304S) substitution in the human ALG6 gene is a common polymorphism and not a causal mutation of CDG-Ic.

A T911C (F304S) substitution in the ALG6 gene involved in congenital disorder of glycosylation type Ic (OMIM 603147) has been described. However, whether the F304S substitution is a common polymorphism or a causal mutation remains unclear. We screened for the T911C substitution in the ALG6 gene in 54 unrelated healthy French individuals. We developed a restriction fragment length polymorphism assay with a mutagenic primer introducing a diagnostic DdeI restriction site. We found 23 heterozygotes (42.6%) and 3 homozygous individuals (5.5%). This result indicates that T911C is a common polymorphism with an allele frequency of 27% in a French population and not a causal mutation of congenital disorder of glycosylation type Ic.

Alleles↗

PubMed2004

Bovine spongiform encephalopathy and Creutzfeldt-Jakob disease: facts and uncertainties underlying the causal link between animal and human diseases.

Following an outbreak of bovine spongiform encephalopathy (BSE) in dairy cows in the United Kingdom (UK), 153 definite and probable human cases of new variant Creutzfeldt-Jakob disease (nvCJD) have been reported, almost exclusively in the UK. Although exposure to the BSE agent is the most plausible interpretation for the occurrence of nvCJD, the causal link between the BSE prion and nvCJD is still debated. This review discusses the pros and cons of nvCJD as a separate nosographic entity, the scientific basis for a correlation between BSE and nvCJD, the validity of the current diagnostic criteria for CJD and nvCJD, the contribution of epidemiology to the detection of a causal relation between BSE and nvCJD, and the present and future directions of the epidemiological research on BSE, CJD and nvCJD.

Animals↗

PubMedDate not supplied

Causal attributions in first-degree relatives of depressed and agoraphobic inpatients.

Causal attributions in 77 first-degree relatives of major depressed, agoraphobic, major depressed and agoraphobic (comorbid), and dysthymic inpatients were studied. The hypothesis that the relatives of comorbid and dysthymic patients should exhibit more "depressogenic" causal attributions for bad events than the relatives of major depressed and agoraphobic patients was partly supported. Relatives of dysthymic patients attributed bad events to more internal causes and assigned more importance to the events themselves than did relatives of major depressed patients. Relatives of patients with major depression and agoraphobia comorbidity attributed bad events to more internal causes than did the relatives of major depressed patients. Statistically controlling for differences in sex, age, social class, and depressive symptom level did not significantly alter the results among the four groups.

Adult↗