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PubMed2005

Causality in cancer epidemiology.

In this review, issues of causality in epidemiologic research with emphasis on the aetiology of human cancer are considered. Principles of assessing causation in epidemiological studies of cancer are distinguished into those concerning an individual study, several studies and a particular person. Strengths and weaknesses of various approaches of documenting carcinogenicity in humans are examined and lists of major established causes of human cancer are presented. The review concludes with estimates of mortality from cancer around the world that can be attributed to specific factors under the light of the current scientific knowledge.

Bias↗

PubMed2006

Two kinds of items in quality of life instruments: 'indicator and causal variables' in the EORTC qlq-c30.

Two kinds of variables may be differentiated within instruments measuring health-related quality of life (HRQOL). Physical symptoms may be called causal variables because their occurrence can cause a change in HRQOL, but poor HRQOL need not necessarily imply that a patient suffers from these symptoms. Other items can be regarded as indicator variables. They reflect the level of HRQOL and a patient with a poor HRQOL is likely to have low scores on all indicator variables. The aim of this study was to test the relationship of the latent HRQOL construct to items and domains on the EORTC QLQ-C30. Confirmatory factor analysis was performed on EORTC QLQ-C30 data from 205 gastrointestinal cancer patients assessed one month after surgery. Functioning scales were established as variables indicating the level of HRQOL whereas all other subscales and items were established as variables causing a change in HRQOL. The model-data fit was satisfactory. Results support the hypothesis that two kinds of variables may be differentiated within HRQOL instruments. Further research should investigate whether both kinds of variables could be combined into a higher order, aggregate score for HRQOL.

Activities of Daily Living↗

PubMed1994

From superstitious behavior to delusional thinking: the role of the hippocampus in misattributions of causality.

Nearly half a century ago B. F. Skinner proposed the hypothesis that human superstitiousness would be equivalent to the 'superstitious' behavior displayed by animals in operant situations involving response-independent reinforcement. Surprisingly, no attempt has ever been made to test this equivalence hypothesis experimentally. In the light of recent evidence for a common neurological basis of both superstitious beliefs held by normal subjects and delusional ideas of psychotic patients, Skinner's hypothesis has become topical again. We present an extension of the hypothesis which assumes dysfunction of the medial temporal lobe, in particular of the hippocampus, to be responsible for conditioned superstitions in animals, for common everyday superstitions, and for schizophrenic delusions. This hypothesis is based on (1) the observation of an enhanced 'superstitious' reactivity in hippocampectomized animals, (2) findings of an increased occurrence of popular superstitions in patients with a temporal-limbic epileptic focus, and (3) morphological and pharmacological evidence for schizophrenic delusions to be causally related to hippocampal damage.

Animals↗

PubMed1996

Causal thinking, biomarkers, and mechanisms of carcinogenesis.

The use of biomarkers is increasing both in acute and chronic disease epidemiology, but the rationale for their introduction is not always firmly established (e.g., when and how their use is scientifically justifiable and cost effective). The use of biomarkers should be considered within the context of causal models in epidemiology, and of the intertwining of causation and pathogenesis. Unlike infectious diseases, for cancer and cardiovascular disease external "necessary" causes have not been identified. Thus, the classification of cancer and other chronic diseases cannot be based on unequivocal criteria such as the "etiologic" classification of infectious diseases. As far as morphology is concerned, "neoplasia" and "anaplasia" are attributes of cancer that cannot be defined in a straightforward way. Tissue pathologies are minimal and difficult to differentiate from normal tissue in some cancers but are obvious in others. From a mechanistic point of view, unless molecular biology discovers specific mechanistic steps in carcinogenesis, which indicate the existence of "necessary" events in carcinogenesis, we cannot adopt an unequivocal definition of cancer. The potential contribution of biomarkers to the elucidation of the pathogenetic process should be considered in the light of such uncertainties. There is a range of indications for biomarkers, from the use of very specific measurements aimed at single molecules, to measurements indicating cumulative exposure to agents with the same mechanism of action. The potential uses of markers in chronic disease epidemiology include (1) exposure assessment in cases in which traditional epidemiologic tools are insufficient (particularly for low doses and low risks); (2) multiple exposures or mixtures, in which the aim is to disentangle the etiologic role of single agents; (3) estimation of the total burden of exposure to chemicals having the same mechanistic target; (4) investigation of pathogenetic mechanisms, and (5) study of individual susceptibility (e.g., metabolic polymorphism, DNA repair).

Animals↗

PubMed2006

Functional connections between auditory cortical fields in humans revealed by Granger causality analysis of intra-cranial evoked potentials to sounds: comparison of two methods.

Knowledge of neural interactions amongst cortical sites is important for understanding higher brain function. We studied such interactions using Granger causality (GC) to analyze auditory event-related potentials (ERPs) recorded directly and simultaneously from two physiologically identified and functionally interconnected auditory areas of cerebral cortex in human neurosurgical patients. Two methods of GC analysis were used and the results compared. Both approaches involved adaptive autoregressive modeling but differed from each other in other ways. Results obtained by using the two methods also differed. Fewer false-positive results were obtained using the method that suppressed the ERP non-stationarity and that expressed the GC as the sum of model coefficients, which suggests that this is the more appropriate approach for analyzing ERPs recorded directly from the human cortex.

Auditory Cortex↗

PubMed2005

Covariation and quantifier polarity: what determines causal attribution in vignettes?

Tests of causal attribution often use verbal vignettes, with covariation information provided through statements quantified with natural language expressions. The effect of covariation information has typically been taken to show that set size information affects attribution. However, recent research shows that quantifiers provide information about discourse focus as well as covariation information. In the attribution literature, quantifiers are used to depict covariation, but they confound quantity and focus. In four experiments, we show that focus explains all (Experiment 1) or some (Experiment 2-4) of the impact of covariation information on the attributions made, confirming the importance of the confound. Attribution experiments using vignettes that present covariation information with natural language quantifiers may overestimate the impact of set size information, and ignore the impact of quantifier-induced focus.

Analysis of Variance↗

PubMed2006

Simplicity and probability in causal explanation.

What makes some explanations better than others? This paper explores the roles of simplicity and probability in evaluating competing causal explanations. Four experiments investigate the hypothesis that simpler explanations are judged both better and more likely to be true. In all experiments, simplicity is quantified as the number of causes invoked in an explanation, with fewer causes corresponding to a simpler explanation. Experiment 1 confirms that all else being equal, both simpler and more probable explanations are preferred. Experiments 2 and 3 examine how explanations are evaluated when simplicity and probability compete. The data suggest that simpler explanations are assigned a higher prior probability, with the consequence that disproportionate probabilistic evidence is required before a complex explanation will be favored over a simpler alternative. Moreover, committing to a simple but unlikely explanation can lead to systematic overestimation of the prevalence of the cause invoked in the simple explanation. Finally, Experiment 4 finds that the preference for simpler explanations can be overcome when probability information unambiguously supports a complex explanation over a simpler alternative. Collectively, these findings suggest that simplicity is used as a basis for evaluating explanations and for assigning prior probabilities when unambiguous probability information is absent. More broadly, evaluating explanations may operate as a mechanism for generating estimates of subjective probability.

Adult↗

PubMed2003

Depressive episodes--evidence for a causal role of primary anxiety disorders?

Anxiety and depressive disorders are common mental disorders in general population, imposing tremendous burden on both affected persons and society. Moreover, comorbidity between anxiety and depressive conditions is high, leading to substantial disability and functional impairment. Findings consistently suggest that anxiety disorders are primary to depression in the majority of comorbid cases. Yet, the question of whether anxiety disorders are risk factors for depression, and potentially even causal risk factors for the first onset of depression, remains unresolved. Recent results have shown that anxiety disorders increase the risk for subsequent depression, and also affect the course of depression, resulting in a poorer prognosis. Further, some results suggest a dose-response-relationship in revealing that a higher number of anxiety disorders and more severe impairment associated with anxiety disorders additionally increase the risk for subsequent depression. The goal of this paper is to review recent literature, summarize implications of previous findings, and suggest directions for future research regarding preventive and intervention strategies.

Anxiety Disorders↗

PubMed2025

Assessing the causal effect of genetically predicted metabolites and metabolic pathways on vitiligo: Evidence from Mendelian randomization and animal experiments.

Vitiligo is a common chronic skin depigmentation disorder that seriously decreases the patients' overall quality of life. Human blood metabolites could contribute to unraveling the underlying biological mechanisms of vitiligo. We used GWAS summary statistics to assess the causal association between genetically predicted 1400 serum metabolites and vitiligo risk by Mendelian randomization (MR). Then, after constructing the mouse model of vitiligo, we did non-targeted metabolomics analysis on the mouse serum and validated MR's pathway enrichment results ulteriorly. In the initial phase, MR analysis revealed causative associations between 36 metabolites and vitiligo risk, including 8 metabolite ratios and 28 individual metabolites (19 known and 9 unknown metabolites). In the validation stage, 7 metabolites were successfully validated. Of the 28 individual metabolites, most are related to lipid metabolism. Genetically predicted higher 4-oxo-retinoic acid showed the strongest protective effect on vitiligo, while the most potent risk effect was the increase in quinate. The metabolites associated with vitiligo risk are mainly enriched in alpha-linolenic acid metabolism, linoleic acid metabolism, arginine biosynthesis and metabolism pathways, validated through the serum metabolomics of vitiligo mouse. By integrating genomics and metabolomics, this study provides new insights into the association between metabolites and vitiligo, highlighting the potential roles of specific metabolites in the pathogenesis of vitiligo. These metabolites associated with vitiligo could serve as new biomarkers, further research could help to reveal how these metabolites influence specific pathways in the development of vitiligo.

Animals↗

PubMed2004

Modeling the causal relationships between symptoms associated with restless legs syndrome and the patient-reported impact of RLS.

The objective of this study is to examine the causal relationships between the symptoms of restless legs syndrome (RLS) and specific clinical and subjective health-related, quality of life consequences. Structural equation modeling was applied to data from a questionnaire-based observational study. The RLS morbidities of decreased functional alertness and emotional distress in our sample of patients appear to be mostly secondary to the sleep disturbance associated with RLS. There was no clear indication of any other feature of RLS affecting these two aspects of RLS morbidity. A primary treatment goal should be the reduction of the sleep disturbance of RLS, both to decrease the RLS-related nocturnal distress and to improve daytime functioning.

Adult↗

PubMed2001

Causal models for road accident fatalities in Yemen.

An identification of the causes of road accident fatalities is becoming more important with the growth of technology, population, number of vehicles and the need for their use. Many authors have addressed the problem in the past but no universal findings have been obtained. The problem tends to be different under different environments and for different geographical regions. The aim of this paper is to develop a model for the analysis and forecasting of road accident fatalities in Yemen considering data restrictions. The proposed data has a particular structure of accident occurrence that has not been reported in any existing research using data in other countries. The available data for the period 1978-1995 is used to build models to understand the nature and extent of the causes of fatalities. Part of the data is used for model building and part of it for test purposes. The issues of correlation and causality have been addressed and multiple collinearity is investigated and dealt with. Two alternative models are proposed based on both statistical grounds and that of practicality in viable decision making. The influence of consuming a locally grown stimulant called Qat on road users has been addressed and it is found that it increases the risk of accidents. This is not the common understanding within the authorities in Yemen as growing and consuming Qat is unregulated.

Accidents, Traffic↗

PubMedDate not supplied

Homocysteine and stroke: evidence on a causal link from mendelian randomisation.

BACKGROUND: Individuals homozygous for the T allele of the MTHFR C677T polymorphism have higher plasma homocysteine concentrations (the phenotype) than those with the CC genotype, which, if pathogenetic, should put them at increased risk of stroke. Since this polymorphism is distributed randomly during gamete formation, its association with stroke should not be biased or confounded. We investigated consistency between the expected odds ratio for stroke among TT homozygotes, extrapolated from genotype-phenotype and phenotype-disease studies, and the observed odds ratio from a meta-analysis of genotype-disease association studies. METHODS: We searched MEDLINE and EMBASE up to June, 2003, for all relevant studies on the association between homocysteine concentration and the MTHFR polymorphism, and until December, 2003, for those on the association between the polymorphism and the risk of stroke. Pooled odds ratios and 95% CI were calculated by random-effects and fixed-effects models. Consistency between expected and observed odds ratios was assessed by interaction test. FINDINGS: 111 studies met the selection criteria. Among 15635 people without cardiovascular disease, the weighted mean difference in homocysteine concentration between TT and CC homozygotes was 1.93 micromol/L (95% CI 1.38 to 2.47). The expected odds ratio for stroke corresponding to this difference based on previous observational studies was 1.20 (1.10 to 1.31). In our genetic meta-analysis (n=13928) the odds ratio for stroke was 1.26 (1.14 to 1.40) for TT versus CC homozygotes, similar to the expected odds ratio (p=0.29). Consistency between the odds ratios was preserved in analyses by age-group, ethnic background, and geographical location. INTERPRETATION: The observed increase in risk of stroke among individuals homozygous for the MTHFR T allele is close to that predicted from the differences in homocysteine concentration conferred by this variant. This concordance is consistent with a causal relation between homocysteine concentration and stroke.

Causality↗

PubMedDate not supplied

Risk factors, causality, and policy initiatives: the case of aluminum and mental impairment.

The question addressed is when can the evidence concerning a health issue be regarded as adequate to implement policy initiatives. The approach is illustrated by comparing evidence about the effects of cigarette smoking with evidence for the aluminum (Al) hypothesis (that Al contributes to mental impairment and especially to Alzheimer's Disease). The criteria for evaluating the evidence are based on the consistency and strength of the association between a putative risk factor and the relevant outcome variable, the likelihood that the relative risk represents a causal relationship, whether possible mechanisms are available, the number of persons affected, and the costs of modifying the risk factor.

Aged↗

PubMed2000

Attributions of causality, responsibility and blame for positive and negative symptom behaviours in caregivers of persons with schizophrenia.

BACKGROUND: Causal, responsibility and blame attributions for positive and negative symptom behaviours were examined in 70 caregivers of persons with schizophrenia. METHODS: The majority of subjects belonged to self-help group organizations. The three types of attributions for positive and negative symptom behaviours were assessed by self-report questionnaires. RESULTS: The extent of patient responsibility did not differ between the two types behaviours. Intentionality and knowledge were equally important in predicting responsibility for positive symptom behaviours, while intent was the most important predictor of responsibility for negative symptom behaviours with the patient capacity playing a significant but minor role. The entailment model was not supported for the two types of behaviours. CONCLUSIONS: Increased attention should be given to responsibility dimensions in assigning moral accountability to the patient. The entailment model should be further explored in problematical caregiving situations.

Adult↗

PubMed2004

Progress in clinical neurosciences: Migraine-stroke: a causal relationship, but which direction?

A significant association between migraine and ischemic stroke has been demonstrated in population and case-control studies. The risk of ischemic stroke appears to be higher in migraine with aura (MWA) than migraine without aura (MwoA). Migraine-stroke comprises a number of distinct entities, including migrainous infarction, in which ischemic stroke occurs during an attack of MWA and migraine-related stroke, in which the causal link is less clear. Migrainous infarction accounts for only one-third of migraine-stroke, strokes may occur during attacks of MwoA, and a number of cerebrovascular disorders may present as MWA or MwoA. Migraine may occur as a consequence of conditions that are known to cause stroke; therefore it remains to be determined whether migraine predisposes to stroke in the absence of any known disease associations, if it is an epiphenomenon of an underlying stroke diathesis, or if it requires the presence of another stroke risk factor to produce cerebral ischemia. Furthermore, it is unclear if ischemia results in migraine more often than migraine results in ischemia. Careful clinical studies that evaluate this bidirectional relationship are needed to determine why migraine patients are subject to a higher risk of ischemic stroke.

Adult↗

PubMed2001

Caries in populations--a theoretical, causal approach.

The focus of this paper is caries in populations. Caries is assessed as a phenomenon and as it occurs in populations. It is observed that in recent literature the notion of causation of caries is restricted to the biological process on the tooth surface. This may be sufficient to explain caries as a phenomenon, but it is argued that a biological causation is insufficient in order to understand caries and its variation in populations. The understanding of the determinants of a population's oral health has been seriously impeded by the absence of a theoretical framework. A framework would be useful to the extent that it would bridge relevant categories for portraying complex causal patterns of caries in populations. An approach to a framework has therefore been outlined, and the idea of such a framework has been confronted with three critical comments. The framework is as yet pragmatic, incomplete, uncertain and fragmented. Yet, even such an approach may invite greater precision in epidemiological concepts about causes of caries than presently prevails. The framework directs attention to health effects of collective phenomena that cannot be reduced to individual attributes. The image proposed in this paper is intended to spur discussion about important aspects of the epidemiology of caries in populations.

Attitude to Health↗

PubMed1994

Individual differences in causal uncertainty.

This article presents a scale that measures chronic individual differences in people's uncertainty about their ability to understand and detect cause-and-effect relationships in the social world: the Causal Uncertainty Scale (CUS). The results of Study 1 indicated that the scale has good internal and adequate test-retest reliability. Additionally, the results of a factor analysis suggested that the scale appears to be tapping a single construct. Study 2 examined the convergent and discriminant validity of the scale, and Studies 3 and 4 examined the predictive and incremental validity of the scale. The importance of the CUS to work on depressives' social information processing and for basic research and theory on human social judgment processes is discussed.

Adult↗

PubMed2000

Causal judgment from contingency information: the interpretation of factors common to all instances.

Participants made judgments about stimulus materials in which there were 2 possible causes of an outcome. One of these was a common factor, a factor present in all instances presented for judgment, and the other was a positive covariate of the outcome. Instead of interpreting the positive covariate as the cause, participants consistently preferred an interpretation in which the common factor was the cause and the positive covariate enabled the cause to produce its effect. Participants' judgments of both interpretations were predicted by the proportion of instances that were confirmatory for the interpretation and not by deltaP. The findings support a hypothesis that people have a multirole conceptualization of causality including, in addition to the roles of cause and effect, that of an enabler, a factor the presence of which ensures that a thing is in a state of readiness to produce a particular effect.

Adult↗