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PubMed2001

Chronic and temporarily activated causal uncertainty beliefs and stereotype usage.

In 3 studies, we examined the hypothesis that the effects of stereotype usage on target judgments are moderated by causal uncertainty beliefs and related accuracy goal structures. In Study 1, we focused on the role of chronically accessible causal uncertainty beliefs as predictors of a target's level of guilt for an alleged academic misconduct offense. In Study 2, we examined the role of chronic causal uncertainty reduction goals and a manipulated accuracy goal; in Study 3, we investigated the role of primed causal uncertainty beliefs on guilt judgments. In all 3 studies, we found that activation of causal uncertainty beliefs and accuracy concerns was related to a reduced usage of stereotypes. Moreover, this reduction was not associated with participants' levels of perceived control, depression, state affect, need for cognition, or personal need for structure. Results are discussed in terms of their implications for the model of causal uncertainty and, more generally, in terms of the motivational processes underlying stereotype usage.

Adult↗

PubMed1990

Causality and the allocation of attention during comprehension.

Recent research has suggested that each statement in a narrative text is understood by relating it to its causal antecedents and consequences and that the text as a whole is understood by finding a causal path linking its opening to its final outcome. Fletcher and Bloom (1988) have proposed that in order to accomplish this goal, while minimizing the number of times long-term memory has to be searched, readers focus their attention on the last clause of a narrative that has causal antecedents but no consequences in the preceding text. As a result, a statement that is followed by a causal antecedent should remain the focus of attention, while the same statement followed by a consequence should not. This prediction was tested and confirmed in three experiments which show that when a target statement is followed by a sentence that includes only causal antecedents, (a) continuation sentences related to it are read more quickly, (b) target words drawn from it are easier to recognize, and (c) subject-generated continuations are more likely to be causally related to it.

Attention↗

PubMed1995

Causal inferences in reading: from immediate activation to long-term memory.

Three different tasks were used to investigate the time course of drawing causal inferences. Participants read passages that contained a causal coherence break that could be resolved by reactivating a concept presented earlier in the passage. In Experiment 1, participants named a probe word that represented the earlier mentioned cause more quickly after encountering the causal coherence break, suggesting that the causal concept had quickly been reactivated. In Experiment 2, participants were slow to read a sentence after the causal coherence break that contradicted the intended inference, indicating that the inference had been encoded and retained in working memory. In Experiment 3, the results of a recall task indicated that the causal link was also included in the long-term memory representation of the text.

Humans↗

PubMed2001

Causal judgments about relations between multilevel variables.

Three experiments presented stimulus information about cause and effect variables taking 3 quantitative values. Judgments tended to vary in accordance with considerations of conditions affecting the validity of causal inference from correlational data: whether causal candidates were presented simultaneously or in a temporal order such that one could affect the other and whether candidates were confounded with each other. The results supported a general hypothesis that causal judgments are moderated in accordance with acquired methodological intuitions. The fourth experiment showed that tendencies in correlation judgment were different from those in causal judgment, further supporting the hypothesis that causal judgment from multilevel variable information is, to some extent, determined by processes or conceptual frameworks specific to the domain of causal cognition.

Adult↗

PubMed2000

Risk factors for a causal intermediate and an endpoint: reconciling differences.

When a risk factor influences the intermediary but not progression to the endpoint, it has been shown that the relative risk estimate for the causal intermediate is identical to that for the endpoint under a single pathway framework. When there are multiple pathways, the relative risk estimate for the endpoint is reduced. The authors examine how the reduction of the effect size from a risk factor's association with the causal intermediate to that with the endpoint relates to the proportion of endpoint cases arising through other pathways, and the measure of effect used. For multiple pathways, all measures of effect are reduced and the reduction increases as the proportion of endpoint cases arising through other pathways increases. For single pathways, the relative rate ratio and odds ratios are reduced. In particular, the reduction in the odds ratio may be dramatic because of the commonness of causal intermediates relative to the endpoint. Comparisons of causal intermediate studies with those for the endpoint should consider the influences of multiple pathways, the prevalence of the causal intermediate, the measure of effect used, and the multiple effects a risk factor may have along the pathway when interpreting the differences observed across the causal chain.

Colorectal Neoplasms↗

PubMed2025

Plasma metabolites mediate the causal relationship between gut microbiota and erectile dysfunction: insights from Mendelian randomization study.

BACKGROUND: While the relationship between gut microbiota and erectile dysfunction (ED) has been reported, the specific pathways involved remain unclear. AIM: This study aims to investigate the causal relationship between gut microbiota and ED, and to identify the potential role of plasma metabolites as mediators. METHODS: Utilizing aggregated genome-wide association study (GWAS) data, a comprehensive two-sample Mendelian randomization (MR) analysis was performed involving 196 gut microbiota taxa, 1400 plasma metabolites and ED. Causal relationships between gut microbiota, plasma metabolites and ED were explored. In addition, mediation analysis was applied to identify the pathway from gut microbiota to ED mediated by plasma metabolites. OUTCOMES: This study reveals that plasma metabolites act as mediators regulating the influence of gut microbiota on ED. RESULTS: MR analysis identified causal relationships between six gut microbial taxa and ED, with Butyrivibrio increasing the risk of ED, while Alistipes, Prevotella 9, Dialister, Marvinbryantia, and LachnospiraceaeUCG010 exhibited protective effects. Additionally, 45 plasma metabolites demonstrated causal associations with ED. Finally, mediation analysis revealed four mediation relationships. Sensitivity analysis indicated no heterogeneity or pleiotropy in this study. CLINICAL IMPLICATIONS: Modulating gut microbiota or targeting specific metabolites may offer new therapeutic approaches for ED, highlighting the potential for microbiome-based interventions. STRENGTHS AND LIMITATIONS: The MR approach and large-scale GWAS data provide robust causal evidence, but the findings are limited by their focus on European populations and lack of experimental validation. Further studies are needed to confirm these mechanisms in diverse cohorts and functional models. CONCLUSION: This study establishes a causal link between gut microbiota, plasma metabolites, and ED, identifying specific microbial taxa and metabolites as key contributors to ED risk. The mediating role of plasma metabolites highlights potential therapeutic strategies, such as probiotics or dietary interventions targeting harmful metabolites.

Mendelian randomization↗

PubMed2025

Causal relationships between antibody-mediated immune responses and acute pancreatitis: Evidence from a genetic study.

Certain specific antibody-mediated immune responses may be associated with acute pancreatitis (AP), but their causal relationship remains uncertain. Therefore, we used bidirectional two-sample Mendelian randomization (MR) to investigate their causal link and potential mediation by inflammatory cytokines. Data for this study were sourced from a large-scale Genome Wide Association Study (GWAS) communal data pool. To explore the causality between antibody-mediated immune responses and AP, we performed two-sample bidirectional MR analyses using 5 approaches: inverse-variance weighted (IVW), MR-Egger, weighted mode, weighted median, and simple mode. We also studied the potential mediating effect of 91 circulating inflammatory cytokines using a two-step MR method. Additionally, sensitivity analyses were conducted using MR-Egger intercept test and Cochran Q test to ensure the robustness of the outcomes. The results of forward MR analysis showed that anti-Epstein-Barr virus (anti-EBV) IgG seropositivity [OR = 0.941; 95% CI, 0.893-0.992; P = .023] and human herpes virus (HHV) 6 IE1A antibody levels [OR = 0.894; 95% CI, 0.816-0.981; P = .017] significantly reduced the risk of AP. The results of the reverse MR analysis revealed a negative correlation between AP and anti-EBV IgG seropositivity [OR = 0.775; 95% CI, 0.605-0.992; P = .043]. Furthermore, none of the 91 circulating inflammatory cytokines could mediate the causal relationship between HHV-6 IE1A antibody levels and the risk of AP. The results of sensitivity analysis confirmed the robustness of these causalities. The current study suggests that HHV-6 IE1A antibody levels are a protective factor against AP, and there is a bidirectional causality between AP and anti-EBV IgG seropositivity. In addition, the mediation analysis results showed that the 91 circulating inflammatory cytokines could not serve as mediators between the 46 antibody-mediated immune responses and AP.

Humans↗

PubMed2025

THE CAUSAL ASSOCIATION OF CARDIOMETABOLIC DISEASES AND SEPSIS-RELATED OUTCOMES: A MENDELIAN RANDOMIZATION AND POPULATION STUDY.

Objective: The causality between cardiometabolic disease (CMD) and sepsis has remained largely unknown. To elucidate this, we conducted a Mendelian randomization (MR) and population study. Methods: First, we used univariable and multivariable MR analyses to investigate causal associations between CMD and sepsis-related outcomes. We obtained genome-wide association study summary from both the MRC Integrative Epidemiology Unit and the FinnGen consortium. Subsequently, a two-step mediation MR analysis was performed to explore mediators. Afterward, we conducted an observational study using the Medical Information Mart for Intensive Care IV database, in which multivariable logistic regression models were utilized to examine the relationship between CMD and sepsis-related outcomes. Results: In the MR study, type 2 diabetes mellitus (OR = 1.058, 95% CI = 1.017-1.100, P = 0.005), obesity (OR = 1.113, 95% CI = 1.057-1.172, P < 0.001), and heart failure (HF) (OR = 1.178, 95% CI = 1.063-1.305, P = 0.002) were independently causally related to sepsis. Obesity (OR = 1.215, 95% CI = 1.027-1.437, P = 0.023) and HF (OR = 1.494, 95% CI = 1.080-2.065, P = 0.015) also showed independent causal associations with sepsis critical care admission. Mediation MR analysis identified 23 blood metabolites potentially causally linked to sepsis ( P < 0.05), yet none mediated the relationship between CMD and sepsis. In the observational study, we found associations between sepsis and several conditions including type 2 diabetes mellitus, obesity, hypertension, stroke, HF, and hyperlipidemia after adjusting for confounding factors. Moreover, hypertension, stroke, HF, coronary artery disease, and hyperlipidemia were linked to sepsis critical care admission. Conclusion: This study has, for the first time, revealed indicative evidence of a causal relationship between CMD and sepsis through observational and genetic evidence. Taken together, clinical attention to sepsis may be warranted among patients with CMD.

Humans↗

PubMed2023

Causal Associations of Sleep Apnea with Alzheimer's Disease and Cardiovascular Disease: a Bidirectional Mendelian Randomization Analysis.

BACKGROUND: Sleep apnea (SA) has been linked to an increased risk of dementia in numerous observational studies; whether this is driven by neurodegenerative, vascular or other mechanisms is not clear. We sought to examine the bidirectional causal relationships between SA, Alzheimer's disease (AD), coronary artery disease (CAD), and ischemic stroke using Mendelian randomization (MR). METHODS: Using summary statistics from four recent, large genome-wide association studies of SA (n=523,366), AD (n=64,437), CAD (n=1,165,690), and stroke (n=1,308,460), we conducted bidirectional two-sample MR analyses. Our primary analytic method was fixed-effects inverse variance weighted MR; diagnostics tests and sensitivity analyses were conducted to verify the robustness of the results. RESULTS: We identified a significant causal effect of SA on the risk of CAD (odds ratio (OR IVW ) =1.35 per log-odds increase in SA liability, 95% confidence interval (CI) =1.25-1.47) and stroke (OR IVW =1.13, 95% CI =1.01-1.25). These associations were somewhat attenuated after excluding single-nucleotide polymorphisms associated with body mass index (BMI) (OR IVW =1.26, 95% CI =1.15-1.39 for CAD risk; OR IVW =1.08, 95% CI =0.96-1.22 for stroke risk). SA was not causally associated with a higher risk of AD (OR IVW =1.14, 95% CI =0.91-1.43). We did not find causal effects of AD, CAD, or stroke on risk of SA. CONCLUSIONS: These results suggest that SA increased the risk of CAD, and the identified causal association with stroke risk may be confounded by BMI. Moreover, no causal effect of SA on AD risk was found. Future studies are warranted to investigate cardiovascular pathways between sleep disorders, including SA, and dementia.

Preprint↗

PubMedDate not supplied

Perceptual causality in children.

Three experiments considered the development of perceptual causality in children from 3 to 9 years of age (N = 176 in total). Adults tend to see cause and effect even in schematic, two-dimensional motion events: Thus, if square A moves toward B, which moves upon contact, they report that A launches B--physical causality. If B moves before contact, adults report that B tries to escape from A--social or psychological causality. A brief pause between movements eliminates such impressions. Even infants in the first year of life are sensitive to causal structure in both contact and no-contact events, but previous research with talking-age children found poor verbal reports. The present experiments used a picture-based forced-choice task to reduce linguistic demands. Observers saw eight different animations involving squares A and B. Events varied in whether or not these agents made contact; whether or not there was a delay at the closest point; and whether they moved rigidly or with a rhythmic, nonrigid "caterpillar" motion. Participants of all ages assigned events with contact to the physical domain and events without contact to the psychological domain. In addition, participants of all ages chose causality more often for events without delay than with delay, but these events became more distinct over the preschool range. The manipulation of agent motion had only minor and inconsistent effects across studies, even though children of all ages considered only the nonrigid motion to be animal-like. These results agree with the view that perceptual causality is available early in development.

Child↗

PubMed2005

A simulation study on the detection of causal mutations from F2 experiments.

A simulation study has been performed to evaluate the power and the rate of false positives for the detection of causal mutations under two different models of analysis. We used an F2 design generated from an F0 population of five sires of line 1 and 40 dams of line 2 to produce an F1 population of 10 sires and 80 dams. Two different locations of the causal mutation and several frequencies of the mutations in the parental populations were considered. The first model included only the genetic configuration of the mutation, while the second model also included the probability of line origin given the neutral markers. Both models performed well when the mutation at the candidate gene was the causal mutation, although a greater power was obtained using the first model, because of its relative simplicity compared to the second one. However, when the candidate gene mutation was a neutral mutation, the second model presented a lower rate of false positives than the first. Moreover, in some cases the second model allowed distinction between the neutral and the causal mutation. The F2 design has a great power to detect quantitative trait loci provided by linkage disequilibrium, but also makes it difficult to discriminate between causal and neutral mutations. Therefore a high percentage of false positives can be expected. The limitations of F2 designs for discriminating between neutral and causal mutations are discussed.

Animals↗

PubMed2004

Theories of conduct disorder: a causal modelling analysis.

BACKGROUND: If a clinician has to make decisions on diagnosis and treatment, he or she is confronted with a variety of causal theories. In order to compare these theories a neutral terminology and notational system is needed. The Causal Modelling framework involving three levels of description - biological, cognitive and behavioural - has previously been used to compare causal accounts for dyslexia and autism. METHOD: In this article we present this framework and explore its application to four causal theories of conduct disorder. We discuss the problems we encountered in this application and evaluate both the framework and the theories of conduct disorder. CONCLUSIONS: It was possible to capture parts of the theories of conduct disorder in the Causal Modelling framework but a multi-model approach may be necessary for the alternative theories of conduct disorder we evaluate. The application of the framework helps to see the relationships among the various theories of aspects of conduct disorder and demonstrates the need for more explicitness in the causal theories.

Child↗

PubMed2006

Causal reasoning in rats.

Empirical research with nonhuman primates appears to support the view that causal reasoning is a key cognitive faculty that divides humans from animals. The claim is that animals approximate causal learning using associative processes. The present results cast doubt on that conclusion. Rats made causal inferences in a basic task that taps into core features of causal reasoning without requiring complex physical knowledge. They derived predictions of the outcomes of interventions after passive observational learning of different kinds of causal models. These competencies cannot be explained by current associative theories but are consistent with causal Bayes net theories.

Animals↗

PubMed2026

Single-cell expression quantitative trait locus Mendelian randomization reveals immune cell-specific causal regulatory networks and actionable targets in polycystic ovary syndrome.

ObjectiveTo systematically investigate whether the pathogenesis of polycystic ovary syndrome (PCOS) is causally related to dysregulated gene expression in specific immune cell subsets, and to evaluate the potential of these causal genes as actionable drug targets.MethodsThis study employed a two-sample Mendelian randomization (MR) framework using publicly available genome-wide association study (GWAS) summary statistics. The participant data included 797 PCOS cases and 140,558 controls (no direct patient recruitment was involved). Instrumental variables were derived from high-resolution immune cell-specific single-cell expression quantitative trait locus (sc-eQTL) data (OneK1K project) across 14 immune cell types. Primary analyses utilized the inverse-variance weighted (IVW) method. Shared causal variants were validated using Bayesian colocalization. Phenome-wide association analysis (PheWAS), external transcriptomic dataset validation (GSE8157), and DrugBank database screening were conducted for pleiotropy assessment and drug repositioning.ResultsMR analysis revealed genome-wide significant causal associations for GLIPR1 in non-classical monocytes (Mono NC) and XBP1 in CD4+ effector memory T cells (CD4 ET) with PCOS risk. Higher GLIPR1 expression was associated with a decreased PCOS risk (OR = 0.669, P = 4.34×10-6), whereas higher XBP1 expression was associated with an increased risk (OR = 1.406, P = 9.53×10-8). Colocalization analysis confirmed that GLIPR1 shares a causal variant with PCOS (PP.H4 = 96.73%). PheWAS and external validation confirmed the safety profile and significant upregulation (P = 0.03) of GLIPR1. Drug repositioning identified SOT-107, a Phase III protein therapy drug, as a potential interacting agent for GLIPR1.ConclusionsThis sc-eQTL MR study reveals immune cell-specific causal regulatory networks in PCOS. GLIPR1 in non-classical monocytes represents a high-confidence protective target, while XBP1 provides suggestive evidence for immune-mediated pathogenesis. The candidate drug SOT-107 highlights theoretical repositioning opportunities, though rigorous preclinical validation remains required.

Female↗

PubMed1994

A first step in total quality management of nursing facility care: development of an empirical causal model of structure, process and outcome dimensions.

While the structure, process, and outcome taxonomy has long been used in the field of health care quality measurement and evaluation, it has not been used in a true causal model which assesses facility level quality. Total quality management and continuous quality improvement call for routinely assessing facility and resident level quality in a causal framework. This paper presents a causal modeling methodology as a more appropriate method for assessing and understanding the inter-relatedness among each of the quality dimensions of Nursing Facility care, and presents how such a causal model directly relates to the notion of continuous quality improvement. The methodology consists of five steps: (1) sample definition and data collection, (2) data reduction through factor analysis, (3) development and testing of a causal model through path analysis, (4) identification of patterns of care through cluster analysis, and (5) integration of the model to both continuous quality improvement and to complex relationships involving quality and organizational variables. The methodology is fully illustrated by using a sample of 104 nursing facilities in Wisconsin in which quality dimensions have been captured through the Quality Assessment Index. The analysis demonstrates that nursing facilities may be substantially benefited by having access to causal linkages which materially affect outcome quality. Management would then have first-hand knowledge of the structural characteristics and the process activities that they may pursue in order to improve outcome quality.

Cluster Analysis↗

PubMed2026

Multi-omics causal inference of childhood asthma triggered by ambient particulate matter.

BACKGROUND: The causal impact of fine particulate matter (PM2.5), an established environmental risk factor, on childhood asthma and its biological mechanisms remain to be elucidated. The objective of the present study was to evaluate the causal association between PM2.5 and childhood asthma and to dissect the mediating role of plasma proteins through a multi-omics integrated Mendelian randomisation (MR) framework. METHODS: Two-sample MR was performed on large-scale genome-wide association data to estimate the causal effect of PM2.5 on childhood asthma. Genes commonly associated with PM2.5 and childhood asthma were screened by transcriptome-wide association study (TWAS) and subjected to enrichment analyses and MR. Mediator proteins were identified by two-step MR. Potential adverse effects were scanned by phenome-wide MR (Phe-MR). RESULTS: MR revealed a significant positive causal effect of PM2.5 on childhood asthma (OR=1.897, 95% CI: 1.063-3.388, p=0.030). TWAS highlighted 70 genes co-expressed in PM2.5 and childhood asthma that were enriched in inflammatory pathways such as lysosome- and leukocyte-mediated immunity. MEAF6 was validated as a protective gene and RNF40 as a risk gene for childhood asthma. Two-step MR identified FUT10 as a positive mediator mediating 19.3% of the causal effect, and CD200 and MANBA as negative mediator proteins. Phe-MR indicated the association of these genes and proteins with multiple other diseases, implying possible adverse effects from therapeutic intervention. CONCLUSION: Long-term PM2.5 exposure is causally linked to childhood asthma with MEAF6, RNF40, CD200, MANBA and FUT10 identified as key molecules. The study provides new evidence for the biological mechanisms linking PM2.5 to childhood asthma.

Journal Article↗

PubMed2003

Audiovisual phenomenal causality.

We report three experiments in which visual or audiovisual displays depicted a surface (target) set into motion shortly after one or more events occurred. A visual motion was used as an initial event, followed directly either by the target motion or by one of three marker events: a collision sound, a blink of the target stimulus, or the blink together with the sound. The delay between the initial event and the onset of the target motion was varied systematically. The subjects had to rate the degree of perceived causality between these events. The results of the first experiment showed a systematic decline of causality judgments with an increasing time delay. Causality judgments increased when additional auditory or visual information marked the onset of the target motion. Visual blinks of the target and auditory clacks produced similar causality judgments. The second experiment tested several models of audiovisual causal processing by varying the position of the sound within the visual delay period. No systematic effect of the sound position occurred. The third experiment showed a subjective shortening of delays filled by a clack sound, as compared with unfilled delays. However, this shortening cannot fully explain the increased tolerance for delays containing the clack sound. Taken together, the results are consistent with the interpretation that the main source of the causality judgments in our experiments is the impression of a plausible unitary event and that perfect synchrony is not necessary in this case.

Adult↗

PubMed2003

A dual-process model of belief and evidence interactions in causal reasoning.

In three experiments, we examined how reasoners' preexisting beliefs about causal relations constrained their evaluation of covariation-based empirical evidence. Reasoners were presented with causal candidates that were a priori rated to be either believable or unbelievable, as well as information regarding the degree to which the cause and the effect covaried. Several findings supported the conclusion that preexisting beliefs about causal relations reflect knowledge of both causal mechanisms and covariation relations, that these sources of knowledge are represented independently and contribute independently to causal judgments, and that the evaluation of new empirical evidence is influenced differently by mechanism-based and covariation-based beliefs. Finally, we observed that reasoners were relatively accurate in evaluating the degree to which their judgments were sensitive to empirical evidence but were less able to judge how much their judgments were influenced by their prior beliefs. We present a dual-process model that provides a descriptive account of the boundary conditions for belief and evidence interactions in causal reasoning.

Adolescent↗