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Social support and occupational stress: a causal analysis.

This study is aimed at gaining insight into the role of social support provided by coworkers and supervisors in the reduction of job-stress. It is emphasized that, despite the inclusion of social support as an important variable in theoretical models of job stress, research on this issue is plagued by a lack of conceptual clarity, disagreement on definitions, and divergent operationalizations. Furthermore, there is little strong empirical evidence for the role of social support in alleviating job stress. Moreover, because of the use of cross-sectional designs, causal interpretations are often impossible. In this study, an attempt was made to assess the causal direction of the relationships between social support, stressors and strains, by employing a longitudinal panel design and LISREL analysis. Subjects consisted of 2034 employees of 21 Dutch companies from the eastern part of the Netherlands. All filled out a questionnaire on organizational stress and social support, and underwent a medical examination. Parts of the sample participated in two follow-up measurements. The results showed that individuals from the highest occupational levels as well as those from the lowest perceived less social support than other individuals. Furthermore, the respondents consistently reported that coworkers provide more support than supervisors. Only in the group with the lower occupational level did social support have a causal effect upon most stressors, indicating that social support indeed reduces role ambiguity, role overload, role conflict and job future uncertainty. However, there was not much evidence for a causal effect of social support by the coworkers upon the stressors.(ABSTRACT TRUNCATED AT 250 WORDS)

Humans↗

Viruses and cancer. Causal associations.

This review first considered some general problems in establishing causal links between a virus and a human cancer and offered some guidelines in the pursuit of this objective. Second, it reviewed the current causal associations for several candidate oncogenic viruses in relation to the tumors with which they are associated. These include Epstein-Barr virus in relation to Burkitt's lymphoma, nasopharyngeal carcinoma, Hodgkin's disease, and non-Hodgkin's lymphoma; hepatitis B and C viruses in relation to hepatocellular carcinoma; human T-cell leukemia/lymphoma virus type 1 and atypical leukemia/lymphoma; and human papilloma viruses in relation to cervical carcinoma. For some, the causal relationship is strong: hepatitis B virus with hepatocellular carcinoma, and human T-cell leukemia/lymphoma virus with adult T-cell leukemia/lymphoma. For one, the causal relationship is moderate: Epstein-Barr virus with African Burkitt's lymphoma. For others it is incomplete or inconclusive: Epstein-Barr virus with Hodgkin's disease and non-Hodgkin's lymphoma, and hepatitis C virus with hepatocellular carcinoma. Current techniques do not permit an answer for some: human papilloma virus with cervical carcinoma.

Animals↗

Causal coherence analysis of heart rate variability and systolic blood pressure variability under mental arithmetic task load.

Causal coherence analysis based on a closed-loop bivariate autoregressive model was applied to heart rate variability and systolic blood pressure (SBP) variability during mental arithmetic tasks to clarify how mental task load affects the linear closed loop interaction between cardiac and vascular systems. Thirteen normal male subjects performed a mental arithmetic task, button press task, and rest task while measuring their RR interval (RRI) and SBP. The mean value in the low frequency (LF) band (0.04-0.15Hz) of the squared causal coherence function from SBP to RRI during the mental arithmetic task was significantly higher than during the other two control tasks. Conversely, the LF band of the squared causal coherence function from RRI to SBP during the mental arithmetic task tended to be lower than during the rest task. These results suggest that mental arithmetic tasks enhance linear causal coupling from the vascular to cardiac system, and conversely weaken that from the cardiac to vascular system.

Adolescent↗

Mendelian randomization and FinnGen analysis of the causal relationship between 473 gut microbiota species and chronic sinusitis.

OBJECTIVE: To investigate the causal associations between Gut Microbiota (GM) and Chronic Sinusitis (CRS) using Mendelian Randomization (MR). METHODS: Genome-Wide Association Study (GWAS) summary statistics for 473&#x2009;GM taxa were obtained from MiBioGen consortium. CRS data (22,099 cases vs. 371,520 controls) were sourced from the FinnGen R12 cohort. Causal effects were estimated via Inverse Variance-Weighted (IVW), MR-Egger, weighted median, and Bayesian-weighted MR methods. Sensitivity analyses (heterogeneity and horizontal pleiotropy tests) were performed to validate robustness. RESULTS: IVW analysis identified 20&#x2009;GM taxa significantly associated with CRS risk (p&#x2009;<&#x2009;0.05). Of these, 7 taxa (e.g., Francisellales, Roseibacillus, Merdibacter massiliensis) exhibited risk-increasing effects, while 13 taxa (e.g., Firmicutes I, Succinivibrionaceae) showed protective effects. Sensitivity analyses confirmed the absence of significant heterogeneity (Cochran's Q p&#x2009;>&#x2009;0.05) or pleiotropy (MR-Egger intercept p&#x2009;>&#x2009;0.05). Bayesian-weighted MR validated 18 causal relationships (posterior probability > 95%), except for RUG420 sp900317985 and UBA7703 (non-significant). CONCLUSIONS: This MR study provides genetic evidence supporting causal roles of specific GM taxa in CRS pathogenesis. These findings highlight the gut-sinus axis as a potential therapeutic target and underscore the utility of large-scale biobanks (e.g., FinnGen) in advancing precision medicine. LEVEL OF EVIDENCE: Level 5. Mendelian Randomized (MR) studies are second only to randomized controlled trials in terms of the level of evidence.

Humans↗

Application of causal discovery of factors driving dissolved oxygen in estuarine environments.

Dissolved oxygen (DO) concentrations in estuarine bottom waters are a manifestation of multiple, interacting physical and biogeochemical processes, yet identifying their independent contributions remains challenging. Here, we analyze monthly water quality monitoring data from eight stations across Long Island Sound from 1994 to 2022 using a causal discovery framework (PCMCI+) and transformation of forcing variables. Our goal is to identify and isolate variables that causally influence bottom DO and improve predictive models by minimizing overfitting and multicollinearity. PCMCI+ reveals surface-layer temperature as the most important and consistent negative driver of bottom DO, followed by stratification. Wind events exhibit only brief relief by advection and mixing, while river discharge shows no direct causal link to DO, making it less influential than previously thought. Biogeochemical variables, including chlorophyll-a (Chl-a), nitrate and nitrite, and particulate carbon, influence DO through both contemporaneous and time-lagged pathways, often with signs that shift depending on the process. The derived models were evaluated by comparing skill scores, mean squared error, and Akaike Information Criterion. Both model types perform well, with coefficient of determination values exceeding 0.90 at multiple stations using only 3-5 predictors. Our analysis reveals that the best causal predictors are surface-layer temperature, stratification, Chl-a, and particle carbon. This approach provides a scalable framework for improving prediction models and understanding the mechanistic links that control the seasonal variability of DO in estuarine systems.

Estuaries↗

Is there a causal relationship between the receipt of blood transfusions and the development of chronic lung disease of prematurity?

The number and total volume of blood transfusions received by premature babies is, after gestational age and birth weight a good predictor of the likelihood of developing chronic lung disease of prematurity (CLD) and retinopathy of prematurity (ROP). Oxidative damage, inflammation and pulmonary infections are also strongly associated with the development of CLD. It is currently not clear whether there is a causal relationship between the receipt of blood transfusions and oxidative damage, infection, inflammation and CLD in these babies. Strong arguments may be made both for and against a causal relationship. The babies who receive blood transfusions are usually smaller than those who do not, and are ventilated, often with high oxygen levels, for a longer period of time. The longer the baby is on a ventilator the more likely it is to develop pulmonary infection and inflammation. All these factors will promote free radical production and oxidative damage irrespective of the receipt of blood transfusion. This would argue against a causal relationship. On the other hand, an argument may be presented which is based on iron promoted free radical generation, infection and fibrosis consequent to the breakdown of haeme released from transfused erythrocytes. Haeme is broken down by haeme oxygenase (HO) to iron, CO and bilirubin. Under normal circumstances the products of HO activity are beneficial to the organism, but when HO activity is excessive, the products are potentially damaging. Free iron, (in the Fe2+ form) if not sequestered with protein or urate, will generate highly toxic free radicals via the Fenton and Heber-Wiess reactions, predispose the tissue to infection and promote fibrosis. The iron chelating ability of the premature baby appears to be limited so that it would be difficult to deal with any increase in free iron production. Free iron will in turn induce HO activity leading to a potentially serious positive feedback process. The lung is particularly sensitive to iron induced HO activity. In addition, HO activity may be enhanced by other events occurring in the premature lung such as the production of proinflammatory cytokines and the reduced level of glutathione. Thus, the possibility of a causal relationship clearly exists and needs to be examined. This can be attempted by measuring the products of HO activity in relation to the receipt of blood transfusions.

Chronic Disease↗

Brain-based mechanisms underlying complex causal thinking.

We use functional magnetic resonance imaging (fMRI) and behavioral analyses to study the neural roots of biases in causal reasoning. Fourteen participants were given a task requiring them to interpret data relative to plausible and implausible causal theories. Encountering covariation-based data during the evaluation of a plausible theory as opposed to an implausible theory selectively recruited neural tissue in the prefrontal and occipital cortices. In addition, the plausibility of a causal theory modulated the recruitment of distinct neural tissue depending on the extent to which the data were consistent versus inconsistent with the theory provided. Specifically, evaluation of data consistent with a plausible causal theory recruited neural tissue in the parahippocampal gyrus, whereas evaluating data inconsistent with a plausible theory recruited neural tissue in the anterior cingulate, left dorsolateral prefrontal cortex, and precuneus. We suggest that these findings provide a neural instantiation of the mechanisms by which working hypotheses and evidence are integrated in the brain.

Adolescent↗

Evaluation of patient-related factors associated with causality, preventability, predictability and severity of hepatotoxicity during antituberculosis [correction of antituberclosis] treatment.

For evaluation the extent of antituberculosis drug-induced hepatotoxicity and also to determine the patient-related factors associated with causality, preventability, predictability and severity of hepatotoxicity induced by antituberculosis medications, a prospective study was conducted on 112 patients in a tertiary care university teaching hospital for three years. Causality, preventability, predictability and severity of hepatotoxicity were determined based on the available standard algorithms. Of 112 patients, 31 (27.7%) demonstrated hepatotoxicity. Two patients died from complications of liver-related illness. The mean duration of treatment before the onset of hepatotoxicity was 16.7+/-3.2 days. Malnutrition was present in 17 of 112 patients. Most of hepatotoxicity (25/31 or 80.6%) occurred within the first month of treatment. Reintroduction of antituberculosis drugs was possible in 29 of 31 patients. Univariate and multivariate analysis did not show significant relationships between the rate of hepatotoxicity with age, sex, nutrition and nationality. Our results showed that hepatotoxicity induced by antituberculosis drugs is a nonpreventable and unpredictable reaction. The causality of this reaction is classified as category A based on European grading of causality. This study noted that the frequency of hepatotoxicity induced by antituberculosis drugs in Iranian patients is higher than other studied populations.

Adolescent↗

Vitalistic causality in young children's naive biology.

One of the key issues in conceptual development research concerns what kinds of causal devices young children use to understand the biological world. We review evidence that children predict and interpret biological phenomena, especially human bodily processes, on the basis of 'vitalistic causality'. That is, they assume that vital power or life force taken from food and water makes humans active, prevents them from being taken ill, and enables them to grow. These relationships are also extended readily to other animals and even to plants. Recent experimental results show that a majority of preschoolers tend to choose vitalistic explanations as most plausible. Vitalism, together with other forms of intermediate causality, constitute unique causal devices for naive biology as a core domain of thought.

Attitude↗

Causal relationship between white matter structural connectivity and epilepsy.

White matter structural connectivity has recently been linked to epilepsy pathogenesis, yet its causal role remains unclear. This study used Mendelian randomization (MR) to investigate the causal relationship between white matter structural connectivity and epilepsy. GWAS summary statistics for white matter structural connectivity were sourced from the UK Biobank, while epilepsy data were obtained from FinnGen R10 and the International League Against Epilepsy (ILAE). Our MR analysis revealed significant causal links between white matter structural connectivity and epilepsy risk. Increased connectivity between the right hemisphere visual and salience/ventral attention networks (RH Vis to RH Sal/VentAttn WMSC) was associated with higher epilepsy risk in FinnGen_R10_FE_STRICT (OR&#xa0;=&#xa0;2.25, 95&#xa0;% CI&#xa0;=&#xa0;1.43-3.56, p&#xa0;<&#xa0;0.01, FDR P&#xa0;=&#xa0;0.019). Conversely, increased connectivity between left and right hemisphere salience/ventral attention networks (LH Sal/VentAttn to RH Sal/VentAttn WMSC) was linked to reduced epilepsy risk in FinnGen_R10_GE_STRICT (OR&#xa0;=&#xa0;0.17, 95&#xa0;% CI&#xa0;=&#xa0;0.07-0.46, p&#xa0;<&#xa0;0.01, FDR P&#xa0;=&#xa0;0.033). A total of 15 nominally significant associations were identified across datasets. These findings suggest a causal relationship between white matter structural connectivity and epilepsy, offering insights into disease mechanisms and potential therapeutic targets.

Humans↗

Shared genetic risk and causal associations between Post-traumatic stress disorder and migraine with antithrombotic agents and other medications.

Post-traumatic stress disorder (PTSD) is a psychiatric disorder that frequently co-occurs with pain disorders including migraine. There are proposed biological, genetic and environmental factors associated with both PTSD and migraine suggesting shared etiology. Genome-Wide Association Studies (GWAS) have been used to identify genomic risk loci associated with various disorders and to investigate genetic overlap between traits. There is a significant genetic correlation between PTSD and migraine with no evidence of a causal relationship that could be attributed to pleiotropy. Cross-disorder genetic analyses were applied to investigate the genetic overlap and causal associations using GWAS summary statistics of PTSD (n&#xa0;=&#xa0;214408), migraine (n&#xa0;=&#xa0;873341) and 23 medication use traits (n&#xa0;=&#xa0;78808-305913) including anti-depressants, anti-migraine preparations and beta-blocking agents. Across the entire genome, anti-thrombotic agents had a significant and negative genetic correlation with PTSD (rG&#xa0;=&#xa0;-0.2, P FDR&#xa0;=&#xa0;0.032) and a positive genetic correlation with migraine (rG&#xa0;=&#xa0;0.26, P FDR&#xa0;=&#xa0;2.23 x 10-8). PTSD showed significant genetic correlation with 11 other medication use traits including beta blocking agents (rG&#xa0;=&#xa0;-0.11, P FDR&#xa0;=&#xa0;0.034). Of the 2495 genomic regions tested, PTSD showed significant local genetic correlation with 12 medication use traits at 43 loci; while migraine showed significant genetic correlation with only anti-inflammatory agents and anti-rheumatic products at locus 12:57522282-57607142 (DAB1) (P&#xa0;<&#xa0;2 x 10-5). The genetic liability to PTSD had a causal effect on increased risk of using pain medication such as opioids (&#x3b2; ivw&#xa0;=&#xa0;0.59, P&#xa0;=&#xa0;5.21 x 10-5) while the genetic liability to migraine had a causal effect on the increased risk of using anti-thrombotic agents (&#x3b2; ivw&#xa0;=&#xa0;0.59, P&#xa0;=&#xa0;1.69 x 10-7). The genes in the genomic regions shared between PTSD and medication use traits were enriched in neural-related pathways such as neuron development, neurogenesis and protein kinase activity. These results provide further insight into the genetically controlled biological and environmental factors underlying the shared etiology between PTSD and migraine. The identified biomarkers can be used as a basis for investigation as potential drug targets for both disorders. These findings are significant for drug re-purposing and treatment of PTSD and migraine using monotherapy.

GWAS↗

Learning, prediction and causal Bayes nets.

Recent research in cognitive and developmental psychology on acquiring and using causal knowledge uses the causal Bayes net formalism, which simultaneously represents hypotheses about causal relations, probability relations, and effects of interventions. The formalism provides new normative standards for reinterpreting experiments on human judgment, offers a precise interpretation of mechanisms, and allows generalizations of existing theories of causal learning. Combined with hypotheses about learning algorithms, the formalism makes predictions about inferences in many experimental designs beyond the classical, Pavlovian cue-->effect design.

Journal Article↗

Sex differences in the genetic and causal relationships between depression, smoking, and alcohol use: the role of socioeconomic status.

Major depressive disorder (MDD), smoking, and drinking frequently co-occur, with evidence suggesting these relationships may differ by sex. However, the direction of causality and the extent of sex-specific associations remain unclear. We investigated sex-specific genetic relationships between MDD and substance use phenotypes using genome-wide association studies (GWAS) from the UK Biobank and publicly available sex-stratified GWAS for MDD and problematic alcohol use (PAU). Causal effects were assessed using bidirectional, sex-stratified Mendelian randomization (MR). We further applied multivariable MR (MVMR) to evaluate the influence of socioeconomic status (SES). Genetic correlation analyses indicated significant shared genetic architecture between MDD and all substance use traits in sex-combined GWAS. In sex-specific analyses, the correlation between cigarettes per day and MDD was significantly stronger in females, and drinks per week were correlated with MDD only in females. MR analyses showed that genetic liability to MDD increased the risk of smoking initiation and PAU in females, and was associated with reduced alcohol drinking frequency in males. In contrast, no tested substance use trait showed evidence of a causal effect on MDD in either sex. MVMR adjusting for SES attenuated the association between MDD and smoking initiation. The effect on PAU in females remained. In males, the negative association between MDD and drinking frequency became non-significant after SES adjustment. These findings reveal sex-specific genetic and causal relationships between smoking, drinking, and MDD, and highlight the role of SES as a potential confounder. Incorporating sex and socioeconomic context is critical when examining these associations.

Humans↗

Tests of the power PC theory of causal induction with negative contingencies.

The power PC theory of causal induction (Cheng, 1997) proposes that causal estimates are based on the power p of a potential cause, where p is the contingency between the cause and effect normalized by the base rate of the effect. Previous tests of this theory have concentrated on generative causes that have positive contingencies with their associated outcomes. Here we empirically test this theory in two experiments using preventive causes that have negative contingencies for their outcomes. Contrary to the power PC theory, the results show that causal judgments vary with contingency across conditions of constant power p. This pattern is consistent, however, with several alternative accounts of causal judgment.

Adult↗

Causal chunking: memory and inference in ongoing interaction.

We propose that people simplify their perceptions of their interactions by organizing them into discrete casual chunks. Once formed, these chunks presumably influence the extent to which people are aware of their influence on others, as well as their impressions of others. We anticipated that people would form self-causal chunks (e.g., my action causes my partner's action) when they possessed an offensive set and other-causal chunks when they possessed a defensive set. We also expected that a self-causal chunking strategy would make salient people's influence on their partners and thereby discourage them from concluding that their partner's behaviors reflected underlying dispositions. In contrast, we anticipated that an other-causal chunking strategy would obscure people's influence on their partners, thereby encouraging them to infer that their partners' behaviors reflected underlying dispositions. We tested these hypotheses by inducing participants to develop either a defensive or an offensive set prior to interacting with another person in a simulated arms race. After the interactions, we assessed the manner in which participants chunked their interactions, as well as their impressions of partners. The results supported our predictions. The implications of these findings for understanding conflict and misunderstanding in interpersonal relations are discussed.

Adult↗

Blickets and babies: the development of causal reasoning in toddlers and infants.

Previous research has suggested that preschoolers possess a cognitive system that allows them to construct an abstract, coherent representation of causal relations among events. Such a system lets children reason retrospectively when they observe ambiguous data in a rational manner (e.g., D. M. Sobel, J. B. Tenenbaum, & A. Gopnik, 2004). However, there is little evidence that demonstrates whether younger children possess similar inferential abilities. In Experiment 1, the authors extended previous findings with older children to examine 19- and 24-month-olds' causal inferences. Twenty-four-month-olds' inferences were similar to those of preschoolers, but younger children lacked the ability to make retrospective causal inferences, perhaps because of performance limitations. In Experiment 2, the authors designed an eye-tracking paradigm to test younger participants that eliminated various manual search demands. Eight-month-olds' anticipatory eye movements, in response to retrospective data, revealed inferences similar to those of 24-month-olds in Experiment 1 and preschoolers in previous research. These data are discussed in terms of associative reasoning and causal inference.

Aging↗

Difficulties in comprehending causal relations among children with ADHD: the role of cognitive engagement.

The present study examined whether time spent in long looks (i.e., >or=15 s), an index of cognitive engagement, would account for differences between children with attention deficit hyperactivity disorder (ADHD) and comparison children in understanding causal relations. Children viewed two televised stories, once in the presence of toys and once in their absence. Dependent variables were visual attention and questions tapping factual information and causal relations. Comparison children answered significantly more causal relations questions than did the children with ADHD, but only in the toys-present condition. Four lines of evidence revealed that the difficulties children with ADHD had in answering causal relations questions in the toys-present condition could be linked specifically to this group's decreased time spent in long looks.

Attention↗

Seeing versus doing: two modes of accessing causal knowledge.

The ability to derive predictions for the outcomes of potential actions from observational data is one of the hallmarks of true causal reasoning. We present four learning experiments with deterministic and probabilistic data showing that people indeed make different predictions from causal models, whose parameters were learned in a purely observational learning phase, depending on whether learners believe that an event within the model has been merely observed ("seeing") or was actively manipulated ("doing"). The predictions reflect sensitivity both to the structure of the causal models and to the size of their parameters. This competency is remarkable because the predictions for potential interventions were very different from the patterns that had actually been observed. Whereas associative and probabilistic theories fail, recent developments of causal Bayes net theories provide tools for modeling this competency.

Achievement↗