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Results for “causality”

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PubMed2003

Coeliac disease: investigation of proposed causal variants in the CTLA4 gene region.

Coeliac disease (CD) is an immune-mediated enteropathy triggered by gluten in genetically predisposed individuals. Patients with CD have an increased prevalence of other autoimmune disorders, including type 1 diabetes (T1D) and Graves' disease (GD). CD shares with these conditions certain HLA susceptibility alleles. A number of studies have also shown association of autoimmune diseases, including CD, with the CD28-cytotoxic T lymphocyte antigen 4 (CTLA4)-inducible costimulator (ICOS) region of chromosome 2q33, but until recently the precise causal variant has remained unknown. Recently, it was shown that, in GD, CT60 (+6230G>A), a single nucleotide polymorphism (SNP) at the end of the CTLA4 transcript, is associated with an alteration in the ratio of splice forms of the CTLA4 gene and that this ratio affects disease susceptibility. A similar but weaker association was found with T1D. There is also an independent association of GD and T1D with the SNP MH30 (-23 327G>C), which possibly affects promoter region function. Hypothesizing that CT60 and MH30 may be causal variants in other autoimmune disorders, we investigated these SNPs in CD using 149 family trios and 100 unrelated/unaffected controls. No association was detected with either SNP using both the transmission disequilibrium test (TDT) and case-control methods. Our study appears to have good power to detect moderate genetic effects, but possibly these SNPs exert too weak an effect on risk of CD to have been detected in our sample. Alternatively, the previously noted association of CD with the CTLA4 gene region may be due to different causal variants. Unlike T1D and GD, CD is not a true autoimmune disease, and CD has different associations at the CTLA4 exon 1 SNP +49G>A from all other autoimmune disorders. MH30, CT60, and other SNPs in the region may still warrant further investigation in other CD samples.

Antigens, CD↗

PubMed2006

Causal connections in the acquisition of an orthographic rule: a test of Uta Frith's developmental hypothesis.

BACKGROUND: In a longitudinal study we tested Frith's causal hypothesis that children first gain orthographic knowledge through reading and then later, as a consequence, through spelling. METHOD: Children from Years 2 and 3 were tested three times over two years on their reading and spelling of pseudo-words which conformed to the conditional orthographic rule, the 'final -e' or 'split-digraph' rule. RESULTS: Cross-lagged panel correlation analyses suggested that the children's success in reading split-digraph words was a causal determinant of their learning to use split-digraphs in spelling, in the 7- to 8-year period and, with one year-group but not with the other, in the 8- to 9-year period. In the 9- to 10-year period children's success in reading no longer seemed to affect their spelling. CONCLUSIONS: These results strongly support Frith's causal hypothesis about the development of orthographic knowledge.

Age Factors↗

PubMed1980

Distress in clients and significant others: the question of causality.

Previous research documenting the association between the level of client disturbance and distress in a significant other has generated two competing causal models. Investigators measuring the level of family burden have suggested that it is the discharged patient who causes distress in the family. Investigators of family factors in patient relapse have suggested that it is the family who disturbs the patient. In this study the relative strengths of these two causal models are compared in a sample of outpatients over a six-month period of time. The data indicate that the significant other is causally predominant in the exacerbation of client disturbance.

Adult↗

PubMed1986

In defense of "lineal causality".

It has often been said that ideas about lineal and circular causality may be theoretically profound, but that the reputed impossibility of lineal causality seems to fly in the face of our experience and our common sense. The above humorous jibe at theory goes straight to the heart of the matter. Bateson's epistemology of lineal and circular causality does not describe our everyday experience. Bateson's epistemology explains our experience.

Adult↗

PubMed1996

Evaluation of gingival and periodontal conditions following causal periodontal treatment in patients treated with nifedipine and diltiazem.

It is established that phenytoin, cyclosporin and some calcium antagonists produce gingival overgrowth, but it is not known how this condition may respond to causal periodontal treatment. In order to find out, a longitudinal study was carried out, over a year, comparing a group of patients who were given nifedipine (NG, n = 18) and another group who were given diltiazem (DG, n = 13) with 2 others: one comprised cardiopathic patients who took no calcium antagonists (CG, n = 12) and the other contained patients who were medically healthy, with moderate periodontitis (HG, n = 12). On their basal visit, they were examined and instructed in oral hygiene, and then given causal periodontal treatment, being seen again at 4 and 8 months, when hygiene instructions were reinforced. They were seen for the last time at 12 months, when they were again examined. Groups NG and DG, on their basal visit, showed larger gum size than groups HG and CG, which was statistically significant; on their final visit, these differences remained only at the interproximal level. The number of patients with gingival overgrowth-taking the average of group HG as a minimal value-was much higher in groups CG (92%), DG (100%) and NG (89%) on the basal visit; on the final visit, the differences remained only in groups DG (85%) and NG (83%). The probing pocket depth reduction was much greater in groups HG and CG than in DG and NG, basically due to a greater gaining on clinical attachment level. The % of sites in which the pocket depth improved by more than 2 mm was 39.8% in HG, 54.5% in CG, 23.7% in DG and 28.7% in NG. The % of sites where the attachment gain by more than 2 mm was 46.2% in HG, 55.5% in CG, 22.8% in DG and 21.4% in NG. The amount of plaque and bleeding on probing, which was similar in all groups on the basal visit, decreased throughout the study, especially between the basal and 2nd visit in groups HG and CG. We have demonstrated that patients that take nifedipine and diltiazem show a larger gum size and their response to causal periodontal treatment is poorer than in the healthy and the cardiac groups.

Analysis of Variance↗

PubMed1999

Cigarette smoking and periodontitis: methodology to assess the strength of evidence in support of a causal association.

Identification of the cause of the development and progression of periodontitis has received extensive attention, with notable advances over the past decade in clinical, microbiological, immunological, biochemical, and behavioral knowledge. However, it is still largely unknown which factors lead to the conversion of non-destructive forms of periodontal disease into destructive forms and disease progression. Chronic adult periodontitis is believed to be influenced by an interaction of host defense and environmental factors. Although these variables have been studied extensively, no study has employed randomized controlled prospective human or randomized controlled community intervention designs, methodologies necessary to prove a variable to be a cause of periodontitis. Owing to the absence of literature employing rigorous experimental design, this article assesses systematically observational, cross-sectional and longitudinal studies to examine the potential causal association between cigarette smoking and periodontitis. The methodology of Sir Bradford Hill's criteria for causation was used as the framework. Results suggest that cigarette smoking is causally associated with periodontitis. That is, cigarette smoking is consistently associated with an increased prevalence/severity of periodontitis and is suspected on theoretical grounds of playing a causal role. Hill's criteria provide a useful methodology to better understand the pathogenesis of periodontal diseases and may be applied to study the pathogenesis of other dental diseases as well.

Adult↗

PubMed2002

Discovery of causal relationships in a gene-regulation pathway from a mixture of experimental and observational DNA microarray data.

This paper reports the methods and results of a computer-based search for causal relationships in the gene-regulation pathway of galactose metabolism in the yeast Saccharomyces cerevisiae. The search uses recently published data from cDNA microarray experiments. A Bayesian method was applied to learn causal networks from a mixture of observational and experimental gene-expression data. The observational data were gene-expression levels obtained from unmanipulated "wild-type" cells. The experimental data were produced by deleting ("knocking out") genes and observing the expression levels of other genes. Causal relations predicted from the analysis on 36 galactose gene pairs are reported and compared with the known galactose pathway. Additional exploratory analyses are also reported.

Animals↗

PubMed2026

Standard tea intake is causally associated with a reduced risk of wet age-related macular degeneration: a Mendelian randomization study.

Researchers have posited that increased consumption of tea and coffee may be associated with more favorable treatment outcomes in patients with age-related macular degeneration (AMD). However, there is no clear evidence regarding the causal associations. To delve deeper into this potential connection, scientists used a rigorous method known as Mendelian randomization (MR). This technique was used to explore the causal impact of tea and coffee consumption on the development or progression of AMD. With the aim of investigating the cause-and-effect relationship between 16 tea- and coffee-consuming subtypes and 3 AMD, we designed a two-sample MR study using comprehensive data from genome-wide association studies (GWAS). The major approach adopted was inverse variance weighting (IVW). Furthermore, we implemented complementary methods like the weighted median (WM), weighted mode, and MR-Egger to strengthen our findings. Sensitivity analyses, including MR-Egger, MR-PRESSO, leave-one-out, and Cochran's Q tests, were used to validate results, explore heterogeneity and pleiotropy, and pinpoint potential biases. Two hundred and sixty-eight instrumental variables were selected for MR analysis. The results showed that standard tea intake may be a protective factor for wet AMD [odds ratio (OR) = 0.7076, 95% confidence interval (CI) = 0.5776-0.8668, P = 8 × 10-4, PFDR = 0.0402]. Sensitivity analysis suggests that the results are robust. Our findings provide genetic evidence that standard tea intake is a protective factor against wet AMD, providing new insights into early risk stratification and prevention strategies for the disease.NEW & NOTEWORTHY This study investigates the potential causal relationship between tea and coffee consumption and age-related macular degeneration (AMD) using Mendelian randomization. Analyzing data from genome-wide association studies, we focused on 16 beverage subtypes and 3 AMD conditions. Our findings suggest that standard tea consumption may protect against wet AMD, with robust evidence supporting this link. The results offer new insights into risk stratification and prevention strategies for AMD, highlighting the importance of dietary factors in eye health.

Mendelian Randomization Analysis↗

PubMed2005

Association of C-reactive protein with blood pressure and hypertension: life course confounding and mendelian randomization tests of causality.

BACKGROUND: C-reactive protein (CRP) has repeatedly been associated with blood pressure and prevalent and incident hypertension, but whether a causal link exists is uncertain. METHODS AND RESULTS: We assessed the cross-sectional relations of CRP to systolic blood pressure, pulse pressure, and prevalent hypertension in a representative sample of >3500 British women aged 60 to 79 years. For both outcomes, substantial associations were observed. However, these associations were greatly attenuated by adjustment for a wide range of confounding factors acting over the life course. We further investigated causality using a Mendelian randomization approach by examining the association of the 1059G/C polymorphism in the human CRP gene with CRP and with blood pressure, pulse pressure, and hypertension. The polymorphism was associated with a robust difference in CRP, and the expectation would be for higher blood pressure and pulse pressure and greater prevalence of hypertension among those carrying the genetic variant associated with higher CRP levels. This was not observed, and the predicted causal effects of CRP on blood pressure, pulse pressure, and hypertension using instrumental variables methods were close to 0, although with wide CIs. CONCLUSIONS: CRP levels are associated with blood pressure, pulse pressure, and hypertension, but adjustment for life course confounding and a Mendelian randomization approach suggest the elevated CRP levels do not lead to elevated blood pressure.

Aged↗

PubMed2026

Systematic Identification of Therapeutic Targets and Repurposed Drugs for Stroke: From Genome Causal Analysis to Multilevel Validation.

BACKGROUND: Stroke is a severe cerebrovascular disease characterized by narrow time windows and complications. This study aimed to identify novel drug targets and repurposed drugs for stroke. METHODS: This study used expression quantitative trait loci data from druggable genes in brain and blood as instrumental variables. Mendelian randomization, colocalization, and phenome-wide Mendelian randomization were applied to evaluate causal relationships and potential side effects, with stroke and ischemic stroke as primary outcomes. Preclinical validation used oxygen-glucose deprivation/reperfusion and middle cerebral artery occlusion/reperfusion models. Pharmacological and behavioral assessments evaluated the therapeutic potential of candidate targets and drugs. Additionally, proteomic sequencing was performed following GGCX (γ-glutamyl carboxylase) overexpression to explore its biological functions. RESULTS: Elevated GGCX expression in brain and blood was potentially causally associated with reduced risk of stroke and ischemic stroke, supported by colocalization evidence, although potential cardiovascular risks could not be excluded. Drug repositioning identified ifenprodil as a candidate agent that reduced infarction volume, improved motor and cognitive functions, and reversed GGCX downregulation in mice. Ifenprodil treatment and GGCX overexpression alleviated oxygen-glucose deprivation/reperfusion-induced injury and upregulated GGCX expression. Mechanistically, GGCX conferred neuroprotection by regulating protein homeostasis, suppressing inflammation, promoting metabolic recovery, and modulating nuclear transcriptional regulation. CONCLUSIONS: This study established a potential causal link between GGCX and stroke risk, particularly ischemic stroke. GGCX represents a promising therapeutic target for ischemic stroke. Targeted GGCX expression upregulation and drug repurposing, particularly ifenprodil, may offer novel therapeutic avenues. Further validation is warranted to assess clinical efficacy and safety.

Animals↗

PubMed2006

The relationship between biogenetic causal explanations and social distance toward people with mental disorders: results from a population survey in Germany.

AIMS: Several studies have found an inverse relationship between people's readiness to endorse biogenetic causal explanations of mental disorder and their desire for social distance from people with mental disorders. The aim of this study is to examine why this may be the case. METHOD: In the spring of 2001, a population survey was carried out among German citizens aged 18 years and older, living in private households. A total of 5025 interviews were conducted, reflecting a response rate of 65.1%. At the beginning of the personal, fully structured interview, respondents were presented with a vignette containing a diagnostically unlabelled psychiatric case history, either depicting a case of schizophrenia or major depressive disorder. Using five-point Likert scales, causal attributions as well as perceived dangerousness, fear and the desire for social distance were assessed. RESULTS: The more respondents endorse a brain disease as a cause, the more dangerous they believe the person with schizophrenia or major depression to be. Respondents who perceive the individual in the vignette as being dangerous express a higher degree of fear and a greater preference for social distance from these individuals. As compared with brain disease, the relationships between heredity and perceived dangerousness are less pronounced for both disorders. CONCLUSIONS: Our analysis showed that endorsing biogenetic explanations decreases the likelihood of social acceptance of people with schizophrenia and major depression. Rejecting behavioural responses in the form of social distance desired from people with schizophrenia and major depression result from cognitive emotional processes in which biogenetic causal attributions are linked to lack of self-control, unpredictability and dangerousness, which, in turn, are associated with fear of these people.

Adolescent↗

PubMed1990

An approach to assessing and facilitating causal language in adults with learning disabilities based on Piagetian theory.

Salient characteristics associated with Piagetian cognitive stages served as the basis for developing a linguistic taxonomy of causal semantic relations. Causal statements from adults with learning disabilities and normally achieving adults were analyzed and organized within this taxonomy. A relationship between Piagetian cognitive stages and verbal expressions of causality was identified. Based on this relationship, principles of Piagetian cognitive theory were used to design assessment and intervention plans for adults with learning disabilities.

Adolescent↗

PubMed2025

Causal associations between inflammatory bowel disease and sepsis: a two-sample Mendelian randomization study.

BACKGROUND: Recent observational studies have revealed an inconclusive correlation between inflammatory bowel disease (IBD) and sepsis, accompanied by an uncertain understanding of the causal relationship between the two. To investigate the causality between IBD and sepsis, we employed a two-sample Mendelian randomization (MR) approach. METHODS: A genome-wide significant threshold (P < 5 × 10-8) was achieved in order to identify single nucleotide polymorphisms (SNPs) as instrumental variables (IVs) for two types of IBD, such as Crohn's disease (CD) and ulcerative colitis (UC). Subsequently, the selected SNPs were assessed in relation to three categories of sepsis, namely sepsis, sepsis (critical care), and sepsis (28-day death in critical care). An inverse-variance weighted (IVW) estimation of MR was conducted, followed by sensitivity analysis on multiple dimensions. RESULTS: There was a significant association between genetic liability to CD (IVW: OR, 1.246; 95% CI, 1.090-1.423; P = 0.0012) with sepsis (28-day death in critical care), but not with sepsis (critical care) and sepsis. Whereas UC showed slightly, yet statistically insignificant, higher risk for sepsis (IVW: OR, 1.031; 95% CI, 0.988-1.064; P = 0.064). CONCLUSION: Our study offers genetic evidence that supports a substantial causal relationship between CD and sepsis (28-day death in critical care). To enhance the specificity and objectivity of future research findings, it is recommended to specify the types of IBD and the severity of sepsis. Furthermore, the genetic risk loci related may become potential drug development targets.

Humans↗

PubMed1980

Causal models and logical inference in epidemiological psychiatry.

The paper examines the nature of causality and how the concept can be interpreted and used in epidemiological psychiatry. The relationship of causality to logical relations is reiterated, and it is emphasized that these relationships in their pure form cannot apply to any one cause of an effect which is the outcome of several causes. In such a case the relation of the cause to the effect is one of weak implication. The fact of weak implication opens the door to the construction of certain causal models, and the possibilities afforded by this situation are illustrated by reference to the work of Brown et al (1975). Weak implication may be an intransitive relationship, and this is shown to invalidate certain ways of testing such models and the conclusions which arise from them.

Female↗

PubMed2004

Causal association between cannabis and psychosis: examination of the evidence.

BACKGROUND: Controversy remains as to whether cannabis acts as a causal risk factor for schizophrenia or other functional psychotic illnesses. AIMS: To examine critically the evidence that cannabis causes psychosis using established criteria of causality. METHOD: We identified five studies that included a well-defined sample drawn from population-based registers or cohorts and used prospective measures of cannabis use and adult psychosis. RESULTS: On an individual level, cannabis use confers an overall twofold increase in the relative risk for later schizophrenia. At the population level, elimination of cannabis use would reduce the incidence of schizophrenia by approximately 8%, assuming a causal relationship. Cannabis use appears to be neither a sufficient nor a necessary cause for psychosis. It is a component cause, part of a complex constellation of factors leading to psychosis. CONCLUSIONS: Cases of psychotic disorder could be prevented by discouraging cannabis use among vulnerable youths. Research is needed to understand the mechanisms by which cannabis causes psychosis.

Adolescent↗

PubMed2002

Causal explanations for common somatic symptoms among women and men.

The purpose of this study was to examine categories of causal attributions assessed by women and men regarding common somatic symptoms. A questionnaire was sent out to a randomly selected sample of 1,500 persons followed by a screening of respondents with symptom experience. To identify groups of individuals considering different causes or causal categories as important, separate cluster analyses were made of ratings for neck/shoulder problems and sore/upset stomach. The results showed similarities between assessed causal categories for the two types of symptoms and that women in this sample were overrepresented, particularly in considering psychological explanations for their symptoms, whereas the men were overrepresented in not considering any of the causes as particularly important. This was discussed in terms of illness severity and an association between psychological and somatic distress in people's experience, such as stress and total workload, and in their subsequent explanatory models suggesting differences in beliefs about a connection between body and mind.

Adult↗

PubMed2002

Do cultural factors affect causal beliefs? Rational and magical thinking in Britain and Mexico.

In two experiments, unusual phenomena (spontaneous destruction of objects in an empty wooden box) were demonstrated to adult participants living in rural communities in Mexico. These were accompanied by actions which had no physical link to the destroyed object but could suggest either scientifically based (the effect of an unknown physical device) or non-scientifically based (the effect of a 'magic spell') causal explanations of the event. The results were compared to the results of the matching two experiments from the earlier study made in Britain. The expectation that scientifically based explanations would prevail in British participants' judgments and behaviours, whereas Mexican participants would be more tolerant toward magical explanations, received only partial support. The prevalence of scientific explanations over magical explanations was evident in British participants' verbal judgments but not in Mexican participants' judgments. In their behavioural responses under the low-risk condition, British participants rejected magical explanations more frequently than did Mexican participants. However, when the risk of disregarding the possible causal effect of magic was increased, participants in both samples showed an equal degree of credulity in the possible effect of magic. The data are interpreted in terms of the relationships between scientific and 'folk' representations of causality and object permanence.

Adult↗

PubMed2002

Do challenging behaviors affect staff psychological well-being? Issues of causality and mechanism.

Little explicit attention has been given to the potential impact of client challenging behavior on staff psychological well-being. Relevant research was critically reviewed according to criteria required to establish a causal relationship. Reasonable evidence was found for an association between challenging behavior and staff stress, and some evidence for temporal precedence. However, few researchers had analyzed data enabling alternative explanations to be eliminated. Thus, empirical evidence of a causal relationship between challenging behavior and staff stress is weak. A fourth causality criterion was addressed by suggestion of a mechanism by which challenging behavior may have its effects. I propose that staff negative emotional reactions mediate the impact of challenging behaviors on staff stress and evaluate research evidence for this theory.

Attitude↗