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Results for “causality”

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At least 811 records · Page 45Linked to original sources

PubMed2003

A causal model of rehabilitation resource use for subjects with spinal cord injury in Taiwan.

OBJECTIVE: The aim of this study was to construct an adequate causal model of rehabilitation resource use based on a Taiwanese rehabilitation database system. DESIGN: Cross-sectional analysis of data from a Taiwanese rehabilitation database system. SUBJECTS: Records from 68 patients (51 men, 17 women; mean age 43 years) with spinal cord injuries were used in the study. METHODS: Path analysis was used to identify a better-fitted model for patients with spinal cord injuries. RESULTS AND CONCLUSION: The results showed that the final causal model fits the data well. The findings also reveal that activities of daily living have the largest total effect on length of stay, whereas subjective well-being and gender have indirect effects on length of stay, mediating through activities of daily living and subjective well-being, respectively. The impact of subjective well-being on the length of stay in hospital for patients with spinal cord injuries deserves special attention, as the quality of life issue plays a vital role in rehabilitation of these patients. The influence of subjective well-being on activities of daily living suggests that therapy targeted at improving patients' subjective well-being is necessary. Additionally, the impact of sexual dysfunction of patients with spinal cord injuries should be investigated further.

Activities of Daily Living↗

PubMed2024

Mendelian randomization study on the causal effect of herpes simplex virus infection on idiopathic pulmonary fibrosis.

BACKGROUND: Previous observational studies have shown that past infection of herpes simplex virus (HSV) is associated with idiopathic pulmonary fibrosis (IPF). The present study aims to identify the causal link between HSV infection (exposure factor) and IPF (outcome factor). RESEARCH DESIGN AND METHODS: To date, the largest publicly available genome-wide association study (GWAS) for HSV infection (1,595 cases and 211,856 controls from Finnish ancestry) and for IPF (1,028 cases and 196,986 controls from Finnish ancestry) were used to perform this two-sample Mendelian randomization (MR) study. RESULTS: We found no significant pleiotropy or heterogeneity of all selected nine HSV infection-associated genetic instrumental variants (IVs) in IPF GWAS dataset. Interestingly, we found that as HSV infection genetically increased, IPF risk increased based on an inverse-variance weighted (IVW) analysis (odds ratio [OR] = 1.280, 95% confidence interval [CI]: 1.048-1.563; p = 0.015) and weighted median (OR = 1.321, 95% CI: 1.032-1.692; p = 0.027). CONCLUSIONS: Our analysis suggests a causal effect of genetically increased HSV infection on IPF risk. Thus, HSV infection may be a potential risk factor for IPF.

Humans↗

PubMed2004

Quality-of-life measurement in clinical trials--the impact of causal variables.

The theory of measurement scales, and in particular multi-item scales, has been extensively developed in educational testing, psychometric testing, personality testing, and consumer research. These scales are usually either based upon traditional psychometric models or modern theory using item response theory. However, clinical measuring instruments, including health-related quality-of-life questionnaires, frequently have different underlying principles and so the adoption of such approaches can be inappropriate. The fundamental statistical distinction between indicator and causal variables can be used to explain why psychometric methods fail. So-called clinimetric approaches may sometimes be more relevant, and clinimetric and psychometric ideas should be combined to yield a suitable measuring instrument. Recognition of the role of causal variables enables informed decisions to be made regarding scale development, validation, and scoring.

Clinical Trials as Topic↗

PubMed2000

Epidemiological risk factors of coronary heart disease are not causal in atherosclerosis.

Logic dictates that for scientific progress in atherogenesis "cause" must be the sole prequisite without which the disease cannot occur. Nor can it be assumed that statistical associations (risk factors) with coronary heart disease (CHD) are causal for atherosclerosis and extrapolations from correlations with CHD incidence to atherosclerosis are invalid. Any factor considered to play a role in atherogenesis requires pathological and experimental evidence consistent with the logic of Koch's specificity of cause and effect. Current epidemiological misuse and manipulation of cause and risk factors are contrary to the basic precepts of scientific logic and the fundamental need for precision in word usage. The term "risk factor", because of the current deeply entrenched false concept of causality has retarded medical progress and should be abandoned. Its adherents, guilty of a disservice to the tenets of their discipline, have also sullied the scientific integrity of medicine as a whole.

Arteriosclerosis↗

PubMed2004

Temporal aggregation bias and inference of causal regulatory networks.

Time course experiments with microarrays have begun to provide a glimpse into the dynamic behavior of gene expression. In a typical experiment, scientists use microarrays to measure the abundance of mRNA at discrete time points after the onset of a stimulus. Recently, there has been much work on using these data to infer causal regulatory networks that model how genes influence each other. However, microarray studies typically have slow sampling rates that can lead to temporal aggregation of the signal. That is, each successive sampling point represents the sum of all signal changes since the previous sample. In this paper, we show that temporal aggregation can bias algorithms for causal inference and lead them to discover spurious relations that would not be found if the signal were sampled at a much faster rate. We discuss the implications of temporal aggregation on inference, the problems it creates, and potential directions for solutions.

Computational Biology↗

PubMed1989

Iron deficiency and behavior: criteria for testing causality.

The association between iron deficiency and poor behavioral-test performance is well established. The question of causality, however, remains unanswered. This paper presents the essential criteria for a valid test of causality. Internal validity is examined in terms of positive and negative findings. Plausibility of the findings requires analyzing the congruency of the results; for example, those who respond to the iron treatment are also those who respond behaviorally. External validity describes the extent to which inferences may be made about other populations or circumstances.

Behavior↗

PubMed1991

Maternal weight gain, infant birth weight, and diet: causal sequences.

The causal sequence maternal nutrition----maternal weight gain----infant birth weight is not sustained by available evidence except under extreme nutritional deprivation. For maternal weight change, diet effects of near starvation are unequivocal. With chronic undernutrition or social deprivation, diet effects are inapparent or modest (conditional on pregnancy stage, diet supplement, and prepregnancy weight). For birth-weight change, diet effects of near starvation are likewise unequivocal and modest with chronic undernutrition or social deprivation. The complete causal sequence has been demonstrated only below a famine threshold. Outside famine, effects are modest (conditional on baseline nutrition, timing, and content of diets, possibly also on infant sex and energy expenditure). High-protein concentrations have produced adverse effects. Micronutrients and consequent fluid retention could have favorable effects. Diet effects on birth weight apparently bypass maternal weight change. Hence, to enhance birth weight, maternal diet appears to deserve more attention than does weight gain.

Birth Weight↗

PubMed1997

Kupffer cells are causally responsible for the mitogenic effect of peroxisome proliferators.

WY-14,643 [4-chloro-6-(2,3-xylidino)pyrimidinylthio-acetic acid] is a well-known non-genotoxic carcinogen and peroxisome proliferator that causes liver cancer in rodents by unknown mechanisms. Its ability to sustain elevated rates of hepatocyte DNA synthesis is most likely pivotal in the ultimate development of tumors. The source of this mitogenic stimulus following treatment of rats with WY-14,643 has been hypothesized to be Kupffer cells, the resident hepatic macrophages, since they are activated by peroxisome proliferators in vivo. Therefore, these studies were designed to determine if Kupffer cells are causally responsible for WY-14 643-induced increases in hepatocyte DNA synthesis in vivo. WY-14,643 (100 mg/kg) increased DNA synthesis 8-fold 24 h after treatment; however, inactivation of Kupffer cells with methyl palmitate, a nonhydrolyzable fatty acid ester and known Kupffer cell inhibitor, completely prevented the mitogenic effect of WY-14,643. On the other hand, the ability of WY-14,643 to induce peroxisomes was not affected by methyl palmitate. These data demonstrate that induction of peroxisomes is not dependent on factors from Kupffer cells and support the idea that stimulation of DNA synthesis and induction of peroxisomes occur via distinct mechanisms. Additionally, WY-14,643 increased liver mRNA transcripts of the hepatocyte mitogen tumor necrosis factor alpha (TNF alpha) more than twofold. This increase was also prevented by inactivating Kupffer cells with methyl palmitate. Therefore, it is concluded that Kupffer cells are causally responsible for WY-14,643-induced increases in hepatocyte DNA synthesis most likely by increasing production of TNF alpha, a hepatic mitogen.

Acyl-CoA Oxidase↗

PubMed2004

The role of the lateral frontal cortex in causal associative learning: exploring preventative and super-learning.

Prediction error--a mismatch between expected and actual outcome--is critical to associative accounts of inferential learning. However, it has proven difficult to explore the effects of prediction error using functional magnetic resonance imaging (fMRI) while excluding the confounding effects of stimulus novelty and incorrect responses. In this event-related fMRI study we used a three-stage experiment generating preventative- and super-learning conditions. In both cases, it was possible to generate prediction error within a causal associative learning experiment while subtracting the effects of novelty and error. We show that right lateral prefrontal cortex (PFC) activation is sensitive to the magnitude of prediction error. Furthermore, super-learning activation in this region of PFC correlates, across subjects, with the amount learned. We thus provide direct evidence for a brain correlate of the surprise-dependent mechanisms proposed by associative accounts of causal learning. We show that activity in right lateral PFC is sensitive to the magnitude, though not the direction, of the prediction error. Furthermore, its activity is not directly explicable in terms of novelty or response errors and appears directly related to the learning that arises out of prediction error.

Adult↗

PubMed1997

Women's caregiving and paid work: causal relationships in late midlife.

Care of an ill or disabled family member or friend is disproportionately done by women and typically is done in late midlife. Because this is-also a time in the life course when women's labor force participation peaks, many women faced with caregiving demands have to decide how to balance them with their employment. In this study we use the National Longitudinal Survey (NLS) of Mature Women to examine the causal relationship between employment and caring for an ill or disabled friend or relative over a three-year period. We find that employment does not affect whether or not women start caregiving, but that women who do start are more likely to reduce employment hours or stop work. Thus, the causal relationship between employment and caregiving in late midlife is largely unidirectional, with women reducing hours to meet caregiving demands.

Caregivers↗

PubMed1985

Loneliness among the elderly: a causal approach.

The purpose of this study was to develop and assess a causal model of loneliness among a national probability sample of noninstitutionalized elderly adults. Path analysis was used to test the causal model. The findings indicated that marital status, self-perceived health status, income, social activity levels, and a sense of social fulfillment directly predict feelings of loneliness. The social fulfillment variable, however, was the most important predictor. An interesting finding was that age had no notable direct or indirect effect on feelings of loneliness.

Age Factors↗

PubMed1997

Association of breastfeeding and stunting in Peruvian toddlers: an example of reverse causality.

BACKGROUND: Child feeding recommendations include breastfeeding beyond 12 months, however, some researchers have reported increased rates of malnutrition in breastfed toddlers. A negative association between growth and breast-feeding may reflect reverse causality; that is, the outcome (growth) is a determinant of the predictor (breastfeeding), and not vice versa. We examined this question with data from 134 Peruvian toddlers. METHODS: A linear regression analysis predicted length at the age of 15 months by length at 12 months, study interval, and 12-14.9-month breastfeeding, complementary food intake, and diarrhoeal incidence. This analysis defined the association between breastfeeding and linear growth. To elucidate the direction of the effect between breastfeeding and linear growth, logistic regression was used to predict the probability of weaning by the end of 14 months. Determinants included weight-for-age (W/A) at 12 months, complementary food intake at 9-11.9 months, and change in diarrhoeal incidence between 9 and 14.9 months. RESULTS: There was a significant (P < 0.01) interaction of breastfeeding, diarrhoeal incidence, and complementary food intake on length at 15 months. Increased breastfeeding was associated with a 1.0 cm decrease in length gain when dietary intake was low and diarrhoeal morbidity was high, implying that breastfeeding is harmful. The logistic analysis, however, demonstrated that the risk of weaning decreased only when W/A and dietary intake were low and diarrhoeal morbidity was high. CONCLUSIONS: The negative association between breastfeeding and linear growth reflected reverse causality. Increased breastfeeding did not lead to poor growth; children's poor growth and health led to increased breastfeeding. Children's health must be considered when evaluating the association of breastfeeding with anthropometric outcomes.

Anthropometry↗

PubMed2001

Is There a Causal Relationship between Iron Deficiency or Iron-Deficiency Anemia and Weight at Birth, Length of Gestation and Perinatal Mortality?

An extensive literature review was conducted to identify whether iron deficiency, iron-deficiency anemia and anemia from any cause are causally related to low birth weight, preterm birth or perinatal mortality. Strong evidence exists for an association between maternal hemoglobin concentration and birth weight as well as between maternal hemoglobin concentration and preterm birth. It was not possible to determine how much of this association is attributable to iron-deficiency anemia in particular. Minimal values for both low birth weight and preterm birth occurred at maternal hemoglobin concentrations below the current cut-off value for anemia during pregnancy (110 g/L) in a number of studies, particularly those in which maternal hemoglobin values were not controlled for the duration of gestation. Supplementation of anemic or nonanemic pregnant women with iron, folic acid or both does not appear to increase either birth weight or the duration of gestation. However, these studies must be interpreted cautiously because most are subject to a bias toward false-negative findings. Thus, although there may be other reasons to offer women supplemental iron during pregnancy, the currently available evidence from studies with designs appropriate to establish a causal relationship is insufficient to support or reject this practice for the specific purposes of raising birth weight or lowering the rate of preterm birth.

Anemia↗

PubMed2026

Causal Relationship of Polyunsaturated Fatty Acids With Mental Disorders: A Systematic Review and Meta-analysis.

CONTEXT: Mental disorders (MDs) pose a important global health challenge, with a complex pathogenesis complicating treatment development. Nutritional interventions, particularly polyunsaturated fatty acids (PUFAs), have gained attention as potential therapeutic options. OBJECTIVE: This Mendelian randomization (MR) meta-analysis aimed to evaluate the potential causal relationship between PUFAs and MDs. DATA SOURCES: Genome-wide association study data were utilized to analyze the association between PUFAs (including omega-3, omega-3 percentage [omega-3%], omega-6, omega-6 percentage [omega-6%], and omega-6 to omega-3 ratio) and 12 major MDs. DATA EXTRACTION: Two-sample MR technology was used to assess the role of PUFAs in MDs. DATA ANALYSIS: The MR analysis revealed that genetically predicted omega-3 was causally linked to MDs, such as obsessive-compulsive disorder, bipolar disorder, schizophrenia, and major depressive disorder. Omega-3% exhibited protective effects against emotional personality disorder. Conversely, omega-6 was inversely correlated with attention-deficit/hyperactivity disorder risk, while a high omega-6 to omega-3 ratio was associated with an increased risk of depression and other mood disorders. CONCLUSION: High omega-3 levels and omega-3% may reduce the risk of MDs, whereas a high omega-6:omega-3 ratio may elevate the risk. These findings highlight the potential of PUFAs, particularly omega-3, in MD prevention and treatment, while underscoring the need for further research into the complex interactions between omega-3 and omega-6. The study provides a scientific foundation for future clinical trials and dietary intervention strategies. SYSTEMATIC REVIEW REGISTRATION: PROSPERO no. CRD42024598472.

Humans↗

PubMed1998

G-estimation of causal effects: isolated systolic hypertension and cardiovascular death in the Framingham Heart Study.

Time-dependent covariates are often both confounders and intermediate variables. In the presence of such covariates, standard approaches for adjustment for confounding are biased. The method of G-estimation allows for appropriate adjustment. Previous studies applying the G-estimation method have addressed effects on all-cause mortality rather than on specific causes of death. In the present study, a method to adjust for censoring by competing risks is presented. The authors used the approach to estimate the causal effect of isolated systolic hypertension on cardiovascular mortality in the Framingham Heart Study, with a 10-year follow-up using data from 1956 to 1970. Arterial rigidity is a major determinant of isolated systolic hypertension and may be a confounder of the relation between isolated systolic hypertension and cardiovascular death. Conversely, isolated systolic hypertension may by itself contribute to stiffening of the vessel wall, and arterial rigidity may therefore also be an intermediate variable in the causal pathway from isolated systolic hypertension to cardiovascular death. While controlling for arterial rigidity and other baseline and time-dependent covariates, isolated systolic hypertension decreased the time to cardiovascular death by 45% (95% confidence interval 3-69).

Adult↗

PubMed1999

Controls who experienced hypothetical causal intermediates should not be excluded from case-control studies.

It has been suggested that controls with adenomatous polyps of the colon and rectum should be excluded from case-control studies of cigarette smoking and colorectal cancer. A claim has been made that the presence of such controls creates a bias toward the null. The polyps are an intermediate step in a hypothetical causal pathway between the exposure and the disease. Thus, the recommendation logically extends to the exclusion of all controls who experienced hypothetical causal intermediates from all case-control studies. It is shown, in the simple case of an exposure that acts solely through the pathway involving the intermediate, that such exclusions create a bias away from the null. The rationale for recommending the detrimental exclusions appears to stem from a variant of the "trohoc fallacy": the mistaken view of case-control studies as comparisons between diseased and healthy groups and not as comparisons between groups that differ by exposure.

Adenoma↗

PubMed2000

Hydrocarbon exposure may cause glomerulonephritis and worsen renal function: evidence based on Hill's criteria for causality.

Many observational and experimental studies point to hydrocarbon exposure as an important pathogenic factor in glomerulonephritis. The findings have made little impact on current concepts and patient care, possibly because the hypothesis of a direct causal effect of the exposure and the hypothesis that the exposure worsens renal function have not been considered separately. This review examines these two hypotheses using Hill's criteria for causality. The results from 14 cross-sectional, 18 case-control studies, two cohort studies, 15 experiments on laboratory animals and two on human beings together with many case reports satisfy all but one of Hill's criteria for both hypotheses. Of particular importance is the finding in the case-control and follow-up studies of an association between degree of exposure and stage of renal disease, and an inverse association between degree of exposure and renal function, indicating that the most important effect of hydrocarbon exposure is its effect on renal function. End-stage renal failure may be preventable in many patients with glomerulonephritis provided a possible exposure to toxic chemicals is discontinued.

Animals↗

PubMed2005

Arthritis in association with human immunodeficiency virus infection in Black African children: causal or coincidental?

OBJECTIVES: To compare human immunodeficiency virus (HIV)-infected and HIV-uninfected children with arthritis of unknown origin to determine whether the association between HIV infection and arthritis is causal or coincidental. METHOD: Retrospective review of 132 children with arthritis who were tested for HIV infection. RESULTS: Thirty-five (27%) of the children were HIV infected and the male to female ratio was 2.5:1 (P = 0.02). Arthritis was the presenting feature of HIV infection in 78% of these children. The remaining 97 (73%) were diagnosed as having juvenile idiopathic arthritis. 'Spondyloarthropathy-like' features were found in 34% of HIV-infected children compared with 5% of uninfected children. CONCLUSION: The high prevalence of HIV infection in 27% of children, the predominance of males and the increased prevalence of 'spondyloarthropathy-like' features, supports a causal relationship between HIV infection and arthritis.

Arthritis↗