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Results for “causality”

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PubMed1999

Causal pathways for incident lower-extremity ulcers in patients with diabetes from two settings.

OBJECTIVE: To determine the frequency and constellations of anatomic, pathophysiologic, and environmental factors involved in the development of incident diabetic foot ulcers in patients with diabetes and no history of foot ulcers from Manchester, U.K., and Seattle, Washington, research settings. RESEARCH DESIGN AND METHODS: The Rothman model of causation was applied to the diabetic foot ulcer condition. The presence of structural deformities, peripheral neuropathy, ischemia, infection, edema, and callus formation was determined for diabetic individuals with incident foot ulcers in Manchester and Seattle. Demographic, health, diabetes, and ulcer data were ascertained for each patient. A multidisciplinary group of foot specialists blinded to patient identity independently reviewed detailed abstracts to determine component and sufficient causes present and contributing to the development of each patient's foot ulcer. A modified Delphi process assisted the group in reaching consensus on component causes for each patient. Estimates of the proportion of ulcers that could be ascribed to each component cause were computed. RESULTS: From among 92 study patients from Manchester and 56 from Seattle, 32 unique causal pathways were identified. A critical triad (neuropathy, minor foot trauma, foot deformity) was present in > 63% of patient's causal pathways to foot ulcers. The components edema and ischemia contributed to the development of 37 and 35% of foot ulcers, respectively. Callus formation was associated with ulcer development in 30% of the pathways. Two unitary causes of ulcer were identified, with trauma and edema accounting for 6 and < 1% of ulcers, respectively. The majority of the lesions were on the plantar toes, forefoot, and midfoot. CONCLUSIONS: The most frequent component causes for lower-extremity ulcers were trauma, neuropathy, and deformity, which were present in a majority of patients. Clinicians are encouraged to use proven strategies to prevent and decrease the impact of modifiable conditions leading to foot ulcers in patients with diabetes.

Adult↗

PubMed2002

Is insulin sensitivity a causal intermediate in the relationship between alcohol consumption and carotid atherosclerosis?: the insulin resistance and atherosclerosis study.

OBJECTIVE: A J-shaped association has been demonstrated between alcohol consumption and atherosclerosis. Insulin resistance, also a risk factor for atherosclerosis, has been shown to have a similar J-shaped association with alcohol intake. This raises the question of whether insulin sensitivity (S(I)) is a causal intermediate in the alcohol-atherosclerosis relationship. RESEARCH DESIGN AND METHODS: The Insulin Resistance Atherosclerosis Study was a multicenter cohort study designed to investigate relationships among S(I), risk factors for cardiovascular disease, and carotid artery atherosclerosis. Using regression analysis, we tested whether adjustment for S(I) attenuated the alcohol-atherosclerosis relationship observed at baseline. RESULTS: A J-shaped association was observed between alcohol consumption and common carotid artery intimal medial thickness. The protective aspect of the alcohol-atherosclerosis relationship was attenuated by 25% after the adjustment for S(I). However, an interaction was observed between alcohol consumption and glucose tolerance (GT) status. In comparison with never drinkers, all levels of alcohol consumption were associated with less atherosclerosis in participants with normal GT status. Participants with impaired GT status (but not diabetes) demonstrated a J-shaped alcohol-atherosclerosis association. All levels of alcohol consumption were associated with more atherosclerosis in participants with diabetes. CONCLUSIONS: S(I) may be a causal intermediate at protective levels of alcohol intake, but an alcohol-GT interaction precluded a definitive conclusion. Moderate alcohol consumption may increase the risk of atherosclerosis in people with diabetes. These findings contrast with previous reports and do not support current recommendations regarding moderate alcohol consumption in people with diabetes. More research is needed to clarify this issue.

Adult↗

PubMed2003

New insights on oxidative stress and diabetic complications may lead to a "causal" antioxidant therapy.

Evidence implicates hyperglycemia-derived oxygen free radicals as mediators of diabetic complications. However, intervention studies with classic antioxidants, such as vitamin E, failed to demonstrate any beneficial effect. Recent studies demonstrate that a single hyperglycemia-induced process of overproduction of superoxide by the mitochondrial electron-transport chain seems to be the first and key event in the activation of all other pathways involved in the pathogenesis of diabetic complications. These include increased polyol pathway flux, increased advanced glycosylation end product formation, activation of protein kinase C, and increased hexosamine pathway flux. Superoxide overproduction is accompanied by increased nitric oxide generation, due to an endothelial NOS and inducible NOS uncoupled state, a phenomenon favoring the formation of the strong oxidant peroxynitrite, which in turn damages DNA. DNA damage is an obligatory stimulus for the activation of the nuclear enzyme poly(ADP-ribose) polymerase. Poly(ADP-ribose) polymerase activation in turn depletes the intracellular concentration of its substrate NAD(+), slowing the rate of glycolysis, electron transport, and ATP formation, and produces an ADP-ribosylation of the GAPDH. These processes result in acute endothelial dysfunction in diabetic blood vessels that, convincingly, also contributes to the development of diabetic complications. These new findings may explain why classic antioxidants, such as vitamin E, which work by scavenging already-formed toxic oxidation products, have failed to show beneficial effects on diabetic complications and may suggest new and attractive "causal" antioxidant therapy. New low-molecular mass compounds that act as SOD or catalase mimetics or L-propionyl-carnitine and lipoic acid, which work as intracellular superoxide scavengers, improving mitochondrial function and reducing DNA damage, may be good candidates for such a strategy, and preliminary studies support this hypothesis. This "causal" therapy would also be associated with other promising tools such as LY 333531, PJ34, and FP15, which block the protein kinase beta isoform, poly(ADP-ribose) polymerase, and peroxynitrite, respectively. While waiting for these focused tools, we may have other options: thiazolinediones, statins, ACE inhibitors, and angiotensin 1 inhibitors can reduce intracellular oxidative stress generation, and it has been suggested that many of their beneficial effects, even in diabetic patients, are due to this property.

Antioxidants↗

PubMed1994

Causal attributions for marital violence and emotional response by women seeking refuge.

The aim was to examine the association between causal attributions for marital violence and emotional reactions of 15 women from two refuges in Northern Ireland. The women who perceived the cause of the violence as stable and uncontrollable scored higher on the Avoidance and Intrusion subscales of the Impact of Events Scale, respectively. In addition, more global causal attributions were associated with higher scores on Intrusion and Avoidance as well as depressive symptomatology as measured by the Beck Depression Inventory. No evidence was, however, found to support the view that these women were engaged in self-blaming (attributions tended to be overwhelmingly external).

Adaptation, Psychological↗

PubMed1987

A simplified logic of causal inference.

This paper provides a simplified method for evaluating the evidence in favour of a causal claim. It analyses the evidence bearing upon such a claim in terms of two questions: Do the putative cause and effect covary, and can alternative non-causal explanations of the relationship be ruled out? The different research designs for assessing covariation are outlined, as are the ways in which these designs permit a researcher to decide between alternative explanations of the relationship.

Depressive Disorder↗

PubMed1990

On doing the "impossible": inferring that a putative causal relationship does not exist.

A simple heuristic is proposed for drawing a warranted inference that a causal relationship does not exist between two events. It is illustrated by a study of the putative indirect causal relationship between Autistic Disorder and the Fragile X syndrome. This study was designed to ensure that a failure to find such a relationship provided good reasons for concluding that it was unlikely there was a relationship between Autistic Disorder and the Fragile X syndrome.

Autistic Disorder↗

PubMed1982

A comparison of alcoholics' and nonalcoholics' causal attributions for drinking behavior.

Alcoholic individuals often are assumed to deny personal responsibility for their alcoholism and to attribute causation to external situational factors. To investigate this assumption, in a 2 x 2 factorial design 20 alcoholics and 20 nonalcoholics made causal attributions for a recent personal drinking episode and for the audiotaped episode of a target individual who was described as either an alcoholic or a nonalcoholic. Results suggested that alcoholic subjects tended to make greater internal attributions for their own drinking than did nonalcoholic subjects. Subjects' attributions for the target individual depended on both the subjects' and targets' drinking histories. The results are discussed in terms of their relevance to models of alcoholism and to actor-observer differences in causal attributions.

Alcohol Drinking↗

PubMed2006

People want to see information that will help them make valid inferences in human causal learning.

According to higher order reasoning accounts of human causal learning (e.g., Lovibond, Been, Mitchell, Bouton, and Frohardt, 2003; Waldmann and Walker, 2005) ceiling effects in forward blocking (i.e., smaller blocking effects when the outcome occurs with a maximal intensity on A+ and AX+ trials) are due to the fact that people are uncertain about the causal status of a blocked cue X in a forward blocking design when the outcome is always fully present on A+ and AX+ trials. This should not be the case for a reduced overshadowing cue Y (B- trials followed by BY+ trials). We tested this hypothesis by asking participants which additional information they preferred to see after seeing all learning trials. Results showed (1) that all participants preferred to see the effect of the blocked cue X over seeing the effect of the reduced overshadowing cue Y (Experiment 1), and (2) that more participants preferred to see the blocked cue X on its own when the outcome on A+ and AX+ trials was fully present than when the outcome on those trials had a submaximalintensity (Experiment 2).

Association Learning↗

PubMed2002

Alignable and nonalignable differences in causal explanations.

Prior research indicates that people may base their causal explanations on distinctive features between an event and a contrasting background instance in which the event did not occur. Research on similarity judgments suggests that there are two types of distinctive features: alignable differences, which are corresponding characteristics of a pair, and nonalignable differences, which are characteristics of one item for which there are no corresponding characteristics in the other. In three experiments, the hypothesis that people's evaluations of causal explanations vary as a function of feature alignment was examined. The results suggest that people will rate explanations differently on the basis of alignable or nonalignable differences, depending on the type of the event, and that alignability depends on the relational structure among the features of the event.

Attitude↗

PubMed2005

Surprise and change: variations in the strength of present and absent cues in causal learning.

It is said that "absence makes the heart grow fonder." But, when and why does an absent event become salient to the heart or to the brain? An absent event may become salient when its nonoccurrence is surprising. Van Hamme and Wasserman (1994) found that a nonpresented but expected stimulus can actually change its associative status-and in the opposite direction from a presented stimulus. Associative models like that of Rescorla and Wagner (1972) focus only on presented cues; so, they cannot explain this result. However, absent cues can be permitted to change their value by assigning different learning parameters to present and absent cues. Van Hamme and Wasserman revised the Rescorla-Wagner model so that the a parameter is positive for present cues, but negative for absent cues; now, changes in the associative strength of absent cues move in the opposite direction as presented ones. This revised Rescorla-Wagner model can thus explain such otherwise vexing empirical findings as backward blocking, recovery from overshadowing, and backward conditioned inhibition. Moreover, the revised model predicts new effects. For example, explicit information about the absence of nonpresented cues should increase their salience (that is, their negative a value should be larger), leading to stronger associative changes than when no explicit mention is made of cue absence. Support for this prediction is detailed in a new causal judgment experiment in which participants rated the effectiveness of different foods' triggering a patient's allergic reaction. Overall, these and other findings encourage us to view human causal learning from an associative perspective.

Adult↗

PubMed2005

Simulations of a modified SOP model applied to retrospective revaluation of human causal learning.

Dickinson and Burke (1996) proposed a modified version of Wagner's (1981) SOP associative theory to explain retrospective revaluation of human causal judgments. In this modified SOP (MSOP), excitatory learning occurs when cue and outcome representations are either both directly activated or both associatively activated. By contrast, inhibitory learning occurs when one representation is directly activated while the other is associatively activated. Finite node simulations of MSOP yielded simple acquisition, overshadowing, blocking, and inhibitory learning under forward contingencies. Importantly, retrospective revaluation was predicted in the form of unovershadowing and backward inhibitory learning. However, MSOP did not yield backward blocking. These predictions are evaluated against the relevant empirical evidence and contrasted with the predictions of other associative theories that have been applied to retrospective revaluation of human causal and predictive learning.

Forecasting↗

PubMed2005

Causal and predictive-value judgments, but not predictions, are based on cue-outcome contingency.

In three experiments, we show that people respond differently when they make predictions as opposed to when they are asked to estimate the causal or the predictive value of cues: Their response to each of those three questions is based on different sets of information. More specifically, we show that prediction judgments depend on the probability of the outcome given the cue, whereas causal and predictive-value judgments depend on the cue-outcome contingency. Although these results might seem problematic for most associative models in their present form, they can be explained by explicitly assuming the existence of postacquisition processes that modulate participants' responses in a flexible way.

Adult↗

PubMed2005

A comparison of forward blocking and reduced overshadowing in human causal learning.

In this study, we directly compared forward blocking with reduced overshadowing in a human causal learning study using an A+, B- (first learning stage), AX+, BY+, KL+ (second learning stage) design. The results showed that reduced overshadowing was significantly stronger than forward blocking. These results are problematic for at least some associative learning models but were predicted on the basis of higher order reasoning accounts of cue competition in human causal learning.

Association↗

PubMed1995

Causal inferences as perceptual judgements.

We analyze how subjects make causal judgements based on contingency information in two paradigms. In the discrete paradigm, subjects are given specific information about the frequency a, with which a purported cause occurs with the effect; the frequency b, with which it occurs without the effect; the frequency c, with which the effect occurs when the cause is absent; and the frequency d, with which both cause and effect are absent. Subjects respond to P1 = a/(a + b) and P2 = c/(c + d). Some subjects' ratings are just a function of P1 while others are a function of delta P = P1-P2. Subjects' post-experiment reports are accurate reflections of which model they use. Combining these two types of subjects results in data well fit by the weighted delta P model (Allan, 1993). In the continuous paradigm, subjects control the purported causes (by clicking a mouse) and observe whether an effect occurs. Because cause and effects occur continuously in time, it is not possible to explicitly pair causes and effects. Rather, subjects report that they are responding to the rate at which the effects occur when they click versus when they do not click. Their ratings are a function of rates and not probabilities. In general, we argue that subjects' causal ratings are judgments of the magnitude of perceptually salient variables in the experiment.

Adult↗

PubMed1989

Selectional processes in causality judgment.

Two experiments illustrate the way in which competition between potential causes occurs when subjects are asked to judge the extent to which an action is the cause of an outcome. In the first experiment, it was found that introducing occurrences of the outcome in the absence of the action reduced causality judgments, but this effect was attenuated if these outcomes were signaled by another stimulus. In the second experiment, a delay between the action and the outcome reduced judgments, but this could be abolished by inserting a stimulus between the action and the outcome. The results are discussed in terms of a view of causality judgment that assumes that such judgments are based on associations between the mental representations of the action and the outcome.

Association Learning↗

PubMed1994

Proguanil plus sulfamethoxazole is not causally prophylactic in the Macaca mulatta--Plasmodium cynomolgi model.

New drugs for causal prophylaxis of malaria are needed. A proguanil/sulfamethoxazole combination was investigated using a rhesus monkey model (Macaca mulatta infected with Plasmodium cynomolgi) to determine whether causal prophylaxis could be achieved. When a five-day regimen of proguanil (40 mg/kg/day) combined with sulfamethoxazole (100 mg/kg/day) was used, infection of all animals (6 of 6) was observed, with an extended prepatent period (median 40 days). Two control animals became infected on days 9 and 23 following sporozoite inoculation. Plasma concentrations indicated that proguanil and sulfamethoxazole were adequately absorbed and metabolized to cycloguanil and N4-acetylsulfamethoxazole, respectively. Analysis of liver biopsy specimens demonstrated that the drugs were present two days following sporozoite inoculation but were not detectable one week later. Proguanil plus sulfamethoxazole does not eliminate exoerythrocytic-stage parasites in the rhesus monkey--P. cynomolgi model.

Animals↗

PubMed1990

Man-made mineral fibers and lung cancer. Epidemiologic evidence regarding the causal hypothesis.

Reviews of the epidemiologic literature point to a causal connection between lung cancer and exposure to airborne man-made mineral fibers. The present critical re-review starts with the requirements for epidemiologic evidence to be informative regarding a hypothesis on cancer etiology. The previous reviews relate lung cancer mortality to exposure that is too recent to be relevant. The relation to relevant (distant) exposure in the available data involves notable confounding by coexposure to other agents in the work environment, by the lower socioeconomic status of the exposed workers, and possibly by smoking. Moreover, analyses of trends in standardized mortality ratios according to timing and duration of exposure involve a lack of mutual comparability between the ratios. Given these problems, the available evidence is inadequate for testing the causal hypothesis. However, reanalyses of the available data, augmentation of the data with reanalyses, and new studies could eliminate the existing inadequacies.

Air Pollutants, Occupational↗

PubMed2026

Genome-wide discovery reveals 30 loci for choroidal thickness and uncovers potential causal links with angle-closure glaucoma.

The choroid is critical for maintaining vision and implicated in several ocular diseases, being the sole source of nutrients and waste removal for the outer retina. Genetic discovery can help elucidate the pathways through which choroidal features influence disease risk. Our meta-analysis of genome-wide association studies (n= 78,682 participants) identified 30 genomic regions, including 20 novel loci, associated with choroidal thickness. Findings suggest inflammatory and vascular processes drive choroidal thickness, with overlapping mechanisms shared with refractive error. Genome-wide independently significant SNPs accounted for 18.7% of the genetic variance in choroidal thickness. Mendelian randomisation analyses showed a causal effect of age-related macular degeneration on choroidal thickness, and suggest a bidirectional causal effect between choroidal thickness and primary angle-closure glaucoma. These findings provide insight into the shared genetic architecture and biological pathways linking choroidal thickness and related diseases.

Canadian Longitudinal Study on Aging↗