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PubMed1987

A graphical approach to the identification and estimation of causal parameters in mortality studies with sustained exposure periods.

In observational cohort mortality studies with prolonged periods of exposure to the agent under study, independent risk factors for death commonly determine subsequent exposure to the study agent. For example, in occupational mortality studies, date of termination of employment is both a determinant of subsequent exposure to the chemical agent under study (since terminated individuals receive no further exposure) and an independent risk factor for death (since disabled individuals tend to leave employment). When a risk factor determines subsequent exposure and is determined by previous exposure, standard analyses that estimate age-specific mortality rates as a function of cumulative exposure can underestimate the true effect of exposure on mortality, whether or not one adjusts for the risk factor in the analysis. This observation raises the question, "Which, if any, empirical population parameter can be causally interpreted as the true effect of exposure in observational mortality studies?" In answer, we offer a graphical approach to the identification and estimation of causal parameters in mortality studies with sustained exposure periods. We reanalyze the mortality experience of a cohort of arsenic-exposed copper smelter workers using our approach and compare our results with those obtained using standard methods. We find an adverse effect of arsenic exposure on all cause and lung cancer mortality, which standard methods failed to detect. The analytic approach introduced in this paper may be necessary to control bias in any epidemiologic study in which there exists a risk factor which both determines subsequent exposure and is determined by previous exposure to the agent under study.

Epidemiologic Methods↗

PubMed2001

A meta-analytic review of coping with illness: do causal attributions matter?

OBJECTIVE: The present meta-analytic review assessed the relations between causal attributions, coping, and psychological adjustment in individuals with physical illnesses or undergoing medical procedures. A theoretical model predicting psychological adjustment was proposed. It was hypothesized that causal attributions would be both directly related to psychological adjustment and indirectly related to psychology adjustment via coping strategies. METHODS: Relevant methodological and statistical information was extracted from 27 target studies. Weighted correlations from 27 studies were used as the unit of analysis to test the theoretical model. RESULTS: Overall, internal, unstable, and controllable attributions were indirectly associated with positive psychological adjustment through the use of Approach and Emotion-Focused coping (P<.01). In addition, stable and uncontrollable attributions were indirectly associated with negative psychological adjustment through the use of Avoidance coping (P<.01). CONCLUSION: These results suggest that attributions guide some motivated cognitions and behaviors within the context of illness, and are related to specific coping strategies. The discussion focuses on the predictive validity of these findings using the proposed theoretical model.

Adaptation, Psychological↗

PubMed2004

Do health causal attributions and coping strategies act as moderators of quality of life in peritoneal dialysis patients?

OBJECTIVE: The present study aimed at testing the relationships between health causal attribution and coping mechanisms with quality of life (QOL) in patients who have end-stage renal disease (ESRD) undergoing a peritoneal dialysis (PD) treatment. It was hypothesized that QOL should be negatively associated with the severity of the disease. Problem-focused coping, internal health-related locus of control (HRLOC) and medical power HRLOC were hypothesized as positive moderators preserving a better QOL, after controlling for the severity of the disease. METHODS: A total of 47 PD patients completed the Kidney Disease Quality of Life (KD-QOL) scale encompassing the Medical Outcomes Study Short-Form (MOS SF-36) self-administered questionnaire, the Multidimensional Health Locus of Control scale and the Ways of Coping Check-List (WCCL) scale. RESULTS: Low scores for all QOL scores were found except for pain dimension, as compared with scores available from a general French population. Globally, QOL was not related to the severity of the disease. Univariate analysis showed that the physical component score (PCS) of QOL was positively associated with internal HRLOC (r=.35; P<.05), and negatively with medical power HRLOC (r=-.36; P<.05). Multivariate analysis adjusting for age confirmed these results. Mental component score (MCS) was negatively associated with the use of emotion-focused coping and seeking social support (r=-.45; P=.001 and r=-.30; P<.05, respectively), the first association persisting in multivariate analysis. Neither PCS nor MCS was linked to the use of problem-focused coping. CONCLUSION: These results suggest that physical QOL is all the more preserved when patients are more convinced that their behaviour can influence their health condition and that psychological QOL is all the more impaired when health condition is perceived as less controllable, requiring emotion-focused coping (avoidance strategies). Health causal attributions and coping act respectively as moderators of physical and psychological components of QOL.

Adaptation, Psychological↗

PubMed1999

Autism and measles, mumps, and rubella vaccine: no epidemiological evidence for a causal association.

BACKGROUND: We undertook an epidemiological study to investigate whether measles, mumps, and rubella (MMR) vaccine may be causally associated with autism. METHODS: Children with autism born since 1979 were identified from special needs/disability registers and special schools in eight North Thames health districts, UK. Information from clinical records was linked to immunisation data held on the child health computing system. We looked for evidence of a change in trend in incidence or age at diagnosis associated with the introduction of MMR vaccination to the UK in 1988. Clustering of onsets within defined postvaccination periods was investigated by the case-series method. FINDINGS: We identified 498 cases of autism (261 of core autism, 166 of atypical autism, and 71 of Asperger's syndrome). In 293 cases the diagnosis could be confirmed by the criteria of the International Classification of Diseases, tenth revision (ICD10: 214 [82%] core autism, 52 [31%] atypical autism, 27 [38%] Asperger's syndrome). There was a steady increase in cases by year of birth with no sudden "step-up" or change in the trend line after the introduction of MMR vaccination. There was no difference in age at diagnosis between the cases vaccinated before or after 18 months of age and those never vaccinated. There was no temporal association between onset of autism within 1 or 2 years after vaccination with MMR (relative incidence compared with control period 0.94 [95% CI 0.60-1.47] and 1.09 [0.79-1.52]). Developmental regression was not clustered in the months after vaccination (relative incidence within 2 months and 4 months after MMR vaccination 0.92 [0.38-2.21] and 1.00 [0.52-1.95]). No significant temporal clustering for age at onset of parental concern was seen for cases of core autism or atypical autism with the exception of a single interval within 6 months of MMR vaccination. This appeared to be an artifact related to the difficulty of defining precisely the onset of symptoms in this disorder. INTERPRETATION: Our analyses do not support a causal association between MMR vaccine and autism. If such an association occurs, it is so rare that it could not be identified in this large regional sample.

Autistic Disorder↗

PubMed2000

Black currant reversion disease--the probable causal agent, eriophyid mite vectors, epidemiology and prospects for control.

Black currant reversion disease and the vector of its causal agent, the black currant gall mite Cecidophyopsis ribis, have been recognised for at least 100 years and are the two most damaging organisms of black currant crops world-wide. However, the molecular characterisation of these two organisms has begun to be determined in only the last few years. The probable causal agent of reversion disease, Black currant reversion associated virus (BRAV), belongs to the genus Nepovirus, has isometric particles c. 28 nm in diameter that contain a single major polypeptide of c. 55 KDa and two polyadenylated ssRNA species of 7700 nt and 6400 nt. Some particle preparations also contain a satellite ssRNA species of 1432 nt. Using immuno-capture RT-PCR and primers based on the genomic RNA of BRAV, this virus was shown to be closely associated with reversion disease. Analysis of Cecidophyopsis mite rDNA, identified rapidly and unambiguously the three known species on Ribes and distinguished four new ones. Resistance to the reversion agent and to the gall mite vector has been introduced into black currant and has given effective control of these respective organisms in the field. These findings and their significance for the ecology, epidemiology and control of variants of these two organisms are reviewed and discussed.

Animals↗

PubMed2000

Is there a causal link between hepatitis B vaccination and multiple sclerosis?

After the publication of case reports of hepatitis B vaccinees with onset or relapse of multiple sclerosis (MS), followed by a media-driven scare campaign in France, the perception that hepatitis B vaccine causes MS has developed. This has led to a fall in the acceptance of hepatitis B vaccination particularly in French-speaking communities which was accelerated by court decisions in favour of vaccination "victims" and the suspension of routine vaccination of pre-adolescents in French schools as a "precautionary measure". This situation has arisen in spite of the absence of scientific data to support a causal link between vaccination and multiple sclerosis. In this article, initially written to inform and reassure employees of one of the vaccine manufacturers, the epidemiological importance of hepatitis B and current knowledge on the aetiology of MS are described. All available data that may throw light on the hypothesis that hepatitis B vaccination is causally linked to MS was reviewed. The conclusion reached on the basis of available data is that the most plausible explanation for the observed temporal association between vaccination and MS is that it is a coincidental association. It is now important to rebuild public confidence in hepatitis B vaccine as well as in vaccination in general.

Adolescent↗

PubMedDate not supplied

Testing the causal role of expectancies in smoking motivation and behavior.

The causal role of outcome expectancies in smoking motivation and behavior was tested in a laboratory experiment. Two expectancy manipulations-Health Consequences Expectancy Increase (HC) and Mood Management Expectancy Challenge (MM)-were crossed in a 2 x 2 factorial design. One hundred twenty-three heavy smokers were randomly assigned to the conditions and shown videotaped interviews of smokers and exsmokers followed by an interview that personalized the information. Both manipulations produced changes in targeted expectancies on at least one of two expectancy instruments. As predicted, only the HC manipulation produced increases in motivation to quit smoking and a reduction in smoking 3 months later. This study provides initial evidence that smoking expectancies play a causal role in smoking motivation, consistent with previous research with alcohol.

Adult↗

PubMed2002

Epidemiologic analyses of risk factors, risk indicators, risk markers, and causal factors. The example of albuminuria and the risk of cardiovascular disease in diabetes.

Much of the practice of modern medicine deals with prevention of the consequences of chronic conditions, including diabetes, hypertension, obesity, asthma, chronic bronchitis, and inflammatory bowel diseases. To achieve this end, identifying people at risk for these consequences and then initiating the appropriate, evidence-based preventive therapies are key. Characterization and study of risk factors are at the core of this effort and represent the only way that high-risk individuals can be identified. These risk factors can be any imagined variable, ranging from a genetic mutation to a blood result, a previous disease, exposure to an infectious agent or toxin, a socioeconomic state, ethnicity, birth weight, or country of origin. All causal factors for an outcome are risk factors for that outcome; reducing these risk factors almost certainly reduces the outcome. The converse is usually not true, however: identification of a risk factor reveals little about its causal connection to the outcome in question, and reducing this risk factor may or may not reduce the outcome. Once high-risk individuals are identified on the basis of their risk factor profile, the relevant clinical question relates to which therapies have been identified clearly that will reduce the risk or the outcome. If modification of the level of the risk factor is considered therapeutically, the question of whether the risk factor is also a good surrogate outcome must be answered. Information regarding whether the risk factor causes the disease is highly desirable; however, it is often unavailable and is not required before making therapeutic decisions.

Albuminuria↗

PubMed1998

Enterovirus infections and insulin dependent diabetes mellitus--evidence for causality.

BACKGROUND: Insulin-dependent diabetes mellitus (IDDM) has a long subclinical period characterised by gradually progressing autoimmune damage of insulin producing beta-cells. Clinical IDDM is manifested when 90% of beta-cells have been destroyed. Several studies have indicated that enterovirus infections, coxsackievirus B (CVB) infections especially, are frequent at the manifestation of clinical IDDM suggesting that they can precipitate the symptoms of IDDM in individuals who already have an advanced beta-cell damage. Recently, the first prospective studies have been published suggesting that enterovirus infections can also initiate the process several years before clinical IDDM. This implies that enterovirus infections may have a crucial role in the pathogenesis of human IDDM. OBJECTIVE: The recent findings have brought up the question whether the time has come when a causal association between enterovirus infections and IDDM could finally be confirmed. This review focuses on this question summarising the current knowledge and the prospects of future research. STUDY DESIGN: Review of the recent progress in studies evaluating the role of enterovirus infections in human IDDM. CONCLUSIONS: The currently available information supports the assumption that the role of enterovirus infections may be more important than previously estimated. Enterovirus infections are obviously associated with increased risk of IDDM, but whether this association reflects causal relationship remains to be confirmed in future studies. Prospective birth-cohort studies will be among the most important ones giving important data on the etiologic fraction of enterovirus infections, the properties of diabetogenic virus variants and the mechanisms of beta-cell damage.

Diabetes Mellitus, Type 1↗

PubMed2003

Nuclear medical PET-study in the causal relationship between mastication and brain function in human evolutionary and developmental processes.

The principal author (Kubote 1995, 1997, 1998, 1999, 2000 a, b) has proposed that chewing food well from infancy will lead to a clear-headed and robust person, following which the same concept has been presented to the general public by the mass media. Unfortunately, however, there does not yet seem to be any direct evidence to support this claim. It is thus necessary to review mastication from the standpoint of the new concept of evidence-based medicine (EBM) and to create a new direction in medicodental research and treatment from the viewpoint of human evolution, because the causal relationship between mastication and brain function has never been clarified either in fossil science research or in the modem scientific bibliography. To confirm the human historical fossil record in regard to the causal relationship between the development of mastication and brain function in human evolutionary processes, the effect of gum chewing on brain reaction was examined in humans by means of a positron-emission tomography (PET) camera (Momose et al. 1997) after an antecubital intravenous injection of H215O. Powerful activation of the cortical cells was demonstrated in multiple cortical areas involving the marginal areas of the bilateral central sulci of the cerebral cortex (Fig. 1), and the activated areas coincided with our previous results in region of interest (ROI) analysis (Momose et al. 1887). Three-dimensionally, numerous cortical cells were shown to form nuclei on relief maps (Fig. 2). As diets and feeding habits changed in a stepwise manner from frugivorous to omnivorous via herbivorous and carnivorous over the lengthy progress of evolution, the brain concomitantly grew and the cranial capacity gradually increased in volume from 500 cm3, food from plant sources to animal sources (700 cm3), and then to both (1500 cm3), during the human evolutionary and developmental processes. Gradual increases in the cranial capacity of human fossils during the developmental stage have been demonstrated also by PET images of the human brain acquired by means of a PET camera and an antecubital intravenous injection of H215O during mastication that showed powerful activation of cortical cells in multiple areas. It could be concluded that human fossils give us concrete information on how to feed our children in the modern human life style from infancy to adulthood, so that we should bring children up by adhering to images of the principal feeding habits discovered during this research on human evolutionary and developmental processes.

Brain↗

PubMed2000

Evidence for cognition without grammar from causal reasoning and 'theory of mind' in an agrammatic aphasic patient.

Understanding the inter-relationship between language and thought is fundamental to the study of human cognition [1] [2] [3]. Some investigators have proposed that propositions in natural language serve to scaffold thinking, by providing, for example, a sequential structure to a massively parallel process [4]. Others have maintained that certain thoughts, such as inferring the mental states of others, termed 'theory of mind' (ToM) reasoning, and identifying causal relationships, necessarily involve language propositions [5]. It has been proposed that ToM reasoning depends upon the possession of syntactic structures such as those that permit the embedding of false propositions within true statements ('Mary knows that John (falsely) thinks chocolates are in the cupboard') [6]. The performance on reasoning tasks of individuals with severe agrammatic aphasia (an impairment of language following a lesion of the perisylvian areas of the language-dominant hemisphere) offers novel insights into the relation between grammar and cognition. We report the unusual case of a patient with agrammatic aphasia of such severity that language propositions were not apparently available at an explicit processing level in any modality of language use. Despite this profound impairment in grammar, he displayed simple causal reasoning and ToM understanding. Thus, reasoning about causes and beliefs involve processes that are independent of propositional language.

Aphasia↗

PubMed2003

Dynamic causal modelling.

In this paper we present an approach to the identification of nonlinear input-state-output systems. By using a bilinear approximation to the dynamics of interactions among states, the parameters of the implicit causal model reduce to three sets. These comprise (1) parameters that mediate the influence of extrinsic inputs on the states, (2) parameters that mediate intrinsic coupling among the states, and (3) [bilinear] parameters that allow the inputs to modulate that coupling. Identification proceeds in a Bayesian framework given known, deterministic inputs and the observed responses of the system. We developed this approach for the analysis of effective connectivity using experimentally designed inputs and fMRI responses. In this context, the coupling parameters correspond to effective connectivity and the bilinear parameters reflect the changes in connectivity induced by inputs. The ensuing framework allows one to characterise fMRI experiments, conceptually, as an experimental manipulation of integration among brain regions (by contextual or trial-free inputs, like time or attentional set) that is revealed using evoked responses (to perturbations or trial-bound inputs, like stimuli). As with previous analyses of effective connectivity, the focus is on experimentally induced changes in coupling (cf., psychophysiologic interactions). However, unlike previous approaches in neuroimaging, the causal model ascribes responses to designed deterministic inputs, as opposed to treating inputs as unknown and stochastic.

Arousal↗

PubMed2003

Malignant melanoma and levodopa in Parkinson's disease: causality or coincidence?

Levodopa is the major drug used in the treatment of patients with Parkinson's disease. However, levodopa continues to be 'contra-indicated' for patients with Parkinson's disease associated with malignant melanoma. Case reports have suggested that levodopa has a causal relationship with malignant melanoma due to their shared dopamine biochemical pathway. Clinical characteristics of 54 patients with both Parkinson's disease and melanoma were analyzed (43 cases from the literature and 11 from our institution). The results suggest that the occurrence of both Parkinson's disease and melanoma in these patients is coincidental rather than causal. It did not appear that the Parkinson's disease patients on levodopa therapy were predisposed to melanoma, nor did levodopa therapy appear to exaggerate melanoma if it were previously present.

Adult↗

PubMed2002

A relational view of causality in normal and abnormal development.

An understanding of developmental phenomena demands a relational or coactive concept of causality, as opposed to a conceptualization that assumes that singular causes can act in isolation. In this article we present a developmental psychobiological systems view of relational (bidirectional, coactional) causality, in which it is proposed that developmental outcomes are a consequence of at least two specific components of coaction from the same or different levels of a developmental system. The levels are genetic, neural, behavioral, and environmental; the latter level includes the cultural, social, and physical aspects of an organism's environment. We show the applicability of this view to the understanding of the development of normal and abnormal behavioral and psychological phenotypes through illustrations from the existing animal and human literature. Finally, we discuss future possibilities and potential stumbling blocks in the implementation of a more fully realized bidirectional, coactional perspective in developmental psychopathological research.

Alcoholism↗

PubMed2002

Intervention research, theoretical mechanisms, and causal processes related to externalizing behavior patterns.

Intervention research with children and adolescents has suffered from a dearth of relevant theoretical grounding and from the lack of a reciprocal "feedback" mechanism by which clinical trials can inform relevant theorizing and conceptualization. There are hopeful signs, however, of increasing confluence between clinical efforts and theoretical models. Indeed, the key issue I discuss is how intervention studies can yield information about developmental and clinical theory as well as mechanisms related to psychopathology. Specific research examples in the field, particularly those emanating from the Multimodal Treatment Study of Children with attention deficit/hyperactivity disorder (MTA study), reveal that probes of moderator and mediator variables can clearly enhance our knowledge of relevant processes and mechanisms. In fact, recent MTA findings have relevance for models of genetic and epigenetic influence on symptomatology related to attentional deficits and hyperactivity. It would be overzealous, however, to make premature claims regarding etiologic variables from intervention research, as treatment studies typically address variables that are causally far "downstream" from primary causal factors and most clinical trials have statistical power that is barely sufficient for main outcome questions, much less mediational linkages. Overall, the field has severely underutilized experimental intervention research to subserve the dual ends of improving the lives of youth and advancing theoretical conceptualization regarding development and psychopathology.

Adolescent↗

PubMedDate not supplied

Estimating the causal effects of treatment.

OBJECTIVE: To provide a relatively non-technical review of recent statistical research on the analysis and interpretation of the results of randomised controlled trials in which there are possibly all three of the following types of protocol violation: non-adherence to allocated treatment, contamination (that is, patients receiving treatments other than the one to which they were allocated) and attrition (missing outcome data). METHODS: The estimation methods involve the use of potential outcomes (counterfactuals) in the definition of a causal effect of treatment and in drawing valid inferences concerning its size. RESULTS: The methods are explained through the use of simple arithmetical expressions involving the counts from three-way contingency tables (Outcome by Treatment Received by Random Allocation). Illustration is provided through the use of a hypothetical data set. CONCLUSIONS: Recent advances in statistical methodology enable one to estimate treatment effects from the results of randomized trials in which the treatment actually received is not necessarily the one to which the patient was allocated. These methods allow one to make adjustments to allow for both non-compliance and loss to follow-up. Even for such a 'broken' randomised trial, inference concerning causal effects is safer than that from data arising from an observational study that never involved random allocation in the first place.

Humans↗

PubMed1997

Causal indicators in quality of life research.

Quality of Life (QOL) questionnaires contain two different types of items. Some items, such as assessments of symptoms of disease, may be called causal indicators because the occurrence of these symptoms can cause a change in QOL. A severe state of even a single symptom may suffice to cause impairment of QOL, although a poor QOL need not necessarily imply that a patient suffers from all the symptoms. Other items, for example anxiety and depression, can be regarded as effect indicators which reflect the level of QOL. These indicators usually have a more uniform relationship with QOL, and therefore a patient with poor QOL is likely to have low scores on all effect indicators. In extreme cases it may seem intuitively obvious which items are causal and which are effect indicators, but often it is less clear. We propose a model which includes these two types of indicators and show that they behave in markedly different ways. Formal quantitative methods are developed for distinguishing them. We also discuss the impact of this distinction upon instrument validation and the design and analysis of summary subscales.

Breast Neoplasms↗

PubMed2002

Second-order backward blocking and unovershadowing in human causal learning.

De Houwer and Beckers (in press, Experiment 1) recently demonstrated that ratings about the relation between a target cue T2 and an outcome are higher when training involves CT1+ and T1T2+ followed by C+ trials than when training involves CT1+ and T1T2+ followed by C- trials. We replicated this study but now explicitly asked participants to rate the causal status of the cues both before and after the C+ or C- trials. Results showed that causal ratings for T2 were significantly higher after C+ trials than before C+ trials and that T2 received significantly lower ratings after C- trials than before C- trials. The results thus provide the first evidence for higher-order unovershadowing and higher-order backward blocking. In addition, the ratings for T1 revealed that first-order backward blocking (i.e., decrease in ratings for T1 as the result of C+ trials) was stronger than first-order unovershadowing (i.e., increase in ratings for T1 as the result of C- trials).

Adult↗