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The social determinants of oral health: new approaches to conceptualizing and researching complex causal networks.

Oral epidemiological research into the social determinants of oral health has been limited by the absence of a theoretical framework which reflects the complexity of real life social processes and the network of causal pathways between social structure and oral health and disease. In the absence of such a framework, social determinants are treated as isolated risk factors, attributable to the individual, having a direct impact on oral health. There is little sense of how such factors interrelate over time and place and the pathways between the factors and oral health. Features of social life which impact on individuals' oral health but are not reducible to the individual remain under-researched. A conceptual framework informing mainstream epidemiological research into the social determinants of health is applied to oral epidemiology. The framework suggests complex causal pathways between social structure and health via interlinking material, psychosocial and behavioural pathways. Methodological implications for oral epidemiological research informed by the framework, such as the use of multilevel modelling, path analysis and structural equation modelling, combining qualitative and quantitative research methods, and collaborative research, are discussed.

Causality↗

Causal cognition in human and nonhuman animals: a comparative, critical review.

In this article, we review some of the most provocative experimental results to have emerged from comparative labs in the past few years, starting with research focusing on contingency learning and finishing with experiments exploring nonhuman animals' understanding of causal-logical relations. Although the theoretical explanation for these results is often inchoate, a clear pattern nevertheless emerges. The comparative evidence does not fit comfortably into either the traditional associationist or inferential alternatives that have dominated comparative debate for many decades now. Indeed, the similarities and differences between human and nonhuman causal cognition seem to be much more multifarious than these dichotomous alternatives allow.

Animals↗

Exploring Causal Links Between 91 Circulating Inflammatory Proteins and Hashimoto's Thyroiditis: A Bidirectional Mendelian Randomization Study.

BACKGROUND: Increasing evidence has linked inflammation to Hashimoto's thyroiditis (HT) etiology. However, the causal role of circulating inflammatory proteins in HT remains uncertain. To investigate this, we conducted a bidirectional Mendelian randomization (MR) study. METHODS: Genetic data for 91 inflammatory proteins and HT were sourced from publicly available GWAS databases. The PhenoScanner database was then searched for pleiotropic SNPs associated with potential confounders. Inverse variance weighted (IVW) analysis was used as the primary analysis, simultaneously supplemented by five sensitivity analyses to strengthen the results. RESULTS: The results revealed that, after false discovery rate (FDR) correction, interleukin (IL)-12p40 was causally associated with increased risk of HT (OR [95% CI] = 1.295 [1.172, 1.431], p = 3.66 × 10-7, PFDR = 3.33×10-5). Conversely, none of the inflammatory proteins was a consequence of HT. CONCLUSION: This study suggests that IL-12p40 is probably one of the factors correlated with HT etiology, contributing to a better understanding of the pathogenesis of HT and underscoring the potential for therapeutic interventions targeting inflammatory proteins.

Humans↗

Perceived causal and treatment factors related to substance abuse: gender differences.

The study aimed to examine gender differences of causal and treatment factors in substance use as perceived by adults who are addicted to drugs in the southern region of Israel. Eighty-one men and a matched group of 81 women recruited from one methadone center and several welfare agencies, average age was about 31 years, about a third immigrated from the former Soviet Union, were administered self-report questionnaires, which measured the following: demographic variables, perceived causal and treatment factors. Results indicated the following: women drug users perceived familial circumstances such as domestic violence or incest to have higher impact on substance abuse than men; men reported curiosity and the influence of addicted friends to have higher impact on substance abuse than women. In addition, women perceived personality characteristics such as willpower to have greater impact on treatment retention than men; men regarded formal and informal social support to have greater impact on treatment retention than women. Results were discussed in light of planning and developing treatment programs.

Adult↗

Evaluating how placebos produce change. Logical and causal traps and understanding cognitive explanatory mechanisms.

The renewed interest in placebo effects from psychological and methodological angles is manifested in two complementary facets: the causal relationship between placebo effects inside and outside of clinical trials and the continual effort to understand how the underlying mechanisms relate to notions of efficacy and effectiveness. The article challenges the premise that placebo effects can be measured precisely enough that variance attributed to "nonspecific" placebo effects can be hierarchically partitioned from variance attributed to other "more specific" elements of therapy and discusses some of the most important recent developments in the understanding of how placebos produce change through cognitive explanatory mechanisms, including efficacy, outcome, and response expectancies; reverse placebo effects; schemas; and biased-information processing. Although much is already known about the complexity of explanatory mechanisms in placebo and expectancy effects, there is still much to do before establishing causal relationships and developing valid treatments based on this knowledge.

Causality↗

A causal model of depression in early adolescents.

The purpose of this study was to test the extent to which a causal model developed from a theoretical formulation of depression was consistent with data obtained from early adolescents, age 12 to 14. In this cross-sectional correlational design, the final sample consisted of 225 adolescents who responded to a demographic data sheet and instruments measuring depression, self-esteem, state anxiety, and perceived stress in classrooms. The causal model was tested via the LISREL 7 program, using a maximum likelihood structural equation model. The results yielded a chi-square (1, N = 225) = .71, p = .401, indicating a good fit of the model to the data. Perceived stress had the strongest direct, indirect, and total effect on depression in early adolescents. Contrary to expectation, self-esteem did not have a direct effect on depression, and girls did not report higher levels of depression than did boys.

Adolescent↗

Causal relationship between educational attainment and the occurrence of venous thromboembolism.

BACKGROUND: The association between educational attainment (EA) and arterial thrombotic disease has been reported, but the causal relationship between EA and venous thromboembolism (VTE) is not clear. We aimed to assess the causal effect of EA on VTE using the two-sample mendelian randomization (MR) method. METHODS: Data mining was conducted on the genome wide association studies (GWAS), with exposure factor EA and outcome factor VTE. Two-sample Mendelian Randomization (TSMR) analysis was conducted, with the results obtained from the random effects inverse variance weighted method (IVW). Use the MR-Egger method for pleiotropy analysis and leave one method for sensitivity analysis to verify the reliability of the data. RESULTS: Genetically predicted decreased EA was associated with a decreased risk of VTE in both the FinnGen consortium and UK Biobank (FinnGen-VTE: OR = 0.848; 95% CI 0.776-0.927; P = 2.84 × 10-4; UKB-VTE OR = 0.996; 95% CI 0.994-0.999; P = 0.008) under a multiplicative random-effects IVW model. Results were consistent in all sensitivity analyses and no horizontal pleiotropy was detected. CONCLUSIONS: The MR technique instructed a potential inverse causative relationship between EA and occurrence of VTE. Therefore, patients with low EA should be more vigilant about the occurrence of VTE.

Venous Thromboembolism↗

The causal relationship between steroid hormones and risk of stroke: evidence from a two-sample Mendelian randomization study.

It is unclear how steroid hormones contribute to stroke, and conducting randomized controlled trials to obtain related evidence is challenging. Therefore, Mendelian randomization (MR) technique was employed in this study to examine this association. Through genome-wide association meta-analysis, the genetic variants of steroid hormones, including testosterone/17β-estradiol (T/E2) ratio, aldosterone, androstenedione, progesterone, and hydroxyprogesterone, were acquired as instrumental variables. Analysis was done on the impact of these steroid hormones on the risk of stroke subtypes. The T/E2 ratio was associated to an elevated risk of small vessel stroke (SVS) according to the inverse variance weighted approach which was the main MR analytic technique (OR, 1.23, 95% CI: 1.05-1.44, p = 0.009). These findings were solid since no heterogeneity nor horizontal pleiotropy were found. The causal association between T/E2 and SVS was also confirmed in the replication study (p = 0.009). Nevertheless, there was no proof that other steroid hormones increased the risk of stroke. According to this study, T/E2 ratio and SVS are causally related. However, strong evidence for the impact of other steroid hormones on stroke subtypes is still lacking. These findings may be beneficial for developing stroke prevention strategies from steroid hormones levels.

Mendelian Randomization Analysis↗

Lines that connect: assessing the causality inference in the case of particulate pollution.

The question of when it would be appropriate to conclude that the associations between particulate pollution and various outcomes (including mortality) should be judged as causal in nature has been difficult and controversial. Although such a judgment must be subject to revision, the volume of new information and new experimental findings has been so great that such a reevaluation is required at frequent intervals. The useful summary by Gamble [PM(2. 5) and Mortality in Long-Term Prospective Cohort Studies: Cause-Effect or Statistical Associations? Environ Health Perspect 106:535-554 (1998)] of the reasons why a causal inference was, in his opinion, not justified provides a basis for reevaluation in the light of new data. Such a reexamination indicates that the associative evidence is now stronger and that the biologic basis for a number of adverse effects has now been demonstrated. All of the useful guideline criteria customarily applied to such questions seem to have been met, although there is still much to be learned about interactive effects and the possibility of statistical thresholds.

Air Pollution↗

Causality and the interpretation of epidemiologic evidence.

There is an ongoing debate regarding how and when an agent's or determinant's impact can be interpreted as causation with respect to some target disease. The so-called criteria of causation, originating from the seminal work of Sir Austin Bradford Hill and Mervyn Susser, are often schematically applied disregarding the fact that they were meant neither as criteria nor as a checklist for attributing to a hazard the potential of disease causation. Furthermore, there is a tendency to misinterpret the lack of evidence for causation as evidence for lack of a causal relation. There are no criteria in the strict sense for the assessment of evidence concerning an agent's or determinant's propensity to cause a disease, nor are there criteria to dismiss the notion of causation. Rather, there is a discursive process of conjecture and refutation. In this commentary, I propose a dialogue approach for the assessment of an agent or determinant. Starting from epidemiologic evidence, four issues need to be addressed: temporal relation, association, environmental equivalence, and population equivalence. If there are no valid counterarguments, a factor is attributed the potential of disease causation. More often than not, there will be insufficient evidence from epidemiologic studies. In these cases, other evidence can be used instead that increases or decreases confidence in a factor being causally related to a disease. Even though every verdict of causation is provisional, action must not be postponed until better evidence is available if our present knowledge appears to demand immediate measures for health protection.

Causality↗

Health and respirable particulate (PM10) air pollution: a causal or statistical association?

Numerous studies have reported weak but statistically significant acute health effects of particulate air pollution. The associations are observed at levels below the current U.S. standard of 150 micrograms/m3 (24 hr). Health effects include acute increased mortality from cardiopulmonary conditions and acute morbidity such as hospital admissions for related diseases. We reviewed recent epidemiology studies to evaluate whether criteria for causality are met, and we conclude that they are not. The weak associations are as likely to be due to confounding by weather, copollutants, or exposure misclassification as by ambient particulate matter (PM). The results from the same metropolitan areas are inconsistent, and PM explains such a small amount of the variability in mortality/morbidity that the association has little practical significance. Finally, experimental chamber studies of susceptible individuals exposed to PM concentrations well above 150 micrograms/m3 provide no evidence to support the morbidity/mortality findings. None of the criteria for establishing causality of the PM/mortality hypothesis are clearly met at ambient concentrations common in many U.S. cities.

Air Pollutants↗

Causality and control: threats to internal validity.

The essence of experimental research is to establish causal relationships between variables and this requires internal validity. An experiment is said to have internal validity when extraneous variables have been controlled. However, there are many threats to internal validity. This article considers 13 of them, providing examples which clarify and help to identify under what conditions these threats may occur. The threats discussed are history, maturation, testing, instrumentation, statistical regression, selection mortality, interactions with selection ambiguity about the direction of causal influence, diffusion of imitation of treatments, compensatory equalization of treatments, compensatory rivalry by respondents receiving less desirable treatments and resentful demoralization of respondents receiving less desirable treatments.

Bias↗

A causal analysis of employment and health in midlife women.

According to the "healthy worker" hypothesis, good health selects women into the employment role; conversely, the social causation hypothesis argues that important social roles such as employment can contribute to health. The relationship between these two variables may be of special concern to women at midlife, as both issues become increasingly salient. In this paper a model hypothesizing a nonrecursive (reciprocal) causal relationship between employment (hours employed) and health was presented. Because of the importance of both employment and health for women at midlife, the model was tested in a sample of 463 women ages 40-64 from a national cross-sectional dataset. Two-stage least squares regression supported the hypothesis that employment and health have a positive reciprocal relationship for women at midlife. In addition, married women and those with a child had better health but were likely to work fewer hours for pay. The same model tested in 21 to 39-year-old women was not significant. The results serve to emphasize the importance of examining assumptions about direction of causality in research on work and well-being at midlife.

Adult↗

Causal influence of car mass and size on driver fatality risk.

OBJECTIVES: This study estimated how adding mass, in the form of a passenger, to a car crashing head-on into another car affects fatality risks to both drivers. The study distinguished the causal roles of mass and size. METHODS: Head-on crashes between 2 cars, one with a right-front passenger and the other with only a driver, were examined with Fatality Analysis Reporting System data. RESULTS: Adding a passenger to a car led to a 14.5% reduction in driver risk ratio (risk to one driver divided by risk to the other). To divide this effect between the individual drivers, the author developed equations that express each driver's risk as a function of causal contributions from the mass and size of both involved cars. Adding a passenger reduced a driver's frontal crash fatality risk by 7.5% but increased the risk to the other driver by 8.1%. CONCLUSIONS: The presence of a passenger reduces a driver's frontal crash fatality risk but increases the risk to the driver of the other car. The findings are applicable to some single-car crashes, in which the driver risk decrease is not offset by any increase in harm to others. When all cars carry the same additional cargo, total population risk is reduced.

Accidents, Traffic↗

Efficiency of retrieval correlates with "logical" reasoning from causal conditional premises.

In two experiments, we examined the prediction that there should be a relation between the speed with which subjects can retrieve potential causes for given effects and their reasoning with causal conditional premises (if cause P, then effect Q). It was also predicted that when subjects are given effects for which there exists a single strongly associated cause, speed of retrieval of a second potential cause should be particularly related to reasoning with invalid logical forms--namely, affirmation of the consequent and denial of the antecedent. In the first experiment, 49 university students were given both retrieval tasks and conditional reasoning problems. The results were generally consistent with the predictions. The second experiment, involving 57 university students, replicated the first, with some methodological variations. The results were also consistent with the predictions. An analysis of the combined results of the two experiments indicated that individual differences in efficiency of retrieval of information from long-term memory did predict performance on the invalid logical forms in the predicted ways. These results strongly support a retrieval model for conditional reasoning with causal premises.

Adult↗

Causal judgment from contingency information: relation between subjective reports and individual tendencies in judgment.

In two experiments, participants made causal judgments from contingency information for problems with different objective contingencies. After the judgment task, the participants reported how their judgments had changed following each type of contingency information. Some reported idiosyncratic tendencies--in other words, tendencies contrary to those expected under associative-learning and normative rule induction models of contingency judgment. These idiosyncratic reports tended to be better predictors of the judgments of those who made them than did the models. The results are consistent with the view that causal judgment from contingency information is made, at least in part, by deliberative use of acquired and sometimes idiosyncratic notions of evidential value, the outcomes of which tend, in aggregate, to be highly correlated with the outcomes of normative procedures.

Adult↗

Causal and conditional inferences: a comment on Cummins (1995)

Cummins (1995) offers an analysis of causal and truth-functional sufficiency and necessity to predict and explain the effects on conditional inferences of two pragmatic factors: alternative causes and disabling conditions. However, the justification of these predictions is inconsistent. This note offers a modified analysis which puts her predictions on a sounder base: it is proposed that alternative causes and disabling conditions affect judgments of argument validity under three different models for the causal conditional.

Causality↗

Serial causation: occasion setting in a causal induction task.

The temporal relations among candidate causes were studied in a causal induction task using a design that is known to produce occasion setting in animal learning preparations. For some subset of the observations, one event, the occasion setter, was accompanied by another event, the conditional cause; for another subset of the observations, the conditional cause occurred alone. The efficacy of the conditional cause depended on whether it was or was not accompanied by the occasion setter. Participants used the occasion setter to modulate their effect expectancy to the conditional cause when the events were presented serially, but not simultaneously. Current causal induction models are unable to account for the full range of effects that we observed; the relative roles of time, attention, and cue distinctiveness are discussed.

Association Learning↗