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Background ADHD symptoms are associated with emotional problems such as depressive and anxiety symptoms from early childhood to adulthood, with the association increasing with age. A shared aetiology and/or a causal relationship could explain their correlation. In the current study, we explore these explanations for the association between ADHD symptoms and emotional problems from childhood to adulthood. Methods Data were drawn from the Twins Early Development Study (TEDS), including 3675 identical and 7063 non-identical twin pairs. ADHD symptoms and emotional symptoms were reported by parents from childhood to adulthood. Self-report scales were included from early adolescence. Five direction of causation (DoC) twin models were fitted to distinguish whether associations were better explained by shared aetiology and/or causal relationships in early childhood, mid-childhood, early adolescence, late adolescence, and early adulthood. Follow-up analyses explored associations for the two subdomains of ADHD symptoms, hyperactivity-impulsivity and inattention, separately. Results The association between ADHD symptoms and emotional problems increased in magnitude from early childhood to adulthood. In the best-fitting models, positive genetic overlap played an important role in this association at all stages. A negative causal effect running from ADHD symptoms to emotional problems was also detected in early childhood and mid-childhood. When distinguishing ADHD subdomains, the apparent protective effect of ADHD symptoms on emotional problems in childhood was mostly driven by hyperactivity-impulsivity. Conclusions Genetic overlap plays an important role in the association between ADHD symptoms and emotional problems. Hyperactivity-impulsivity may protect children from emotional problems in childhood, but this protective effect diminishes after adolescence. [ABSTRACT FROM AUTHOR]

Although health disparities among same-sex attracted compared to heterosexual individuals are typically explained by minority stress, there is limited evidence for a causal effect. This study investigated whether same-sex attraction was causally associated with psychological distress and risky sexual behavior using sociosexual behavior as a proxy. The sample comprised monozygotic and dizygotic twins and their non-twin siblings (n = 2036, 3780 and 2356, respectively) genotyped and assessed for same-sex attraction, psychological distress (anxiety and depressive symptoms), and risky sexual behavior. Causal influences were investigated with same-sex attraction as the predictor and psychological distress and risky sexual behavior as the outcomes in two separate Mendelian Randomization-Direction of Causation (MRDoC) models using OpenMx in R. The MRDoC model improves on the Mendelian Randomization and Direction of Causation twin models by allowing analyses of variables with similar genetic architectures, incorporating polygenic scores as instrumental variables and specifying pleiotropy and residual covariance. There were significant causal influences flowing from same-sex attraction to psychological distress and risky sexual behavior (standardized coefficients = 0.13 and 0.16; 95% CIs 0.03–0.23 and 0.08–0.25, respectively). Further analyses also demonstrated causal influences flowing from psychological distress and risky sexual behavior toward same-sex attraction. Causal influences from same-sex attraction to psychological distress and risky sexual behavior may reflect minority stress, which reinforces ongoing measures to minimize social disparities. Causal influences flowing in the opposite direction may reflect rejection sensitivity, stigma-inducing outcomes of risky sexual behavior, and recall bias; however, further research is required to specifically investigate these processes. [ABSTRACT FROM AUTHOR]

Previous genetically informed studies have uncovered likely causal relationships between mental health problems and self-harm but resulting causal estimates may be biased due to unmediated pleiotropy. By fitting Mendelian Randomization - Direction of Causation (MR-DoC) models that explicitly model pleiotropy, we investigated the effect of four quantitatively measured mental health problems - major depressive disorder (MDD), schizophrenia, attention-deficit hyperactivity disorder (ADHD), and insomnia, on non-suicidal self-harm (NSSH) and suicidal self-harm (SSH), separately. We used data of 12,723 twins (56.6% females) in the Twins Early Development Study. Besides substantial pleiotropy, we found effects from child-rated depressive symptoms to both NSSH (β = 0.194, 95% CIs: 0.131, 0.257) and SSH (β = 0.210, 95% CIs: 0.125, 0.295). Similarly, effects flowed from parent-rated depressive symptoms to NSSH (β = 0.092, 95% CIs: 0.004, 0.181) and SSH (β = 0.165, 95% CIs: 0.051, 0.281). We did not find evidence of aetiological difference between NSSH and SSH. [ABSTRACT FROM AUTHOR]

This paper discusses some procedures developed in recent work in machine learning for inferring causal direction from observational data. The role of independence and invariance assumptions is emphasized. Several familiar examples, including Hempel’s flagpole, problem are explored in the light of these ideas. The framework is then applied to problems having to do with explanatory direction in non-causal explanation. [ABSTRACT FROM AUTHOR]

Introduction: The amyloid cascade hypothesis predicts that amyloid-beta (Aβ) aggregation drives tau tangle accumulation. We tested competing causal and non-causal hypotheses regarding the direction of causation between Aβ40 and Aβ42 and total Tau (t-Tau) plasma biomarkers., Methods: Plasma Aβ40, Aβ42, t-Tau, and neurofilament light chain (NFL) were measured in 1,035 men (mean = 67.0 years) using Simoa immunoassays. Genetically informative twin modeling tested the direction of causation between Aβs and t-Tau., Results: No clear evidence that Aβ40 or Aβ42 directly causes changes in t-Tau was observed; the alternative causal hypotheses also fit the data well. In contrast, exploratory analyses suggested a causal impact of the Aβ biomarkers on NFL. Separately, reciprocal causation was observed between t-Tau and NFL., Discussion: Plasma Aβ40 or Aβ42 do not appear to have a direct causal impact on t-Tau. In contrast, Aβ aggregation may causally impact NFL in cognitively unimpaired men in their late 60s., Competing Interests: Conflicts No authors reported a conflict of interest.

Determining (1) the direction of causation and (2) the size of causal effects between two constructs is a central challenge of the scientific study of humans. In the early 1990s, researchers in behavioral genetics invented what was termed the direction of causation (DoC) model to address exactly these two concerns. The model claims that for any two traits whose mode of inheritance is sufficiently different, the direction of causation can be ascertained using a sufficiently large genetically informative sample. Using a series of simulation studies, we demonstrate a major challenge to the DoC model, namely that it is extremely sensitive to even tiny amounts of non-shared confounding. Even under ideal conditions for the DoC model (a large sample, N = 10,000), a large causal relationship (e.g., a causal correlation of .50) with very different modes of inheritance between the two traits (e.g., a pure AE model for one trait and a pure CE model for another trait) and a modest degree (correlation of .10) of non-shared confounding between the two traits results in the choice of the wrong causal models and estimating the wrong causal effects. [ABSTRACT FROM AUTHOR]

Our ordinary causal concept seems to fit poorly with how our best physics describes the world. We think of causation as a time-asymmetric dependence relation between relatively local events. Yet fundamental physics describes the world in terms of dynamical laws that are, possible small exceptions aside, time symmetric and that relate global time slices. My goal in this paper is to show why we are successful at using local, time-asymmetric models in causal explanations despite this apparent mismatch with fundamental physics. In particular, I will argue that there is an important connection between time asymmetry and locality, namely: understanding the locality of our causal models is the key to understanding why the physical time asymmetries in our universe give rise to time asymmetry in causal explanation. My theory thus provides a unified account of why causation is local and time asymmetric and thereby enables a reply to Russell's famous attack on causation. [ABSTRACT FROM AUTHOR]

The Physical Intentionality Thesis claims that dispositions share the marks of psychological intentionality; therefore, intentionality is not exclusively a mental phenomenon. Beyond the standard five marks, Alexander Bird introduces two additional marks of intentionality that he argues dispositions do not satisfy: first, thoughts are extrinsic; second, the direction of causation is that objects cause thoughts, not vice versa. In response, this paper identifies two relevant conceptions of extrinsicness, arguing that dispositions show deep parallels to thoughts on both conceptions. Then, it shows that Bird's discussion of direction of causation overlooks complexities of dispositionality and intentionality that problematize apparent differences between thoughts and dispositions. The paper ends with a discussion of why we find these parallels between thoughts and dispositions. [ABSTRACT FROM AUTHOR]

Previous research suggests an association between hyperactivity-impulsivity – one of the two behavioural dimensions that form attention deficit hyperactivity disorder – and the temperament characteristic of novelty seeking. We aimed to examine etiological links underlying the co-occurrence between these behaviours using a general population sample of 668 twin pairs, ages 7-10, for whom we obtained parent ratings in middle childhood; and pilot longitudinal data on 76 children. Structural equation modelling confirmed a shared genetic etiology (genetic correlation, rD=.81; 95% confidence intervals [CI]= .34-1.00) and showed that much (64%) of the covariation can be accounted for by shared genetic effects. In addition, causal paths were modelled between the two behaviours; 12% of the variance in novelty seeking at age 7 was accounted for by hyperactive-impulsive behaviors at the same age. The causal effects model fits with the current characterization of hyperactive-impulsive behaviors reflecting a heightened need for stimulation. This has important implications for the management of hyperactive-impulsive behaviors in clinical settings.

The direction of causation between measures of disrupted sleep, anxiety and depression is not well understood. Under certain conditions, cross-sectional analysis based on genetically informative data can provide important information about the direction of causation between variables. Two community-based samples of 7235 Australian twins aged 18-87 years were mailed an extensive questionnaire that covered a wide range of personality and behavioral measures. Included were self-report measures of disrupted sleep, as well as symptoms of anxiety and depression. Among all females, modeling the direction of causation did not support the hypothesis of sleep having a direct causal impact on risk of anxiety or depression. Among older females, we found evidence that both anxiety and depression interact reciprocally with disrupted sleep, whereas among younger women both anxiety and depression appear to have a causal impact on sleep. Results for males were equivocal. The nosological implications of our findings are discussed. [ABSTRACT FROM AUTHOR]

Traditional theories of political participation have emphasized its social and normative components; however, recent evidence suggests that political participation has a strong additive genetic component. Accordingly, it is necessary to reevaluate the traditional empirical findings and begin to integrate the two approaches. To do so, a variety of analyses were conducted that explore the modes of genetic and environmental transmission. I find that the empirical estimates of the relationships between the phenotypic level traits are highly consistent with what has been found in the traditional literature, the vast majority of the variance in political participation that is accounted for by the predictor variables is being accounted for at the genetic level, and not at the environmental level. Thus, the current findings suggest that the empirical results found in prior studies are quite likely very accurate. However, the interpretation of those empirical findings, as well as the subsequent theoretical implications, require serious revision. [ABSTRACT FROM PUBLISHER]

Is the common cause principle merely one of a set of useful heuristics for discovering causal relations, or is it rather a piece of heavy duty metaphysics, capable of grounding the direction of causation itself? Since the principle was introduced in Reichenbach’s groundbreaking work The Direction of Time (1956), there have been a series of attempts to pursue the latter program—to take the probabilistic relationships constitutive of the principle of the common cause and use them to ground the direction of causation. These attempts have not all explicitly appealed to the principle as originally formulated; it has also appeared in the guise of independence conditions, counterfactual overdetermination, and, in the causal modelling literature, as the causal markov condition. In this paper, I identify a set of difficulties for grounding the asymmetry of causation on the principle and its descendents. The first difficulty, concerning what I call the vertical placement of causation, consists of a tension between considerations that drive towards the macroscopic scale, and considerations that drive towards the microscopic scale—the worry is that these considerations cannot both be comfortably accommodated. The second difficulty consists of a novel potential counterexample to the principle based on the familiar Einstein Podolsky Rosen (EPR) correlations in quantum mechanics. [ABSTRACT FROM AUTHOR]

Abstract: There is ongoing debate whether the efficiency of local cognitive processes leads to global cognitive ability or whether global ability feeds the efficiency of basic processes. A prominent example is the well-replicated association between inspection time (IT), a measure of perceptual discrimination speed, and intelligence (IQ), where it is not known whether increased speed is a cause or consequence of high IQ. We investigated the direction of causation between IT and IQ in 2012 genetically related subjects from Australia and The Netherlands. Models in which the reliable variance of each observed variable was specified as a latent trait showed IT correlations of −0.44 and −0.33 with respective Performance and Verbal IQ; heritabilities were 57% (IT), 83% (PIQ) and 77% (VIQ). Directional causation models provided poor fits to the data, with covariation best explained by pleiotropic genes (influencing variation in both IT and IQ). This finding of a common genetic factor provides a better target for identifying genes involved in cognition than genes which are unique to specific traits. [Copyright &y& Elsevier]