The longitudinal rank-order stability of cognitive ability increases dramatically over the lifespan. Multiple theoretical perspectives have proposed that genetic and/or environmental mechanisms underlie the longitudinal stability of cognition, and developmental trends therein. However, the patterns of stability of genetic and environmental influences on cognition over the lifespan largely remain poorly understood. We searched for longitudinal studies of cognition that reported raw genetically-informative longitudinal correlations or parameter estimates from longitudinal behavior genetic models. We identified 150 combinations of time points and measures from 15 independent longitudinal samples. In total, longitudinal data came from 4,538 monozygotic twin pairs raised together, 7,777 dizygotic twin pairs raised together, 34 monozygotic twin pairs raised apart, 78 dizygotic twin pairs raised apart, 141 adoptive sibling pairs, and 143 non-adoptive sibling pairs, ranging in age from infancy through late adulthood. At all ages, cross-time genetic correlations and shared environmental correlations were substantially larger than cross-time nonshared environmental correlations. Cross-time correlations for genetic and shared environmental components were low during early childhood, increased sharply over child development, and remained relatively high from adolescence through late adulthood. Cross-time correlations for nonshared environmental components were low across childhood and increased gradually to moderate magnitudes in adulthood. Increasing phenotypic stability over child development was almost entirely mediated by genetic factors. Time-based decay of genetic and shared environmental stability was more pronounced earlier in child development. Results are interpreted in reference to theories of gene-environment interaction and correlation.
Intelligence; Cognitive Abilities; Longitudinal Studies; Developmental Behavioral Genetics; Rank-Order Stability
Brady and Kendall (1992) concluded that although anxiety and depression in youth are meaningfully linked, there are important distinctions, and additional research was needed. Since then, studies of anxiety-depression comorbidity in youth have increased exponentially. Following a discussion of comorbidity, we review existing conceptual models and propose a multiple pathways model to anxiety-depression comorbidity. Pathway 1 describes youth with a diathesis for anxiety, with subsequent comorbid depression resulting from anxiety-related impairment. Pathway 2 refers to youth with a shared diathesis for anxiety and depression, who may experience both disorders simultaneously. Pathway 3 describes youth with a diathesis for depression, with subsequent comorbid anxiety resulting from depression-related impairment. Additionally, shared and stratified risk factors contribute to the development of the comorbid disorder, either by interacting with disorder-related impairment or by predicting the simultaneous development of the disorders. Our review addresses descriptive and developmental factors, gender differences, suicidality, assessments, and treatment-outcome research as they relate to comorbid anxiety and depression, and to our proposed pathways. Research since 1992 indicates that comorbidity varies depending on the specific anxiety disorder, with Pathway 1 describing youth with either social phobia or separation anxiety disorder and subsequent depression, Pathway 2 applying to youth with co-primary generalized anxiety disorder and depression, and Pathway 3 including depressed youth with subsequent social phobia. The need to test the proposed multiple pathways model and to examine (a) developmental change and (b) specific anxiety disorders is highlighted.
comorbidity; anxiety; depression; children; adolescents; youth
In their recent article, N. Spillane and G. Smith (2007) suggested that reservation-dwelling American Indians have higher rates of problem drinking than do either non–American Indians or those American Indians living in nonreservation settings. These authors further argued that problematic alcohol use patterns in reservation communities are due to the lack of contingencies between drinking and “standard life reinforcers” (SLRs), such as employment, housing, education, and health care. This comment presents evidence that these arguments were based on a partial review of the literature. Weaknesses in the application of SLR constructs to American Indian reservation communities are identified as is the need for culturally contextualized empirical evidence supporting this theory and its application. Cautionary notes are offered about the development of literature reviews, theoretical frameworks, and policy recommendations for American Indian communities.
American Indians; alcohol; problem drinking; reservation
The relationship between religion and morality has long been hotly debated. Does religion make us more moral? Is it necessary for morality? Do moral inclinations emerge independently of religious intuitions? These debates, which nowadays rumble on in scientific journals as well as in public life, have frequently been marred by a series of conceptual confusions and limitations. Many scientific investigations have failed to decompose “religion” and “morality” into theoretically grounded elements; have adopted parochial conceptions of key concepts—in particular, sanitized conceptions of “prosocial” behavior; and have neglected to consider the complex interplay between cognition and culture. We argue that to make progress, the categories “religion” and “morality” must be fractionated into a set of biologically and psychologically cogent traits, revealing the cognitive foundations that shape and constrain relevant cultural variants. We adopt this fractionating strategy, setting out an encompassing evolutionary framework within which to situate and evaluate relevant evidence. Our goals are twofold: to produce a detailed picture of the current state of the field, and to provide a road map for future research on the relationship between religion and morality.
cognitive science of religion; moral foundations theory; prosocial behavior; cultural evolution
There are dramatic individual differences among adolescents in how and when they become sexually active adults, and “early” sexual activity is frequently cited as a cause of concern for scientists, policymakers, and the general public. Understanding the causes and developmental impact of adolescent sexual activity can be furthered by considering genes as a source of individual differences. Quantitative behavioral genetics (i.e., twin and family studies) and candidate gene association studies now provide clear evidence for the genetic underpinnings of individual differences in adolescent sexual behavior and related phenotypes. Genetic influences on sexual behavior may operate through a variety of direct and indirect mechanisms, including pubertal development, testosterone levels, and dopaminergic systems. Genetic differences may be systematically associated with exposure to environments that are commonly treated as causes of sexual behavior (gene-environment correlation). Possible gene-environment correlations pose a serious challenge for interpreting the results of much behavioral research. Multivariate, genetically-informed research on adolescent sexual behavior compares twins and family members as a form of “quasi-experiment”: How do twins who differ in their sexual experiences differ in their later development? The small but growing body of genetically-informed research has already challenged dominant assumptions regarding the etiology and sequelae of adolescent sexual behavior, with some studies indicating possible positive effects of teenage sexuality. Studies of gene × environment interaction may further elucidate the mechanisms by which genes and environments combine to shape the development of sexual behavior and its psychosocial consequences. Overall, the existence of heritable variation in adolescent sexual behavior has profound implications for environmentally-oriented theory and research.
To behave adaptively, we must learn from the consequences of our actions. Doing so is difficult when the consequences of an action follow a delay. This introduces the problem of temporal credit assignment. When feedback follows a sequence of decisions, how should the individual assign credit to the intermediate actions that comprise the sequence? Research in reinforcement learning provides two general solutions to this problem: model-free reinforcement learning and model-based reinforcement learning. In this review, we examine connections between stimulus-response and cognitive learning theories, habitual and goal-directed control, and model-free and model-based reinforcement learning. We then consider a range of problems related to temporal credit assignment. These include second-order conditioning and secondary reinforcers, latent learning and detour behavior, partially observable Markov decision processes, actions with distributed outcomes, and hierarchical learning. We ask whether humans and animals, when faced with these problems, behave in a manner consistent with reinforcement learning techniques. Throughout, we seek to identify neural substrates of model-free and model-based reinforcement learning. The former class of techniques is understood in terms of the neurotransmitter dopamine and its effects in the basal ganglia. The latter is understood in terms of a distributed network of regions including the prefrontal cortex, medial temporal lobes cerebellum, and basal ganglia. Not only do reinforcement learning techniques have a natural interpretation in terms of human and animal behavior, but they also provide a useful framework for understanding neural reward valuation and action selection.
Reinforcement learning; sequential choice; temporal credit assignment
Researchers have found that, compared to European Americans, African Americans report later initiation of drinking, lower rates of use, and lower levels of use across almost all age groups. Nevertheless, African Americans also have higher levels of alcohol problems than European Americans. After reviewing current data regarding these trends, we provide a theory to understand this apparent paradox as well as to understand variability in risk among African Americans. Certain factors appear to operate as both protective factors against heavy use and risk factors for negative consequences from use. For example, African American culture is characterized by norms against heavy alcohol use or intoxication, which protects against heavy use but which also provides within group social disapproval when use does occur. African Americans are more likely to encounter legal problems from drinking than European Americans, even at the same levels of consumption, perhaps thus resulting in reduced consumption but more problems from consumption. There appears to be one particular group of African Americans, low-income African American men, who are at the highest risk for alcoholism and related problems. We theorize that this effect is due to the complex interaction of residential discrimination, racism, age of drinking, and lack of available standard life reinforcers (e.g., stable employment and financial stability). Further empirical research will be needed to test our theories and otherwise move this important field forward. A focus on within group variation in drinking patterns and problems is necessary. We suggest several new avenues of inquiry.
African American; alcohol use; alcohol problems; socioeconomic status; discrimination
Discovering the stress-buffering effects of social relationships has been one of the major findings in psychobiology in the last century. However, an understanding of the underlying neurobiological and psychological mechanisms of this buffering is only beginning to emerge. An important avenue of this research concerns the neurocircuitry that can regulate the activity of the hypothalamic-pituitary-adrenocortical (HPA) axis. The present review is a translational effort aimed at integrating animal models and human studies of the social regulation of the HPA axis from infancy to adulthood, specifically focusing on the process that has been named social buffering. This process has been noted across species and consists of a dampened HPA axis stress response to threat or challenge that occurs with the presence or assistance of a conspecific. We describe aspects of the relevant underlying neurobiology when enough information exists and expose major gaps in our understanding across all domains of the literatures we aimed to integrate. We provide a working conceptual model focused on the role of oxytocinergic systems and prefrontal neural networks as two of the putative biological mediators of this process, and propose that the role of early experiences is critical in shaping later social buffering effects. This synthesis points to both general future directions and specific experiments that need to be conducted to build a more comprehensive model of the HPA social buffering effect across the lifespan that incorporates multiple levels of analysis: neuroendocrine, behavioral, and social.
stress; social support; early caregiving; oxytocin; prefrontal cortex
Frick at al. (2013) presented a comprehensive and well-articulated review of studies relevant to the validity and utility of using callous-unemotional traits to subtype the diagnosis of conduct disorder. Like definitions of subtypes of conduct disorder in previous versions of the DSM, the available evidence on the validity of the new subtypes of conduct disorder in DSM-5 based on callous-unemotional traits is thin. Nonetheless, the target article makes a compelling argument for further study of callous-unemotional and related traits to better understand the heterogeneity of conduct disorder. In particular, the possibilities that callous-unemotional traits may facilitate understanding of etiology and psychobiological mechanisms, and help predict the prognosis and treatment outcomes of children with conduct disorder deserve greater study. Future research must be stronger than previous research, however, in using more appropriate samples of children with CD along with more informative designs, and in conducting analyses to directly test the incremental validity of callous-unemotional traits as a subtyping variable beyond the severity or aggressiveness of CD.
This meta-analysis reviewed 126 published empirical articles over the past 50 years describing associations between marital relationship quality and physical health in over 72,000 individuals. Health outcomes included clinical endpoints (objective assessments of function, disease severity, and mortality; subjective health assessments) and surrogate endpoints (biological markers that substitute for clinical endpoints, such as blood pressure). Biological mediators included cardiovascular reactivity and hypothalamic-pituitary-adrenal axis activity. Greater marital quality was related to better health, with mean effect sizes from r = .07 to .21, including lower risk of mortality, r = .11, and lower cardiovascular reactivity during marital conflict, r = −.13, but not daily cortisol slopes or cortisol reactivity during conflict. The small effect sizes were similar in magnitude to previously found associations between health behaviors (e.g., diet) and health outcomes. Effect sizes for a small subset of clinical outcomes were susceptible to publication bias. In some studies, effect sizes remained significant after accounting for confounds such as age and socioeconomic status. Studies with a higher proportion of women in the sample demonstrated larger effect sizes, but we found little evidence for gender differences in studies that explicitly tested gender moderation, with the exception of surrogate endpoint studies. Our conclusions are limited by small numbers of studies for specific health outcomes, unexplained heterogeneity, and designs that limit causal inferences. These findings highlight the need to explicitly test affective, health behavior, and biological mechanisms in future research, and focus on moderating factors that may alter the relationship between marital quality and health.
marriage; marital quality; health; morbidity; mortality; meta-analysis
Over the last decade, a normative framework for making causal inferences, Bayesian Probabilistic Causal Networks, has come to dominate psychological studies of inference based on causal relationships. The following causal networks—[X→Y→Z, X←Y→Z, X→Y←Z]—supply answers for questions like, “Suppose both X and Y occur, what is the probability Z occurs?” or “Suppose you intervene and make Y occur, what is the probability Z occurs?” In this review, we provide a tutorial for how normatively to calculate these inferences. Then, we systematically detail the results of behavioral studies comparing human qualitative and quantitative judgments to the normative calculations for many network structures and for several types of inferences on those networks. Overall, when the normative calculations imply that an inference should increase, judgments usually go up; when calculations imply a decrease, judgments usually go down. However, two systematic deviations appear. First, people’s inferences violate the Markov assumption. For example, when inferring Z from the structure X→Y→Z, people think that X is relevant even when Y completely mediates the relationship between X and Z. Second, even when people’s inferences are directionally consistent with the normative calculations, they are often not as sensitive to the parameters and the structure of the network as they should be. We conclude with a discussion of productive directions for future research.
Causal Inference; Causal Structures; Bayes Nets; Markov Assumption; Discounting; Explaining Away; Conditional Reasoning; Logical Arguments
Martel (2013) proposed a meta-theory, based on sexual selection theory and broad evolutionary psychological (EP) principles, to account for well-known sex differences in the emergence of common behavioral and certain internalizing disorders across childhood and adolescence, respectively. This Comment first enumerates several strengths and then offers two primary critiques about Martel’s proposal. Martel provides an exceptional, integrative review that organizes several disparate literatures that hold promise to enhance understanding of such sex differences. At the same time, I raise critical questions regarding EP generally, and sexual selection theory specifically, as the meta-theoretical framework chosen to bind together these different influences and mechanisms as drivers of the sex difference in different psychopathologies. Indeed, it is not clear that EP is necessary—nor does it provide unique explanatory power—to explicate the emergence of sex differences in internalizing and externalizing disorders among youth. Moreover, Martel’s EP-based proposal pertains to adolescent-onset depression and social phobia but does not provide an explanation for known sex differences in other common childhood-onset and early adult-onset anxiety disorders.
The “Flynn effect” refers to the observed rise in IQ scores over time, resulting in norms obsolescence. Although the Flynn effect is widely accepted, most approaches to estimating it have relied upon “scorecard” approaches that make estimates of its magnitude and error of measurement controversial and prevent determination of factors that moderate the Flynn effect across different IQ tests. We conducted a meta-analysis to determine the magnitude of the Flynn effect with a higher degree of precision, to determine the error of measurement, and to assess the impact of several moderator variables on the mean effect size. Across 285 studies (N = 14,031) since 1951 with administrations of two intelligence tests with different normative bases, the meta-analytic mean was 2.31, 95% CI [1.99, 2.64], standard score points per decade. The mean effect size for 53 comparisons (N = 3,951) (excluding three atypical studies that inflate the estimates) involving modern (since 1972) Stanford-Binet and Wechsler IQ tests (2.93, 95% CI [2.3, 3.5], IQ points per decade) was comparable to previous estimates of about 3 points per decade, but not consistent with the hypothesis that the Flynn effect is diminishing. For modern tests, study sample (larger increases for validation research samples vs. test standardization samples) and order of administration explained unique variance in the Flynn effect, but age and ability level were not significant moderators. These results supported previous estimates of the Flynn effect and its robustness across different age groups, measures, samples, and levels of performance.
Flynn effect; IQ test; intellectual disability; capital punishment; special education
The inverse relation between serotonin and human aggression is often portrayed as “reliable,” “strong,” and “well-established” despite decades of conflicting reports and widely recognized methodological limitations. In this systematic review and meta-analysis we evaluate the evidence for and against the serotonin deficiency hypothesis of human aggression across four methods of assessing serotonin: (a) cerebrospinal fluid levels of 5-hydroxyindoleacetic acid (CSF 5-HIAA), (b) acute tryptophan depletion, (c) pharmacological challenge, and (d) endocrine challenge. Results across 175 independent samples and over 6,500 total participants were heterogeneous, but, in aggregate, revealed a small, inverse correlation between central serotonin functioning and aggression, anger, and hostility, r = −.12. Pharmacological challenge studies had the largest mean weighted effect size, r = −.21, and CSF 5-HIAA studies had the smallest, r = −.06, p = .21. Potential methodological and demographic moderators largely failed to account for variability in study outcomes. Notable exceptions included year of publication (effect sizes tended to diminish with time) and self-versus other-reported aggression (other-reported aggression was positively correlated to serotonin functioning). We discuss four possible explanations for the pattern of findings: unreliable measures, ambient correlational noise, an unidentified higher-order interaction, and a selective serotonergic effect. Finally, we provide four recommendations for bringing much needed clarity to this important area of research: acknowledge contradictory findings and avoid selective reporting practices; focus on improving the reliability and validity of serotonin and aggression measures; test for interactions involving personality and/or environmental moderators; and revise the serotonin deficiency hypothesis to account for serotonin’s functional complexity.
serotonin; 5-HT; aggression; anger; hostility
Rumination, defined as repetitive thinking about negative information, has been found to lead to serious maladaptive consequences, including longer and more severe episodes of major depression. In this review, we present and discuss research findings motivated by the formulation that individual differences in cognitive processes that control how information is processed influence the likelihood that thoughts will become repetitive and negative. A number of studies have demonstrated that a tendency to ruminate (i.e., trait rumination) is related to difficulties updating working memory (WM) and disengaging from and forgetting no-longer-relevant information. Other investigators have documented that trait rumination is also associated with an enhanced ability to ignore distracting information and to more stable maintenance of task-relevant information. In contrast to trait rumination, a state of rumination has been found to be related to widespread deficits in cognitive control. In this paper we discuss how the current accounts of control functioning cannot explain this pattern of anomalous control functioning. To explain these findings, including unexpected and contradictory results, we present an attentional scope model of rumination that posits that a constricted array of thoughts, percepts, and actions that are activated in WM or available for selection from LTM affects the control functioning of trait ruminators. This model explains, at a cognitive level, why rumination is particularly likely to arise when individuals are in a negative mood state; it also accounts for a number of findings outside of the rumination-control literature and generates several novel predictions.
Emotion expression is an important feature of healthy child development that has been found to show gender differences. However, there has been no empirical review of the literature on gender and facial, vocal, and behavioral expressions of different types of emotions in children. The present study constitutes a comprehensive meta-analytic review of gender differences, and moderators of differences, in emotion expression from infancy through adolescence. We analyzed 555 effect sizes from 166 studies with a total of 21,709 participants. Significant, but very small, gender differences were found overall, with girls showing more positive emotions (g = −.08) and internalizing emotions (e.g., sadness, anxiety, sympathy; g = −.10) than boys, and boys showing more externalizing emotions (e.g., anger; g = .09) than girls. Notably, gender differences were moderated by age, interpersonal context, and task valence, underscoring the importance of contextual factors in gender differences. Gender differences in positive emotions were more pronounced with increasing age, with girls showing more positive emotions than boys in middle childhood (g = −.20) and adolescence (g = −.28). Boys showed more externalizing emotions than girls at toddler/preschool age (g = .17) and middle childhood (g = .13) and fewer externalizing emotions than girls in adolescence (g = −.27). Gender differences were less pronounced with parents and were more pronounced with unfamiliar adults (for positive emotions) and with peers/when alone (for externalizing emotions). Our findings of gender differences in emotion expression in specific contexts have important implications for gender differences in children’s healthy and maladaptive development.
Emotion expression; Gender/sex differences; Observational studies; Emotional development; Contextual factors
Maintaining attention for more than a few seconds is essential for mastering everyday life. Yet, our ability to stay focused on a particular task is limited, resulting in well-known performance decrements with increasing time on task. Intriguingly, such decrements are even more likely if the task is cognitively simple and repetitive. The attentional function that enables our prolonged engagement in intellectually unchallenging, uninteresting activities has been termed “vigilant attention.” Here we synthesized what we have learnt from functional neuroimaging about the mechanisms of this essential mental faculty. To this end, a quantitative meta-analysis of pertinent neuroimaging studies was performed, including supplementary analyses of moderating factors. Furthermore, we reviewed the available evidence on neural time-on-task effects, additionally considering information obtained from patients with focal brain damage. Integrating the results of both meta-analysis and review, a set of mainly right-lateralized brain regions was identified that may form the core network subserving vigilant attention in humans, including dorsomedial, mid- and ventrolateral prefrontal cortex, anterior insula, parietal areas (intraparietal sulcus, temporo-parietal junction), and subcortical structures (cerebellar vermis, thalamus, putamen, midbrain). We discuss the potential functional roles of different nodes of this network as well as implications of our findings for a theoretical account of vigilant attention. It is conjectured that sustaining attention is a multi-component, non-unitary mental faculty, involving a mixture of (i) sustained/recurrent processes subserving task-set/arousal maintenance and (ii) transient processes subserving the target-driven reorienting of attention. Finally, limitations of previous studies are considered and suggestions for future research are provided.
sustained attention; alertness; vigilance; meta-analysis; ALE
Previous research has clearly established associations between low socioeconomic status (SES) and poor youth physical health outcomes. This article provides an overview of the main pathways through which low SES environments come to influence youth health. We focus on two of the most prevalent chronic health problems in youth today, asthma and obesity. We review and propose a model that encompasses (1) multiple levels of influence, including the neighborhood, family and person level, (2) both social and physical domains in the environment, and finally (3) dynamic relationships between these factors. A synthesis of existing research and our proposed model draw attention to the notion of adverse physical and social exposures in youth’s neighborhood environments altering family characteristics and youth psychosocial and behavioral profiles, thereby increasing youth’s risk for health problems. We also note the importance of acknowledging reciprocal influences across levels and domains (e.g., between family and child) that create self-perpetuating patterns of influence that further accentuate the impact of these factors on youth health. Finally, we document that factors across levels can interact (e.g., environmental pollution levels with child stress) to create unique, synergistic effects on youth health. Our model stresses the importance of evaluating influences on youth’s physical health not in isolation but in the context of the broader social and physical environments in which youth live. Understanding the complex relationships between the factors that link low SES to youth’s long-term health trajectories is necessary for the creation and implementation of successful interventions and policies to ultimately reduce health disparities.
socioeconomic status; youth; asthma; obesity; family; neighborhood; social environment; physical environment
Major life stressors, especially those involving interpersonal stress and social rejection, are among the strongest proximal risk factors for depression. In this review, we propose a biologically plausible, multilevel theory that describes neural, physiologic, molecular, and genomic mechanisms that link experiences of social-environmental stress with internal biological processes that drive depression pathogenesis. Central to this social signal transduction theory of depression is the hypothesis that experiences of social threat and adversity up-regulate components of the immune system involved in inflammation. The key mediators of this response, called proinflammatory cytokines, can in turn elicit profound changes in behavior, which include the initiation of depressive symptoms such as sad mood, anhedonia, fatigue, psychomotor retardation, and social-behavioral withdrawal. This highly conserved biological response to adversity is critical for survival during times of actual physical threat or injury. However, this response can also be activated by modern-day social, symbolic, or imagined threats, leading to an increasingly proinflammatory phenotype that may be a key phenomenon driving depression pathogenesis and recurrence, as well as the overlap of depression with several somatic conditions including asthma, rheumatoid arthritis, chronic pain, metabolic syndrome, cardiovascular disease, obesity, and neurodegeneration. Insights from this theory may thus shed light on several important questions including how depression develops, why it frequently recurs, why it is strongly predicted by early life stress, and why it often co-occurs with symptoms of anxiety and with certain physical disease conditions. This work may also suggest new opportunities for preventing and treating depression by targeting inflammation.
early life stress; social threat; cytokines; mechanisms; disease
Cognitive impairments are now widely acknowledged as an important aspect of major depressive disorder (MDD), and it has been proposed that executive function (EF) may be particularly impaired in patients with MDD. However, the existence and nature of EF impairments associated with depression remain strongly debated. While many studies have found significant deficits associated with MDD on neuropsychological measures of EF, others have not, potentially due to low statistical power, task impurity, and diverse patient samples, and there have been no recent, comprehensive, meta-analyses investigating EF in patients with MDD. The current meta-analysis uses random effects models to synthesize 113 previous research studies that compared participants with MDD to healthy control participants on at least one neuropsychological measure of EF. Results of the meta-analysis demonstrate that MDD is reliably associated with impaired performance on neuropsychological measures of EF, with effect sizes ranging from d = 0.32–0.97. While patients with MDD also have slower processing speed, motor slowing alone cannot account for these results. In addition, some evidence suggests that deficits on neuropsychological measures of EF are greater in patients with more severe current depression symptoms, and those taking psychotropic medications, while evidence for effects of age was weaker. The results are consistent with the theory that MDD is associated with broad impairment in multiple aspects of EF. Implications for treatment of MDD and theories of EF are discussed. Future research is needed to establish the specificity and causal link between MDD and EF impairments.
executive function; major depressive disorder; meta-analysis
For the last century, there has been a continuing debate about the nature of emotion. In the most recent offering in this scientific dialogue, Lench, Flores, and Bench (2011) report a meta-analysis of emotion induction research and claim support for the natural kind hypothesis that discrete emotions (e.g., happiness, sadness, anger, and anxiety) elicit specific changes in cognition, judgment, behavior, experience, and physiology. In this paper, we point out that Lench et al. (2011) is not the final word on the emotion debate. First, we point out that Lench et al.’s findings do not support their claim that discrete emotions organize cognition, judgment, experience, and physiology because they did not demonstrate emotion-consistent and -specific directional changes in these measurement domains. Second, we point out that Lench et al.’s findings are in fact consistent with the alternative (a psychological constructionist approach to emotion). We close by appealing for a construct validity approach to emotion research, which we hope will lead to greater consensus on the operationalization of the natural kind and psychological construction approaches, as well as the criteria required to finally resolve the emotion debate.
emotion; natural kinds; psychological construction; construct validity; meta-analysis
Age is the only social category identifying subgroups that everyone may eventually join. Despite this, and despite the well-known growth of the older population, age-based prejudice remains an under-studied topic in social psychology. This paper systematically reviews the literature on ageism, highlighting extant research on its consequences and theoretical perspectives on its causes. We then identify a crucial gap in the literature: potential intergenerational tensions, speculating how a growing older population—and society’s efforts to accommodate it—might stoke intergenerational fires, particularly among the younger generation. Presenting both sides of this incipient issue, we review relevant empirical work that introduces reasons for both optimism and pessimism concerning intergenerational relations within an aging society. We conclude by suggesting future avenues for ageism research, emphasizing the importance of understanding forthcoming intergenerational dynamics for the benefit of the field and broader society.
We propose a new version of the “theory theory” grounded in the computational framework of probabilistic causal models and Bayesian learning. Probabilistic models allow a constructivist but rigorous and detailed approach to cognitive development. They also explain the learning of both more specific causal hypotheses and more abstract framework theories. We outline the new theoretical ideas, explain the computational framework in an intuitive and non-technical way, and review an extensive but relatively recent body of empirical results that supports these ideas. These include new studies of the mechanisms of learning. Children infer causal structure from statistical information, through their own actions on the world and through observations of the actions of others. Studies demonstrate these learning mechanisms in children from 16 months to 4 years old and include research on causal statistical learning, informal experimentation through play, and imitation and informal pedagogy. They also include studies of the variability and progressive character of intuitive theory change, particularly theory of mind. These studies investigate both the physical and psychological and social domains. We conclude with suggestions for further collaborative projects between developmental and computational cognitive scientists.
Cognitive Development; Bayesian Inference; Theory of Mind; Causal Knowledge; Intuitive Theories
Although psychology is the science of mental life and behavior, it has paid little attention to the means by which mental life is translated into behavior. One domain where links between cognition and action have been explored is the manipulation of objects. This article reviews psychological research on this topic, with special emphasis on the tendency to grasp objects differently depending on what one plans to do with the objects. Such differential grasping has been demonstrated in a wide range of object manipulation tasks, including grasping an object in a way that reveals anticipation of the object's future orientation, height, and required placement precision. Differential grasping has also been demonstrated in a wide range of behaviors, including one-hand grasps, two-hand grasps, walking, and transferring objects from place to place as well as from person to person. The populations in whom the tendency has been shown are also diverse, including nonhuman primates as well as human adults, children, and babies. Meanwhile, the tendency is compromised in a variety of clinical populations and in children of a surprisingly advanced age. Verbal working memory is compromised as well if words are memorized while object manipulation tasks are performed; the recency portion of the serial position curve is reduced in this circumstance. In general, the research reviewed here points to rich connections between cognition and action as revealed through the study of object manipulation. Other implications concern affordances, Donders' Law, and naturalistic observation and the teaching of psychology.
Action; Cognition; Motor Control; Object Manipulation; Planning; Reaching
Our first review paper on the occasion of the centennial anniversary of Gestalt psychology focused on perceptual grouping and figure-ground organization. It concluded that further progress requires a reconsideration of the conceptual and theoretical foundations of the Gestalt approach, which is provided here. In particular, we review contemporary formulations of holism within an information-processing framework, allowing for operational definitions (e.g., integral dimensions, emergent features, configural superiority, global precedence, primacy of holistic/configural properties) and a refined understanding of its psychological implications (e.g., at the level of attention, perception, and decision). We also review four lines of theoretical progress regarding the law of Prägnanz—the brain’s tendency of being attracted towards states corresponding to the simplest possible organization, given the available stimulation. The first considers the brain as a complex adaptive system and explains how self-organization solves the conundrum of trading between robustness and flexibility of perceptual states. The second specifies the economy principle in terms of optimization of neural resources, showing that elementary sensors working independently to minimize uncertainty can respond optimally at the system level. The third considers how Gestalt percepts (e.g., groups, objects) are optimal given the available stimulation, with optimality specified in Bayesian terms. Fourth, Structural Information Theory explains how a Gestaltist visual system that focuses on internal coding efficiency yields external veridicality as a side-effect. To answer the fundamental question of why things look as they do, a further synthesis of these complementary perspectives is required.
Gestalt; holism; simplicity versus likelihood; dynamical systems; information theory