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
Burt (2009) recently published a meta-analysis of twin studies on behaviors associated with childhood psychopathologies, concluding that the finding that traits associated with attention-deficit/hyperactivity disorder (ADHD) were the only behaviors that did not show a significant influence of shared environment (C) was surprising. We agree, highlighting four methodological issues that may account for this finding: (a) the use of nonlinear transformations to normalize skewed data; (b) low power to detect C and the subsequent presentation of reduced models; (c) the negative confounding of dominant genetic (D) and C influences in twin models with data exclusively from monozygotic and dizygotic twin pairs reared together; and (d) the correction used for contrast effects (a form of rater bias), which may lead to an overestimate of additive genetic (A) or D parameters at the expense of C. We offer suggestions for future research to address these issues, and we emphasize the need for additional research to examine possible shared environmental factors related to ADHD.
ADHD; twin studies; heritability; objective data; meta-analysis
The dominance behavioral system (DBS) can be conceptualized as a biologically-based system which guides dominance motivation, dominant and subordinate behavior, and responsivity to perceptions of power and subordination. A growing body of research suggests that problems with the DBS are evident across a broad range of psychopathologies. We begin by describing psychological, social, and biological correlates of the dominance behavioral system (DBS). Extensive research suggests that externalizing disorders, mania-proneness, and narcissistic traits are related to heightened dominance motivation and behaviors. Mania and narcissistic traits also appear related to inflated self-perceptions of power. Anxiety and depression are related to subordination and submissiveness, as well as a desire to avoid subordination. Models of the DBS have received support from research with humans and animals; from self-report, observational, and biological methods; and using naturalistic and experimental paradigms. Limitations of available research include the relative lack of longitudinal studies using multiple measures of the DBS and the absence of relevant studies using diagnosed samples to study narcissistic personality disorder and bipolar disorder. We provide suggestions for future research on the DBS and psychopathology, including investigations of whether the DBS can be used to differentiate specific disorder outcomes; the need for more sophisticated biological research; and the value of longitudinal dynamical research. Implications of using the DBS as a tool in clinical assessment and treatment are discussed.
There is ample empirical evidence for an asymmetry in the way that adults use positive versus negative information to make sense of their world; specifically, across an array of psychological situations and tasks, adults display a negativity bias, or the propensity to attend to, learn from, and use negative information far more than positive information. This bias is argued to serve critical evolutionarily adaptive functions, but its developmental presence and ontogenetic emergence have never seriously been considered. Here, we argue for the existence of the negativity bias in early development, evident especially in research on infant social referencing but also in other developmental domains. We discuss ontogenetic mechanisms underlying the emergence of this bias, and explore not only its evolutionary but also its developmental functions and consequences. Throughout, we suggest ways to further examine the negativity bias in infants and older children, and we make testable predictions that would help clarify the nature of the negativity bias during early development.
Negativity bias; Affective asymmetry; Social-cognitive development; Emotion; Social referencing
Nearly 80% of children in the U.S. have at least one sibling, indicating that the birth of a baby sibling is a normative ecological transition for most children. Many clinicians and theoreticians believe the transition is stressful, constituting a developmental crisis for most children. Yet, a comprehensive review of the empirical literature on children’s adjustment over the transition to siblinghood (TTS) has not been done for several decades. The current review summarized research examining change in firstborns’ adjustment to determine whether there was evidence that the TTS was disruptive for most children. Thirty studies addressing the transition to siblinghood were found and of those studies, the evidence did not support a crisis model of developmental transitions, nor was there overwhelming evidence of consistent changes in firstborn adjustment. Although there were decreases in children’s affection and responsiveness toward mothers, the results were more equivocal for many other behaviors (e.g., sleep problems, anxiety, aggression, regression). An inspection of the scientific literature indicated there are large individual differences in children’s adjustment and that the TTS can be a time of disruption, an occasion for developmental advances, or a period of quiescence with no noticeable changes. The TTS may be a developmental turning point for some children that portends future psychopathology or growth depending on the transactions between children and the changes in the ecological context over time. A developmental ecological systems framework guided the discussion of how child, parent, and contextual factors may contribute to the prediction of firstborn children’s successful adaptation to the birth of a sibling.
Siblings; Infants; Parenting; Behavior Problems; Family; Birth of a Sibling
Use of prescription stimulants by normal healthy individuals to enhance cognition is said to be on the rise. Who is using these medications for cognitive enhancement, and how prevalent is this practice? Do prescription stimulants in fact enhance cognition for normal healthy people? We review the epidemiological and cognitive neuroscience literatures in search of answers to these questions. Epidemiological issues addressed include the prevalence of nonmedical stimulant use, user demographics, methods by which users obtain prescription stimulants, and motivations for use. Cognitive neuroscience issues addressed include the effects of prescription stimulants on learning and executive function, as well as the task and individual variables associated with these effects. Little is known about the prevalence of prescription stimulant use for cognitive enhancement outside of student populations. Among college students, estimates of use vary widely but, taken together, suggest that the practice is commonplace. The cognitive effects of stimulants on normal healthy people cannot yet be characterized definitively, despite the volume of research that has been carried out on these issues. Published evidence suggests that declarative memory can be improved by stimulants, with some evidence consistent with enhanced consolidation of memories. Effects on the executive functions of working memory and cognitive control are less reliable but have been found for at least some individuals on some tasks. In closing, we enumerate the many outstanding questions that remain to be addressed by future research and also identify obstacles facing this research.
amphetamine; enhancement; neuroethics; psychopharmacology; stimulant
Longitudinal, epidemiological studies have identified robust risk factors for youth antisocial behavior, including harsh and coercive discipline, maltreatment, smoking during pregnancy, divorce, teen parenthood, peer deviance, parental psychopathology, and social disadvantage. Nevertheless, because this literature is largely based on observational studies, it remains unclear whether these risk factors have truly causal effects. Identifying causal risk factors for antisocial behavior would be informative for intervention efforts and for studies that test whether individuals are differentially susceptible to risk exposures. In this paper, we identify the challenges to causal inference posed by observational studies and describe quasi-experimental methods and statistical innovations that may move us beyond discussions of risk factors to allow for stronger causal inference. We then review studies that use these methods and we evaluate whether robust risk factors identified from observational studies are likely to play a causal role in the emergence and development of youth antisocial behavior. For most of the risk factors we review, there is evidence that they have causal effects. However, these effects are typically smaller than those reported in observational studies, suggesting that familial confounding, social selection, and misidentification might also explain some of the association between risk exposures and antisocial behavior. For some risk factors (e.g., smoking during pregnancy, parent alcohol problems) the evidence is weak that they have environmentally mediated effects on youth antisocial behavior. We discuss the implications of these findings for intervention efforts to reduce antisocial behavior and for basic research on the etiology and course of antisocial behavior.
antisocial behavior; causal inference; risk factors; quasi-experimental designs
Insomnia is prevalent, causing severe distress and impairment. This review focuses on illuminating the puzzling finding that many insomnia patients misperceive their sleep. They overestimate their sleep onset latency (SOL) and underestimate their total sleep time (TST), relative to objective measures. This tendency is ubiquitous (although not universal). Resolving this puzzle has clinical, theoretical, and public health importance. There are implications for assessment, definition, and treatment. Moreover, solving the puzzle creates an opportunity for "real world" applications of theories from clinical, perceptual, and social psychology as well as neuroscience. Herein we evaluate thirteen possible resolutions to the puzzle. Specifically, we consider the possible contribution, to misperception, of: (1) features inherent to the context of sleep (e.g., darkness); (2) the definition of sleep onset which may lack sensitivity for insomnia patients; (3) insomnia being an exaggerated sleep complaint; (4) psychological distress causing magnification; (5) a deficit in time estimation ability; (6) sleep being misperceived as wake; (7) worry and selective attention toward sleep-related threats; (8) a memory bias influenced by current symptoms and emotions, a confirmation bias/belief bias or a recall bias linked to the intensity/recency of symptoms; (9) heightened physiological arousal; (10) elevated cortical arousal; (11) the presence of brief awakenings; (12) a fault in neuronal circuitry; and (13) there being two insomnia subtypes (one with and one without misperception). The best supported resolutions were misperception of sleep as wake, worry, and brief awakenings. A deficit in time estimation ability was not supported. We conclude by proposing several integrative solutions.
sleep; insomnia; perception; measurement; polysomnography; comorbidity
Tobacco addiction and chronic pain represent two highly prevalent and comorbid conditions that engender substantial burdens upon individuals and systems. Although interrelations between pain and smoking have been of clinical and empirical interest for decades, research on the topic of pain, nicotine, and tobacco smoking has increased dramatically over the past five years. We conceptualize the interaction of pain and smoking as a prototypical example of the biopsychosocial model. Accordingly, the current review extrapolated from behavioral, cognitive, affective, biomedical, and social perspectives to propose causal mechanisms that may contribute to the observed comorbidity between these two conditions. Research in the broad area of pain and smoking was first dichotomized into investigations of either "effects of smoking on pain" or "effects of pain on smoking." We then integrated the extant literature to present a reciprocal model of pain and smoking that is hypothesized to interact in the manner of a positive feedback loop, resulting in greater pain, increased smoking, and the maintenance of tobacco addiction. Finally, we proposed directions for future research, and discussed clinical implications for smokers with comorbid pain disorders. We observed modest evidence to support the notions that smoking may be a risk factor in the multifactorial etiology of some chronically painful conditions, and that the experience of pain may come to serve as a potent motivator of smoking. We also found that whereas animal studies yielded consistent support for direct pain-inhibitory effects of nicotine and tobacco smoke, results from human studies were much less consistent. Future research in the emerging area of pain and smoking has the potential to inform theoretical and clinical applications with respect to tobacco smoking, chronic pain, and their comorbid presentation.
pain; nicotine; tobacco; smoking; chronic pain; mechanisms
Among people exposed to major psychological stressors in early life, there are elevated rates of morbidity and mortality from chronic diseases of aging. The most compelling data come from studies of children raised in poverty or maltreated by their parents, who show heightened vulnerability to vascular disease, autoimmune disorders, and premature mortality. These findings raise challenging theoretical questions. How does childhood stress get under the skin, at the molecular level, to affect risk for later diseases? And how does it incubate there, giving rise to diseases several decades later? Here we present a Biological Embedding Model, which attempts to address these questions by synthesizing knowledge across several behavioral and biomedical literatures. This model maintains that childhood stress gets “programmed” into macrophages through epigenetic markings, post-translational modifications, and tissue remodeling. As a consequence these cells are endowed with pro-inflammatory tendencies, manifest in exaggerated cytokine responses to challenge and decreased sensitivity to inhibitory hormonal signals. The model goes on to propose that over the lifecourse, these pro-inflammatory tendencies are exacerbated by behavioral proclivities and hormonal dysregulation, themselves the products of exposure to early stress. Behaviorally, the model posits that childhood stress gives rise to excessive threat vigilance, mistrust of others, poor social relationships, impaired self-regulation, and unhealthy lifestyle choices. Hormonally, early stress confers altered patterns of endocrine and autonomic discharge. This milieu amplifies the pro-inflammatory environment already instantiated by macrophages. Acting in concert with other exposures and genetic liabilities, the resulting inflammation drives forward pathogenic mechanisms that ultimately foster chronic disease.
Stress; inflammation; cortisol; HPA axis; childhood; heart disease; epigenetics
A meta-analysis examined the extent to which socio-structural and psycho-cultural characteristics of societies correspond with how much gender and ethnic/racial groups differ on their support of group-based hierarchy. Robustly, women opposed group-based hierarchy more than men did and members of lower-power ethnic/racial groups opposed group-based hierarchy more than members of higher-power ethnic/racial groups. As predicted by social dominance theory, gender differences were larger, more stable, and less variable from sample to sample than differences between ethnic/racial groups. Subordinate gender and ethnic/racial group members disagreed more with dominants in their views of group-based hierarchy in societies that can be considered more liberal and modern (e.g., emphasizing individualism and change from traditions), as well as in societies that enjoyed greater gender equality. The relations between gender and ethnic/racial groups are discussed and implications are developed for social dominance theory, social role theory and biosocial theory, social identity theory, system justification theory, realistic group conflict theory and relative deprivation theory.
Social dominance; gender and arbitrary groups; cross-cultural; meta-analysis
In 1912, Max Wertheimer published his paper on phi motion, widely recognized as the start of Gestalt psychology. Because of its continued relevance in modern psychology, this centennial anniversary is an excellent opportunity to take stock of what Gestalt psychology has offered and how it has changed since its inception. We first introduce the key findings and ideas in the Berlin school of Gestalt psychology, and then briefly sketch its development, rise, and fall. Next, we discuss its empirical and conceptual problems, and indicate how they are addressed in contemporary research on perceptual grouping and figure-ground organization. In particular, we review the principles of grouping, both classical (e.g., proximity, similarity, common fate, good continuation, closure, symmetry, parallelism) and new (e.g., synchrony, common region, element and uniform connectedness), and their role in contour integration and completion. We then review classic and new image-based principles of figure-ground organization, how it is influenced by past experience and attention, and how it relates to shape and depth perception. After an integrated review of the neural mechanisms involved in contour grouping, border-ownership, and figure-ground perception, we conclude by evaluating what modern vision science has offered compared to traditional Gestalt psychology, whether we can speak of a Gestalt revival, and where the remaining limitations and challenges lie. A better integration of this research tradition with the rest of vision science requires further progress regarding the conceptual and theoretical foundations of the Gestalt approach, which will be the focus of a second review paper.
Gestalt; grouping principles; figure-ground organization; neural mechanisms; vision science
A. C. Moss and I. P. Albery (2009) presented a dual-process model of the alcohol-behavior link, integrating alcohol expectancy and alcohol myopia theory. Their integrative theory rests on a number of assumptions including, first, that alcohol expectancies are associations that can be activated automatically by an alcohol-relevant context, and second, that alcohol selectively reduces propositional reasoning. As a result, behavior comes under the control of associative processes after alcohol consumption. We agree with the second but not with the first assumption, based on theoretical and empirical arguments. Although in some cases expectancies may involve a simple association, they are propositional in nature. We demonstrate that this assertion is supported by existing literature cited in Moss and Albery. Moreover, six recent studies consistently demonstrated that under circumstances where executive control is impaired (either as a stable individual difference or under the acute influence of alcohol), associative processes, over and above expectancies, predict alcohol-related behavior. Taken together, the evidence strongly suggests a fundamental distinction between expectancies and associations in memory: effects of propositional expectancies and executive functions are impaired under the acute influence of alcohol but memory associations are not. This difference in perspective not only has theoretical implications, but also leads to different predictions regarding acute alcohol effects in society.
Dual-Process Theories; Automatic and Controlled Processes; Acute Alcohol Effects
There are many reports of relations between age and cognitive variables and of relations between age and variables representing different aspects of brain structure, and a few reports of relations between brain structure variables and cognitive variables. These findings have sometimes led to inferences that the age-related brain changes cause the age-related cognitive changes. Although this conclusion may well be true, it is widely recognized that simple correlations are not sufficient to warrant causal conclusions, and other types of correlational information, such as mediation and correlations between longitudinal brain changes and longitudinal cognitive changes, also have limitations with respect to causal inferences. These issues are discussed, and the existing results on relations of regional volume, white matter hyperintensities, and DTI measures of white matter integrity to age and to measures of cognitive functioning are reviewed. It is concluded that at the current time the evidence that these aspects of brain structure are neuroanatomical substrates of age-related cognitive decline is weak. The final section contains several suggestions concerned with measurement and methodology that may lead to stronger conclusions in the future.
The commentaries on my article contain a number of points with which I disagree, but also several with which I agree. For example, I continue to believe that the existence of many cases in which between-person variability does not increase with age indicates that greater variance with increased age is not inevitable among healthy individuals up to about 80 years of age. I also do not believe that problems of causal inferences from correlational information are more severe in the cognitive neuroscience of aging than in other research areas; instead, I contend that neglect of these problems has led to confusion about neurobiological underpinnings of cognitive aging. I agree that researchers need to be cautious in extrapolating from cross-sectional to longitudinal relations, but I also note that even longitudinal data are limited with respect to their ability to support causal inferences.
Salthouse (2011) critically reviewed cross-sectional and longitudinal relations among adult age, brain structure, and cognition (ABC), and identified problems in interpretation of the extant literature. His review, however, misses several important points. First, there is enough disparity among the measures of brain structure and cognitive performance to question the uniformity of B and C vertices of the ABC triangle. Second, age differences and age changes in brain and cognition are often nonlinear. Third, variances and correlations among measures of brain and cognition frequently vary with age. Fourth, cross-sectional comparisons among competing models of ABC associations cannot disambiguate competing hypotheses about the structure and the range of directed and reciprocal relations between changes in brain and behavior. Based on these observations, we offer the following conclusions. First, individual differences among younger adults are not useful for understanding the aging of brain and behavior. Second, only multivariate longitudinal studies, age-comparative experimental interventions, and a combination of the two will deliver us from the predicaments of the ABC triangle described by Salthouse (2011). Mediation models of cross-sectional data represent age-related differences in target variables but fail to approximate time-dependent relations, and thus do not elucidate the dimensions and dynamics of cognitive aging.
brain; aging; cognition; longitudinal; mediation