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Genes in ContextGene–Environment Interplay and the Origins of Individual Differences in Behavior
Abstract
Interactions between genes and the environment are a critical feature of development. Insights into the dynamic interplay between these factors have come from laboratory studies exploring experience-dependent changes in gene function, which illustrate the importance of environmental factors in determining activity of the genome. These studies have implications for our understanding of the origins of individual differences in behavior and may provide new ways of thinking about the transmission of traits across generations. Here we will highlight how these new findings illustrate the importance of putting genes in context.
... Between-person differences can be due to variations in the genetic code (genotype) between people, such as alterations in a single nucleic acid for a specific set of coding instructions (a single nucleotide polymorphism or SNP in a specific gene), or epigenetic modifications to an individual's DNA (Slavich & Cole, 2013). Epigenetic modifications are any changes in the DNA that do not involve changes to the nucleic acids in the gene sequence itself (Champagne & Mashoodh, 2009). Genotype variations or epigenetic modifications can result in between-person differences in the degree or amount of gene expressed and protein produced, or changes in the structure of the protein itself; both can have important implications for the function of tissues and cells. ...
... For instance, individuals with a specific variation in a specific gene may be more susceptible to harmful or beneficial features of the environment; those factors could include environmental (pollution exposure, drought, infectious illness exposures) and social (socioeconomic status, quality of family relationships, stress exposure) factors. When different genotypes have different responses to a specific environmental factor, this is known as a gene X environment interaction (Champagne & Mashoodh, 2009). In a recent example from two large epidemiological studies (Multi-Ethnic Study of Atherosclerosis, Framingham Cohort 2), for individuals with a specific SNP in the EBF1 gene (which codes for a protein involved in gene transcription in B-cells), greater selfreported exposure to chronic psychological stress was related to surrogate CVD endpoints including greater waist circumference, fasting glucose, prevalence of diabetes, and a marker of atherosclerosis; but only among White participants (Singh et al., 2014). ...
... Among the annotation categories associated with train_avgmo under 28 Si, we also find KEGG_MM_FATTY_ACID_METABOLISM (p < 5.7 × 10 −8 ). There is extensive literature on the effect of ionizing radiation on fatty acid metabolism (Alfaia et al., 2007;Chukwuemeka et al., 2012;Mims et al., 2015;Rae et al., 2015). For KEGG_MM_RETINOL_METABOLISM (p < 1.6 × 10 −6 ), there is evidence that retinoids reduce cellular apoptosis following irradiation (Vorotnikova et al., 2004); other studies have also found involvement of retinol in molecular or cellular responses to irradiation (Ross and Kempner, 1993). ...
... We find that alterations in environmental conditions and environmental challenges other than irradiation also have the potential to alter behavioral and cognitive performance and their genetic basis, an observation consistent with previous findings (Champagne and Mashoodh, 2009;Beery and Kaufer, 2015). Stressful events (such as intrusive urine collection) have a strong effect on the actual behavioral and cognitive performance (Kurien et al., 2004). ...
Behavioral and cognitive traits have a genetic component even though contributions from individual genes and genomic loci are in many cases modest. Changes in the environment can alter genotype–phenotype relationships. Space travel, which includes exposure to ionizing radiation, constitutes environmental challenges and is expected to induce not only dramatic behavioral and cognitive changes but also has the potential to induce physical DNA damage. In this study, we utilized a genetically heterogeneous mouse model, dense genotype data, and shifting environmental challenges, including ionizing radiation exposure, to explore and quantify the size and stability of the genetic component of fear learning and memory-related measures. Exposure to ionizing radiation and other external stressors altered the genotype–phenotype correlations, although different behavioral and cognitive measures were affected to different extents. Utilizing an integrative genomic approach, we identified pathways and functional ontology categories associated with these behavioral and cognitive measures.
... Moreover, person-environment interaction is a long-standing theme in behavioral sciences (Lewin, 1935). Reflected in the genetic research, the perspective of gene and environment interaction has also emerged as one of the most widely studied topics (Belsky & Pluess, 2009;Champagne & Mashoodh, 2009;Moffitt, Caspi, & Rutter, 2006). Studies found that genes typically work in tandem with environmental factors in modulating human attitudes and behaviors. ...
... The person-environment interaction perspective suggests that behavior is a function of the interactive effect of the person and the environment (Lewin, 1935). Genetics research has also shown that genes interact with environmental factors in shaping human behavior (Belsky & Pluess, 2009;Champagne & Mashoodh, 2009;Moffitt, Caspi, & Rutter, 2006). In the organizational behavior literature, the gene-environment interaction perspective was adopted to study the moderating role of social environments in adolescences on genetic influences on leadership (Zhang, Ilies, & Arvey, 2009). ...
... Moreover, person-environment interaction is a long-standing theme in behavioral sciences (Lewin, 1935). Reflected in the genetic research, the perspective of gene and environment interaction has also emerged as one of the most widely studied topics (Belsky & Pluess, 2009;Champagne & Mashoodh, 2009;Moffitt, Caspi, & Rutter, 2006). Studies found that genes typically work in tandem with environmental factors in modulating human attitudes and behaviors. ...
... The person-environment interaction perspective suggests that behavior is a function of the interactive effect of the person and the environment (Lewin, 1935). Genetics research has also shown that genes interact with environmental factors in shaping human behavior (Belsky & Pluess, 2009;Champagne & Mashoodh, 2009;Moffitt, Caspi, & Rutter, 2006). In the organizational behavior literature, the gene-environment interaction perspective was adopted to study the moderating role of social environments in adolescences on genetic influences on leadership (Zhang, Ilies, & Arvey, 2009). ...
This study examined how a dopamine genetic marker, DRD4 7 Repeat allele, interacted with early life environmental factors (i.e., family socioeconomic status, and neighborhood poverty) to influence job change frequency in adulthood using a national representative sample from the United States. The dopamine gene played a moderating role in the relationship between early life environments and later job change behaviors, which was meditated through educational achievement. In particular, higher family socioeconomic status was associated with higher educational achievement, and thereafter higher frequency of voluntary job changes and lower frequency of involuntary job changes; such relationships were stronger (i.e., more positive or negative) for individuals with more DRD4 7R alleles. In contrast, higher neighborhood poverty was associated with lower educational achievement, and thereafter lower frequency of voluntary job change and higher frequency of involuntary job change; such relationships were again stronger (i.e., more positive or negative) for individuals with more DRD4 7R alleles. The results demonstrated that molecular genetics using DNA information, along with early life environmental factors, can bring new insights to enhance our understanding of job change frequency in individuals' early career development. (PsycINFO Database Record
... A number of molecular mechanisms have been shown to contribute to glucocorticoid desensitization, including decreased expression of the GR gene and increased expression of pro-inflammatory transcription factors that inhibit expression of the GR gene (Barnes & Adcock, 2009). Some basic definitions and terminology about gene expression are in order at this point (see also, Champagne &Mashoodh, 2009, andOchs &Golemis, 2003, for a basic tutorial on gene expression). Gene expression refers to a multi-step process through which a gene leads to a functional gene product (typically a protein). ...
... A number of molecular mechanisms have been shown to contribute to glucocorticoid desensitization, including decreased expression of the GR gene and increased expression of pro-inflammatory transcription factors that inhibit expression of the GR gene (Barnes & Adcock, 2009). Some basic definitions and terminology about gene expression are in order at this point (see also, Champagne &Mashoodh, 2009, andOchs &Golemis, 2003, for a basic tutorial on gene expression). Gene expression refers to a multi-step process through which a gene leads to a functional gene product (typically a protein). ...
... Importantly, these changes reflected permanently altered gene expression (epigenetic programming), with consequences for the next generation's parenting behavior (Champagne & Meaney, 2007). These studies suggest that similarities in traits between parents and offspring involve far more than the inheritance of genes (Champagne & Mashoodh, 2009). Recently, it has been shown in a rat study that low-quality maternal care (that is, low levels of maternal licking and grooming) affects not only the pups' stress physiology but also their brain morphology, in a way that on the face of it seemed disadvantageous (lower neural density), but that actually enhanced learning and memory processes under stressful conditions. ...
... Genetics are here to stay. Creating a division between genes and environment will not help our understanding of the processes that lead to individual differences; the interaction between genes and environment is a critical feature of development (Champagne & Mashoodh, 2009). ...
In the past decades, the effects of parenting and the rearing environment have been seriously queried by behavioral genetic research. The current generation of genetic studies ascribes more influence to parenting, seeking to answer specific questions of shared and non-shared environment and directed at the interplay between nature and nurture (gene–environment interaction, GxE). We present results from our research on dopamine-related genes as an illustration of the difference between “genetic risk” and “differential susceptibility” as frameworks for the interpretation of GxE effects in both children and parents, and we argue that dopamine-related genes may play a part in explaining differential susceptibility to the rearing environment. The growing evidence for environmental impact on gene expression (i.e., epigenetic programming) underlines the significance of parenting. Implications for family science are discussed.
... Moreover, we still know very little about the links among heritable behaviors, decisions, and traits and the processes underlying such effects. That is, despite the great progress that has been made in the areas of molecular genetics, and especially the rapidly developing field of epigenetics (i.e., the study of heritable alterations in gene expression caused by mechanisms other than changes in DNA sequences; for a review, see, e.g., Champagne andMashoodh [2009] andMeaney [2008]), these areas are probably many years away from providing insights into the heritability of choice and judgment. A noteworthy illustration of this conclusion is provided by the influential finding of Caspi et al. (2003), who identified a specific gene-by-environment interaction whereby a genetic disposition to depression produces depression only among those experiencing great stress. ...
... While the recent advancements in the field of genetics, and, in particular, epigenetics (for a review, see, e.g., Champagne and Mashoodh [2009] and Szyf et al. [2008]) suggest that environmental (nurture) factors can affect gene expression and corresponding behavioral tendencies, the scope of our investigation and the extension to judgment and choice would require a significant extrapolation of current epigenetic research. Indeed, explaining how epigenetic (gene expression) changes might create a propensity to not/compromise appears much more complex than accounting for the impact of licking rat pups on their epigenetic characteristics (Champagne 2008). ...
While constructed preferences have received a great deal of attention, there has been virtually no research regarding the genetic basis of consumer judgment and choice. In this research, we examine a wide range of previously unexplored heritable effects on consumer choices and judgments. Moreover, whereas prior research on heritable traits has typically employed a piecemeal approach, demonstrating each heritable trait separately, we propose an alternative way to simultaneously explore common mechanisms and links among heritable traits and behaviors. Using a classic twins study design, we find a large heritable effect on preferences for (a) compromise (but not dominating) options, (b) sure gains, (c) an upcoming feasible, dull assignment, (d) maximizing, (e) utilitarian options, and (f) certain products. Conversely, we do not find significant heritable effects regarding judgment heuristics, discounting, and other decision problems. We tentatively propose that the pattern of findings might reflect a generic heritable individual difference relating to “prudence.” We discuss the implications of our research with respect to the determinants of preferences and future research on heritable aspects of judgment and choice.
... Therefore, even when some early methylation marks are lost during development, their early ontogenetic effects can significantly influence cell and tissue differentiation with a cascade of consequences for later development. Thus, DNA methylation modifications caused by early socio-structural and ecological exposures have the potential to modify the pace of reproductive maturation and reproductive outcomes [69][70][71][72][73][74]. ...
Adolescent pregnancy (occurring < age 20) is considered a public health problem that creates and perpetuates inequities, affecting not only women, but societies as a whole globally. The efficacy of current approaches to reduce its prevalence is limited. Most existing interventions focus on outcomes without identifying or addressing upstream social and biological causes. Current rhetoric revolves around the need to change girls’ individual behaviours during adolescence and puberty. Yet, emerging evidence suggests risk for adolescent pregnancy may be influenced by exposures taking place much earlier during development, starting as early as gametogenesis. Furthermore, pregnancy risks are determined by complex interactions between socio-structural and ecological factors including housing and food security, family structure, and gender-based power dynamics. To explore these interactions, we merge three complimentary theoretical frameworks: “Eco-Social”, “Life History” and “Developmental Origins of Health and Disease”. We use our new lens to discuss social and biological determinants of two key developmental milestones associated with age at first birth: age at girls’ first menstrual bleed (menarche) and age at first sexual intercourse (coitarche). Our review of the literature suggests that promoting stable and safe environments starting at conception (including improving economic and social equity, in addition to gender-based power dynamics) is paramount to effectively curbing adolescent pregnancy rates. Adolescent pregnancy exacerbates and perpetuates social inequities within and across generations. As such, reducing it should be considered a key priority for public health and social change agenda.
... Scholars in the social sciences have urged for a paradigm shift in the approach to studying biological and environmental influences on human development with some arguing they be conceptualized as closely interrelated or even inseparable rather than viewed as separate and competing factors (e.g., Champagne & Mashoodh, 2009;Dodge, 2004;Lerner, 2006;Meaney, 2001;Spencer et al., 2009). Moving beyond the "versus" paradigm when considering biology ("nature") and environment ("nurture") has been similarly echoed by those speaking to the importance of practitioner understanding of disease etiology (Sonuga-Barke, 2010). ...
Mental health researchers emphasize the importance of practitioner understanding of biology-environment interplay. Accordingly, our goal of the study described in this article was to understand students’ preconceptions and misconceptions about biological and environmental influences on development through investigating their conceptions of epigenetics. Using a short-term longitudinal design, we explored preservice helping professionals’ conceptions and misconceptions pertaining to epigenetics within the framework of a graduate level human development course. Baseline knowledge about epigenetics was low. Students developed multiple misconceptions about epigenetics and how the phenomenon relates to biological and environmental influences on human development. Students reported feeling highly efficacious for detecting and resolving misconceptions related to biology-environment interactions but varied in their perceptions of interest for learning about the content. Findings support the use of open-ended questions to detect misconceptions about epigenetics and are discussed in light of how to teach students about this phenomenon. Overall, this research speaks to the importance of understanding the misconceptions students believe and instructional strategies that may assist in correcting them.
... Finally, we found a main effect of children's genotype on their own DAT1 methylation at M5, with a higher level of methylation on children with DAT1 10/10 genotypes. Overall, our results confirmed previous studies suggesting that environmental and genetic factors may have both a main and interactive effect on children's methylation status [31,98]. Interestingly, our results suggested that children's genotypes moderate children's methylation in response to maternal (but not paternal) psychological profiles. ...
Parental psychopathological risk is considered as one of the most crucial features associated with epigenetic modifications in offspring, which in turn are thought to be related to their emotional/behavioral profiles. The dopamine active transporter (DAT) gene is suggested to play a significant role in affective/behavioral regulation. On the basis of the previous literature, we aimed at verifying whether children's DAT1 polymorphisms moderated the relationship between parents' psychological profiles, children's emotional/behavioral functioning, and DAT1 methylation in a normative sample of 79 families with school-age children (Ntot = 237). Children's biological samples were collected through buccal swabs, while Symptom CheckList -90 item Revised, Adult Self Report, and Child Behavior Check-List/6-18 was administered to assess parental and children's psychological functioning. We found that higher maternal externalizing problems predicted the following: higher levels of children's DAT1 methylation at M1, but only among children with 10/10 genotype; higher levels of methylation at M2 among children with 10/10 genotype; while lower levels for children with a 9-repeat allele. There was also a positive relationship between fathers' externalizing problems and children's externalizing problems, only for children with a 9-repeat allele. Our findings support emerging evidence of the complex interplay between genetic and environmental factors in shaping children' emotional/behavioral functioning, contributing to the knowledge of risk variables for a child's development and psychological well-being.
... Other important aspects to consider in translational psychiatry are the role of sex and individual differences in disease pathogenesis (Qureshi & Mehler, 2010), and their impact on G × E (Champagne & Mashoodh, 2009). For instance, different strategies for coping with environmental stressors in males and females may cause the differential prevalence of CNS disorders between the sexes (Schwandt et al., 2010), as has already been reported in schizophrenia for certain dopaminergic genes (Karl & Arnold, 2014). ...
Currently becoming widely recognized, personalized psychiatry focuses on unique physiological and genetic profiles of patients to best tailor their therapy. However, the role of individual differences, as well as genetic and environmental factors, in human psychiatric disorders remains poorly understood. Animal experimental models are a valuable tool to improve our understanding of disease pathophysiology and its molecular mechanisms. Due to high reproduction capability, fully sequenced genome, easy gene editing, and high genetic and physiological homology with humans, zebrafish (Danio rerio) are emerging as a novel powerful model in biomedicine. Mounting evidence supports zebrafish as a useful model organism in CNS research. Robustly expressed in these fish, individual, strain, and sex differences shape their CNS responses to genetic, environmental, and pharmacological manipulations. Here, we discuss zebrafish as a promising complementary translational tool to further advance patient‐centered personalized psychiatry.
... Research suggests that depression and anxiety are correlated with a number of epilepsy attributes such as age of seizure onset, seizure frequency, and medications [13,14]. Although this might suggest that epilepsy associated variables account for psychopathology there is an important interplay between biology and the environment that shapes development [15]. Thus, in order to fully understand risk factors for psychopathology in children with epilepsy we also need to consider contextual factors. ...
Epilepsy is the number one neurological disorder in children in western society. Childhood epilepsy is highly comorbid with psychopathology. Although neurological and biological factors may partially explain the increased risk of psychopathology in children with epilepsy, social contextual factors are also important to understanding development of psychopathology in children with epilepsy. The current paper examines the development of children with epilepsy utilizing Bronfenbrenner's micro-, meso-, exo-, and macrosystem social contexts. Negative interpersonal interactions within the microsystems and the ripple effect of social context at the other levels may contribute to increased risk for psychopathology.
... Epigenetics deals with virtually everything that happens to the expressed genes in the phenotype during stages of the lifespan, for example, prenatal, postnatal, childhood, lifetime social experiences, diet, nutrition, exposure to toxins, lifestyle, behavior, stress and environment, and how these impact the expression of genes. [7][8][9][10][11][12] The phenotypic expression differs in each individual depending on which part of the DNA (genes) is being expressed, based on past exposures, experiences and impressions, knowledge of which is embedded in the genes in the form of these epigenetic modifications. The phenotype is dynamic and always changing. ...
Ayurveda is a traditional system of medicine originated in the ancient Vedic times of India. This body of knowledge is found in well-documented texts such as the Charaka Samhita and Sushruta Samhita, and describes physiology and interrelated systems of the body, variations in human constitution, surgery, herbal use, and health-promoting recommendations. Ayurveda is translated as the "Science of Life;" Ayus = Life, and Veda = knowledge/science. The principles and treatment modalities have endured over time. For Ayurveda to be appreciated by Western medical researchers, this traditional system of medicine needs to be understood in terms of modern science. The current theories of physiology that support Ayurvedic approaches need to be explored. Herein, one approach of how the realm of epigenetics can help elucidate the mechanisms of Ayurveda has been described.
... Epigenetics with the Greek prefix epi; meaning over, outside of, or around, is concerned with studying the genetic effects which are not encoded in the DNA sequence of an organism but may result from external factors that switch genes on and off and hence affecting the cellular gene expression. Such effects may or may not be inherited but using the terminology "epigenetics" to describe heritable processes is a matter of debate [4][5][6][7][8]. ...
The interaction between environmental factors and genetic vulnerability plays a major role in the development of mood disorders. Episodes of bipolar disorder could be considered as the outcome of the battle between stress and the individual's ability to cope with; a fact that proposes a role of epigenetics in its pathogenesis and pathophysiology. Although the molecular studies on methylation of DNA and histone modification in cases of bipolar disorder are still inadequate but the role of stress in developing the disorder and the therapeutic efficacy of mood stabilizers in controlling its episodes highlight the potential influence of epigenetic variation on its occurrence. Limited availability of human brain tissue for conducting researches represents a great obstacle in replicating the findings on animal models of mood disorders in humans as humans do differ from animals in their response to environmental factors whether on the subcellular, cellular, organ, or individualistic levels; nevertheless some ongoing research on DNA methylation seems to be very promising in settling the impact of epigenetics on the development of bipolar disorder with a potential role in empowering psychiatrists in helping their patients and controlling its episodes.
... 235). Other important aspects of gen-environment interplay are gene-environment correlations and gen-environment interactions (F. A. Champagne & Mashoodh, 2009;Rutter et al., 2006), but a detailed discussion of these issues is beyond the scope of this paper. ...
The present work proposes an evolutionary model of externalising personality that defines variation in this broad psychobiological phenotype resulting from genetic influences and a conditional adaptation to high-risk environments with high extrinsic morbidity-mortality. Due to shared selection pressure, externalising personality is co-adapted to fast life history strategies and maximises inclusive fitness under adverse environmental conditions by governing the major trade-offs between reproductive versus somatic functions, current versus future reproduction, and mating versus parenting efforts. According to this model, externalising personality is a regulatory device at the interface between the individual and its environment that is mediated by two overlapping psychobiological systems, that is, the attachment and the stress-response system. The attachment system coordinates interpersonal behaviour and intimacy in close relationships and the stress-response system regulates the responsivity to environmental challenge and both physiological and behavioural reactions to stress. These proximate mechanisms allow for the integration of neuroendocrinological processes underlying inter-individual differences in externalising personality. Hereinafter I further discuss the model’s major implications for personality psychology, psychiatry and public health policy.
... More recently, Caspi et al. (2003) explored the roles of a variation in a gene that alters serotonin levels and exposure to stressful life events across a 20-year period in determining the risk of depression (Champagne and Mashoodh, 2009). ''Individuals with one or two copies of the short allele of the 5-HT T promoter polymorphism exhibited more depressive symptoms, diagnosable depression, and suicidality in relation to stressful life events than individuals homozygous for the long allele. ...
The arrival of modern brain imaging technologies has provided new opportunities for examining the biological essence of human intelligence as well as the relationship between brain size and cognition. Thanks to these advances, we can now state that the relationship between brain size and intelligence has never been well understood. This view is supported by findings showing that cognition is correlated more with brain tissues than sheer brain size. The complexity of cellular and molecular organization of neural connections actually determines the computational capacity of the brain. In this review article, we determine that while genotypes are responsible for defining the theoretical limits of intelligence, what is primarily responsible for determining whether those limits are reached or exceeded is experience (environmental influence). Therefore, we contend that the gene-environment interplay defines the intelligent quotient of an individual.
... The enduring impact of the critique is supported by modern biology, which rejects a dichotomy between genetic and environmental effects. The current guiding principle is that genetic determinants of phenotypical behavioral and physiological traits depend on an interaction of genes and the environment in which those genes operate (Champagne & Mashoodh, 2009;Crews, 2011; see also Volume 1, Chapters 11 and 18, this handbook). Such epigenetic mechanisms are becoming increasingly evident as key players in learning and memory (Lattal & Wood, 2013). ...
Pavlovian conditioning is a fundamental mechanism guiding behavioral change. It enables organisms to adjust to their environments and facilitates their interactions with ecologically relevant resources, conspecifics, and threats. Associative learning is extraordinarily common, and even exists among invertebrates with remarkably simple nervous systems. The biological and evolutionary foundations of conditioning are built on studies of a diversity of species that encounter unique, species-specific ecological problems. These foundations were established as long-standing historical debates about the relative contributions of nature and nurture took place. Resolution on the issue is ongoing and is aided by incorporating ethological and evolutionary perspectives into studies of animal learning. Researchers of Pavlovian conditioning have long offered special insight into these questions because their work involves studying reflexive or unconditioned responses (UR) and the ways that experience alters how these responses occur. In this chapter we review the outcome of ethologically and evolutionary-based investigations of Pavlovian conditioning. We seek to bring together information about all of the major biologically informed perspectives on conditioning, including consideration of the evolutionary origins of conditioning, the biological functions of conditioning, as well as ecological, adaptationist, and behavioral systems approaches. We begin with a brief overview of the historical debate about learning and instinct because it provides the historical context for the ethological and evolutionary perspectives offered in this chapter.
... The enduring impact of the critique is supported by modern biology, which rejects a dichotomy between genetic and environmental effects. The current guiding principle is that genetic determinants of phenotypical behavioral and physiological traits depend on an interaction of genes and the environment in which those genes operate (Champagne & Mashoodh, 2009;Crews, 2011; see also Volume 1, Chapters 11 and 18, this handbook). Such epigenetic mechanisms are becoming increasingly evident as key players in learning and memory (Lattal & Wood, 2013). ...
Investigators of conditioning phenomena at the behavioral level have always sought to identify general principles or processes. That effort has been challenged by instances of learning that are specific to the responses, stimuli, and reinforcers involved in a particular instrumental or Pavlovian conditioning situation. This chapter reviews the theoretical and empirical efforts that have been pursued to integrate specialized conditioning effects into a general theory, and then illustrates how evidence from naturalistic learning paradigms offers a more ecologically and evolutionarily relevant basis for identifying adaptive specializations of learning and the developing general theories of learning.
... A host of different studies have now provided evidence that environmental cues can affect these intermediary factors, thereby affecting gene expression. These types of effects are called epigenetic effects, and it is now known that such effects have important implications for a variety of different physical and emotional outcomes (Champagne & Mashoodh, 2009). They also help elucidate how environmental events have biological implications. ...
This chapter focuses on the stability-change issue in personality, as well as the organization of personality variables and their utility in predicting mortality among older adults. Scholars are using personality variables to predict important outcomes in older adulthood, particularly mortality. With respect to the former, intriguing new findings have permitted a deeper and more complex understanding of personality development in older adulthood, which is especially true with respect to stability and change in personality traits over long-term periods. The Hooker–McAdams model is important for the field of personality psychology in general because it provides a broader framework than that of the big five, which is too strongly attached to structure approaches, particularly the trait approach. The effects of change in personality and health may work both ways. A change in personality may also have a protective effect on health. People who increase in conscientiousness or decrease in neuroticism may enjoy a concomitant increase in physical health or, more likely, stability in his or her good health trajectory.
... When the human genome was first revealed, there were few genetic markers of disorders identified, but instead it was found that most disorders were polygenic, and most gene-environment interactions produced remarkable transformations and differing outcomes in individuals. This has led to the birth of epigenetics [187,188]. In recognizing these complex interrelationships, many different combinations of alleles could produce similar types of disorders, especially when it comes to disorders affecting learning and behaviour. ...
... Most G Â E research on adolescents examined extreme environments such as childhood trauma and maltreatment, sexual abuse or threatening life events [25,47,48]. More common factors such as conflicts in the family and peer victimization as well as positive parenting have been investigated in interaction with multiple polymorphisms related to serotonin, dopamine, and oxytocin [21,22,[49][50][51][52][53][54]. We look at perceived parenting as represented by five dimensions [20]: perceived support, proactive control (i.e., consistent rule setting), psychological control (i.e., intrusive type of control, parents manipulate thoughts, emotions and feelings of the adolescent), punishment, and harsh punishment (i.e., physical punishment), in interaction with the above mentioned VNTRs. ...
Background:
Parenting dimensions are associated with depressive symptoms in adolescents. We investigated the role of perceived parenting dimensions and gene-environment interactions between these perceived parenting dimensions and five well-known variable number of tandem repeats (VNTRs): 5-HTTLPR, STin2, DAT1, DRD4, and MAO-A, in depressive symptoms.
Methods:
From a non-clinical sample of 1111 Belgian adolescents (mean age: 13.79 years, SD=.94; 51% boys), 1103 adolescents consented for genetic research. Five VNTRs were analyzed using DNA from saliva samples. Perceived parenting dimensions (i.e., support, proactive control, psychological control, punishment, and harsh punishment) were examined using self-report scales completed by adolescents and their parents. Depressive symptoms were investigated using the CES-D self-report scale. Statistical analyses were performed in R using linear regression.
Results:
Parental support, as perceived by the adolescent, was negatively associated with depressive symptoms (CES-D) and psychological control was positively associated with these symptoms. The only interaction effect withstanding correction for multiple testing was observed for 5-HTTLPR and the difference in proactive control as perceived by adolescents in comparison to parents. Short-allele carriers showed more depressive symptoms when there was a higher discrepancy in proactive control as perceived by adolescents versus parents.
Conclusions:
Our results suggest that perceived parenting dimensions are associated with depressive symptoms, as measured by the CES-D. We only found modest evidence for 5-HTTLPR as a moderator in the association between the difference in perception of proactive control (adolescents vs. parents) and depressive symptoms.
... This phenomenon is often referred to as the way that " poverty gets under the skin." About fi ve years ago, early research identifi ed abnormal levels of, and fl uctuations in, cortisol (the "stress" hormone) as the primary underlying mechanism (McEwen and Gianaros 2010 ; Champagne and Mashoodh 2009 ;Seeman et al. 2010 ). More recently, given that stress-related, elevated levels of cortisol in the mother can affect the placenta, researchers have focused on the potential negative effects of maternal stress on fetal outcomes. ...
This chapter focuses on how intergenerational mobility is affected by children’s earliest life experiences from conception through preschool. These experiences are important because of their effects on outcomes later in life. One consequence is that intervening early is the most cost-effective way to put a child on course to pass through the gates that determine adult success and thereby reduce differences in mobility among children born in different circumstances. Using a life-cycle model, we examine the evidence on trends in factors that affect child development. The evidence we assess leads to the conclusion that opportunity and mobility are declining for lower and even middle class children as changes in family life, parenting practices, economic inequality, unresponsive social institutions, and increasingly economically homogeneous neighborhoods all point to a serious decline in the factors that are associated with greater mobility. We conclude that the decline in opportunity and mobility for current generations of American children is likely the biggest negative effect of the continuing U.S. inequality boom in income, wealth, and consumption. The paper ends by outlining a series of policies that would help restore opportunity in America by intervening early in the life course.
... In order to understand the role and workings of DNA in an individual's life, we might take the illustrative example that genes can be likened to books, categorized and arranged in a library. Books and DNA are both ''waiting to be read'' [8]. If a book is difficult to reach or is hidden, it may not be read. ...
Recent research provides evidence that early life experience plays a critical role in human development, as it also has a role in susceptibility to disease in later life. However, the mechanism of how this works remains largely in question, though it is crucial to consider the complex interaction between genes and environment which is a critical feature of development and which gives rise to individual differences in behaviour. Studies on the gene/environment interplay have given rise to the new field of research called epigenetics. Epigenetics is a mechanism that regulates gene expression, without incurring any change in the underlying DNA sequence. It relies instead on the chemical modification of DNA and histone proteins. Epigenetic findings from human and animal studies suggest that changes, such as DNA methylation, are involved not only in cellular differentiation but also in the modulation of genome function in response to early life experience affecting gene function as well as phenotype. In this article we review some recent studies regarding gene–environment interplay. These studies provide new ways of thinking about the transmission of traits across generations and provide implications for our understanding of the origins of individual differences in behaviour. Understanding how the environment impacts the working of the genome could have massive implications on how we approach solving current diseases and think about inheritance.
... can alter a developmental trajectory" making meaningless any linear regression studies of nature and nurture. Genes are always "genes in context", "contextdependent catalysts of cellular changes, rather "controllers" of developmental progress and direction" (Nijhout, 1990: 444), susceptible to be reversed in their expression by individual's experiences during development (Champagne and Mashoodh, 2009). ...
The rise of molecular epigenetics over the last few years promises to bring the discourse about the sociality and susceptibility to environmental influences of the brain to an entirely new level. Epigenetics deals with molecular mechanisms such as gene expression, which may embed in the organism "memories" of social experiences and environmental exposures. These changes in gene expression may be transmitted across generations without changes in the DNA sequence. Epigenetics is the most advanced example of the new postgenomic and context-dependent view of the gene that is making its way into contemporary biology. In my article I will use the current emergence of epigenetics and its link with neuroscience research as an example of the new, and in a way unprecedented, sociality of contemporary biology. After a review of the most important developments of epigenetic research, and some of its links with neuroscience, in the second part I reflect on the novel challenges that epigenetics presents for the social sciences for a re-conceptualization of the link between the biological and the social in a postgenomic age. Although epigenetics remains a contested, hyped, and often uncritical terrain, I claim that especially when conceptualized in broader non-genecentric frameworks, it has a genuine potential to reformulate the ossified biology/society debate.
... Elegant experimental studies have shown deficiencies of early rearing to effect lifelong behavioral alterations in laboratory animals via epigenetic modifications of the hypothalamic-pituitaryadrenal system (Champagne & Mashoodh 2009, Meaney 2010, although relatively little research has yet been done in humans or in relation to G × E. One exception is recent work relevant to posttraumatic stress disorder (PTSD), which was previously predicted by an interaction of early childhood trauma with polymorphic variation in FKBP5, a protein involved in the regulation of glucocorticoid receptor binding and function (Binder et al. 2008, Xie et al. 2010. In follow-up work, Klengel and colleagues (2013) found exposure to trauma in early life to be associated with demethylation of DNA proximal to a glucocorticoid response element in FKBP5, an effect that was specific to persons carrying one of the FKBP5 variants previously linked to risk of PTSD. ...
With the advent of increasingly accessible technologies for typing genetic variation, studies of gene-environment (G×E) interactions have proliferated in psychological research. Among the aims of such studies are testing developmental hypotheses and models of the etiology of behavioral disorders, defining boundaries of genetic and environmental influences, and identifying individuals most susceptible to risk exposures or most amenable to preventive and therapeutic interventions. This research also coincides with the emergence of unanticipated difficulties in detecting genetic variants of direct association with behavioral traits and disorders, which may be obscured if genetic effects are expressed only in predisposing environments. In this essay we consider these and other rationales for positing G×E interactions, review conceptual models meant to inform G×E interpretations from a psychological perspective, discuss points of common critique to which G×E research is vulnerable, and address the role of the environment in G×E interactions.
... However, the existence of instructions on how to build proteins does not guarantee that those instructions will be carried out. The dierence is well framed by way of a metaphor due to Champagne & Mashoodh (2009). They describe DNA sequences as being like books precisely arranged in a library. ...
On average, children from less economically privileged households have lower levels of educational attainment than their higher income peers, and this association has important implications for intergenerational mobility and equality of opportunity. Using a large national data set that recently added information on genetic markers, this paper shows that the income-achievement relationship varies greatly across groups of children with different versions of a single gene, monoamine oxidase A (MAOA). For children with one variant of MAOA, increases in household income have the expected large positive association with college enrollment, college graduation, and total years of schooling completed. For children with another variant of MAOA, who comprise over half of the population, there is virtually no relationship between economic background and educational attainment. These results hold when the interactive effects are identified using MAOA variation between full biological siblings, which genetic principles assure is as good as randomly assigned. Implications for policy design and future research are discussed.
... The modern synthesis of the laws of heredity, adaptation and evolution [30], which assumes that chance generates genetic diversity and that natural selection favors the most adaptive solutions, is no longer effective at explaining some scientific observations [31][32][33][34][35][36]. During the last decade, epigenetics has established much evidence of this ineffectiveness of the modern synthesis for questions concerning transgenerational transmission [37][38][39][40][41][42], the influence of the environment [43][44][45][46][47], the impact of chemical substances [48,49] with consequences for behavior [50][51][52] or for the risk of disease [53][54][55][56][57][58]. ...
Korzybski's general semantics recommends considering living beings as organisms-as-a-whole in their environment. Our cognitive abilities, specific to the human species, have thus to be taken into account. In this framework we establish a semantic similarity between particular stressful events of the 20th century and AIDS in which the immune-deficiency-caused is semiotically seen as a biological state of disarmament of the organism. It then appears that: These observations suggest that AIDS could benefit from some collusion by the neuro-immune system because of positive learning of the semiotic concept of disarmament, thus making the terrain favorable to the germ in response to intense stress. The disease would then result from a conditioning process based on semiotics and involve some confusion at the level of the unconscious cognitive system between disarmament toward outside the body and disarmament toward inside the body. This hypothesis is discussed within a multidisciplinary perspective considering the specificities of our modern lifestyles, the cybernetic ability of signs to control metabolism and behavior, and the recent advances of epigenetics and cognition sciences. This hypothesis may explain the multiple cross-species transmissions of the immunodeficiency virus into humans during the 20th century. Further research is suggested for evaluating this hypothesis.
... Finally, the increased focus on the importance of gene x environment interactions (Champagne and Mashoodh, 2009) in determining dispositional differences in LHSs has emerged (Belsky and Pluess, 2009;Ellis and Boyce, 2008). There are a number of possible ways in which gene x environment interactions could play a role in the development of dispositional LHSs. ...
Following a model that is inclusive of both dispositional and situational influences on life-history behaviors and attitudes, the effect of life expectancies on aggression and generativity was examined. Consistent with the hypotheses it was found that shorter life expectancies led to an increase in the desire to aggress and a decrease in the desire to engage in generative behaviors. The results are discussed in terms of how life history theory can be used to frame research on person-situation interactions.
... The size and direction of environmental effects on behavioral phenotypes vary with the genotype, resulting in gene by environment interactions on behavior (Kafkafi et al., 2005;Spires and Hannan, 2005;Tucci et al., 2006b;Valdar et al., 2006). Environmental variables, such as those discussed in this section and the section below can have epigenetic effects on behavioral phenotypes (Champagne and Mashoodh, 2009;Holmes et al., 2005;Shepard et al., 2009;Spires and Hannan, 2005). Thus, two animals of the same genotype reared under different conditions may show different phenotypes (Branchi and Ricceri, 2002;Champagne and Meaney, 2007;Mueller and Bale, 2008) as can their F1 and F2 offspring (Curley et al., 2009 ...
Genetically modified mice are used to study the neurobiological basis of normal behavior and have been developed as models of human neurodegenerative and psychiatric disorders. These genetically modified mice show changes in gene expression in particular brain regions and altered behavior. The analysis of behavioral abnormalities in genetically modified mice through behavioral phenotyping is essential to determine the functional effects of genetic manipulations on the brain. Once a mouse model of a neural disorder has been established, novel treatments, including pharmacotherapy, immunotherapy, gene therapy, or behavioral therapy may be tested to restore the mouse to “normal.” However, many factors have the potential to confound the results of behavioral studies and these have led to questions about the validity and reliability of mouse models of neural disorders. The mouse itself must be considered, as issues such as the specificity of genetic manipulations, the supplier of the mice, their health, sex, and sensory or motor impairments may influence experimental findings. Environmental factors, including prenatal experience, housing conditions, and the social environment, also have the potential to affect the results. Furthermore, the laboratory environment, including the testing room, the light:dark (L:D) cycle, and the process of handling and habituating the mice to the test apparatus, may influence their behavior. The testing apparatus may lead to confounds through lack of standardization of design, poor reliability, and errors in automated recording of behavior. Finally, the experimenters themselves may influence the results because of inexperience, differences in following a protocol, and errors in recording data. This chapter outlines sources of error in the use of mouse models and suggests the ways in which these errors can be reduced to improve the reliability and validity of mouse models of human neurodegenerative and neuropsychiatric disorders.
... While this accomplishment was indeed signifi cant, it marks an important milestone rather than the end of an era of exploration into the molecular underpinnings of the human brain. Borrowing a metaphor from Champagne and Mashoodh, unexpressed genes are like books sitting unread on the shelves of a library: only when a gene is expressed does it have any causal eff ects, just as a book must be lift ed from a shelf and read before its contents can reach an audience (Champagne & Mashoodh, 2009). Indeed, " although genetics supply the basic blueprint for brain development, experience adjusts the genetic plan for the brain and shapes the architecture of its neural circuits , according to the needs and distinctive environment of the individual " (Nelson & Sheridan, in press). ...
... Although DNA methylation is just one of an array of epigenetic mechanisms , it is the one regarded as most stable and most representative of the broader epigenetic modification of a given locus (Hochberg et al., 2010). For comprehensive reviews of this rapidly expanding field of study, readers are referred to Champagne and Mashoodh (2009), Cole (2009), Curley, Jensen, Mashoodh, and Champagne (2010), Hochberg et al. (2010), and Meaney (2010). Our working hypothesis in the current study was that early experience leaves a mark on the epigenome that, in turn, leads to stable changes in expression of genes critical for human development and health (Szyf, McGowan, & Meaney, 2008). ...
Fifteen-year-old adolescents (N = 109) in a longitudinal study of child development were recruited to examine differences in DNA methylation in relation to parent reports of adversity during the adolescents' infancy and preschool periods. Microarray technology applied to 28,000 cytosine-guanine dinucleotide sites within DNA derived from buccal epithelial cells showed differential methylation among adolescents whose parents reported high levels of stress during their children's early lives. Maternal stressors in infancy and paternal stressors in the preschool years were most strongly predictive of differential methylation, and the patterning of such epigenetic marks varied by children's gender. To the authors' knowledge, this is the first report of prospective associations between adversities in early childhood and the epigenetic conformation of adolescents' genomic DNA.
... debate is rendered highly questionable by recent discoveries in genetics. Although our genes remain the same, the expression of those genes, i.e. whether those genes are turned on or off, is hugely influenced by the environment throughout life (Champagne and Mashoodh, 2009). Indeed, the activation and deactivation of genes within the nuclei of neurons is precisely the pathway via which the environment makes long-term changes to our synapses during learning (McClung and Nestler, 2008). ...
THE STUDY OF SOCIOECONOMIC STATUS (SES) AND THE BRAIN FINDS ITSELF IN A CIRCUMSTANCE UNUSUAL FOR COGNITIVE NEUROSCIENCE: large numbers of questions with both practical and scientific importance exist, but they are currently under-researched and ripe for investigation. This review aims to highlight these questions, to outline their potential significance, and to suggest routes by which they might be approached. Although remarkably few neural studies have been carried out so far, there exists a large literature of previous behavioural work. This behavioural research provides an invaluable guide for future neuroimaging work, but also poses an important challenge for it: how can we ensure that the neural data contributes predictive or diagnostic power over and above what can be derived from behaviour alone? We discuss some of the open mechanistic questions which Cognitive Neuroscience may have the power to illuminate, spanning areas including language, numerical cognition, stress, memory, and social influences on learning. These questions have obvious practical and societal significance, but they also bear directly on a set of longstanding questions in basic science: what are the environmental and neural factors which affect the acquisition and retention of declarative and nondeclarative skills? Perhaps the best opportunity for practical and theoretical interests to converge is in the study of interventions. Many interventions aimed at improving the cognitive development of low SES children are currently underway, but almost all are operating without either input from, or study by, the Cognitive Neuroscience community. Given that longitudinal intervention studies are very hard to set up, but can, with proper designs, be ideal tests of causal mechanisms, this area promises exciting opportunities for future research.
... Even in the expanding scholarship on genetics, current work recognizes that our genetic code is more changeable and influenced by the environment than we might expect. Champagne and Mashoodh's (2009) article, aptly titled, "Genes in Context" illustrates the dynamic complexities well. Mahoney's (2005) constructivist approach reflects a nonlinear dynamic and complex view of behavior, with a stronger emphasis on social context. ...
In the early 1970s, both my academic career and the psychology subdiscipline within kinesiology began as "social psychology and physical activity. "Since then, sport and exercise psychology research has shifted away from the social to a narrower biopsycho-(no social) approach, and professional practice has focused on the elite rather than the larger public. Psychology can contribute to an integrative and relevant professional discipline by going back to the future as social psychology and physical activity and by incorporating three of C. H. McCloy's themes (a) evidence-based practice, (b) beyond dualisms, and (c) commitment to public service. Our scholarship must move beyond dualisms to recognize complexities and connections and be truly scholarship for practice. Social psychology and physical activity can serve the public by advocating for inclusive, empowering physical activity programs that promote health and well being for all.
Die Umweltepigenetik erforscht, wie sich Umweltfaktoren auf die Expression des Genoms auswirken und damit auf Körper, Gesundheit und Krankheit. Dabei geht es um den Einfluss materieller Faktoren, wie etwa von Umweltgiften und Nahrungsmitteln, aber auch darum, wie soziale Erfahrungen die Genexpression verändern können. Die Umweltepigenetik konzipiert den Körper damit als ‚biosozial‘ und schafft Möglichkeitsräume, um die Auswirkungen unterschiedlicher Lebensumwelten auf die Biologie des Körpers zu untersuchen. Am Beispiel von Experimenten, die die epigenetischen Effekte ‚mütterlicher Fürsorge‘ erforschen, untersucht dieser Artikel die Potentiale, aber auch die Herausforderungen einer solchen epigenetischen Perspektive auf den Körper. Der Artikel zeigt, dass trotz eines Aufweichens der Grenzen zwischen Biologie und Sozialem traditionelle Kategorien sozialer Differenz, wie etwa Geschlecht und Schichtzugehörigkeit, häufig überraschend statisch und deterministisch gefasst werden.
Abstract: An inchoate yet sanguine picture is emerging for a more brain-related epiphenomenal foundation for the understanding and treatment of psychiatric disorders. We review germane advances and impediments in this regard. Encouraging findings in tracking certain anomalous genetic conditions from their origins to effects on neurological structures and functions (strong biologism) are discussed; findings from neuroimaging research are likewise noteworthy, but the search continues for delineation of pathological biomarkers from neuroimaging data. The nature of genetic mediation of adverse environmental effects on the brain and behavior are beginning to be understood in relation to the expanding area of epigenetics. We opine that an extant synthesis of neurobiological and epigenetic information warrants serious and increasing dialogue regarding biologically
based diagnoses, treatments, and preventive strategies.
Keywords: Strong biologism · Psychiatric diagnoses · Environmental and genetic determinants · Epigenetics
This paper considers whether expanding access to center-based early childhood education (ECE) will reduce economic inequality later in life. A strong evidence base indicates that ECE is effective at improving young children's academic skills and human capital development. We review evidence that children from low-income families have lower rates of preschool enrollment than their more affluent peers. Our analysis indicates that increasing enrollments for preschoolers in the year before school entry is likely to be a worthy investment that will yield economic payoffs in the form of increased adult earnings. The benefits of even a moderately effective ECE program are likely to be sufficient to offset the costs of program expansion, and increased enrollment among low-income children may reduce later economic inequality.
The incidence of global obesity and Type 2 diabetes has increased and is predicted to rise to 30% of the global population. Diet and lifestyle factors are incapable to resolve the increased incidence for obesity and diabetes in various populations of the world. Developing countries have come to the forefront because of the higher diabetic
epidemic. The urbanization may possibly provide an explanation for the global diabetic epidemic. In Western countries the metabolic syndrome and non alcoholic fatty liver disease (NAFLD) have reached 30 % of the population and now at present NAFLD afflicts 20% of developing populations. Western diets and sedentary lifestyles cause metabolic
disorders in developing countries which may increase neurodegenerative diseases by the disrupted metabolism of xenobiotics in urban populations. In developing countries access to high calorie diets in urban areas down regulate liver nuclear receptors that are responsible for glucose, lipid and toxicological sensing and interrupt the metabolism
of xenobiotics that become toxic to various tissues such as the pancreas, heart, kidney, brain and liver. Xenobiotics in urban areas induce epigenetic changes that involve chromatin remodelling by alterations in transcriptional regulators with modification of histones. Dysfunction of nuclear receptors such as the calorie sensitive sirtuin 1
(Sirt 1) gene involves abnormal nutrient metabolism with insulin resistance, NAFLD, energy balance and circadian rhythm disorders. In obesity and diabetes insulin resistance has been connected to poor xenobiotic metabolism with the toxic affects of increased xenobiotic transport to the brain associated with neurodegeneration. Dietary
interventions to increase xenobiotic metabolism are likely to reduce oxidative stress and neuroendocrine disease in developing countries. Prevention programs are an important goal of international health organizations and in developing countries the plans to adapt a healthy diet, active lifestyle and reduced exposure to xenobiotics are important to manage the global epidemic for obesity and diabetes.
This paper provides an overview of historical and current standard scientific practices for investigating the evolution of behavior. I argue that Evolutionary Psychology (EP) ignores its historical precedents—ethology and the instinct critics—and while acknowledging current perspectives—epigenetics and developmental systems theories—does so only in terms of lip service. In particular, EP does not investigate the dynamic interplay between genes and context that is essential for understanding the development and evolution of behavior. Thus, EP does not conform to the rigorous standards of biology or psychology, is often unresponsive to methodological critiques, skirts theoretical controversies, and is disconnected from a large body of scholarship on issues surrounding the evolution of behavior.
Researchers have become increasingly interested in uncovering how genetic factors work together with the peer environment in influencing development. This article offers an overview of the state of knowledge. It first describes the different types of gene‐environment correlations (rGE) and gene‐environment interactions (GxE) that are of relevance for understanding the role of peer relations as well as the two main methodologies of genetically informed research, that is, the quantitative genetic approach and molecular genetics. This is followed by an overview of recent studies that examined different mechanisms of gene‐environment interplay involving peer relations in childhood and adolescence. The article concludes with an outline of future directions in genetically informed peer relations research as well as the implications for theory and practice.
In the early 1970s, both my academic career and the psychology subdiscipline within kinesiology began as “social psychology and physical activity.” Since then, sport and exercise psychology research has shifted away from the social to a narrower bio-psycho-(no social) approach, and professional practice has focused on the elite rather than the larger public. Psychology can contribute to an integrative and relevant professional discipline by going back to the future as social psychology and physical activity and by incorporating three of C. H. McCloy's themes (a) evidence-based practice, (b) beyond dualisms, and (c) commitment to public service. Our scholarship must move beyond dualisms to recognize complexities and connections and be truly scholarship for practice. Social psychology and physical activity can serve the public by advocating for inclusive, empowering physical activity programs that promote health and well being for all.
The now-classic article "What Is Temperament? Four Approaches" by H. H. Goldsmith et al. (1987) brought together originators of four prominent temperament theories—Rothbart, Thomas and Chess, Buss and Plomin, and Goldsmith—to address foundational questions about the nature of temperament. This article reviews what has been learned about the nature of temperament in the intervening 25 years, It begins with an updating of the 1987 consensus definition of temperament that integrates more complex current findings. Next, 4 "progeny" trained in the original temperament traditions assess contributions of their respective approaches. The article then poses essential questions for the next generation of research on the fundamentals of temperament, including its structure, links with personality traits, interaction with context, and change and continuity over time.
Objective. There is growing recognition that antisocial behaviors are produced by a combination of environmental and genetic factors. Research has revealed that environmental and genetic factors work interactively and often moderate the effects of the other. Method. We test for gene–environment interactions in the current study by examining whether neighborhood disadvantage interacts with two dopamine receptor genes (DRD2 and DRD4) to predict three different antisocial measures: adolescent victimization, contact with delinquent peers, and involvement in violent delinquency. Results. Analysis of male respondents drawn from the National Longitudinal Study of Adolescent Health revealed that the association between the two dopamine genes and the measures of antisocial outcomes tended to be stronger in disadvantaged neighborhoods. Conclusions. Antisocial outcomes appear to be affected by gene–environment interactions between dopaminergic genes and neighborhood disadvantage.
The present chapter deals with a variety of topics related to causality. In the last four chapters, I focused on brain processes, especially related to hemispheric specialization, and on systems theory. In this chapter and the next, I examine epigenesis. Before beginning, I touch on the question of causality, in general. It has a storied history, and Aristotle proposed a classic model of four causes. The model is still referred to, and the study of causality is still important in philosophy (Beebee, Hitchcock, & Menzies, 2009). Tinbergen (1963) proposed a powerful model of causation also involving four types. It includes developmental processes, and is quite applicable to the present work. In contrast, the Aristotelian model has led to differing applications in psychology, and until there is a standard understanding of its pertinence, it is best to use more contemporary models. The present work adopts a biopsychosocial and relational metaframe in understanding behavior, and these types of models can integrate Tinbergen’s four questions and expand upon them. As for even more general models, I refer to the four forces in physics and draw parallels with different levels of coherence in sociality, in particular.
An important challenge for the Department of Defense (DOD) science and technology (S&T) programs is to avoid technological surprise resulting from the exponential increase in the pace of discovery and change in S&T worldwide. The nature of the military threat is also changing, resulting in new military requirements, some of which can be met by technology. Proper shaping of the S&T portfolio requires predicting and matching these two factors well into the future. Some examples of technologies which have radically affected the battlefield include the Global Positioning System coupled with inexpensive hand held receivers, the microprocessor revolution which has placed the power of the Internet and satellite communications into the hands of soldiers in the field, new sensing capabilities such as night vision, the use of unmanned vehicles, and composite materials for armor and armaments. Some of these new technologies came from military S&T, some from commercial developments and still others from a synthesis of the two sectors; but all were based on advances in the underlying sciences. Clearly, leaders and planners in military S&T must keep abreast of such developments and look ahead as best they can. Since World War II, predictions of S&T for enabling military capabilities have occurred periodically. A study chartered by the Army Air Force1 in 1947 predicted a broad range of developments in aeronautics and air power, and the study process has been a model for such forecasts ever since. Projections in S&T have been issued for many years by the National Research Council (NRC) of the National Academies, and the NRC occasionally publishes decadal studies for specific disciplines. NRC committee reports for astronomy and astrophysics, for example, go back every 10 years to at least 1964.
Recent years have seen an explosion of biologically based studies, interventions, and explanations for most mental disorders. Indeed, the mantra that mental disorders are brain disorders is frequently stated and certainly is at least partially true. Yet, the current landslide of information, produced with new extraordinary technologies, has resulted in limited clarity. The area of mental disorders remains laden with deficient, contradictory, and unproven explanations and treatments. One common rationale for this state is the failure to translate new scientific findings into practise. A more defensible and encompassing explanation focuses on the very basic conceptualizations and definitions of these disorders. Patently powerful methodologies can be no better or worse than the clarity of the problems under study. Numerous examples of definitional and diagnostic problems exist that have led to the lack of clarity and application of research findings. Alternative research strategies are discussed with a focus on the high-risk paradigm. A series of studies of a single characteristic of individuals at risk for problems with alcohol is presented. (PsycINFO Database Record (c) 2012 APA, all rights reserved)
We systematically mistreat psychological phenomena, both logically and clinically. This article explores three contentions: that the dominant discourse in modern cognitive, affective, and clinical neuroscience assumes that we know how psychology/biology causation works when we do not; that there are serious intellectual, clinical, and policy costs to pretending we do know; and that crucial scientific and clinical progress will be stymied as long as we frame psychology, biology, and their relationship in currently dominant ways. The arguments are developed with emphasis on misguided attempts to localize psychological function via neuroimaging, misunderstandings about the role of genetics in psychopathology, and unfortunate constraints on health-care policy and clinical service delivery. A particular challenge, articulated but not resolved in this article, is determining what constitutes adequate explanation in the relationship between psychology and biology.
The three-way connection between DNA methylation, gene activity and chromatin structure has been known for almost two decades. Nevertheless, the molecular link between methyl groups on the DNA and the positioning of nucleosomes to form an inactive chromatin configuration was missing. This review discusses recent experimental data that may, for the first time, shed light on this molecular link. MeCP2, which is a known methylcytosine-binding protein, has been shown to possess a transcriptional repressor domain (TRD) that binds the corepressor mSin3A. This corepressor protein constitutes the core of a multiprotein complex that includes histone deacetylases (HDAC1 and HDAC2). Transfection and injection experiments with methylated constructs have revealed that the silenced state of a methylated gene, which is associated with a deacetylated nucleosomal structure, could be relieved by the deacetylase inhibitor, trichostatin A. Thus, methylation plays a pivotal role in establishing and maintaining an inactive state of a gene by rendering the chromatin structure inaccessible to the transcription machinery.
In a prospective-longitudinal study of a representative birth cohort, we tested why stressful experiences lead to depression
in some people but not in others. A functional polymorphism in the promoter region of the serotonin transporter (5-HT T) gene
was found to moderate the influence of stressful life events on depression. Individuals with one or two copies of the short
allele of the 5-HT T promoter polymorphism exhibited more depressive symptoms, diagnosable depression, and suicidality in
relation to stressful life events than individuals homozygous for the long allele. This epidemiological study thus provides
evidence of a gene-by-environment interaction, in which an individual's response to environmental insults is moderated by
his or her genetic makeup.
Here we report that increased pup licking and grooming (LG) and arched-back nursing (ABN) by rat mothers altered the offspring epigenome at a glucocorticoid receptor (GR) gene promoter in the hippocampus. Offspring of mothers that showed high levels of LG and ABN were found to have differences in DNA methylation, as compared to offspring of 'low-LG-ABN' mothers. These differences emerged over the first week of life, were reversed with cross-fostering, persisted into adulthood and were associated with altered histone acetylation and transcription factor (NGFI-A) binding to the GR promoter. Central infusion of a histone deacetylase inhibitor removed the group differences in histone acetylation, DNA methylation, NGFI-A binding, GR expression and hypothalamic-pituitary-adrenal (HPA) responses to stress, suggesting a causal relation among epigenomic state, GR expression and the maternal effect on stress responses in the offspring. Thus we show that an epigenomic state of a gene can be established through behavioral programming, and it is potentially reversible.
Transgenerational effects of environmental toxins require either a chromosomal or epigenetic alteration in the germ line.
Transient exposure of a gestating female rat during the period of gonadal sex determination to the endocrine disruptors vinclozolin
(an antiandrogenic compound) or methoxychlor (an estrogenic compound) induced an adult phenotype in the F1 generation of decreased spermatogenic capacity (cell number and viability) and increased incidence of male infertility. These
effects were transferred through the male germ line to nearly all males of all subsequent generations examined (that is, F1 to F4). The effects on reproduction correlate with altered DNA methylation patterns in the germ line. The ability of an environmental
factor (for example, endocrine disruptor) to reprogram the germ line and to promote a transgenerational disease state has
significant implications for evolutionary biology and disease etiology.
Monozygous twins share a common genotype. However, most monozygotic twin pairs are not identical; several types of phenotypic discordance may be observed, such as differences in susceptibilities to disease and a wide range of anthropomorphic features. There are several possible explanations for these observations, but one is the existence of epigenetic differences. To address this issue, we examined the global and locus-specific differences in DNA methylation and histone acetylation of a large cohort of monozygotic twins. We found that, although twins are epigenetically indistinguishable during the early years of life, older monozygous twins exhibited remarkable differences in their overall content and genomic distribution of 5-methylcytosine DNA and histone acetylation, affecting their gene-expression portrait. These findings indicate how an appreciation of epigenetics is missing from our understanding of how different phenotypes can be originated from the same genotype.
• DNA methylation
• epigenetics
• histones
Stress responses in the adult rat are programmed early in life by maternal care and associated with epigenomic marking of the hippocampal exon 1(7) glucocorticoid receptor (GR) promoter. To examine whether such epigenetic programming is reversible in adult life, we centrally infused the adult offspring with the essential amino acid L-methionine, a precursor to S-adenosyl-methionine that serves as the donor of methyl groups for DNA methylation. Here we report that methionine infusion reverses the effect of maternal behavior on DNA methylation, nerve growth factor-inducible protein-A binding to the exon 1(7) promoter, GR expression, and hypothalamic-pituitary-adrenal and behavioral responses to stress, suggesting a causal relationship among epigenomic state, GR expression, and stress responses in the adult offspring. These results demonstrate that, despite the inherent stability of the epigenomic marks established early in life through behavioral programming, they are potentially reversible in the adult brain.
Variations in maternal behavior are associated with differences in estrogen receptor (ER)-alpha expression in the medial preoptic area (MPOA) and are transmitted across generations such that, as adults, the female offspring of mothers that exhibit increased pup licking/grooming (LG) over the first week postpartum (i.e. high LG mothers) show increased ERalpha expression in the MPOA and are themselves high LG mothers. In the present studies, cross-fostering confirmed an association between maternal care and ERalpha expression in the MPOA; the biological offspring of low LG mothers fostered at birth to high LG dams show increased ERalpha expression in the MPOA. Cross-fostering the biological offspring of high LG mothers to low LG dams produces the opposite effect. We examined whether the maternal programing of ERalpha expression is associated with differences in methylation of the relevant ERalpha promoter. Levels of cytosine methylation across the ERalpha1b promoter were significantly elevated in the adult offspring of low, compared with high, LG mothers. Differentially methylated regions included a signal transducer and activator of transcription (Stat)5 binding site and the results of chromatin immunoprecipitation assays revealed decreased Stat5b binding to the ERalpha1b promoter in the adult offspring of low, compared with high, LG mothers. Finally, we found increased Stat5b levels in the MPOA of neonates reared by high, compared with low, LG mothers. These findings suggest that maternal care is associated with cytosine methylation of the ERalpha1b promoter, providing a potential mechanism for the programming of individual differences in ERalpha expression and maternal behavior in the female offspring.
Alterations in gene expression in the suicide brain have been reported and for several genes DNA methylation as an epigenetic regulator is thought to play a role. rRNA genes, that encode ribosomal RNA, are the backbone of the protein synthesis machinery and levels of rRNA gene promoter methylation determine rRNA transcription.
We test here by sodium bisulfite mapping of the rRNA promoter and quantitative real-time PCR of rRNA expression the hypothesis that epigenetic differences in critical loci in the brain are involved in the pathophysiology of suicide. Suicide subjects in this study were selected for a history of early childhood neglect/abuse, which is associated with decreased hippocampal volume and cognitive impairments. rRNA was significantly hypermethylated throughout the promoter and 5' regulatory region in the brain of suicide subjects, consistent with reduced rRNA expression in the hippocampus. This difference in rRNA methylation was not evident in the cerebellum and occurred in the absence of genome-wide changes in methylation, as assessed by nearest neighbor.
This is the first study to show aberrant regulation of the protein synthesis machinery in the suicide brain. The data implicate the epigenetic modulation of rRNA in the pathophysiology of suicide.
In animal models, variations in early maternal care are associated with differences in hypothalamic-pituitary-adrenal(HPA) stress response in the offspring, mediated via changes in the epigenetic regulation of glucocorticoid receptor (GR) gene (Nr3c1) expression.
To study this in humans, relationships between prenatal exposure to maternal mood and the methylation status of a CpG-rich region in the promoter and exon 1F of the human GR gene (NR3C1) in newborns and HPA stress reactivity at age three months were examined.
Prenatal exposure to increased third trimester maternal depressed/anxious mood was associated with increased methylation of NR3C1 at a predicted NGFI-A binding site. Increased NR3C1 methylation at this site was also associated with increased salivary cortisol stress responses at 3 months, controlling for prenatal SRI exposure, postnatal age and pre and postnatal maternal mood.
The methylation status of a CpG-rich region of the NR3C1 gene, including exon 1F, in genomic DNA from cord blood mononuclear cells was quantified by bisulfite pyrosequencing in infants of depressed mothers treated with a serotonin reuptake inhibitor antidepressant (SRI) (n = 33), infants of depressed nontreated mothers (n = 13) and infants of non depressed/non treated mothers (n = 36). To study the functional implications of the newborn methylation status of NR3C1 in newborns, HPA function was assessed at three months using salivary cortisol obtained before and following a non noxious stressor and at a late afternoon basal time.
Methylation status of the human NR3C1 gene in newborns is sensitive to prenatal maternal mood and may offer a potential epigenetic process that links antenatal maternal mood and altered HPA stress reactivity during infancy.
Childhood maltreatment elevates risk for antisocial behavior, depression, and other problems over the life span, but a subset of maltreated individuals avoids maladaptive development and shows resilience. Resilience reflects a dynamic confluence of factors that promotes positive adaptation despite exposure to adverse experiences. Recent replicated findings of gene-environment interactions (abbreviated G × E) involving maltreatment have identified two genes, monoamine oxidase A (MAOA) and serotonin transporter (5-HTT), that moderate the association between childhood maltreatment and psychopathology. Accordingly, G × E raise new questions about potential biological mechanisms by which some individuals are able to cope adaptively and function relatively well despite experiencing early adversity. We summarize advances toward greater specification of G × E mechanisms, including genetic and environmental moderation of G × E effects and imaging genomics that provide clues regarding resilience processes in development.
Relationships between genes and social behavior have historically been construed as a one-way street, with genes in control. Recent analyses have challenged this view by discovering broad alterations in the expression of human genes as a function of differing socio-environmental conditions. The emerging field of social genomics has begun to identity the types of genes subject to social regulation, the biological signaling pathways mediating those effects, and the genetic polymorphisms that moderate socio-environmental influences on human gene expression.
When scientists opened up the human genome, they expected to find the genetic components of common traits and diseases. But they were nowhere to be seen. Brendan Maher shines a light on six places where the missing loot could be stashed away.
Prenatal stress is associated with an increased vulnerability to neurodevelopmental disorders, including autism and schizophrenia. To determine the critical time window when fetal antecedents may induce a disease predisposition, we examined behavioral responses in offspring exposed to stress during early, mid, and late gestation. We found that male offspring exposed to stress early in gestation displayed maladaptive behavioral stress responsivity, anhedonia, and an increased sensitivity to selective serotonin reuptake inhibitor treatment. Long-term alterations in central corticotropin-releasing factor (CRF) and glucocorticoid receptor (GR) expression, as well as increased hypothalamic-pituitary-adrenal (HPA) axis responsivity, were present in these mice and likely contributed to an elevated stress sensitivity. Changes in CRF and GR gene methylation correlated with altered gene expression, providing important evidence of epigenetic programming during early prenatal stress. In addition, we found the core mechanism underlying male vulnerability may involve sex-specific placenta responsivity, where stress early in pregnancy significantly increased expression of PPARalpha (peroxisome proliferator-activated receptor alpha), IGFBP-1 (insulin-like growth factor binding protein 1), HIF3alpha (hypoxia-inducible factor 3a), and GLUT4 (glucose transporter 4) in male placentas but not females. Examination of placental epigenetic machinery revealed basal sex differences, providing further evidence that sex-specific programming begins very early in pregnancy, and may contribute to the timing and vulnerability of the developing fetus to maternal perturbations. Overall, these results indicate that stress experience early in pregnancy may contribute to male neurodevelopmental disorders through impacts on placental function and fetal development.
Naturally occurring variations in maternal care alter the expression of genes that regulate behavioral and endocrine responses to stress, as well as hippocampal synaptic development. These effects form the basis for the development of stable, individual differences in stress reactivity and certain forms of cognition. Maternal care also influences the maternal behavior of female offspring, an effect that appears to be related to oxytocin receptor gene expression, and which forms the basis for the intergenerational transmission of individual differences in stress reactivity. Patterns of maternal care that increase stress reactivity in offspring are enhanced by stressors imposed on the mother. These findings provide evidence for the importance of parental care as a mediator of the effects of environmental adversity on neural development.
To test for differential effects of early environment on the problem-solving of bright and dull rats, a group of each was reared in an "enriched" environment and in an "unstimulating" one. Bright and dull control animals were reared under usual laboratory conditions. As tested by the Hebb-Williams maze, enrichment facilitated learning ability in dull rats, but not bright ones. A restricted environment markedly handicapped members of the bright strain, but produced no impairment in the dull group. A neurophysiological explanation is suggested.
Epidemiological studies suggest that environmental adversity can alter parental care and thus influence child development. We addressed the question of whether stressors can directly affect parental behavior using a rodent model of stable, individual differences in maternal behavior.
Lactating rat mothers were characterized as high or low in pup-directed licking/grooming (LG) behavior, rebred, and subjected to 7 days of intermittent stress or control conditions during gestation. Female rats were mated a third time without any subsequent intervention. Maternal behavior, oxytocin receptor (OTR) binding, and offspring behavior were examined.
Stress reduced OTR levels and pup LG of high LG mothers to levels comparable with those of low LG mothers. The adult offspring of the gestational stress/high LG mothers resembled those of low LG mothers on behavioral measures of anxiety and maternal behavior, as well as OTR levels. The results of the third mating revealed an enduring effect of gestational stress on both mother and offspring maternal LG.
These findings suggest that stress can directly alter maternal care through the neuroendocrine systems that normally regulate this behavior. Thus, the effects of environmental adversity can be transmitted across generations through a nongenomic mechanism involving maternal care.
Monozygotic (MZ) twin concordance for a range of psychiatric conditions is rarely 100%. It has been suggested that epigenetic factors, such as DNA methylation, may account for a proportion of the variation in behavioral traits observed between these genetically identical individuals. In this study we have quantitatively assessed the methylation status of two CpG sites in the promoter region of the COMT gene in 12 MZ twins-pairs discordant for birth weight, but otherwise clinically unaffected. DNA was obtained at age 5-years using buccal swabs, and modified using sodium-bisulfite treatment. Methylation profiles were assessed using Pyrosequencing, a technology enabling the precise degree of methylation to be assessed at any CpG site. We found that the degree of methylation at the two CpG sites was highly correlated, but there was considerable variation in the concordance of methylation levels between MZ twin-pairs. Some MZ twin-pairs showed a high degree of methylation concordance, whereas others differed markedly in their methylation profiles. Such epigenetic variation between genetically identical individuals may play a key role in the etiology of psychopathology, and explain the incomplete phenotypic concordance observed in MZ twins.
DNA methylation is a covalent chemical modification of DNA catalyzed by DNA methyltransferases (DNMTs). DNA methylation is associated with transcriptional silencing and has been studied extensively as a lifelong molecular information storage mechanism put in place during development. Here we report that DNMT gene expression is upregulated in the adult rat hippocampus following contextual fear conditioning and that DNMT inhibition blocks memory formation. In addition, fear conditioning is associated with rapid methylation and transcriptional silencing of the memory suppressor gene PP1 and demethylation and transcriptional activation of the synaptic plasticity gene reelin, indicating both methyltransferase and demethylase activity during consolidation. DNMT inhibition prevents the PP1 methylation increase, resulting in aberrant transcription of the gene during the memory-consolidation period. These results demonstrate that DNA methylation is dynamically regulated in the adult nervous system and that this cellular mechanism is a crucial step in memory formation.
Epidemiological evidence increasingly suggests that environmental exposures early in development have a role in susceptibility to disease in later life. In addition, some of these environmental effects seem to be passed on through subsequent generations. Epigenetic modifications provide a plausible link between the environment and alterations in gene expression that might lead to disease phenotypes. An increasing body of evidence from animal studies supports the role of environmental epigenetics in disease susceptibility. Furthermore, recent studies have demonstrated for the first time that heritable environmentally induced epigenetic modifications underlie reversible transgenerational alterations in phenotype. Methods are now becoming available to investigate the relevance of these phenomena to human disease.
Cross-fostering studies in the rat have illustrated the importance of the postnatal environment in mediating the transmission of maternal licking/grooming (LG) from mother to offspring. The authors addressed the question of how postweaning social conditions can alter the patterns of maternal behavior. Juvenile female offspring of high LG and low LG mothers were placed in either standard, enriched, or impoverished postweaning environments for 50 consecutive days and then mated and observed with their own litters. Analysis of LG behavior indicated that the effect of postweaning environment was dependent on the level of postnatal mother-infant interaction. Postweaning isolation reduced exploratory behavior, maternal LG, and oxytocin receptor binding in the offspring of high LG mothers, whereas social enrichment enhanced exploration, LG behavior, and oxytocin receptor binding of low LG offspring. These effects were also transmitted to the next generation of offspring. Thus, maternal LG and the neural mechanisms that regulate this behavior exhibited a high degree of plasticity in response to changes in environment both within and beyond the postnatal period, with implications for the transmission of behavioral response to novelty and maternal care across generations.
The transmission of traits across generations has typically been attributed to the inheritance by offspring of genomic information from parental generations. However, recent evidence suggests that epigenetic mechanisms are capable of mediating this type of transmission. In the case of maternal care, there is evidence for the behavioral transmission of postpartum behavior from mothers to female offspring. The neuroendocrine and molecular mediators of this transmission have been explored in rats and implicate estrogen-oxytocin interactions and the differential methylation of hypothalamic estrogen receptors. These maternal effects can influence multiple aspects of neurobiology and behavior of offspring and this particular mode of inheritance is dynamic in response to environmental variation. In this review, evidence for the generational transmission of maternal care and the mechanisms underlying this transmission will be discussed as will the implications of this inheritance system for offspring development and for the transmission of environmental information from parents to offspring.