The Emotional Foundations of Personality

by Kenneth L Davis

  MODERN GENETICS, EPIGENETICS, AND THE HERITABILITY OF PERSONALITY TRAITS

  We have already noted how investigators have been able to select for a variety of emotional-personality traits in animals (see Chapters 8–10). During the past half century, one of the most remarkable scientific achievements has been an in-depth understanding of the genetic foundations of our human nature, which is remarkably similar to that of all other mammals, with clear relationships as we go further down the evolutionary ladder or, more correctly, into the thickets of the evolutionary bush. Although it was once thought that we had at least a hundred thousand genes, with improvements in technology it fell to less than a quarter of that. Still, for most of our DNA, which contains more than 3 billion base pairs, only a small fraction are protein-coding sequences, with lots of pseudogenes (or junk DNA, as some called it) whose functions are not known, perhaps much of it being nonfunctional residues from the past, although some may facilitate protein synthesis by participating in gene regulation and expression (for a more detailed discussion, see Pennisi, 2012).

  According to current estimates, there are at least twenty-two thousand human protein-coding genes, with the first draft of the human genome published on February 12, 2001 (and refined considerably since then, with the genomes of many individual humans being added to the library). This has opened up the Pandora’s box of estimating the genetic contributions to many human/animal traits. Indeed, investigators are finally beginning to seek the genetic sources of various psychological traits, including the foundations of the various personality dimensions we have been discussing. We also note that the remarkable similarities in genomes across mammalian species again coaxes us to accept that we share many similarities with other mammals, including our emotional foundations, which need to be integrated into the human sciences (e.g., Panksepp et al., 2016). Indeed, genetic research on emotional traits, including personality dimensions in animals, may help clarify the foundations of our own temperamental nature. It is becoming ever clearer that certain personality traits can be inherited, and not simply from the specific genes one inherits but also by the transmission of the environmentally induced epigenetic changes in our genomes.

  This story gets very complex when we consider that there are various epigenetic mechanisms that control the extent to which individual genes are expressed. During development, diverse environmental experiences, including drugs, sex, and many other life experiences, can modify the intensity of gene expressions. Remarkably, these epigenetic factors can tune our genetic orchestras to better fit the environments in which we live, and they can lead to personality changes as well as mental health issues—from increased resilience to troublesome emotional imbalances, often so extreme as to be considered psychiatric problems.

  One of the great surprises of the epigenetic revolution of the past decade is the diverse ways gene regulation can be modified indirectly by environmental events (i.e., without changing the genetic code itself), and many of these effects can be passed from parents to children. In a manner of speaking, the “sins” and vicissitudes of parents can epigenetically affect their children, while positive emotional support can facilitate thriving. For instance, child abuse can leave epigenetically induced emotional scars, while well-tuned, devoted parenting can promote resilience in children. There is abundant work ranging from autism to attention-deficit hyperactive disorder (Panksepp, 2007b, 2008b) highlighting the possible long-term neurobiological consequences of rearing.

  GENE REGULATION: PATHS TO BEHAVIORAL AND PERSONALITY TRAITS

  The genetic and neuroscience revolutions of the past century have been the most seminal events in understanding our fundamental nature and our place in the living order. To reiterate, since 1953, the year the structure of DNA was decoded, genetic knowledge has touched all aspects of living creatures, including the sources of human and animal personalities. With the genetic revolution, we now have great assurance that the recipe for life is very similar across all mammals, indeed, all species. To a substantial degree all personality traits are heritable, with many linked to the genes we inherit and many others linked to the ability of our gene expression patterns to change dynamically, based on epigenetics. One of the most exciting outgrowths of the modern genetic revolution is the illumination of how epigenetics (inherited and/or acquired) can impact the emotional-affective foundations of personality (for a superb review, see Weaver, 2014). The view of simple genetic determinism has been replaced with the understanding that inheritance is no longer as predetermined as it was once thought to be. Genetic science has finally revealed the joint roles of nature and nurture in guiding who we are and who we can become. And in personality theory, ruthless biological reductionism needs now to be supplemented with novel forms of environmental relativism.

  In brief, the variety in the DNA sequences of our reproductive cells, called single nucleotide polymorphisms (SNPs, pronounced “snips”), provides diverse avenues for genetic changes. When rare and deleterious, they are typically called mutations, but when common (e.g., promoting trait variability), they are called SNPs. When transmitted to children, these variations can fine-tune the underlying emotional/affective tools for living that control personality styles—both strengths and weaknesses. A great number of SNPs have been discovered that contribute to behavioral and psychological effects, including various pathways to personality styles, psychobehavioral resilience, and susceptibility to mental/psychiatric disorders. There are genes that can control the intensity of people’s emotional traits, such as susceptibility to anger and aggression, through well-studied mechanisms, such as the intensity of serotonin transmission in the brain (Craig & Halton, 2009), and other genes may lead to psychopathic tendencies (for an intriguing, emotional autobiography of a famous scientist who discovered that he had inherited such tendencies, see Fallon, 2013). While many genetic variants promote very specific temperamental changes, others lead to pervasive, life-damaging progressions.

  THREE ROADS TO EPIGENETIC CONTROL OF PERSONALITY AND EMOTIONAL DISORDERS

  Beside the sequence of nucleotides of DNA and RNA that code for amino acids in proteins, there are three major epigenetic modes of transmission. A fact that is critical for understanding such processes is that DNA is tightly packaged in a chromatin matrix within the nucleus of all cells—in a sense, DNA strands are integrated within (“wound around”) a complex protein (histone and DNA) matrix that can control the extent to which DNA can be transcribed into proteins. There are three main ways that the extent of protein synthesis can be controlled: (1) the interaction of histones with DNA can be modified in various ways (e.g., histone acetylation or deacetylation), effecting rates of gene expression; (2) the chromatin matrix can be remodeled so as to modify various gene transcription factors; and (3) direct DNA methylation that can be a highly stable influence on gene expression. Each of these epigenetic regulatory processes can last a lifetime and change the intensity with which translation of DNA to RNA and ultimately protein synthesis can proceed, without any change in the DNA code itself. Thus, from a functional brain perspective, epigenetics has revealed that various factors contribute to neural development and plasticity, which ultimately can impact diverse brain processes, including the affective-emotional networks that undergird the major global personality dimensions that psychologists and neuroscientists study.

  Let us consider an example: a rare childhood disorder called Rett’s syndrome, characterized by Andreas Rett, a pediatrician in Vienna who first published his observations in 1966. Rett’s syndrome, once thought to be an autistic spectrum disorder, typically inflicts girls, with the first symptoms, appearing at about a year of age, being loss of coherent hand movements, loss of language and social skills, and cognitive delays. Such children, doomed to a rapid regression of initial development, have severe life-long behavioral and psychological problems, including disturbing emotional symptoms, such as inconsolable crying, screaming fits, and avoidance of social contact, combined with impaired motor coordination.

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bsp; This tragic disorder, with a prevalence of about 1 in 10,000 births, arises from a genetic abnormality of a specific gene, MECP2 (methyl CpG-binding protein 2). Amir et al. (1999) discovered that most of the problems in Rett’s syndrome arose from the dysfunction of this gene, whose protein product is essential for the broad regulation of the expression of various genes—this one gene plays a critical role in the epigenetic regulation of gene expressions that promote maturation. Thus, a pervasive developmental disorder emerges when this gene is dysfunctional. It is currently believed that correction of epigenetic changes in such children at an early age may prevent progression of the disorder (for a fuller description of the varieties of such developmental disorders, see Peterson and Panksepp, 2004).

  A second example is the increasing evidence for epigenetic mechanisms in the development of substance abuse, for example, cocaine addiction. Coca leaves have been chewed by South American Andean natives for at least three thousand years (Biondich & Joslin, 2016), but use of whole leaves does not produce dependence, as indicated by the development of tolerance or withdrawal symptoms (Weil, 1981). However, the chemical isolation of cocaine from the leaves led to what has become a drug of abuse, with vulnerability to addiction determined roughly half by genetic and half by nongenetic factors (Nestler, 2014).

  The ancestral roots of cocaine’s dopaminergic reward properties have been confirmed by demonstrating cocaine-induced conditioned place preference in crayfish (Panksepp & Huber, 2004), an invertebrate species predating humans by 600 million years. It is likely that cocaine addiction, both in humans and as studied experimentally in rodents, incorporates such evolutionarily conserved brain substrates for reward, which are embedded within motivational subcortical brain systems shared homologously by all mammals. Better understanding the cross-species affective reward properties of our primary emotions is essential for understanding the motivational and behavioral changes associated with addiction, as well as exploring potential treatments for such emotional imbalances.

  One of the dangers of cocaine use is the relatively rapid onset of addiction, with about 5 percent of first-time cocaine users becoming addicted by a 24-month follow-up (O’Brien & Anthony, 2005). Cocaine addiction is further characterized by drug craving and relapses—despite severe physical and social consequences—that can persist for a lifetime and outlast long periods of abstinence, suggesting the occurrence of long-lasting changes in the brain, including evidence for changes in gene expression (Robison & Nestler, 2011).

  As discussed above, chromatin consists of DNA and the histone proteins that DNA is tightly coiled around. Histone acetylation allows the chromatin structure to relax and thereby facilitates gene expression. Based on the study of mouse models, it is widely thought that chromatin modification is central to the epigenetic brain changes observed in drug addiction (for a readable review, see McQuown & Wood, 2010). An acute dose of cocaine induces a process of increased histone acetylation that is balanced by corresponding deacetylation and reverts to control levels within three hours. Elevated increases in histone acetylation induced by the inhibition of histone deacetylase enzymes increase the rewarding effects of cocaine, as demonstrated by enhanced conditioned place preference even at low cocaine doses. Conversely, experimentally induced overexpression of histone deacetylase enzymes dramatically decreases cocaine’s rewarding properties, as measured by conditioned place preference, providing further support that histone acetylation and deacetylation mechanisms promote the reward and behavioral changes associated with cocaine addiction (Kumar et al., 2005). Importantly, it is through chronic, not acute, cocaine exposure that a complex epigenetic process emerges, dramatically reducing histone deacetylation and providing a major mechanism for increasing the rewarding properties and associated behavior changes of cocaine addiction. Thus, the behavioral and reward changes observed in cocaine addiction may largely be the result of reducing histone deacetylation rather than directly increasing histone acetylation (Renthal et al., 2007). Eventually, such findings may lead to new treatments able to “undo” the epigenetic changes of cocaine addiction.

  BEHAVIORAL, EMOTIONAL, AND PSYCHIATRIC EPIGENETICS

  Perhaps the most extensive animal research in behavioral epigenetics is the work of Michael Meaney’s group at McGill University (e.g., Anacker, O’Donnell, & Meaney, 2014; Turecki & Meaney, 2016). The findings are straightforward: Rat mothers spend a lot of time licking and grooming their newborn pups during the first week of life. In general, pups that received abundant maternal touch exhibited resilience in a variety of behavioral situations, while those that did not were much more stress sensitive. Indeed, major epigenetic changes from lack of maternal care—altered expressions of a wide range of genes—were identified in neurons of the major stress axis of the brain: the hypothalamic-pituitary-adrenal system, which controls how well humans and animals can cope with a variety of environmental challenges. Such changes were clearly detrimental to young rats. Indeed, a remarkable aspect of the work lies in the demonstration that some of the adverse effects could be reversed in adulthood with pharmacological agents that could reverse early epigenetic changes (Weaver, Meaney, & Szyf, 2006).

  Such work has implications for understanding comparable processes in humans and other primates as highlighted in a special issue of the journal Hormones and Behavior (Fleming, Lévy & Lonstein, 2016) devoted to the effect of “external regulators” such as maternal care on infant physiology, especially brain development and the resulting socioemotional developmental changes that ensue, namely, “the negative long-term consequences of the absence of needed caregiving (e.g., neglect) or the presence of harmful/aversive caregiving (e.g., physical abuse)” that “are translatable across species” (Drury, Sánchez, & Gonzalez, 2016, p. 182). Clearly, there is a possibility for cross-species translations in how negative caregiving (child maltreatment) impacts many brain and bodily processes that can have lasting negative impact on mental and physical health.

  Such animal studies may have direct implications for optimal human childcare. For instance, Brody, Yu, Chen, Beach, and Miller (2016) have analyzed how negative family environments impacted diverse health issues, highlighting how parental depression when children are becoming adolescents (e.g., age eleven) can forecast accelerated epigenetic aging at age twenty, and how such deleterious effects could be ameliorated by a family-centered prevention program that sought to enhance supportive parenting and the explicit strengthening of family relationships. A total of almost four hundred families were studied, and the conclusion was that enhanced parenting guidance “can buffer the [negative] biological residue of life” (Brody et al., 2016, p. 567) in at-risk families.

  Although direct translations from animal infant care often do not translate directly to humans, licking and grooming in rats may have consequences similar to attentive loving touch in humans. Indeed, Pickles, Sharp, Hellier, and Hill (2017), who had previously shown that prenatal depression and anxiety were related to diminished maternal stroking of infants, with various negative child outcomes at 29 weeks and 2.5 years (Sharp et al., 2012), evaluated whether such effects could be replicated in a much larger sample. They reported “long-term [beneficial] effects of early maternal stroking” (p. 325) on child anxiety, depressive, and aggressive symptoms. No doubt there are many psychological mirroring processes in children, and one might expect that premature infants may be especially at risk for negative epigenetic modifications. In fact, Montirosso et al., (2016) documented how preterm infants may exhibit abnormal methylation of key genes: Not only did preemies exhibit elevated negative emotionality, but Montirosso et al. also observed changes in methylation patterns of the gene SLC6A4 that were predictive of greater negative emotionality.

  Of course, there are a large number of possible mechanisms for both positive and adverse epigenetic effects (see, e.g., Gaudi, Guffanti, G., Fallon, & Macciardi, 2016). Of all the neuromodulator candidates, perhaps the most evidence has been collected for oxytocin. For instance, Haas et al., (2016) focused on the moun
ting evidence that oxytocin genes, which have long been associated with animal sociability, might exhibit epigenetic modifications of DNA methylation, as measured in human saliva samples. They found that people exhibiting lower oxytocin DNA methylation, which may indicate higher oxytocin expression, displayed better ability to detect facial emotional expressions, as well as more secure attachment styles. With modern brain imaging, they also found higher regional cortical arousal during emotional perspective-taking exercises in such individuals than in those whose methylation pattern indicated diminished oxytocin activity.

  Modern molecular genetics will eventually impact both psychiatric diagnostics and the development of new treatments, heralding a new field of psychiatric epigenetics. Just as with animal models, there is increasing evidence that early emotional and physical traumas can promote the development of dysfunctional brain circuits, which partly reflect epigenetic changes resulting from life challenges as well as transgenerational effects, especially as arising from early life stressors (Gröger et al., 2016), which may lead to the development of various preventive measures and resilience-promoting interventions that arise directly from our understanding of epigenetics (Shrivastava & Desousa, 2016). As already noted, some of the adverse epigenetic effects can even be reversed by administration of drugs that can “erase” the adverse epigenetic markers (Weaver et al., 2006).