Michael J. Beatty and Paola Pascual-Ferrá

11Genetics and communication competence

Abstract: Behavioral genetics research has indicated that a wide range of social behaviors and behavioral patterns are functions of neurobiological structures that are partly determined by genetic inheritance. Aspects of social behaviors associated with the dimensions of communication competence are among them. This chapter reviews the relevant research and theory.

Keywords: genetic inheritance, neurobiological moderators, studies of twins, genetics, message processing

Everyday experience is probably sufficient to lead to the conclusion that some people are more competent than others in social situations. Even casual observation reveals that, at one end of the continuum are articulate, witty, confident, and appropriately responsive communicators that balance listening and talk time, and seem interesting as well as interested in others. At the other end of the continuum, their less competent counterparts struggle to maintain conversations, behave either in reticent or arrogant ways, say little or dominate conversations, and either use inappropriate humor or demonstrate no sense of humor whatsoever. One theoretically compelling set of questions concerns factors that account for differences among communicators with respect to communicator competence. Is competence acquired or learned through observation of others or through direct experience? Can social competence be taught to everyone or just those pre-disposed toward competence? Is social competence merely a behavioral manifestation of inborn neurobiological functions due to genetic inheritance or other purely biological sources such as prenatal exposure to particular hormones? Although it might be tempting to simply conclude that communication competence consists of patterns of behavior that are shaped by nature and nurture, a scientific treatment of the issue requires somewhat more precision regarding the relative contributions of biology and social experience.

In this chapter, we lay out the broader biological and evolutionary context for understanding communication competence within a genetic inheritance paradigm, we review research findings and relevant evidence, and, finally, we suggest directions for future research and theory regarding communication competence. However, such an endeavor entails a set of assumptions about the purpose of the discipline of communication, which can be understood within a broader conceptual orientation.

1Conceptual orientation

As a point of departure, it is relevant to the ensuing discussion that our conceptual orientation is that the discipline of communication should be viewed as the scientific study of the ways in which people construct, use, and respond to messages. Within this framework, communication competence constitutes just one type of message production process to be explained scientifically. However, four dimensions of the treatment of communication competence in this chapter require explanation to put the discussion of potential genetic contributions to individual differences in communication competence in proper perspective.

1.1A scientific perspective

Beatty and Pence (2010: 3–4) remarked that

A commitment to scientific explanation often runs counter to the widespread remedial impulse in our discipline. A commitment to scientific explanation requires that competing theories are evaluated and endorsed first and foremost on the basis of predictive power … Conclusions drawn from treatment studies or skills programs are often cited as evidence against biologically-based positions but inspection of studies cited usually reveals serious design flaws and/or effects that are small enough to fit within the parameters of variance in a construct not explained by the theoretical models being challenged.

Certainly, the discipline of communication has a strong tradition anchored in undergraduate courses designed to improve student skills in contexts such as public speaking and group discussion. Indeed, that tradition is alive and well today with most communication departments regularly offering multiple sections of public speaking. Although theory has become increasingly prevalent in undergraduate curricula, many members of our profession continue to be invested in skills training and confidence-building as the justification for communication programs. Despite the appeal of claims to substantially improve students’ competence and reduce their apprehension about communicating, program assessments must com-port to the principles of experimental design, free of threats to internal validity such as selection effect, maturation effect, history effect, regression to the mean, instrument decay or any interactions among these threats (e.g., Campbell and Stanley 1963). A commitment to scientific explanation disallows the use of results from unscientific assessments and anecdotal observations derived from one’s teaching experience as evidence that communication behaviors are substantially moldable rather than hardwired.

In addition to matters regarding the criteria for evaluating evidence, a scientific approach strives toward a complete accounting of the communication behavior of interest. The ultimate goal in science is to construct models that completely explain phenomena. Einstein’s classic equation,E=mc2 accounts completely for E (i.e., energy). It does not merely account for 20 % of the variance in energy. Similarly, adopting a scientific perspective on communication leads to the goal of complete and comprehensive understanding of the communication-related phenomenon of interest, in this case communication competence. This point is important because it accounts for what might be seen as a preoccupation with variance accounted for in genetic-related models of human behavior. Mere statistical significance, while often indicating that a research paradigm is promising, is insufficient from the complete explanation standpoint. This point also underscores the emphasis on measurement and psychometric improvement, and on statistical corrections until measures can be refined. As will be discussed, the lack of predictive power is often attributable to imperfect measurement but can be easily misinterpreted as indicating an inadequate theoretical model.

1.2Primacy of biological/genetic factors as exogenous variables

Social experience and learning approaches to the acquisition of social competence and those based in genetic inheritance do not start on equal footing. As Beatty, McCroskey, and Valencic (2001: 1) observed

whatever the exact point in time we believe life begins during pregnancy, there is consensus that we are biological beings long before we are social beings. If it were proven beyond any doubt that we are programmed through genetic inheritance and prenatal care such that every aspect of our social behavior were determined, there would be no need for any additional speculation regarding why we communicate in the ways we do.

More recently, Beatty and Pence (2010: 4) made the same point, asserting that “explanations relying on social experience are necessary only to the extent that evidence indicates that humans are not already ‘hardwired’ … at birth.” The point is not that sufficient evidence exists to establish that individual differences in patterns of communication are already hardwired at birth but, rather, that humans are not likely blank states, and that thresholds of genetic inheritance and purely biological substrates of communicative performance should be established before assuming that other social constructs are necessary. At present, it is fair to say that theories that rely on influence of social environment to explain how humans come to communicate as they do seem to treat humans as blank slates.

Clues to the primacy of genetic inheritance, however, can be gleaned from the work of scientists studying primates, humankind’s closest biological relatives, in their natural environment (e.g., Goodall 1986). Social interaction is not limited to humans. Chimpanzees, for example, engage in a wide range of social behavior with varying degrees of success among individuals. They comfort and seek comfort after experiencing pain, when fearful, or subsequent to loss. They warn others of impending danger. Smaller chimpanzees solicit the aid of larger chimpanzees in response to bullies. Moreover, bands of male chimpanzees organize and carry out raids on neighboring bands over food, water, territorial encroachment, and breeding opportunities. Assuming that chimpanzees living in isolation are not influenced by media, the social interaction as pattern of behavior central to survival for primates seems to emanate from a natural impulse, social organization, and therefore the need for communication, facilitated survival of humans in much the same way as it has for other primates (Pinker 2002). It seems reasonable, therefore, to work from the assumption that the basic template for patterns of communication are in place before the individual confronts social contingencies.

In discussing the potential influence of genetic inheritance on the development of communication competence, it is important to distinguish between monomorphic and polymorphic genes. Monomorphic genes are responsible for differences between species (Pinker 2002). As Pinker (2002: 119) put it, they are why humans “grow bigger than a squirrel”. Humans and gorillas, for instance, are 95 percent similar in terms of monomorphic genes. Slight differences matter, as our monomorphic genes are 90 percent similar to salamanders. Polymorphic genes are responsible for individual differences within species. Thus, the language instinct that differentiates us from most other living things is due to monomorphic genes but individual differences among humans with respect to communication would be traceable to polymorphic genes.

The distinction between monomorphic and polymorphic gene effects is central to the way the treatment of genetics and communication competence is framed in this chapter. Monomorphic genes, such as FOXP2 (Vicario 2013), are thought to underlie differences in language development between humans and other species. From that perspective, FOXP2 might be described as a generic antecedent to human communication competence in the broad sense. However, as we alluded to at the outset, within the discipline of communication the term communication competence refers to the ability to construct messages that facilitate goal-achievement and also fulfill social appropriateness expectations rather than merely the ability to construct well-formed sentences. That is, it is possible to clearly articulate a sentence composed of correctly-used words and conforming to the rules of grammar and syntax but from a strategic perspective be ineffective and inappropriate to the occasion. It is the possible contribution of genetic inheritance to individual differences in communication competence in the sense of effectiveness and appropriateness that is of interest in this chapter. As such, polymorphic rather than monomorphic gene effects such as those associated with FOXP2 are most relevant to the present discussion. Although a few researchers have speculated that FOXP2 might have polymorphic implications of differences in language acquisition (Vicario 2013), no studies have yet been conducted to investigate the possibility nor has theorizing included strategic aspects such as effectiveness and appropriateness within interpersonal contexts. Therefore, a comprehensive review of research linking the FOXP2 gene to general language development in humans is beyond the scope and purpose of this chapter.

1.3Effects of genetic inheritance on behavior is indirect (mediated)

A common misconception about genetically based models of human behavior is that specific behaviors are directly influenced by a specific gene (Nelson 2004). However, most attempts to model the influence of genes on human behavior propose that brain structures and processes, which are the product of multiple genes – often interacting in the statistical sense, mediate gene effects on behavior. As Zuckerman (1995: 331–332) noted, “we do not inherit personality traits or even behavior mechanisms as such. What is inherited are chemical templates that produce and regulate proteins involved in the structure of nervous systems and neurotransmitters, enzymes, and hormones that regulate them … we are born with different reactivity of brain structures and levels of regulators.” In the communication literature, Zuckerman’s observation is manifest in Beatty’s (2005) mediated effects model, which specified the genetic inheritance leads to neurobiological characteristics, which lead to particular traits, which in turn implement specific behavior in response to situational demands. Within this framework, individual communicative acts, whether competent or incompetent, occur because the demands of the social situation excite particular neurobiological systems that implement the observed behavior. Differences in verbal plans and enacted behaviors, therefore, are due to differences in the thresholds for triggering various neurobiological processes underlying situational assessment, strategic planning, and particular action (For a detailed discussion of these processes, see Beatty, McCroskey, and Valencic 2001).

Making sense out of the statistical associations between genetic inheritance and behavior requires a sound grasp of the statistical characteristics of mediated models. Readers familiar with mediated effects models understand that the correlation between any two variables at the beginning and end of a causal chain are equal to the product of all the correlations between variables included in the chain. In terms of Beatty’s (2005) model, the correlation between the presence/absence of the requisite genes and behavior is equal to the product of: 1. the correlation between presence/ absence of the requisite genes and neurobiological characteristics, 2. the correlation between neurobiological characteristics and the behavior relevant trait, and 3. the correlation between the behavior relevant trait and the particular behavior. As such, even if each correlation between components of the model were .70, the correlation between presence or absence of the specified genes and a particular behavior would be comparatively smaller, .343.

Moreover, calculations for expected degrees of association between genetic inheritance and behavior are further complicated if multiple genes or multiple neuro-biological dimensions are required to account for variables in causal chains. This is particularly true if antecedent variables in models interact. Frequently, the brain structures and processes underlying patterns of behavior are products of complex interactions among multiple genes (For a discussion, see Beatty et al. 2002). Ultimately, it is important to note that genetic inheritance is likely to be more significant about the origin of individual differences in the antecedents to behavior and less informative about particular behavioral choices.

1.4Genetic effects depend on cognitive operations underlying message planning

Based on the assumption that if genetic inheritance contributes to individual differences in communication competence, its effects are mediated by brain structures/ processes, the relative influence of genetic inheritance likely depends on the type of cognitive operations underlying particular message strategies. For example, messages enacted in response to social demands can be spontaneously crafted, requiring multiple complex cognitive operations associated with constructing responses to novel stimuli. Some of these operations would be goal-setting, assessment of social expectations, construction of alternative strategies, considering possible consequences of each alternative, and language choice and selecting the alternative. According to computational theory (Chomsky 1975), the human mind is sufficiently powerful to execute all of the required computations rapidly enough to competently engage in social interaction. On the other hand, communication scholars have noted that much social interaction is routine (see Berger 2002). Therefore, knowledge structures, or prepared chunks of dialogue are essentially downloaded for implementation for the sake of efficiency. The theoretical foundation for this view resides in dynamic memory theory (Schank 1999). Clearly, everyday social interaction involves discourse that varies in degree to the extent it is spontaneously constructed or prepared and ritualistic. However, assessing the potential role of genetic inheritance of (in)competent performance in social situations requires attention to the level of preparedness of messages because the brain regions that implement the cognitive operations underlying spontaneous message construction differ from those underlying recall and implementation of knowledge structures (Beatty and Heisel 2007).

2Methodological issues in behavioral genetics

Behavioral geneticists have employed studies of twins to provide indirect tests of the potential effects of genetic inheritance on traits, patterns of behavior, and specific acts. The study of twins is informative about genetic inheritance because “monozygotic (MZ) twin pairs are genetically identical whereas dizygotic (DZ) pairs share only 50 percent of their genes” (Hughes and Cutting 1999: 429). Comparing the “within-pair correlations therefore provides an estimate of the proportion of trait variance attributable to genetic influences, the heritability of the trait” (Hughes and Cutting 1999: 429). Traits, patterns of behavior, and specific behavioral responses that are highly heritable are identifiable on the basis of high correlations for identical (MZ) twins on the construct and relatively low correlations for fraternal (DZ) twins. Heritability coefficients are calculated on the bases of MZ and DZ correlations.

The traditional formula for calculating heritability (h2), developed by Falconer (1989), was based on two assumptions: 1. MZ twins share 100 percent of their genes, and 2. gene effects are additive. Additive genes are responsible for the variation in a trait or behavior transmissible from parents to offspring. In contrast, non-additive gene effects define the variance in a trait or behavior not directly inherited from parents. Generally speaking, when the trait or behavior is fairly narrow in scope or unidimensional, nonadditive gene effects are most often attributed to gene by environment interaction (Lykken 1995). However, in complex traits and behavior, such as those underlying individual differences in communication competence, nonadditive gene effects might suggest gene × gene interactions. Broad heritability refers to the sum of additive and nonadditive effects.

If the construct of interest is the product of nonadditive gene effects, Falconer’s formula, h2 =2(R_MZ –R_DZ), where R_MZ represents the MZ correlation and R_DZ represents the DZ correlation, inflates the heritability estimates. This in turn deflates the effects estimated for shared environment. Two observations about the overall body of research on twins tend to mitigate concern about nonadditive gene effects on social interaction variables in general. First, studies such as Tellegen et al. (1988) observed only additive effects when data were coded according to whether twin-pairs were 1. MZ verses DZ, and 2. raised together or raised apart. Second, DZ correlations across 35 studies of twins looking at various dimensions of interpersonal affiliation were only slightly less than half of the magnitude of MZ correlations. In the face of clear evidence the gene effects are nonadditive or in cases where DZ correlations are borderline, many researchers adopt conservative approaches to calculating h2, the most popular of which consists of simply using the MZ correlations as the estimate of h2 (Lykken 1995).

When gene effects are decidedly additive, it is possible to calculate the effects of shared environmental effects (c2) from twins data, c2 =R_MZ –h2, and nonshared environmental effects, e2 =1–R_MZ (Plomin 1986). Shared environment is relatively straightforward, representing common family, educational, and social background. Nonshared environment, on the other hand, is somewhat misleading in that it does not merely consist of the unique experiences of each twin. Statistically speaking, nonshared environment estimates also contain the “residual term” (Rushton et al. 1986: 1195). In other words, in addition to unique social experiences, nonshared environment consists of all sorts of errors, including measurement error. Given the formula for e2, errors that alternate R_MZ are deposited in nonshared environment effects estimates. Therefore, as Beatty and Pence (2010: 9) pointed out, “unique social experiences that affect one twin but not the other would be represented in the nonshared environment component but a nonzero estimate of the nonshared environment isn’t sufficient to establish that such effects took place.” When gene effects are nonadditive, however, estimates of shared environment effects are compromised because nonadditive gene effects implicate possible gene × environment interaction rather than main effects for the environment.

During initial behavior genetics research, data were sorted into 2 (MZ twins/ DZ twins) by 2 (raised together/raised apart) matrices to tease out genetic inheritance effects from shared environment effects. However, as Zuckerman (1994: 245) observed, “There is little difference between the correlations for identical twins who were raised apart and those raised together.” Other researchers (e.g., Lykken 1995) point to that basic finding as a rationale for dropping the distinction regarding whether twins are raised together or apart from formulae for estimating heritability.

3Studies of twins pertaining to communication competence

Beatty and associates (2002) meta-analyzed the studies of twins involving social interaction variables that also have been cited in major professional journals in communication and scholarly reference texts. Their literature search included an electronic search using PsychInfo, Biological Abstracts, Bioethics Online, EBSCO-host, Eric, Healthstar, and the General Science Index database, a review of research journals that published studies of twins, and a scan of the reference lists of all articles retrieved through the electronic searches and scanning of journals. After deleting duplications and narrowing the study sample to research that reported quantitative results, Beatty et al. (2002) settled on 40 studies that covered 20 different social interaction constructs, which could be sorted into three broad categories: 1. interpersonal affiliation, 2. social anxiety, and 3. aggressiveness. In their meta-analysis, Beatty et al. (2002) applied constructive criteria for calculating h2, using the R_MZ as the estimate. They reported mean heritability effects computed on disattenuated correlations of .70 for interpersonal affiliation studies, .65 for social anxiety studies, and .58 for aggressiveness studies that included verbal aggression in some studies. Importantly, Beatty et al. (2002) found no difference due to whether data were self-report or observer-based and they found genetic inheritance effects were stronger as the age of study participants increased. This finding for age as a moderator was consistent with genetic effects unfolding and becoming more manifest with time but inconsistent with the notion that experience across a lifespan moderates genetic inheritance.

Although many of the 26 studies contained in the interpersonal affiliation cluster represented broad personality variables related to social interaction (e.g., extra-version) or behaviors, such as talkativeness, which might actually be characteristic of incompetent communicators, nine studies focused on variables that are conceptually relevant to communication competence. In addition to McGuire et al.’s (1994) study of social competence, the other studies in the nine-study cluster just mentioned examined self-monitoring (Dworkin 1979), perspective-taking (Hughes and Cutting 1999), wit (Beatty, Marshall, and Rudd 2001), spontaneous conversation (Goldsmith and Gottesman 1981), empathy (Mathews et al. 1981), sociability (Matheny and Dolan 1980), and pleasantness (Losoya et al. 1997). These studies, the variable studied, the measurement approach used, sample size, and the disattenuated R_MZ and R_DZ correlations reported in Beatty et al. (2002) for each study are presented in Table 1. Based on the preceding discussion of methodological issues provided in this chapter, the data displayed in Table 1 lead to three informative albeit tentative propositions.

First, the average sample weighted R_MZ correlation for the study results presented is .60 (N = 2744, K = 9), indicating a substantial effect of genetic inheritance, with R_MZ and R_DZ for social competence, in particular, indicating a slightly stronger genetic inheritance effect (i.e., R_MZ = .65, R_DZ = .20). Second, the average sample weighted R_DZ was .18, far less than half of the R_MZ correlation. This result suggests nonadditive gene effects. It is, therefore, possible that genetic inheritance and environment interact to produce patterns of social behavior and orientations associated with communication competence. Third, strong influences of genetic inheritance were not restricted to variables measured via self-report scales. The pattern of R_MZ and R_DZ correlations examined in this chapter is similar to those for social anxiety reported in Beatty et al (2002), which included one study focused on social composure (R_MZ = .69, R_DZ = .28).

4Neurobiological moderators

Self-regulation or self-control of emotional impulses is considered central to social competence in general (e.g., Eisenberg and Fabes 1992). Certainly, the ability to censor inappropriate comments and remarks that are likely to produce results counter to a communicator’s interaction goals plays an important role in communication competence. Furthermore, the ability to regulate counterproductive emotions such as anger, fear, or even too much enthusiasm, supports effective and appropriate communicative behavior. In this regard, a large body of neuroscience research suggests that functional properties of the prefrontal cortex (PFC) produce stable individual differences in the ability to self-regulate emotion and behavior (for comprehensive general reviews, see Davidson 2000, 2004; for reviews focused specifically on social interaction, see Pence et al. 2011).

Although increased electrical activity in either the left or right side of the PFC can be produced when specific emotional states are induced (e.g., Harmon-Jones and Siegelman 2001), self-regulation or self-control is heavily dependent on differences between resting alpha range (8–13 HZ) electrical activity in the two sides of the PFC (Davidson 2000). Self-regulatory ability is greatest in those in which electrical activity is symmetrical. In part, the theoretical significance of anterior PFC functional asymmetry for genetic perspectives on communication competence resides in the fact that empirical relationships between social interaction variables, including social competence, are based on resting levels of asymmetry in the anterior region of the PFC rather than levels stimulated by situationally induced states. Meta-analysis of 12 studies (Pence et al. 2011) indicated that differences in electrical activity in the left and right anterior region, even when individuals are not engaged in social interaction, account for substantial amounts of variance in traits and social behaviors (average r = .44), with all of the variance in correlations across studies attributable to sampling error.

Within the set of studies examined in Pence et al., one investigated the relationship between anterior cortex asymmetry and perspective-taking (Sabbagh and Flynn 2006) while another focused on anterior cortex asymmetry and social competence in children (Fox et al. 1995). The attenuated correlations were −.49 and −.47, respectively, indicating the greater the asymmetry in anterior cortex functioning, the lower the perspective-taking ability and social competence.

Two lines of research support the proposition that baseline (a)symmetry in the functioning of the anterior cortex represents a neurobiological trait or substrate underlying individual differences in social interaction: 1. the magnitude of test-retest correlations for resting and asymmetry are quite high and consistent with expectations regarding stable traits (Davidson 2000), and 2. consistent baseline levels of asymmetry in the anterior cortex, correlated with affectivity, have been observed in infants with 4 months of birth (e.g., Davidson and Fox 1982). Thus, inborn functional differences in between the left and right side of the anterior cortex presumed to be constructions of genetic programs (Davidson 2000) moderate emotional reactions and impulses to behave in a particular way.

The finding that symmetry in the anterior cortex correlated with prosocial orientations and behaviors, whereas antisocial orientations and reactions are associated with asymmetry (Pence et al. 2011), is not entirely novel. Communication scholars have long been interested in the effects of overall brain hemisphericity on communication competence in general (Sellers and Stacks 1990), as well as on specific competencies such as decoding facial displays of emotion (Floyd and Mikkelson 2003). However, in the past decade, researchers have become attentive to localized areas, especially within the PFC, in attempts to map the neurobiological processes underlying cognitive processes involved in the construction, use, and reception of interpersonal messages.

In addition to baseline functioning as a neurobiological substrate relevant to communication competence, individual differences in activation potential or arousability (Strelau 1994) appear to be associated with traits relevant to interpersonal communication and social behavior. For example, adapting messages to interaction partners requires that sources are able to construct a reasonably accurate version of partners’ perspectives on the topic under discussion. Heisel and Beatty (2006) found that activity in both the orbitofrontal and dorsolateral cortex implements perspective-taking attempts. Moreover, they detected individual differences in the amount of activation in those regions.

The major regions of the brain theoretically involved in deploying knowledge structures involve memory. Fluent, effective, and socially appropriate responses that are basically downloaded require rapid matching of memory packet to the situation recall of the particular alternative choices, selection of the most effective and appropriate response from all of the alternatives, and uploading the knowledge structures into memory in the first place requires considerable powers of memory. Research indicates that memory capacity and recall ability are facets of intelligence, which is among the most genetically inheritable individual differences (Eysenck 1986).

As important as neurobiological structures/processes are as moderators of genetic effects when routine conversation permits the use of knowledge structures, genetically inherited functioning associated with general and verbal intelligence probably has more profound effects when social situations demand spontaneously crafted messages. In such cases, fluency and other dimensions of effectiveness cannot be acquired through rehearsal. Lai and colleagues (2001) identified a gene (FOXP2) responsible for triggering the cascade of genes necessary for language fluency. Defects in FOXP2 preclude the acquisition of fluency regardless of preparation and practice. Moreover, even within the population of communicators with normal FOXP2 genes, variation in the ability to respond to novel situational demands, communication-related or otherwise, correlated with activity in the dorso-lateral PFC when responding to novel tasks. Measuring electrical activity in the cortex while participants constructed verbal plans in response to an unfolding compliance-gaining scenario, Beatty and Heisel (2007) found that significant increases in dorsolateral PFC occurred when novel social influence strategies were required. Deficits in the ability to access dorsolateral PFC involvement would be expected to inhibit spontaneous message construction.

Eysenck (1995: 98–99, 240–242) summarized experiments designed to examine individual differences based on the ability to generate creative verbal responses. Using a variation of the free word association test introduced by Galton (1879), these studies suggest that individual differences exist in the proclivity to respond spontaneously and creatively rather than normatively or in a routine manner to verbal tasks, and that these differences have some genetic foundation. Mednick (1962) observed that in a word association task, for example, most individuals respond with a word that appears frequently in the sample of responses compiled from other participants’ responses. However, a sizeable number of participants respond in ways that are unique, pairing responses to stimulus words that either do not appear or only rarely occur in the entire database. These individual differences are not random. Unique or novel responses to stimulus words occur more frequently for participants that score low on a measure of socialization (Eysenck’s P), which studies of twins indicate is highly heritable (Eysenck 1986).

5Summary

In this chapter, we reviewed the evidence, albeit indirect, regarding the role of genetic inheritance in the production of messages that vary with respect to competent communication. The results of twin studies of variables related to competent communication as well as social competence itself consistently indicate a sizable effect of genetic inheritance. Although the evidence does not support the proposition that competence is mostly heritable, models of communication competence will fall far short of comprehensive explanation if the possible role of genetic inheritance is overlooked. The present chapter outlined the issues that require attention to fully consider the degree to which individual differences in communication competence are heritable.

References

Beatty, Michael J. 2005. Fallacies in the textual analysis of the communibiological literature. Communication Theory 15. 456–457.

Beatty, Michael J. and Alan D. Heisel. 2007. Spectrum analysis of cortical activity during verbal planning: Physical evidence for the formation of social interaction rituals. Human Communication Research 33. 48–63.

Beatty, Michael J., Alan D. Heisel, Alice E. Hall, Timothy R. Levine and Betty H. La France. 2002. What can we learn from the study of twins about genetic and environmental influences on interpersonal affiliation, aggressiveness, and social anxiety: A meta-analytic study. Communication Monographs 69. 1–18.

Beatty, Michael J., Lenora A. Marshall and Jill E. Rudd. 2001 A twins study of communicative adaptability: Heritability of individual differences. Quarterly Journal of Speech 87(4). 366– 377.

Beatty, Michael J., James C. McCroskey and Kristin M. Valencic. 2001. The Biology of Communication: A Communibiological Perspective. Cresskill, NJ: Hampton Press.

Beatty, Michael J. and Michelle E. Pence. 2010. Verbal aggressiveness as an expression of selected biological influences. In: Theodore A. Avtgis and Andrew S. Rancer (eds.), Arguments, Aggression, and Conflict: New Directions in Theory and Research, 3–25. New York: Routledge.

Berger, Charles R. 2002. Goals and knowledge structures in social interaction. In: Mark L. Knapp and John A. Daly (eds.), Handbook of Interpersonal Communication (3rd ed.), 181–212. Thousand Oaks, CA: Sage.

Campbell, Donald T. and Julian C. Stanley. 1963. Experimental and Quasi-Experimental Designs for Research. Boston: Houghton Mufflin.

Chomsky, Noam. 1975. Reflections on Language. New York: Pantheon.

Davidson, Richard J. 2000. The neuroscience of affective style. In: Michael S. Gazzaniga (ed.), The New Cognitive Neurosciences (2nd ed.), 1149–1159. Cambridge, MA: MIT Press.

Davidson, Richard J. 2004. What does the prefrontal cortex “do” in affect: Perspectives on frontal EEG asymmetry research. Biological Psychology 67. 219–233.

Davidson, Richard J. and Nathan A. Fox. 1982. Asymmetrical brain activity discriminates between positive and negative affective stimuli in human infants. Science 218. 1235–1239.

Dworkin, Robert H. 1979. Genetic and environmental influences on person–situation interactions. Journal of Research in Personality 13. 155–168.

Eisenberg, Norman and Richard A. Fabes. 1992. Emotion, regulation, and the development of social competence. In: Margaret S. Clark (ed.), Emotion and Social Behavior, 119–150. Newbury Park, CA: Sage.

Eysenck, Hans J. 1986. Can personality study ever be scientific? Journal of Social Behavior and Personality 1. 3–19.

Eysenck, Hans J. 1995. Genius: The Natural History of Creativity. Cambridge, UK: Cambridge University Press.

Falconer, Douglas S. 1989. Introduction to Quantitative Genetics. New York: Wiley.

Fox, Nathan A., Kenneth H. Rubin, Susan D. Calkins, Timothy R. Marshall, Robert J. Coplan, Stephen W. Porges, James M. Long and Shannon Stewart. 1995. Frontal activation asymmetry and social competence at four years of age. Child Development 66. 1770–1784.

Floyd, Kory and Alan C. Mikkelson. 2003. Effect of brain laterality on accuracy of decoding facial displays of emotion. Communication Quarterly 51. 417–435.

Galton, Francis. 1879. Psychometric experiments. Brain 2. 149–162.

Goldsmith, H. Hill and Irving I. Gottesman. 1981. Origin of variation in behavioral styles: A longitudinal study of temperament in young twins. Child Development 52. 91–103.

Goodall, Jane. 1986. The Chimpanzees of Gomba: Patterns of Behavior. Cambridge, MA: Harvard University Press.

Harmon-Jones, Eddie and Jonathan Siegelman. 2001. State anger and prefrontal brain activity; Evidence that insult-related relative left-prefrontal activation is associated with experienced anger and aggression. Journal of Personality and Social Psychology 80. 797–803.

Heisel, Alan D. and Michael J. Beatty. 2006. Are cognitive representations of friends’ request refusals implemented in the orbitofrontal and dorsolateral prefrontal cortices?: A cognitive neuroscience approach to “theory of mind” in relationships. Journal of Social and Personal Relationships 23. 249–265.

Hughes, Claire and Alexandra L. Cutting. 1999. Nature, nurture, and individual differences in early understanding of mind. Psychological Science 10. 429–432.

Lai, Cecilia S. L., Simon E. Fisher, Jane A. Hurst, Faraneh Vargha-Khadem and Anthony P. Monaco. 2001. A forkhead-domain gene is mutated in severe speech and language disorders. Nature 413. 519–523.

Losoya, Sandra H., Suzanne Callor, David C. Rowe and H. Hill Goldsmith. 1997. Origins of family similarity in parenting: A study of twins and adoptive siblings. Developmental Psychology 33. 1012–1023.

Lykken, David T. 1995. The Antisocial Personalities. Hillsdale, NJ: Lawrence Erlbaum.

Matheny, Adam P. and Anne B. Dolan. 1980. A twin study of personality and temperament during middle childhood. Journal of Research in Personality 14. 224–234.

Mathews, Karen A., Daniel Batson, Joseph Horn and Ray Rosenman. 1981. “Principles in his nature which interest him in the fortunes of others …”: The heritability of empathic concern for others. Journal of Personality 49. 237–247.

McGuire, Shirley, Jenae M. Neiderhiser, David Reiss, E. Mavis Hetherington and Robert Plomin. 1994. Genetic and environmental influences on perceptions of self‐worth and competence in adolescence: A study of twins, full siblings, and step‐siblings. Child Development 65. 785– 799.

Mednick, Sarnoff. 1962. The associative basis of the creative process. Psychological Review 69. 220–232.

Nelson, Christian K. 2004. Classifying communibiology’s texts: Implications for genre theory. Communication Theory 14. 141–165.

Pence, Michelle E., Alan D. Heisel, Amber Reinhart, Yan Tian and Michael J. Beatty. 2011. Resting prefrontal cortex asymmetry and communication apprehension, verbal aggression, and other social interaction constructs: A meta-analytic review. Communication Research Reports 28. 287–295.

Pinker, Steven. 2002. The Blank Slate: The Modern Denial of Human Nature. New York: Viking.

Plomin, Robert. 1986. Behavioral genetic methods. Journal of Personality 54. 226–261.

Rushton, J. Philippe, David W. Fulker, Michael C. Neale, David K. B. Nias and Hans J. Eysenck. 1986. Altruism and aggression: The heritability of individual differences. Journal of Personality and Social Psychology 50. 1192–1198.

Sabbagh, Mark A. and Jessica Flynn. 2006. Mid-frontal EEG alpha asymmetries predict individual differences in one aspect of theory of mind: Mental state decoding. Social Neuroscience 1. 299–308.

Schank, Roger C. 1999. Dynamic Memory Revisited. Cambridge, UK: Cambridge University Press.

Sellers, Daniel E. and Don W. Stacks. 1990. Toward a hemispheric processing approach to communication competence. Journal of Social Behavior and Personality 5. 45–59.

Strelau, Jan. 1994. The concept of arousal and arousability as used in temperament studies. In: John E. Bates and Theodore D. Wachs (eds.), Temperament: Individual Differences in the Interface with Biology and Behavior, 117–141. Washington, DC: American Psychological Association.

Tellegen, Auke, David T. Lykken, Thomas J. Bouchard, Kimerly J. Wilcox, Nancy L. Segal and

Stephen Rich. 1988. Personality similarity in twins reared apart and together. Journal of Personality and Social Psychology, 54. 1031–1039.

Vicario, Carmelo M. 2013. FOXP2 gene and language development: The molecular substrate of the gestural-origin theory of speech? Frontiers in Behavioral Neuroscience, 7. 1–3.

Zuckerman, Marvin. 1994. Behavioral Expressions and Biosocial Bases of Sensation-Seeking. New York: Cambridge University Press.

Zuckerman, Marvin. 1995. Good and bad humors: Biochemical bases of personality and its disorders. Psychological Science 6. 325–332.