Miserliness is heritable

Despite numerous folk sayings about miserly people, the genetic and environmental architecture of the character trait of miserliness has been very rarely studied to date. We administered six items of the miserliness scale to 1110 pairs of South Korean twins aged 12- to 25-years (M = 18.0, SD = 3.3). Model-fitting analyses indicated that 28% (95% CI: 21–34%) and 72% (95% CI: 66–79%) of individual difference in miserliness were attributable to genetic and unique environmental influences, respectively. Common family environmental effects were negligible, consistent with a large body of behavioral genetic literature on personality. Sex differences in the magnitude of genetic and environmental factors in miserliness were not significant.     

On genes,environments and human development: A commentary to Goossens

Using the example of adolescent loneliness, Goossens (this issue) presented an outline of integral research programmes in European developmental psychology. Integral research programmes should combine longitudinal analysis with state-of-the-art methods from the neurosciences and use the gene×environment approach to track differential susceptibility to the environment. In my commentary, I suggest using control variables in gene–environment studies to rule out spurious associations, to make the studies more developmentally sensitive, and to stress the need for replication of gene–environment findings. I offer two hypothetical models for developmentally sensitive gene–environment studies on adolescent loneliness, namely a social cognition model and a social rejection model.     

The genetic and environmental relationship between Cloninger's dimensions of temperament and character

The purpose of this study was to determine whether Cloninger's revised 7-factor model of personality showed incremental validity over his four dimensions of temperament. A sample of 2517 Australian twins aged over 50 between 1993 and 1995 returned completed self-reported measures of Self-directedness, Cooperativeness, and Self-transcendence from Cloninger's Temperament and Character Inventory. Many of these twins had participated in a 1988 study containing Cloninger's temperament measures of Harm Avoidance, Novelty Seeking, Reward Dependence and Persistence. Contrary to theoretical expectations, univariate analyses revealed that familial aggregation for the character dimensions could be entirely explained by additive gene action alone. Although temperament explained 26, 37 and 10% of additive genetic variance in Self-directedness, Cooperativeness and Self-transcendence, respectively, seven genetic factors were required to explain the genetic variance among the TPQ dimensions, and almost all of the non-shared environmental variance was unique to each dimension of character. Our results indicate that the inclusion of all seven dimensions in a taxonomy of personality is warranted.     

Language evolution as a Darwinian process: computational studies

This paper presents computational experiments that illustrate how one can precisely conceptualize language evolution as a Darwinian process. We show that there is potentially a wide diversity of replicating units and replication mechanisms involved in language evolution. Computational experiments allow us to study systemic properties coming out of populations of linguistic replicators: linguistic replicators can adapt to specific external environments; they evolve under the pressure of the cognitive constraints of their hosts, as well as under the functional pressure of communication for which they are used; one can observe neutral drift; coalitions of replicators may appear, forming higher level groups which can themselves become subject to competition and selection.

Hedonic possibilities and heritability statistics

Several influential psychologists have attempted to estimate to what extent human happiness levels are directly controlled by genes by comparing the happiness levels of identical twins raised apart. If we discover that the happiness levels of identical twins raised apart tend to be closer than the happiness levels of fraternal twins raised apart, this is taken as evidence that average happiness levels are largely controlled by genes. However, if it turns out that identical twins' happiness levels tend to be substantially different, as different as fraternal twins raised apart, it has been argued that this implies that the environment largely determines happiness levels. I contend that this interpretation of the data rests on a set of questionable, closely related assumptions: a) that pairs of identical twins raised apart are raised in substantially different environments; b) that genetically identical twins aren't identical in other pertinent ways; and c) that average levels of affect that are correlated with certain sets of genes in the environments the twin studies were conducted in will be correlated with those genes in other relevant environments because those genes govern average affect levels. In this paper, I will show that these assumptions are false and explain how to properly go about investigating the contingent causal links between genes and happiness. In the end, I argue that there is no good evidence that our genes delimit our hedonic potential and that the fact that this misinterpretation of the data has been widely disseminated is potentially harmful to human well-being.     

Genetic polymorphisms predict national differences in life history strategy and time orientation

The existence of a genetic factor behind group-level differences in life history strategy (LHS) has long been disputed. A number of recent studies suggest that some polymorphisms in the androgen receptor gene AR, the dopamine receptor gene DRD4, and the 5-HTTLPR VNTR of the serotonin transporter gene are associated with risk acceptance versus prudence and a short-term versus long-term time orientation, which are important aspects of LHS. We integrated studies from diverse nations reporting the prevalence of these three polymorphisms for many countries. We collected national indices for each of the three polymorphisms and found that they define a strong, single factor, yielding a single LHS-related, national genetic index. As expected, this index is strongly associated with reported national measures of LHS and time orientation, even after controlling for socioeconomic variables. The genetic effect seems especially strong across societies with high socioeconomic inequality.