Genetic and Environmental Structure of Altruism Characterized by Recipients in Relation to Personality

Background and Objectives: Altruism is a form of prosocial behavior with the goal of increasing the fitness of another individual as a recipient while reducing the fitness of the actor. Although there are many studies on its heterogeneity, only a few behavioral genetic studies have been conducted to examine different recipient types: family members favored by kin selection, the dynamic network of friends and acquaintances as direct reciprocity, and strangers as indirect reciprocity. Materials and Methods: This study investigated the genetic and environmental structure of altruism with reference to recipient types measured by the self-report altruism scale distinguished by the recipient (the SRAS-DR) and examine the relationship to personality dimensions measured by the NEO-FFI with a sample of 461 adult Japanese twin pairs. Results: The present study shows that there is a single common factor of altruism: additive genetic effects explain 51% of altruism without a shared environmental contribution. The genetic contribution of this single common factor is explained by the genetic factors of neuroticism (N), extraversion (E), openness to experience (O), and conscientiousness (C), as well as a common genetic factor specific to altruism. Only altruism toward strangers is affected by shared environmental factors. Conclusions: Different types of altruistic personality are constructed by specific combinational profiles of general personality traits such as the Big Five as well as a genetic factor specific to altruism in each specific way.

A Common Genetic Influence on Human Intensity Ratings of Sugars and High-Potency Sweeteners

The perception of sweetness varies among individuals but the sources of this variation are not fully understood. Here, in a sample of 1,901 adolescent and young adults (53.8% female; 243 MZ and 452 DZ twin pairs, 511 unpaired individuals; mean age 16.2 ± 2.8, range 12–26 years), we studied the variation in the perception of sweetness intensity of two monosaccharides and two high-potency sweeteners: glucose, fructose, neohesperidine dihydrochalcone (NHDC), and aspartame. Perceived intensity for all sweeteners decreased with age (2–5% per year) and increased with the history of otitis media (6–9%). Males rated aspartame slightly stronger than females (7%). We found similar heritabilities for sugars (glucose: h2 = 0.31, fructose: h2 = 0.34) and high-potency sweeteners (NHDC: h2 = 0.31, aspartame: h2 = 0.30); all were in the modest range. Multivariate modeling showed that a common genetic factor accounted for >75% of the genetic variance in the four sweeteners, suggesting that individual differences in perceived sweet intensity, which are partly due to genetic factors, may be attributed to a single set of genes. This study provided evidence of the shared genetic pathways between the perception of sugars and high-potency sweeteners.

NPSR1 Gene Is Associated with Reduced Risk of Rheumatoid Arthritis

Objective.Neuropeptide S receptor 1 (NPSR1) is a G protein-coupled receptor involved in immune response and is associated with several inflammatory diseases. We investigated the possible contribution of several polymorphisms in the intronic region of NPSR1 to rheumatoid arthritis (RA).Methods.Genotyping of 7 single-nucleotide polymorphisms (SNP) was performed in a total of 1232 patients with RA and 983 healthy controls of Spanish white origin by real-time polymerase chain reaction technology, using the TaqMan 5′-allele discrimination assay.Results.One out of the 7 SNP analyzed (rs740347) was associated with RA [p after Bonferroni correction (pBNF) = 1.2 × 10−3, OR 0.73]. An association was also observed with rheumatoid factor-positive and shared epitope-positive RA (pBNF = 0.011, OR 0.73; pBNF = 0.037, OR 0.75, respectively).Conclusion.Our results show that variations in the NPSR1 intronic region are associated with low risk in patients with RA, supporting other evidence that this locus represents a common genetic factor in inflammatory diseases.

Fear and Attitudes Towards Torture and Preventive War

This paper examines the association between individuals' beliefs that the world is a dangerous place and their support for a variety of national security policies. We find that the source of the covariance between perceived danger and support for aggressive national security policies is primarily due to a common genetic factor. Latent genetic factors that influence individuals' perception of danger also appear to influence their positions on policies purported to alleviate such danger. Covariation between individuals' experiences and genes suggests that priming messages alone do not drive the covariation between feelings of danger and acceptance of policy changes.

A common genetic factor explains the association between psychopathic personality and antisocial behavior

Background. Both psychopathic personality traits and antisocial behavior are influenced by genetic as well as environmental factors. However, little is known about how genetic and environmental factors contribute to the associations between the psychopathic personality traits and antisocial behavior.Method. Data were drawn from a longitudinal population-based twin sample including all 1480 twin pairs born in Sweden between May 1985 and December 1986. The twins responded to mailed self-report questionnaires at two occasions: 1999 (twins 13–14 years old), and 2002 (twins 16–17 years old).Results. A common genetic factor loaded substantially on both psychopathic personality traits and antisocial behavior, whereas a common shared environmental factor loaded exclusively on antisocial behavior.Conclusions. The genetic overlap between psychopathic personality traits and antisocial behavior may reflect a genetic vulnerability to externalizing psychopathology. The finding of shared environmental influences only in antisocial behavior suggests an etiological distinction between psychopathic personality dimensions and antisocial behavior. Knowledge about temperamental correlates to antisocial behavior is important for identification of susceptibility genes, as well as for possible prevention through identification of at-risk children early in life.

Genetics of testosterone and the aggression-hostility-anger (AHA) syndrome: a study of middle-aged male twins

The aim of this study was to determine the genetic contribution to the variation in testosterone and the aggression-hostility-anger (AHA) syndrome in middle-aged twins. Moreover, the relation between testosterone and this syndrome, and possible common genetic mechanisms were investigated. Towards this end, blood samples were collected at two time points; the AHA syndrome was measured using three questionnaires: the Buss-Durkee Hostility Inventory with seven subscales, the Jenkins Activity Survey and the Spielberger State-Trait Anger Scale. The results showed substantial heritabilities for testosterone (approximately 60%) and moderate to fair heritabilities for the nine measures of the AHA syndrome (23–53%). The best fitting model for testosterone at two time points included a small age component and additive genetic and unique environmental factors, while a multivariate analysis of the nine AHA subscales resulted in an independent pathway model with two common additive genetic and two common unique environmental factors. No correlation between the common genetic factor influencing testosterone and the AHA subscales was found. We did, however, detect a negative correlation between the common environmental factor underlying testosterone and both common environmental factors influencing the nine AHA subscales, which may reflect a tendency for testosterone levels to rise and hostility to drop (or vice versa) after repeatedly experiencing success (or failure). Twin Research (2000) 3, 266–276.