Accepted Manuscript

Title: Genetic and Environmental Contributions to Children’s

Prosocial Behavior: Brief Review and New Evidence from a
Reanalysis of Experimental Twin Data

Author: Ariel Knafo-Noam Dana Vertsberger Salomon Israel

PII: S2352-250X(17)30162-8
DOI: http://dx.doi.org/doi:10.1016/j.copsyc.2017.08.013
Reference: COPSYC 538

To appear in:

Received date: 4-6-2017

Revised date: 30-6-2017
Accepted date: 3-8-2017

Please cite this article as: A. Knafo-Noam, D. Vertsberger, S. Israel, Genetic and
Environmental Contributions to Children’s Prosocial Behavior: Brief Review and
New Evidence from a Reanalysis of Experimental Twin Data, COPSYC (2017),
http://dx.doi.org/10.1016/j.copsyc.2017.08.013

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• Twin research shows, a genetic contribution to variability in children’s prosocial behavior
• Genetic effects are found across measures and cultures
• The association between sharing and comforting reflects overlapping genetic effects
• Molecular genetic evidence using genome-wide and polygenic measures is needed
• Gene-environment interaction and gene-environment correlations are reviewed

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Genetic and Environmental Contributions to Children’s Prosocial Behavior: Brief

Review and New Evidence from a Reanalysis of Experimental Twin Data

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Ariel Knafo-Noam

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Dana Vertsberger

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Salomon Israel

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Psychology Department, The Hebrew University of Jerusalem
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Abstract

Children’s prosocial behaviors show considerable variability. Here we discuss the genetic

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and environmental contributions to individual differences in children’s prosocial

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behavior. Twin research systematically shows, at least from the age of 3 years, a genetic

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contribution to individual differences in prosocial behavior, both questionnaire-based and

observed. This finding is demonstrated across a wide variety of cultures. We discuss the

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possibility that different prosocial behaviors have different genetic etiologies. A re-

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analysis of past twin data shows that sharing and comforting are affected by overlapping

genetic factors at age 3.5 years. In contrast, the association between helping and
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comforting is attributed to environmental factors. The few molecular genetic studies of

children’s prosocial behavior are reviewed, and we point out genome-wide and polygenic
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methods as a key future direction. Finally, we discuss the interplay of genetic and
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environmental factors, focusing on both gene X environment interactions and gene-

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environment correlations.
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 Introduction

Children start helping, sharing with, and comforting others at a very early age[1,

2]. When voluntary and intended to benefit others, such behaviors are referred to as

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prosocial behaviors[3]. Despite this early emergence, prosocial behaviors also show

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considerable variation; some children willingly sacrifice personal resources and help

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others while some children do not. Studies have linked individual differences to many

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factors, including parenting, peers, school variables, and temperament[3,4]. Here we

discuss the genetic and environmental contributions to individual differences in

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children’s prosocial behavior, reviewing both quantitative and molecular genetic research

(see [6] for a broader discussion of morality genetics in children and adults).
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Quantitative Genetic Designs

The most frequently used method to assess genetic contributions to prosocial

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behavior relies on comparing behavioral similarity in monozygotic (MZ) twins, who

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share virtually 100% of their genes, and dizygotic (DZ) twins, who share on average 50%
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of the genetic variance. Assuming both twin types received equally similar environments,
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greater MZ twin similarity indicates a genetic basis for a phenotype (heritability[5]).

Substantial DZ twin similarity beyond what would be expected by genetic relatedness

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indicates shared environment effects, environmental influences making siblings similar,

while twin differences not due to genetic differences indicate the contribution of non-

shared environmental effects and measurement error. Importantly, these estimates are

contingent upon the context, culture, age and population from which they are derived.

Twin studies in infancy and early childhood show relatively low heritability

estimates and substantial shared environment effects on prosocial behavior[6]. For

Page 4 of 25
example, 19-25 month-olds’ observed prosocial helping toward their mothers in a

simulated distress experiment showed share environmental influence and no genetic

effect[7].

Starting at age three, research shows more clearly the importance of genetics to

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prosocial behavior. This was replicated with questionnaire (parent, teacher, and self-

report) data from samples of diverse cultural backgrounds (Israel[8], Nigeria[9], South

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Korea[10], the USA[11], and the United Kingdom[12]). Research using observational

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measures is rarer. One study[13] found only environmental contributions to

experimentally observed sharing behavior in seven year-olds. Aggregating across six

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laboratory-based behaviors in 3.5 year-old twins, we found modest heritability estimates

for compliant (following request) (34%) and self-initiated (without request) prosocial
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behaviors (43%), with nonshared environment accounting for the remaining variance[14],

indicating that genetic findings are not limited to questionnaire-based research.

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Longitudinal designs enable study of the changing roles of genetics and the
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environment within the same individuals. A study of observed prosocial acts[15] found
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that the magnitude of genetic and environmental effects varied across ages among
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American 14 to 36 month-olds. While most of the variance was due to the nonshared

environment, genetic effects dropped first and then tended to rise and shared environment
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effects tended to fall during early development. This general pattern of increasing

heritability and dropping shared environment has also been observed throughout

childhood and into adolescence. Using UK parent-rated prosocial behavior[6] it was

found that heritability increased from 26-37% at age two years to 60-62% at age seven

years. At the same time, shared environment effects became less important with age. A

Page 5 of 25
similar pattern was found[16] (cross-sectionally) from later childhood to early-mid

adolescence. However, another UK study[12] found no change in magnitude of genetic

influence from mid to late adolescence, suggesting an age dependent boundary/limit on

this developmental process. For potential explanations for the pattern of increasing

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heritability and decreasing shared environment effects, which has also been reported for

empathy[15] , general cognitive abilities[17] and other traits, see previous review[18].

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Complexity of Prosocial Behavior

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Up until now, we have largely treated prosocial behavior as a unitary concept. Most

of the research cited above has used broad questionnaires, assessing a global prosocial
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behavior dimension. However, prosocial behavior should be seen as a multifaceted,

complex trait[4, 19]. First, at the behavioral level sharing, helping and comforting do not
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always correlate, suggesting that the behaviors reflect different psychological factors[20].

Second, different aspects of prosocial behavior have different social correlates, such as
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parenting and attachment[21, 22].

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One way to address the complexity of individual differences in prosocial behavior

is to look simultaneously, within the same children, at phenotypic, genetic, and

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environmental contributions to the associations among different aspects of prosocial

behavior. In one study[23], different aspects of mother-reported prosociality (sharing,

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social concern, kindness, helping, and empathic concern) in seven-year old Israeli twin

children all inter-correlated positively, consistent with the notion of an overall underlying

prosociality trait. Importantly, each aspect of prosociality also had substantial variance

not accounted for by the global prosociality factor. The common prosociality factor was

highly heritable (69%), while there were also genetic effects specific to each of the facets.

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This last finding suggested that one reason for which different prosocial behaviors only

partially overlap is that there are unique genetic factors that separately contribute to

different prosocial aspects.

To further illustrate this complexity, we reanalyzed our previous data[14].

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Methodological details appear elsewhere[24, 25]. Six experimental situations tested 3.5 year-

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old Israeli twins’ helping, sharing, and comforting[26].

The different behaviors showed different genetic and environmental contributions

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(Figure 1). In the case of helping, similar MZ and DZ correlations (note to Figure 1) indicated

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shared environment effects (when analyzed separately from self-initiated helping, compliant

helping did show higher MZ correlations). The positive correlation was larger among MZ
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twins in both sharing and comforting, suggesting a genetic influence. In the case of

comforting, MZ twins correlated positively, while DZ twins did not correlate at all, which
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could indicate a non-additive genetic effect.

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Comforting correlated with both sharing, r = .20, p < .05, and helping, r = .23,
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p<.01, while sharing and helping did not correlate with each other, r = .04, ns. A bivariate
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genetic analysis indicated the presence of a non-shared environment correlation between

helping and comforting (re=.21, 95% confidence interval (CI)=.05-.35). A genetic

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correlation between comforting and sharing, rg=.50, CI=.20-.1.00, indicated that

overlapping genetic factors contribute to the comforting-sharing association. These

results show the complex nature of prosociality and its genetic etiology.

Molecular Genetic Studies of Prosocial Behavior

Page 7 of 25
 While twin studies demonstrate a phenotype’s heritability, they are uninformative

regarding the specific biological processes involved. For this, we turn to molecular genetic

studies. Research on the associations between specific genetic polymorphisms and prosocial

behavior has largely taken a candidate gene approach, selecting polymorphisms for analysis

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based on putative links between the behavior and the biological mechanisms which give rise

to it[18]. Most candidate gene studies of social phenotypes have focused on a few

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neurotransmitter systems in adults[18, 27]: the dopaminergic system, involved with executive

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function, learning and reward[28]; the oxytocinergic and vasopressinergic systems, involved

in social bonding and affiliative behaviors[29]; and the serotonergic system, involved in

mood and emotional regulation[30, 31]. an

The few molecular genetic studies of children’s prosociality have found some support
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for the role of genes in the oxytocin-vasopressin system. The G allele of the rs53576 single
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nucleotide polymorphism (SNP, variation in a single “letter” of the genetic code) of the
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oxytocin receptor gene (OXTR) was associated with Chinese children’s higher helping and
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comforting, but not sharing, behaviors towards experimenters[32]. Importantly, this SNP was

found in a recent meta-analysis[33] to be associated with a broad dimension of sociality

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(including extraversion, empathy, and social isolation). In Chinese adolescents, another

OXTR SNP, rs2254298, was associated with self-reported prosocial tendencies, an effect
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mediated via moral evaluation of behaviors[34]. Variation in the promoter region of the

AVPR1a gene which codes for the arginine vasopressin 1a receptor has been associated with

observed sharing behavior in Israeli 3.5 year old twin children[35]. Using parent reports of

older children’s prosocial behavior, an American study marginally replicated this finding[36].

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 Although intriguing, candidate gene findings have been criticized for several

reasons[18], including relatively small samples, not controlling for differences in allele

frequencies in subsamples of different ancestry, and lack of replication. Although it has not

been tested directly, the genetic architecture of prosocial behavior, like other complex traits,

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genes[37] is likely not based on a few genes with large effects, but rather on additive and

interactive small effects across many genes. A more recent approach includes the hypothesis-

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free study of genetic variation in hundreds of thousands of loci across the genome. Naturally,

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such genome-wide research necessitates very large samples, typically tens of thousands of

participants. The most relevant study to-date is a genome-wide-association-study of empathy

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(n=46,861), where genetic variation across the genome accounted for 12% of the variance in

self-reported empathy[38]. Such genome-wide approaches, and in addition the utilization of

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polygenic scores (i.e., combining the effects of many genetic polymorphisms[39]) hold

promise for elucidating the polygenic architecture of prosocial behavior.

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Gene-Environment Interactions
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Although until now we have discussed the role of genetics and the environment

separately, the two do not operate independently. Gene x Environment interactions (GxE)
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are indicated when individuals with certain genotypes are affected by the environment

differently than other individuals, and vice versa[40, 41]. Several molecular genetic
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studies have demonstrated evidence for GxE, but only a few studied children. For

example, variation in a functional variable number tandem repeat in the third exon of the

dopamine receptor D4 gene (DRD4) interacted with parenting[14] and attachment[42] to

predict prosocial behavior. Importantly, such associations do not necessarily generalize

across studies and different environmental factors; in one study the DRD4 polymorphism

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was associated with sharing with peers, but did not interact with parenting in predicting

sharing[43]). In another study, DRD4 did not interact with being preferred by peers to

predict prosocial behavior[44].

Another GxE approach examines how environments moderate the contribution of

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genetic effects. Heritability of parent-rated prosocial behavior in 3-year old Israeli twins

was estimated as much lower when twins had no additional siblings than when they

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did[8]. In a Nigerian study the relative contribution of environmental factors to

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adolescents’ prosocial behavior was higher in families low in cohesiveness than in

cohesive families[9]. Finally, a study of Canadian first graders showed that

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environmental influences played a stronger role than genetic influences in prosocial

leadership when children had many friends, suggesting that the quality of the social
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environment moderates genes’ influence[45]. Importantly, the differential heritability

observed in different ages[6] could also indicate that the role of genes becomes different
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as children’s social environment changes, for example as they move to larger social
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groups when transitioning to schools.

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Gene-Environment Correlations
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Gene-environment correlations (rGE) are another major way in which genetic and

environmental influences are interrelated[46, 47]. Passive rGE occurs when one family
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member provides an environmental input (e.g., parenting) that is influenced by genetic

factors that overlap with genetic effects on the child’s behavior[48]. Such association

between children’s genes and the environment they receive indicates that some

correlations observed between parenting and children’s behavior may reflect the shared

genetics of family members[49]. Although studies have yet to test this in the context of

Page 10 of 25
prosocial behavior, the AVPR1A gene, which has been associated with preschoolers'

sharing[35] has also been associated with mothers’ parenting[50], suggesting it may be a

promising candidate for research into passive rGE.

Children also affect their environment in a way corresponding with their own

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genotype, a process termed evocative rGE. One way to address this is by seeing whether

siblings with different genotypes (e.g., DZ twins) receive different parenting that is

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associated with differences in their own, genetically-influenced behavior. For example,

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using a twin design, the associations between children’s prosocial behavior and the

parenting they received were largely accounted for by genetic overlap between parenting
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and genetic differences between twins in prosocial behavior[51] . Moreover, children’s

genetically-influenced prosocial behavior evoked prosocial behavior and easy-going

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behaviors in their peers[52].

Children are also active agents in their prosocial development. Their genetically-
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influenced prosocial behavior can lead them to select environments (e.g., peer networks)
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that will suit their own behavior; a process called active rGE. One study demonstrating
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active rGE reported that a common genetic factor related both to children’s tendency to
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be prosocial leaders as well as to their quantity of friendships[45] (as these were

reciprocated friendships, evocative rGE might be at play too.) Both active and evocative
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rGE affect the input children receive from their environment. To the extent that such

experiences (e.g., parenting or peer reaction) also affect the developing child,

environmental differences in these genetically mediated environmental exposures can

accumulate and amplify the initial differences in prosociality. This process of genetically

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mediated selection into specific environments could also be one explanation for the

observed increase in the heritability of prosocial behavior[53].

Conclusions

Interest in prosocial development is on the rise[54]. Extant research strongly supports

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the role of genetics in individual differences in prosocial behavior, although genetic

effects are dependent on age, content of behavior (sharing, helping or comforting), and

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additional, environmental variables. However, research addressing the complex network

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of rGE and GxE[55] is still needed. Epigenetics, modifications in the DNA that do not

affect the DNA sequence but alter gene expression[56, 57, 58] are another potentially
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important way for future research on how environments and genes work together in

prosocial development.
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Prosocial behavior is a complex trait, likely to be influenced by many genes with

small effects[37]. Only recently has research begun to unravel the ways by which the
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interplay of genes and environments account for variation in prosocial behavior, delineate
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different aspects of prosocial behavior, and link prosocial behavior with other
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psychological processes, such as theory of mind, empathy, personality traits and values.
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The way all of these variables relate and interact at the psychological and brain level is a

fascinating quest for our understanding of the noble side of human nature.
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Page 12 of 25
 Acknowledgments

This research was supported by grants from the Israel Science Foundation (31/06,
1670/13). The authors thank all the families who participated in the Longitudinal Israeli
Study of Twins.

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Page 18 of 25
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**American adults were tested on methylation levels (a type of epigenetic modification)

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Figure 1.

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Genetic and Environmental Variance Component Estimates in Different Prosocial Behaviors

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Note: Sharing, helping and comforting were each tested twice, once in a self-initiated setting, and once following a request, and
standardized scores were then averaged separately for each of pair of tasks. When possible, we used finer coding (e.g., not only
presence of sharing, but also amount shared) than the original study[26]. Twin correlations for helping, sharing, and comforting, were
.23, .24, and .57, respectively for MZ twins (N=61 pairs), and .22, .15, and .04 for DZ twins (N=91 pairs). The genetic effect on
helping and the shared environment effects on sharing and comforting could be dropped off the model without affecting model fit. All
effects portrayed in the figure had 95% confidence intervals above zero. Additional information on the analyses can be obtained from
the authors.

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Conflict of interest: None

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