Stability and Change in Temperament During Adolescence.pdf

Journal of Personality and Social Psychology

Stability and Change in Temperament During Adolescence

Jody M. Ganiban

George Washington University

Kimberly J. Saudino

Boston University

Jennifer Ulbricht

George Washington University

Jenae M. Neiderhiser and David Reiss

George Washington University Medical School

This study assessed genetic and environmental contributions to temperament during adolescence within

the Nonshared Environment and Adolescent Development project (NEAD; D. Reiss, J. M. Neiderhiser,

E. M. Hetherington, & R. Plomin, 2000). NEAD is a national study that includes twins and other sibling

types who vary in regard to genetic relatedness. Seven hundred twenty sibling pairs (aged 12.1–13.5

years) participated at Time 1, and 395 sibling pairs (aged 14.7–16.2 years) participated again at Time 2.

At both Times, mothers and fathers rated their children’s temperament (emotionality, activity, sociability,

and shyness). At Times 1 and 2, genetic and nonshared environmental factors accounted for variance in

temperament, whereas shared environmental contributions were negligible. However, at Time 1, genetic

contributions were inflated, and shared environmental contributions were masked if sibling contrast

effects were not taken into account. At Time 2, sibling interaction effects had little impact on estimates

of genetic and environmental contributions to temperament. Last, temperament stability was primarily

explained by genetic factors, whereas both genetic and nonshared environmental factors accounted for

change.

Keywords: temperament, adolescence, genes, twins, stepfamilies

Temperament has long been identified as a factor that affects

adjustment during adolescence. Specific temperament characteris-

tics have been linked to alcohol use and substance abuse (e.g.,

Colder & Chassin, 1997; Cloninger, Sigvardsson, & Bohman,

1988) and interact with a wide range of risk and protective factors

during adolescence (e.g., Davies & Windle, 2001; Lynam et al.,

2000). Temperament characteristics that emerge during early

childhood are also predictive of behavioral outcomes during ado-

lescence and young adulthood (Newman, Caspi, Moffitt, & Silva,

1997). Because temperament plays an important role in adolescent

development, factors that contribute to individual differences in

temperament as well as to stability and change in temperament

during this critical time require attention. Numerous studies have

examined temperament stability; however, most studies have been

confined to children younger than 12 years of age (Roberts &

DelVecchio, 2000). Moreover, few studies have focused upon

understanding sources of stability and change in temperament

during adolescence. Such information is crucial to understanding

the malleability of temperament and, in turn, whether temperament

itself can be targeted as a source of intervention. The current article

examines the degree to which genetic and environmental factors

contribute to temperament during early and late adolescence and to

stability and change throughout adolescence.

Temperament is defined as biologically based individual differ-

ences in emotional and physiological reactivity and regulation that

are expressed through children’s negativity and positive emotion-

ality, activity level, sociability, and shyness (Buss & Plomin, 1984;

Rothbart & Bates, 1998). Studies conducted with young children

generally find that individual differences in temperament appear

early in life and demonstrate increasing stability from infancy to

the preschool years (Rothbart & Bates, 1998). For example, Le-

mery, Goldsmith, Klinnert, and Mrazek (1999) reported that spe-

cific temperament characteristics undergo progressive change dur-

ing infancy, but from the toddler to preschool periods, they are

moderately stable. By middle to late childhood, temperament

characteristics also demonstrate moderate stability, with estimates

ranging from .35 to .41 for most characteristics (Roberts &

DelVecchio, 2000). During late childhood and adolescence, re-

search has focused primarily upon personality, rather than upon

temperament. Similar to temperament characteristics, personality

characteristics exhibit moderate stability between the ages of 12

and 30 years, with average cross-age correlations between .47 and

.57 (Roberts & DelVecchio, 2000). Furthermore, Roberts and

DelVecchio (2000) noted that stability continues to increase after

age 30 years and peaks after 50 years, leading to population

correlation estimates as high as .75. These findings are consistent

with more recent studies that included large community samples

(Roberts, Caspi, & Moffitt, 2001; Shiner, Masten, & Tellegen,

2002).

Jody M. Ganiban and Jennifer Ulbricht, Department of Psychology,

George Washington University; Kimberly J. Saudino, Department of Psy-

chology, Boston University; Jenae M. Neiderhiser and David Reiss, Center

for Family Research, George Washington University Medical School.

Jenae M. Neiderhiser is now at the Department of Psychology, Penn-

sylvania State University, and David Reiss is now at the Child Study

Center, Yale University.

Correspondence concerning this article should be addressed to Jody M.

Ganiban, Department of Psychology, George Washington University, 2125

G Street, NW, Washington, DC 20052. E-mail: ganiban@gwu.edu

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2008, Vol. 95, No. 1, 222–236

0022-3514/08/$12.00 DOI: 10.1037/0022-3514.95.1.222

ADOLESCENCE AND TEMPERAMENT

223

These studies suggest that temperament and personality become

increasingly fixed and, thus, less malleable. When characteristics

appear highly stable, it is frequently assumed that such stability

reflects the expression of endogenous characteristics, including

those that are genetically influenced (McCrae et al., 2000). How-

ever, environmental factors can also explain continuity. It is plau-

sible that stable temperament or personality characteristics are

produced by the cumulative effects of experiences or environmen-

tal pressures, such as the internalization of emotion display rules,

the acquisition of new coping strategies, or becoming embedded

within a stable social environment. Likewise, both genetic and

environmental mechanisms can be used to account for changes in

temperament and personality. For example, new genes may be

activated with puberty, causing changes in reactions and behavior.

Changes in one’s environment may also stimulate outward

changes in temperament or personality (Rothbart, Ahadi, & Evans,

2000).

Findings from twin studies are consistent with a genetic expla-

nation for continuity. Cross-sectional studies indicate that even in

infancy, temperament is genetically influenced (e.g., Silberg et al.,

2005) and that heritability estimates tend to increase from infancy

to early childhood (Nigg & Goldsmith, 1994). In one study,

Goldsmith, Buss, and Lemery (1997) detected moderate to large

genetic contributions for two indices of negative emotionality

(social fearfulness, anger proneness), activity level, and interest/

persistence during the toddler period. However, during the pre-

school years, moderate genetic contributions (heritability estimates

ranged from .41 to .58) were found more consistently for all

temperament dimensions, including positivity (i.e., surgency),

negative affectivity, and effortful control. Fewer studies have

focused upon adolescents. One exception is the Nonshared Envi-

ronment and Adolescent Development project (NEAD; Reiss, Nei-

derhiser, Hetherington, & Plomin, 2000), which includes twins as

well as full-, half-, and unrelated siblings. Analyses that included

just the monozygotic (MZ) and dizygotic (DZ) twins consistently

detected moderate to large genetic contributions to variance in

negative emotionality, activity, sociability, and shyness during

early adolescence (Saudino, McGuire, Reiss, Hetherington, & Plo-

min, 1995). In a more recent analysis of the NEAD data, Loehlin,

Neiderhiser, and Reiss (2003) examined genetic contributions to

personality and adjustment dimensions. Again, moderate to large

heritability estimates were found for each dimension when only

twins were included in the analyses. Similarly, adult twin studies

on personality have reported high heritability estimates for extra-

version (i.e., .41–.58), neuroticism (i.e., .41–.58), and conscien-

tiousness (i.e., .38–.53; Bouchard & McGue, 2003).

Few longitudinal analyses have examined genetic and environ-

mental contributions to continuity in temperament or personality.

In one twin study, Gillespie, Evans, Wright, and Martin (2004)

obtained self-reports of personality at ages 12, 14, and 16 years.

Their analyses indicated that continuity in most personality char-

acteristics is explained by additive genetic factors. They also noted

that genetic factors contributed to changes in temperament, per-

haps reflecting the activation of new genes during puberty. How-

ever, most changes were explained by environmental factors. In a

second study with young adults, McGue, Bacon, and Lykken

(1993) estimated genetic and environmental contributions to per-

sonality within adult twins between the ages of 20 to 30 years and

also found that genetic factors accounted for most of the observed

stability. In a subsequent, larger study that used the Finnish Twin

Registry, Viken, Rose, Kaprio, and Koskenvuo (1994) similarly

reported that genetic factors primarily explained personality sta-

bility, whereas nonshared environmental factors accounted for

changes in temperament across adulthood. In addition, they found

little evidence of new genetic effects upon personality character-

istics after age 40 years. These studies all indicate that a common

set of genetic factors account for stability in temperament from

adolescence through adulthood. However, although change in per-

sonality is explained by environmental factors during adulthood,

both genetic and environmental factors may play a role in changes

during adolescence. Therefore, the relative influences of both

factors on changes in temperament may wax and wane over time.

More longitudinal studies during transition points such as adoles-

cence are needed to determine whether this is true and to contrib-

ute to a more comprehensive developmental theory of tempera-

ment.

Although twin studies point to significant genetic contributions

to temperament stability, a different picture emerges when nontwin

samples are assessed. For example, within the first wave of NEAD,

estimates of genetic and environmental contributions to activity

and shyness significantly differed for the twin and nontwin sibling

groups. In both cases, nonshared environmental factors explained

most variance within the nontwin sibling groups, whereas genetic

contributions were negligible (Saudino et al., 1995). Within

NEAD, genetic contributions to personality characteristics also

dropped significantly when twins were excluded from analyses

pertaining to personality characteristics (Loehlin et al., 2003).

Nontwin adoption studies also routinely yield lower heritability

estimates for temperament and personality characteristics than do

twin studies (Caspi, 1998; Goldsmith et al., 1997). For example,

the Colorado Adoption Project examined the temperament of

adopted children from ages 9 to 16 years through self-, parent, and

teacher reports. There was little evidence of genetic contributions

between the ages of 9 and 12 years when parents reported on their

children’s emotionality, activity, sociability, and attention (Gagne,

Saudino, & Cherny, 2003). Self-reports obtained when the adopt-

ees were 16 years old also yielded low heritability estimates

(Plomin, Corley, Caspi, Fulker, & DeFries, 1998). However,

teacher reports of the adoptees’ negative emotionality did yield

heritability estimates that ranged from .19 to .49 ( M .36) from

9 to 12 years of age (Gagne et al., 2003).

In summary, studies that do not include twins tend to generate

lower heritability estimates for temperament than do studies that

include twins. These discrepancies have been attributed to nonad-

ditive genetic influences on temperament (Plomin et al., 1998) or

to sibling-interaction effects (Saudino et al., 1995). Nonadditive

genetic effects are caused by interactions between alleles at the

same locus (dominance) or across different loci (epistasis). Such

effects are unpredictable, and their detection relies upon the inclu-

sion of MZ twins within the study sample. Because MZ twins are

genetically identical, their phenotypes are also identical for both

genetic dominance and epistasis. However, DZ twins and full

siblings, on average, have only a 25% chance of inheriting the

same set of alleles at a locus, whereas half siblings have little

chance of inheriting the same alleles and, thus, dominant genetic

influences. The potential of inheriting the same epistatic effects is

even less predictable and harder to detect given that siblings have

a low chance of inheriting the same alleles at the same loci, let

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GANIBAN, SAUDINO, ULBRICHT, NEIDERHISER, AND REISS

alone across loci. Consequently, only studies that include MZ

twins along with other sibling groups or relatives have sufficient

power to detect nonadditive genetic effects. There is increasing

evidence from twin and extended twin kin studies (i.e., twins and

their siblings, parents) that nonadditive and additive genetic factors

contribute to personality characteristics (e.g., Eaves et al., 1999;

Finkel & McGue, 1997; Keller, Coventry, Heath, & Martin, 2005;

Lake, Eaves, Maes, Heath, & Martin, 2000). Eaves, Heath, Neale,

Hewitt, and Martin (1998) further demonstrated that nonadditive

genetic contributions to personality may be best explained by

epistasis, rather than dominance. Thus, nontwin studies may un-

derestimate genetic influences on temperament because they do

not have the power to identify nonadditive genetic contributions.

Sibling-interaction effects may also be an important source of

discrepancies between twin and nontwin studies. These effects

were initially conceptualized to describe and measure the social-

izing influences siblings have on each others’ phenotypes (Carey,

1986; Eaves, 1976). Specifically, some siblings may imitate each

other or encourage each other to become more similar over time

(i.e., sibling assimilation). Other siblings may strive to distinguish

themselves by behaving differently and actually become less sim-

ilar to each other over time (i.e., sibling contrast or competition).

When this occurs, sibling interaction becomes an environmental

factor that affects the phenotype of each sibling and, thus, sibling

similarity. However, the degree to which siblings become more

similar to or different from each other may be influenced by their

genetic relatedness (Eaves, 1976). Because MZ twins share the

same genotype, any influence MZ twins have on each other will be

correlated with their genetic makeup (i.e., an MZ twin is socialized

by a cotwin who has the same genetic makeup). However, for

stepsiblings who are not genetically related, their influences upon

each other are not correlated with their genetic makeups. As a

result, sibling interactions will have a greater influence on sibling

similarity for sibling pairs who demonstrate the lowest levels of

genetic relatedness than for sibling pairs who demonstrate highest

levels of genetic relatedness. Because sibling-interaction effects on

phenotypes can depend on sibling relatedness, they can also mimic

nonadditive genetic effects when sibling-contrast effects are

present or mimic shared environmental effects when sibling as-

similation is present.

More pertinent to the current investigation, however, is the

application of the sibling-interaction model to account for and

assess rater bias in parents’ reports of their children’s tempera-

ments (e.g., Goldsmith et al., 1997; Neale & Stevensen, 1989;

Saudino, Cherny, & Plomin, 2000). For example, some parents

may be predisposed to focus on sibling differences and to ignore

sibling similarities (i.e., sibling contrast). Other parents may focus

on sibling similarities and ignore sibling differences (i.e., sibling

assimilation). Either tendency can lead to inaccurate assessments

of true sibling similarities or differences and affect estimates of

genetic and environmental contributions to behavior. Again, it is

expected that such report biases influence perceptions of similar-

ities or differences more for siblings who demonstrate lower levels

of genetic relatedness than for siblings who demonstrate higher

levels of relatedness. Thus, sibling contrast could mimic nonaddi-

tive effects, whereas sibling assimilation could mimic shared en-

vironmental effects.

Sibling-interaction effects are difficult to detect in twin-only

samples. Rietveld, Posthuma, Dolan, and Boomsma (2003) esti-

mated that a sample of 500 MZ and 1,000 DZ twins would be

required to detect a sibling-interaction effect with an absolute

magnitude of .15. Therefore, it is possible that the higher genetic

estimates found in twin-only studies may, in part, reflect the

impact of nonmeasured sibling-interaction effects. However, stud-

ies that include twins along with other sibling types, such as

NEAD, have greater power to detect sibling-interaction effects.

Saudino et al. (1995) examined sibling-contrast versus assimilation

effects for mother and father reports of adolescent temperament

during early adolescence within NEAD. They did not find assim-

ilation effects for MZ twins but detected significant contrast ef-

fects for parents’ reports of their adolescents’ emotionality, activ-

ity level, shyness, and sociability. Their results suggest that

sibling-interaction effects partially accounted for nonadditive ge-

netic contributions to the ratings and that they also masked the

contributions of family-wide experiences to temperament. Other

studies have detected significant contrast effects within infant and

toddler populations for difficult temperament (Silberg et al., 2005)

and for activity and shyness (Saudino et al., 2000; Saudino, Wertz,

Gagne, & Chawla, 2004).

In summary, current studies indicate that nonadditive genetic

factors contribute to temperament and personality and that sibling-

interaction effects exist. Both factors could explain discrepancies

between the findings of twin and nontwin studies. Specifically,

many twin studies that focus on personality do not include contrast

effects in their analytical model or lack sufficient power to detect

sibling-interaction effects. Conversely, nonadditive genetic effects

may not be detectable within studies that do not include MZ twins.

Therefore, studies that include both twins and nontwin sibling

groups are particularly suited to estimate the relative importance of

both genetic and contrast effects on temperament ratings. NEAD

affords this opportunity because it includes twin and nontwin

sibling pairs. In the current study, we revisit and extend the

findings of Saudino et al. (1995), who examined genetic contribu-

tions and sibling-interaction effects within NEAD’s first wave of

data collection. In the current report, we include a second set of

temperament ratings made 3 years after the initial assessment and

examine factors that contribute to stability and change in temper-

ament at this later time point.

Method

Participants

NEAD represents a nationwide sample of two-parent families

that included never-divorced families and stepfamilies. Several

inclusion criteria were used to select families: (a) family had two

adolescent same-sex siblings no more that 4 years apart in age

( M 1.61 1.29 years apart); and (2) family was in existence for

at least 5 years prior to the first Time 1 ( M 8.9 3.7 years of

marriage). At Time 1, 720 families participated. At Time 1, the

adolescent children ( N 1,420) ranged in age from 13.5 2.0

years (Child 1) to 12.1 1.3 years (Child 2). Participating families

were grouped into one of the following six sibling categories, in

one of the two family types (i.e., never divorced or stepfamily):

MZ twin pairs ( n 93), dizygotic DZ twin pairs ( n 99), and full

sibling (FI) pairs ( n 95) from never divorced families and full

sibling (FS) pairs ( n 182), half sibling (HS) pairs ( n 109), and

genetically unrelated sibling (US) pairs ( n 130) residing in

ADOLESCENCE AND TEMPERAMENT

225

stepfamilies. For the three sibling pair types within the stepfami-

lies, we matched the age of the oldest child and age spacing

between siblings across families to maximize their comparability.

At Time 2, 395 families from Time 1 participated. This subset

of Time 1 families included 63 MZ twin pairs, 75 DZ twin pairs,

and 58 FI pairs from nondivorced families and 95 FS pairs, 60 HS

pairs, and 44 US pairs residing in stepfamilies. In all, 790 children

participated at Time 2 and ranged in age from 16.2 2.1 years

(Child 1) to 14.7 1.9 years (Child 2). The decrease in the number

of participating families from Time 1 to Time 2 was not due to

attrition. Rather, only families with both adolescents still residing

at home for at least half of the time with both parents were eligible

to participate at Time 2. Of the ineligible families, 15% experi-

enced a divorce; in 79% cases one or both of the adolescents had

moved out of the home, and the remaining 6% were unable to be

classified. At Time 2, 91% of eligible families participated. There

were no mean differences in the demographic characteristics (par-

ents’ education, family income, gender of the siblings, and age

difference between siblings) for families who participated at both

Times 1 and 2 versus those who only participated at Time 1. In

regard to temperament, children who participated in the study at

Times 1 and 2 were rated by their mothers as slightly more

sociable than were children who only participated at Time 1.

However, no differences were found between the fathers’ temper-

ament ratings of each group. For the 27 eligible families who

refused to participate at Time 2, analyses indicated significant

main effects for age and variables related to age (i.e., the

adolescents were older and received less parental monitoring)

when compared with eligible families who chose to participate

at Time 2.

logical adjustment, as well as parental mental health, marital

quality, and stability.

Measures

The EAS Temperament Survey–Parent Form (Buss & Plomin,

1984) includes 20 descriptive statements that assess children’s

negative emotionality, activity level, sociability, and shyness.

Mothers and fathers completed the EAS for each adolescent sib-

ling in the study. For each statement, parents were asked to rate the

degree to which it described their children over the past 2 weeks,

using a 5-point Likert scale. At Time 1, the alphas for the EAS

ratings averaged .73 (range .60–.81) for mothers and .72 (range

.61–.81) for fathers. The average alphas for ratings at Time 2 were

.75 (range .64–.87) for mothers, and .70 (range .56–.81) for

fathers.

Analyses

Preliminary analyses. The following potential confounding

variables were regressed from the temperament ratings: maternal

age, child age, age differences between nontwin siblings, child

gender, and Child Age Child Gender interaction (McGue &

Bouchard, 1984). Next, the means and standard deviations were

computed for the study variables, and the distribution of each

variable was examined for normality. The temperament subscales

demonstrated significant skew. Therefore, we ranked the residu-

alized temperament ratings and normalized them across the entire

sample, using procedures described by Blom (1958). This strategy

for dealing with skewed data has been used in previous behavioral

genetic analyses (e.g., Eaves et al., 1997). The raw transformed

data were used in the model-fitting analyses. These data-analytic

methods differ from those of Saudino et al. (1995). In this earlier

report of the Time 1 NEAD data, Saudino et al. (1995) used

double-entered, unranked data and variance/covariance matrices in

the model-fitting analyses. The current analyses also included 41

additional sibling pairs that were not available at the time of the

original report.

Twin/sibling intraclass correlations. We computed intraclass

twin/sibling correlations to explore whether additive genetic (A),

dominant genetic (D), shared environmental (C), and nonshared

environmental (E) factors contribute to children’s temperament

characteristics and to assess potential sibling-interaction effects.

For each sibling group, temperament ratings for Sibling 1 were

correlated with those for Sibling 2. We double entered data for

these analyses to guard against the possibility that the original

designations of siblings as 1 or 2 were not random.

Genetic contributions are inferred if the magnitude of intraclass

correlations closely parallels the genetic relatedness of the sibling

pairs. If this was the case, then correlations would be highest for

sibling pairs that are the most genetically similar (e.g., MZ twins,

who share 100% of their genes) and lowest for sibling pairs that

are least genetically similar (US siblings, who share 0% of their

genes). If the MZ twin correlation is approximately twice as large

as the DZ twin and full sibling correlations, then additive genetic

contributions are inferred. If this difference is larger, nonadditive

genetic contributions may be present as well. The presence of

environmental factors that cause sibling similarity (i.e., shared

environment) are inferred if the intraclass twin/sibling correlations

Twin Zygosity

Twins were rated for physical similarity (e.g., eye and hair

color) by the interviewer, by the parents, and with self-reports

using a questionnaire designed for adolescents (Nichols & Bilbro,

1966). If any differences in physical characteristics were reported

(e.g., eye color, hair color) or if respondents reported that people

never were confused about the identity of the twins, the twin pair

was classified as dizygotic. Ten of the twin pairs could not be

classified as either monozygotic or dizygotic and were excluded

from these analyses (7% of the twin pairs). Questionnaire methods

of assigning zygosity have been found to be at least 90% accurate

when compared with tests of single-gene markers in blood pheno-

types (Nichols & Bilbro, 1966; Spitz et al., 1996).

Procedures

At Time 1, each family participated in two 3-hour home visits

during which family members were interviewed, completed ques-

tionnaires, and were observed during interactions. The home visits

were scheduled 2 weeks apart. At Time 2, families were visited

once by one interviewer. Both parents and the two adolescents

completed questionnaires and were videotaped during each visit.

Additional questionnaire data were obtained from take-home ques-

tionnaires, which were mailed ahead and collected by the inter-

viewer. At Times 1 and 2, data were gathered from the children

and both parents regarding the children’s temperament character-

istics; relationship with siblings, parents, and peers; and psycho-

226

GANIBAN, SAUDINO, ULBRICHT, NEIDERHISER, AND REISS

are greater than would be predicted by genetic relatedness. Shared

experiences, such as the same household environment or being

raised by the same parents, may account for sibling similarities that

are independent of genetic relatedness. Nonshared environment

encompasses the unique experiences of siblings that make them

different from each other (e.g., having different peers, being in

different classrooms, and even differential parental treatment), as

well as measurement error. Because MZ twins share 100% of their

genes and are reared in the same family, any deviation from a

correlation of 1.0 for this sibling group indicates nonshared envi-

ronmental influences.

We also examined the pattern of intraclass twin/sibling corre-

lations for evidence of sibling-contrast effects. If parents exagger-

ated true differences between siblings, sibling contrast would be

greatest for the least genetically related sibling pairs. This would

result in greater increases in variance and deflation of intraclass

sibling correlations for the least genetically related sibling pairs

(Carey, 1986; Eaves, 1976). Therefore, MZ twin correlations that

are more than two times those of DZ twin or full sibling correla-

tions could be caused by sibling-contrast effects. The presence of

significant negative twin/sibling correlations would also provide

strong evidence of sibling-contrast effects, as they would indicate

that parents’ ratings of one sibling are in opposition to the ratings

of the other sibling.

Biometric model fitting. We used model fitting to estimate

genetic and environmental contributions to each temperament di-

mension (Neale & Cardon, 1992). We used a Cholesky model to

assess genetic and environmental contributions to temperament

ratings at Times 1 and 2 and covariance between both time points

(see Figure 1). This model includes latent additive genetic (A1,

A2), nonadditive genetic (D1, D2), shared environmental (C1, C2),

and nonshared environmental (E1, E2) factors. Variance in Time 1

ratings is explained by latent factors A1, D1, C1, and E1. Squaring

paths a 11 ,d 11 ,c 11 , and e 11 can be used to estimate genetic and

environment contributions to these ratings. Variance in Time 2

ratings, however, is explained by factors unique to the Time 2

ratings (i.e., A2, D2, C2, E2) and by latent factors associated with

Time 1 ratings (i.e., A1, D1, C1, E1). Summing the squares of

paths from these latent factors to the Time 2 ratings can be used to

estimate genetic (a 21 2

a 22 2

d 21 2

d 22 2 ), shared environmen-

e 22 2 )

contributions to variance in the Time 2 ratings. This variance can

be further decomposed into variance that is shared with the Time

1 ratings and variance that is unique to Time 2. Shared variance

between Times 1 and 2 provides an estimate of temperament

stability, whereas variance unique to Time 2 provides an estimate

of change.

Some paths in Figure 1 were fixed. Specifically, the paths

between additive genetic factors (A1, A2) for Siblings 1 and 2

were set to 1.0 for MZ twin pairs, .50 for DZ twin pairs and full

sibling pairs, .25 for half siblings, and 0 for unrelated siblings. The

paths between nonadditive genetic factors (D1, D2) for the siblings

were also fixed to 1.0 for MZ twin pairs, .25 for DZ and full sibling

pairs, and 0 for half sibling and unrelated sibling pairs. For all

sibling groups, the path between shared environmental factors (C1,

C2) for the siblings was set to 1.0.

The Cholesky model assumes that nonadditive genetic effects

reflect dominance, rather than epistasis. Eaves et al. (1998) re-

c 22 2 ), and nonshared environmental (e 21 2

a 21

d 21

e 11

e 21

a 21

d 21

e 11

e 21

c 11

d 11

c 21

a 22

d 22

c 22

e 22

d 11

c 21

a 22

d 22

c 22

e 22

a 11

Te mperament

Time 1

Sibling 1

Te mperam

Time 1

Sibling 2

ent

Te mperament

Time 2

Sibling 1

Te mperament

Time 2

Sibling 2

Figure 1. Cholesky model for estimating additive genetic (A1, A2), nonadditive genetic (D1, D2), shared

environmental (C1, C2), and nonshared environmental (E1, E2) contributions to temperament ratings at Times

1 and 2. Genetic and environmental correlations between siblings are represented by double-headed arrows. The

paths between A1 for Siblings 1 and 2 and between A2 for Siblings 1 and 2 were set to 1.0 for monozygotic

twins, .50 for dizygotic twins and full siblings, .25 for half siblings, and .00 for unrelated siblings. The paths

between D1 for Siblings 1 and 2 and between D2 for Siblings 1 and 2 were set to 1.0 for monozygotic twins,

.25 for dizygotic twins and full siblings, and .00 for half siblings and unrelated siblings. Paths between C1 for

Siblings 1 and 2 and between C2 for Siblings 1 and 2 were set to 1.0 for all sibling groups. All paths were

constrained to be equal for Siblings 1 and 2.

tal (c 21 2

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