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Gene ics o Pe cei ed Family In e ac ion F om 12 o 17 Yea s o Age
© Sp inge Science+Business Media, LLC, pa o Sp inge Na u e 2019
Published e sion
Sil en oinen, Ka i; Su, Jinni; Pulkkinen, Lea; Ba , Pe e ; Rose, Richa d J.; Dick,
Danielle M.; Kap io, Jaakko
Sil en oinen, K., Su, J., Pulkkinen, L., Ba , P., Rose, R. J., Dick, D. M., & Kap io, J. (2019). Gene ics
o Pe cei ed Family In e ac ion F om 12 o 17 Yea s o Age. Beha io Gene ics, 49(4), 366-375.
h ps://doi.o g/10.1007/s10519-019-09960-z
2019
Vol:.(1234567890)
Beha io Gene ics (2019) 49:366–375
h ps://doi.o g/10.1007/s10519-019-09960-z
1 3
ORIGINAL RESEARCH
Gene ics o Pe cei ed Family In e ac ion F om 12 o17 Yea s o Age
Ka iSil en oinen1 · JinniSu2· LeaPulkkinen3· Pe e Ba 2· Richa dJ.Rose4· DanielleM.Dick2,5,6·
JaakkoKap io7,8
Recei ed: 26 Oc obe 2018 / Accep ed: 13 May 2019 / Published online: 24 May 2019
© Sp inge Science+Business Media, LLC, pa o Sp inge Na u e 2019
Abs ac
We analyzed how he e ec s o gene ic and en i onmen al ac o s on he pe cep ions o amily in e ac ion change om ea ly
o la e adolescence. The da a we e collec ed by pos al su eys on Finnish wins (N = 4808) a 12, 14 and 17yea s o age
and analyzed using gene ic win modeling. Addi i e gene ic ac o s explained a modes sha e o he a ia ion in pe cei ed
ela ional suppo (a2 = 0.30 in boys and 0.18 in gi ls) and ela ional ensions (a2 = 0.13 and 0.14, espec i ely) a 12yea s
o age, wi h he p opo ions becoming la ge h ough 17yea s o age (a2 = 0.53 in boys and 0.49 in gi ls o ela ional sup-
po ; a2 = 0.35 in boys and 0.33 in gi ls o ela ional ensions). Simul aneously, he ole o en i onmen sha ed by co- wins
dec eased. These indings sugges ha he associa ions be ween pe cei ed amily in e ac ion and o he ac o s in adul hood
should be in e p e ed wi h cau ion, because hey pa ly e lec gene ic backg ound, whe eas in childhood, hey may p o ide
mo e eliable in o ma ion on pa en al cha ac e is ics.
Keywo ds Family in e ac ion· Adolescen s· Twins· Gene ics
In oduc ion
P e ious s udies ha e shown ha he psychosocial amily
en i onmen has impo an in luences on o sp ing, includ-
ing e ec s on men al heal h (Yap and Jo m 2015), heal h
beha io s such as physical ac i i y (Bee s e al. 2010), and
o he heal h- ela ed ou comes such as body mass index
(BMI) (Sokol e al. 2017). The e is con incing e idence,
howe e , ha he psychosocial amily en i onmen canno
be conside ed as a pu ely en i onmen al ac o , since i also
e lec s he gene ic backg ound o he child. A e iew by
Klah and Bu (2014) demons a ed ha he amily en i on-
men , as epo ed by child en, shows mode a e he i abili y
when es ima ed by using a gene ic win design. The psy-
chosocial amily en i onmen has many aspec s and can be
de ined in di e en ways, bu he quali y o he pa en –child
ela ionship and how o sp ing pe cei e hei amily a mos-
phe e ha e been ega ded as pa icula ly impo an and a e
used especially in he p e ious beha io al gene ic s udies
(Klah and Bu 2014). Thus, a pa o he a ia ion in he
amily en i onmen as measu ed by pa en ing and amily
in e ac ion as pe cei ed by child en is because o in e -indi-
idual gene ic di e ences.
The e a e a leas h ee possible mechanisms explain-
ing his gene ic componen behind he pe cei ed amily
Handling Edi o : Yoon-Mi Hu , PhD.
Elec onic supplemen a y ma e ial The online e sion o his
a icle (h ps ://doi.o g/10.1007/s1051 9-019-09960 -z) con ains
supplemen a y ma e ial, which is a ailable o au ho ized use s.
* Ka i Sil en oinen
ka i.sil [email p o ec ed]
1 Depa men o Social Resea ch, Uni e si y o Helsinki, P.O.
Box18, FIN-00014Helsinki, Finland
2 Depa men o Psychology, Vi ginia Commonweal h
Uni e si y, Richmond, VA, USA
3 Depa men o Psychology, Uni e si y o Jy askyla,
Jy askyla, Finland
4 Depa men o Psychological andB ain Sciences, Indiana
Uni e si y, Blooming on, IN, USA
5 Depa men o Human andMolecula Gene ics, Vi ginia
Commonweal h Uni e si y, Richmond, VA, USA
6 College Beha io al andEmo ional Heal h Ins i u e, Vi ginia
Commonweal h Uni e si y, Richmond, VA, USA
7 Ins i u e o Molecula Medicine (FIMM), Uni e si y
o Helsinki, Helsinki, Finland
8 Depa men o Public Heal h, Uni e si y o Helsinki,
Helsinki, Finland
367Beha io Gene ics (2019) 49:366–375
1 3
en i onmen . Fi s , he e is s ong e idence based on bo h
win and molecula gene ic s udies ha he gene ic makeup
o pa en s a ec s hei beha io and in u n he amily en i-
onmen (Mile a-Sei z e al. 2016). Because child en inhe i
genes om hei pa en s, a co ela ion be ween he geno ype
o child en and hei amily en i onmen esul s, which is
called he passi e gene–en i onmen co ela ion (Ja ee and
P ice 2007). Second, child en can e oke eac ions om hei
pa en s due o hei pe sonali y and o he ac o s ha a e
gene ically in luenced. Fo example, a Swedish win s udy
ound ha ex e nalizing p oblems in child en, which showed
s ong he i abili y, e oked c i icism om hei mo he s
(Na usy e e al. 2011). Finally, child en may expe ience he
same en i onmen al exposu es di e en ly because o di -
e ences in pe sonali y. Since gene ic ac o s a e known o
explain indi idual di e ences in pe sonali y in childhood
(Spengle e al. 2012), di e en pe cep ions o he amily
en i onmen can gene a e gene ic di e ences in he pe -
cei ed amily en i onmen .
The he i abili y es ima es o he pe cei ed amily en i-
onmen may change, howe e , om childhood o adul hood.
Based on he p e ious li e a u e, adolescence is cha ac e -
ized by dec easing dependence on pa en s, widening social
ne wo ks, s onge in luence o pee s and inc eased sen-
sa ion seeking which may lead o inc eased isk beha io
(Ahmed e al. 2015; Kil o d e al. 2016). These changes can
modi y he he i abili y es ima es o he pe cei ed amily
en i onmen h ough changing gene–en i onmen co ela-
ions. A p e ious me a-analysis o mainly c oss-sec ional
s udies on he he i abili y o he amily en i onmen ound
ha when based on child en’s own epo s, he in luence
o en i onmen al ac o s sha ed by co- wins dec eased
and he in luence o en i onmen al ac o s unique o each
win inc eased du ing aging; he e ec o gene ic ac o s
emained oughly s able (Klah and Bu 2014). This esul
is consis en wi h he dec easing in luence o pa en s and
inc easing in luence o pee s du ing adolescence. Howe e ,
he e is also e idence ega ding physiological ai s such as
BMI (Sil en oinen e al. 2016) and many psychological ai s
such as in elligence and men al heal h indica o s (Be gen
e al. 2007) ha he in luence o gene ic ac o s inc eases
du ing adolescence. A possible eason is ha he in luence
o he passi e gene–en i onmen co ela ion dec eases and
is pa ly eplaced by he ac i e o e oca i e gene–en i on-
men co ela ions when child en ac i ely shape hei en i-
onmen o e oke eac ions om o he pe sons such as hei
pee s (Ma ceau e al. 2016). This p ocess is demons a ed
by mul iple s udies showing ha en i onmen al exposu es
show mode a e he i abili y (Kendle and Bake 2007). Fu -
he , because o inc easing independence, pe sonali y ac-
o s may mo e s ongly shape how adolescen s in e p e
en i onmen al exposu es as compa ed o younge child en.
Thus, i could also be expec ed ha he in luence o gene ic
ac o s on how adolescen s expe ience he amily en i on-
men inc eases du ing his de elopmen al pe iod.
We a e awa e o wo longi udinal win coho s which ha e
examined he ole o gene ic ac o s on he pe cei ed amily
en i onmen o e his ansi ional pe iod, bu hese s udies
ha e p oduced somewha inconsis en esul s. Bo h o he
s udies we e based on o sp ing a ings o he amily en i-
onmen , bu he measu emen ins umen s used di e ed. A
US win s udy ound ha he ole o gene ic ac o s inc eased
om 11 o 14yea s o age in boys and gi ls using a pa -
en –child ela ionship ques ionnai e (McGue e al. 2005). A
ollow-up s udy on his same coho ound ha he gene ic
a ia ion inc eased and he sha ed en i onmen al a ia ion
dec eased un il 17yea s o age; his inc easing gene ic a i-
a ion was s ongly co ela ed wi h gene ic a ia ion al eady
p esen a 12yea s o age (Ludeke e al. 2013). In con as ,
a UK win s udy using h ee measu es o he amily en i-
onmen (household chaos, pa en al discipline and pa en al
eelings) ound no sys ema ic change in he ole o gene ic
and sha ed en i onmen al ac o s om nine un il 16yea s o
age (Hannigan e al. 2017a). Fu he , in his UK s udy, he
gene ic co ela ions be ween he ages we e low. Thus, mo e
longi udinal esea ch is needed o cla i y how gene ic and
en i onmen al in luences on amily in e ac ion may change
ac oss de elopmen .
In his s udy, we analyzed how he gene ic a chi ec u e o
pe cei ed amily in e ac ion changes om 12 o 17yea s o
age by using a longi udinal Finnish win da ase . Two indica-
o s o amily in e ac ion, ela ional suppo and ela ional
ensions, we e used. We ocused on hese wo dimensions o
amily in e ac ion because hey cap u e posi i e and nega-
i e aspec s o amily in e ac ion and ha e been shown o
be p edic i e o adolescen psychosocial ou comes (La en-
d esse e al. 2010; Sil en oinen e al. 2014). We analyzed
bo h he change in gene ic and en i onmen al a ia ion o
amily in e ac ion and how gene ic and en i onmen al ac-
o s explained he s abili y o he pe cep ion o amily in e -
ac ion om ea ly o la e adolescence.
Da a andme hods
The s udy coho was de i ed om he longi udinal
FinnTwin12 s udy co e ing all Finnish wins bo n in
1983–1987 (Kap io e al. 2002). The names and pos al
add esses o he wins and hei pa en s we e ecei ed
om he Finnish popula ion egis y by iden i ying ami-
lies wi h wo child en bo n o he same mo he on he
same day (3136 win amilies, supplemen a y Fig.1). In
esponse o an in i a ion o ake pa in he s udy, 86% o
amilies indica ed hei willingness and e u ned a ques ion-
nai e (on he bi h, childhood and ea ly school yea s o he
wins) and consen o m. A e e u n o he ques ionnai e,
368 Beha io Gene ics (2019) 49:366–375
1 3
u he baseline ques ionnai es we e sen o he pa en s and
wins. The baseline win ques ionnai e was sen o bo h co-
wins indi idually in he au umn o he yea hey eached
he age o 11–12yea s (mean age: 11.42yea s; ange:
11.41–11.43yea s). Zygosi y was de e mined based on
ques ionnai e i ems on he physical simila i y and con us-
abili y o appea ance a school age and, i needed, was sup-
plemen ed by school pho og aphs and ques ions o pa en s.
The eliabili y o his me hod was alida ed in a sample o
295 same-sex win pai s using DNA; zygosi y was con-
i med among 97% o he pai s, showing good eliabili y
o his me hod (Jelenko ic e al. 2011). A e emo ing 264
wins wi h unknown zygosi y and 226 wins who we e no
a ailable o did no espond o he su ey, we had 4920 alid
esponses (49% gi ls), including 2456 comple e win pai s
om which 34% we e monozygo ic (MZ), 33% same-sex
dizygo ic (SSDZ) and 33% opposi e-sex dizygo ic wins
(OSDZ). This ep esen s 78% o all Finnish wins in hese
bi h coho s. Simul aneously when he i s ques ionnai e
o wins was sen , a ques ionnai e was sen o hei pa en s
asking o beha io al a ings o he wins and amily in e -
ac ions. This amily ques ionnai e yielded alid esponses
om 2320 amilies (74% o all amilies). A second su ey,
a he mean age o 14.0yea s ( ange: 13.9–14.9yea s; 4523
alid esponses; 72% o all wins), was sen o hose wins
who esponded o he i s su ey and a hi d su ey, a he
mean age o 17.6yea s ( ange 17.2–19.5yea s; 4041 alid
esponses; 64% o all wins), was sen o hose wins who
esponded o he second su ey.
I ems in he amily in e ac ion ques ionnai e asked
whe he he amily was (1) wa m, ca ing; (2) c ea i e, sup-
po i e; (3) us ing, unde s anding; (4) open; (5) s ic ; (6)
unjus ; (7) con lic ed; and (8) indi e en . A 5-poin scale
(1 = i s comple ely, 2 = mainly, 3 = somewha , 4 = mainly
no , 5 = no a all) was used (Na usk and Pulkkinen 1994).
The a ings we e e-coded such ha o all a iables highe
alues indica e be e amily in e ac ions. The same ques-
ions we e used in he ques ionnai es sen o wins a 12,
14 and 17yea s o age as well as o pa en s when hei win
child en we e 12yea s o age. Twins we e ins uc ed o ill
in he ques ionnai e independen ly, bu pa en s we e asked
o do i oge he . In mos o hese amilies, he wins’ mo he
(60%) o mo he and a he join ly (35%) comple ed his
amily ques ionnai e. Thus, in nea ly all cases, he mo he
had an impo an ole in he a ings, bu he a he may ha e
also con ibu ed o hese a ings. The pa en s we e asked
o conside all child en when making he a ings; hus, he
pa en al a ings a e he same o bo h co- wins.
The ini ial ac o analyses showed a 2- ac o solu ion
(supplemen a y Table1). A all ages and in bo h boys and
gi ls, he eigen alues dec eased less han one o he hi d
ac o ; oge he , he i s wo ac o s explained 54–65% o
he o al a ia ion. When we analyzed he ac o loadings
o he un- o a ed solu ions, we ound ha i ems 5–8 loaded
nega i ely on he i s ac o , indica ing ha hese i ems c e-
a e ano he dimension (supplemen a y Table2). The ac o
loadings we e la gely simila a all ages, o bo h boys and
gi ls and when using ei he o sp ing o pa en al epo s. To
c ea e mo e in e p e able esul s, in he u he analyses we
conduc ed wo sepa a e 1- ac o solu ions: o i ems 1–4 we
in e p e o indica e ela ional suppo and 5–8 o indica e
ela ional ensions. This s a egy allowed us o analyze he
co ela ions be ween hese wo dimensions o amily in e -
ac ion. When using hese wo 1- ac o solu ions, he ac o s
explained 55–73% o he a ia ion; i em 5 (s ic ) did no i
well on ei he measu e educing he explained a ia ion by
10–14%, and was hus excluded om u he analyses (sup-
plemen a y Table3).
We hen calcula ed he ac o sco es o ela ional sup-
po and ela ional ensions sepa a ely by using he 1- ac-
o solu ions such as also in he p e ious s udies using his
ques ionnai e (La end esse e al. 2010; Sil en oinen e al.
2014). The C onbach α- alues a ied be ween 0.71 and
0.87 o ela ional suppo and be ween 0.57 and 0.69 o
ela ional ensions, sugges ing good in e nal consis ency o
hese measu es (supplemen a y Table3). The sys ema ically
lowe C onbach α- alues o ela ional ensions was a ec ed
by a smalle numbe o i ems han was used o ela ional
suppo because o he emo al o one i em (s ic ). In he
desc ip i e analyses, we used sum a iables o show how
he pe cei ed amily in e ac ion changed om 12 o 17yea s
o age. The sco es a ied om 4 o 20 o ela ional sup-
po and 3–15 o ela ional ensions. Howe e , o make he
esul s compa able, we ans o med bo h o a y be ween
0 and 100 whe e highe alues indica e be e suppo and
less ensions. All wins ha ing missing o any i em we e
emo ed om he analyses o ela ional suppo (i ems 1–4)
and ela ional ensions (i ems 6–8). The numbe o alid
measu es in wins dec eased om 4799 o ela ional en-
sions and 4808 o ela ional suppo a 12yea s o age o
3997 and 3988, espec i ely, a 17yea s o age (supplemen-
a y Fig.1). The numbe o comple e win pai s ha ing hese
measu es a each age by sex and zygosi y a e a ailable in
supplemen a y Table4.
The da a we e analyzed using gene ic win modeling
based on he compa isons o simila i y be ween MZ and
dizygo ic (DZ) wins. MZ wins ha e i ually he same gene
sequence whe eas DZ wins sha e, on a e age, 50% o hei
gene ic a ia ion (Pos huma e al. 2003). Uni a ia e models
we e i s used o decompose he ai a ia ion in pe cei ed
amily in e ac ions in o h ee a iance componen s: addi i e
gene ic ac o s (A) including he e ec s o all loci on he ai
(co ela ion 1.0 wi hin MZ and 0.5 wi hin DZ co- wins),
sha ed en i onmen (C) including he e ec s o all en i-
onmen al ac o s making co- wins simila (co ela ion 1.0
wi hin bo h MZ and DZ co- wins) and unique en i onmen
369Beha io Gene ics (2019) 49:366–375
1 3
(E) including he e ec s o all en i onmen al ac o s mak-
ing co- wins di e en (co ela ion 0 bo h wi hin MZ and
DZ co- wins), along wi h measu emen e o (Fig.1a). We
ound s a is ically signi ican co ela ions be ween age and
ela ional suppo a 14yea s o age ( = − 0.05; p = 0.021),
whe eas he co ela ion was ma ginally signi ican o ela-
ional suppo a 12yea s (p = 0.078) and ela ional en-
sions a 14yea s o age (p = 0.054). Howe e , o make he
esul s sys ema ic, we adjus ed he esul s o exac age a all
measu emen s because o he wise he age e ec would ha e
been modeled as a pa o sha ed en i onmen al a ia ion.
DZ co ela ions we e sys ema ically highe han hal o he
MZ co ela ions, sugges ing he p esence o sha ed en i-
onmen al ac o s (supplemen a y Table4). Thus, we used
an addi i e gene ic/sha ed en i onmen al/unique en i on-
men al (ACE) model in he analyses. The model i s a is ics
o he gene ic win models a e p esen ed in supplemen a y
Table5. The assump ions o gene ic win models applied
well, as seen in he good i o he ACE models as compa ed
wi h he sa u a ed models; he model i di e ence was only
s a is ically signi ican o ela ional ensions a 17yea s o
age (p = 0.013), bu his can also be due o mul iple es -
ing since i is la ge han he Bon e oni co ec ed p alue
(p = 0.008 o 6 es s). We only ound s a is ically signi ican
sex-speci ic gene ic e ec s o ela ional suppo (p = 0.046)
and ensions (p = 0.009) a 12yea s o age, bu he OSDZ
co ela ions we e also somewha lowe han he SSDZ co e-
la ions a he o he ages, suppo ing he sex-speci ic gene ic
e ec (supplemen a y Table4). Thus, o ha e he in e nally
consis en esul s, we allowed sex-speci ic gene ic e ec s a
all ages. Di e ences be ween boys and gi ls we e highly s a-
is ically signi ican excep o ela ional ensions a 12yea s
o age. Thus, we s a i ied all u he analyses by sex.
Following he uni a ia e models, we decomposed he
co a ia ion be ween he wo dimensions o amily in e -
ac ion a same ages as well as o each measu e be ween
di e en ages by using bi a ia e Cholesky decomposi ion
(Fig.1b). This me hod makes no assump ions abou he
unde lying gene ic a chi ec u e bu decomposes he a i-
ance and co- a iance in he da a in o a se ies o unco ela ed
gene ic and en i onmen al ac o s. Using his me hod, we
calcula ed gene ic and en i onmen al co ela ions be ween
ela ional ensions and ela ional suppo a each age (c oss-
ai co ela ions) as well as be ween hese measu es a di -
e en ages (c oss-age co ela ions). Fu he , we calcula ed
how much sha ed gene ic and en i onmen al ac o s explain
he o al co ela ions.
The gene ic win models we e i ed using he OpenMx
package, e sion 3.0.2, o R s a is ical so wa e (Neale e al.
2016). The maximum likelihood es ima ion was used o es i-
ma e he pa ame e s and hei 95% con idence in e als (CI).
Fo desc ip i e s a is ics, s a is ical es s we e pe o med
using linea eg ession models by S a a/SE 13.1 o Win-
dows s a is ical so wa e (S a aCo p, College S a ion, TX,
USA). In he s a is ical es s, he e ec o in a-pai co -
ela ions on s anda d e o s (i.e. sampling win pai s a he
han independen indi iduals) was aken in o accoun by he
clus e op ion in S a a (Williams 2000).
Resul s
Table1 p esen s he desc ip i e s a is ics o amily in e -
ac ion by sex and zygosi y. The o sp ing a ings o ela-
ional suppo declined om 12 o 17yea s o age by 8.3
poin s (95% CI 7.4–9.3) in boys and by 10.8 poin s (95%
CI 9.8–11.7) in gi ls. A he same ime, he s anda d de ia-
ions (SD) o ela ional suppo inc eased in boys and gi ls.
Fo ela ional ensions, he esul s we e less sys ema ic:
while in gi ls he a ings dec eased by 4.2 poin s (95% CI
3.2–5.3), in boys he di e ence was no s a is ically signi i-
can (p = 0.80). Some dec ease in SD o ela ional ensions
we e seen in boys and gi ls. Pa en s epo ed less ela ional
ensions [7.8 poin s (95% CI 7.0–8.7) in boys and 5.3 poin s
(95% CI 4.4–6.2) in gi ls] bu also epo ed ela ional sup-
po o be lowe [2.0 poin s (95% CI 1.2–2.7) in boys and
3.0 poin s (95% CI 2.2–3.8) in gi ls] han hei win chil-
d en epo ed a 12yea s o age. MZ wins expe ienced
A
C
E
ACEACE
RT1RS1
(A)
(B)
=1 MZ / 0.5 DZ
=1 MZ and DZ
=0 MZ and DZ
ace
ACE
ace
ACE
RT1RT2
Fig. 1 Analy ical models: a Uni a ia e addi i e gene ic (A), sha ed
en i onmen (C) and unique en i onmen (E) model o ela ional en-
sions (RT1 o i s and RT2 o second win); b Bi a ia e Cholesky
decomposi ion (p esen ed o one win only) o addi i e gene ic co -
ela ion ( A), sha ed en i onmen al co ela ion ( C) and unique en i-
onmen al co ela ion ( E) be ween RT and ela ional suppo (RS)
370 Beha io Gene ics (2019) 49:366–375
1 3
sligh ly be e ela ional suppo and less ela ional en-
sions han DZ wins. The di e ences we e s a is ically
signi ican (0.71–1.3 poin s; p- alues 0.002–0.039 when
adjus ed o sex) excep o ela ional ensions a 12yea s
o age (p = 0.065). Gi ls epo ed be e ela ional suppo
(1.7 poin s 95% CI 0.94–2.52) and less ela ional ensions
(2.5 poin s 95% CI 1.6–3.5) a 12yea s o age han boys.
Howe e , his di e ence disappea ed a 14yea s o age,
and a 17yea s o age, gi ls epo ed less ela ional suppo
(1.3 poin s 95% CI 0.2–2.4) and mo e ela ional ensions
(2.1 poin s 95% CI 1.1–3.1) han boys. Only mino di e -
ences we e ound in SD be ween MZ and DZ wins. In he
compa isons o SSDZ and OSDZ wins, bo h means and
SDs we e e y simila (da a no shown bu a e a ailable
on eques ). The pa en al a ings o amily in e ac ion when
hei o sp ing we e 12yea s o age co ela ed modes ly
wi h he o sp ing a ings a he same age [ = 0.32 (95%
CI 0.29–0.34) o ela ional suppo and = 0.24 (95% CI
0.22–0.27) o ela ional ensions]. These co ela ions some-
wha dec eased when using o sp ing a ings a 14 [ = 0.27
(95% CI 0.25–0.30) and = 0.20 (95% CI 0.18–0.23), espec-
i ely] and 17yea s o age [ = 0.20 (95% CI 0.17–0.23) and
= 0.17 (95% CI 0.13–0.20), espec i ely], bu he dec ease
was no subs an ial.
Table2 p esen s he esul s o uni a ia e modeling
(Fig.1a). We allowed he means o di e be ween MZ
and DZ wins in he gene ic win models because o he
abo emen ioned zygosi y mean di e ences. In ela ional
suppo , addi i e gene ic, sha ed en i onmen al and unique
en i onmen al ac o s explained oughly equal sha es o
he a ia ion a 12yea s o age in boys, whe eas in gi ls,
sha ed en i onmen al ac o s we e mo e impo an and
explained nea ly hal o he a ia ion. The ole o gene ic
ac o s became mo e impo an o e ime, explaining a ound
hal o he a ia ion o ela ional suppo a 17yea s o age
in boys and gi ls. In ela ional ensions o bo h boys and
gi ls, he ole o gene ic ac o s was less impo an han
sha ed and unique en i onmen al ac o s a 12yea s o
age. Howe e , gene ic ac o s became mo e impo an o e
ime and a 17yea s o age explained oughly one- hi d o
he a ia ion. The e was some o e lap in he 95% CIs o
pa ame e s, bu gene ally he di e ences be ween he ages
we e s a is ically highly signi ican o ela ional suppo
(Δ-2LL = 63.4, Δd. . = 12, p < 0.00001) and ela ional en-
sions (Δ-2LL = 50.4, Δd. . = 12, p < 0.00001).
Finally, we analyzed he co ela ions be ween he o -
sp ing a ings o ela ional suppo and ela ional ensions
(c oss- ai co ela ions) as well as how hese dimensions
o amily in e ac ion co ela e be ween ages (c oss-age co -
ela ions) (Table3). As expec ed, he c oss-age co ela ions
we e highes be ween he closes ages (12 s. 14yea s and
14 s. 17yea s) bu emained mode a e ( ≤ 0.42). Gene ally,
he co ela ions we e simila in boys and gi ls. The co ela-
ions be ween ela ional suppo and ela ional ensions we e
lowes a 12yea s o age, inc easing un il 17yea s o age o
0.54 in boys and 0.65 in gi ls. When we decomposed hese
co ela ions in o gene ic and en i onmen al co ela ions
using Cholesky decomposi ion (Fig.1b), he highes co -
ela ions we e gene ally ound o sha ed en i onmen al ac-
o s. Mos o hese exceeded 0.60, and some exceeded 0.90.
Sha ed en i onmen al ac o s also explained an impo an
sha e o he c oss- ai and c oss-age co ela ions. Addi i e
gene ic co ela ions we e mos ly signi ican ly posi i e and
explained a pa o hese ai co ela ions. Howe e , mos
o hem we e lowe han sha ed en i onmen al co ela ions.
One o he addi i e gene ic co ela ions was nega i e leading
o he nega i e p opo ion o explained a ia ion, bu i was
no s a is ically signi ican . Gene ally, unique en i onmen al
c oss-age co ela ions we e small, and a ound hal o hem
we e no s a is ically signi ican . Fo c oss- ai co ela ions,
Table 1 Means and s anda d
de ia ions (SD) o amily
in e ac ion by age, sex and
zygosi y
a The scales a e ans o med o ange be ween 0 and 100
Boys Gi ls
All MZ wins DZ wins All MZ wins DZ wins
Mean SD Mean SD Mean SD Mean SD Mean SD Mean SD
Rela ional suppo a
12yea s o age 84 14 85 13 84 14 86 14 87 14 85 14
14yea s o age 80 15 80 15 79 15 79 18 80 17 78 18
17yea s o age 76 17 77 17 76 17 75 19 77 19 74 19
Pa en al epo a age 12 82 13 82 12 82 13 83 13 84 12 82 13
Rela ional ensionsa
12yea s o age 81 18 82 17 81 18 84 16 85 16 83 16
14yea s o age 79 17 81 17 79 17 80 16 82 16 79 16
17yea s o age 82 16 83 15 81 16 80 16 81 15 79 16
Pa en al epo a age 12 89 12 89 11 89 12 89 12 90 12 89 12
371Beha io Gene ics (2019) 49:366–375
1 3
unique en i onmen al co ela ions we e la ge han hose
o c oss-age co ela ions, bu hey we e s ill smalle han
sha ed en i onmen al and gene ic c oss- ai co ela ions.
Discussion
In his s udy based on a longi udinal Finnish win da ase ,
we ound ha gene ic ac o s explained an inc easing sha e
o he a ia ion o pe cei ed amily in e ac ion om 12 o
17yea s o age measu ed as ela ional suppo and ela ional
ensions. The esul s on he in luence o gene ic ac o s on
amily in e ac ion a e no su p ising, and u he mo e, a
gene ic componen has been ound no only o amily en i-
onmen (Klah and Bu 2014) bu also o li e e en s and
social suppo (Kendle and Bake 2007), which ha e been
adi ionally ega ded as pa o one’s en i onmen . We
ound mode a e gene ic co ela ions be ween he a ings o
amily in e ac ion om 12 o 17yea s o age. The US s udy
based on he Minneso a Twin Coho also ound inc eas-
ing gene ic a ia ion and gene ic co ela ions om 11 o
17yea s o age when hey analyzed pa en –child ela ion-
ships (Ludeke e al. 2013; McGue e al. 2005). In his US
coho , bo h he i abili y es ima es and gene ic co ela ions
we e, howe e , highe han wha we ound o pa en al en-
sions, which was due o a lesse ole o sha ed en i onmen al
ac o s. The UK win s udy using he measu es o household
chaos, pa en al discipline and pa en al eelings ound ha
gene ic ac o s explained a smalle and sha ed en i onmen-
al ac o s explained a la ge p opo ion o a ia ion han
in ou s udy (Hannigan e al. 2017a). This UK s udy di -
e ed om bo h ou esul s and he esul s o he US s udy
because no sys ema ic inc ease in he ole o gene ic ac o s
was obse ed and he gene ic co ela ions we e gene ally
o small magni ude. Ou esul s also di e om he esul s
o p e ious me a-analysis o mainly c oss-sec ional s udies
inding ha he e ec o gene ic ac o s emained oughly
s able du ing adolescence (Klah and Bu 2014). Howe e ,
i is no ewo hy ha di e en measu es o amily en i on-
men we e used in hese h ee longi udinal coho s and se -
e al di e en measu es o amily en i onmen we e used in
he me a-analysis o c oss-sec ional s udies. I is unce ain
whe he hese di e ences a e because o he di e ences in
he measu es o amily en i onmen , con ex ual di e ences
o whe he hey e lec o he di e ences be ween he coho s.
In addi ion o gene ic ac o s, sha ed en i onmen al ac-
o s also explained an impo an sha e o he a ia ion in
amily in e ac ion, especially a 12yea s o age. This sug-
ges s ha especially among child en, he a ings o amily
in e ac ion e lec he cha ac e is ics o pa en ing and less
so he child en’s own pe cep ions o pa en ing cha ac e -
is ics. This conclusion is u he suppo ed by ou esul s
ha sha ed en i onmen al co ela ions we e subs an ial and
explained in gene al a la ge sha e o c oss-age co ela ions
han gene ic ac o s. Ou esul s on he impo ance o he
sha ed en i onmen in he s abili y o e ages somewha
Table 2 Rela i e p opo ions
o addi i e gene ic, sha ed
en i onmen al and unique
en i onmen al ac o s wi h
95% con idence in e als (CI)
explaining he a ia ion in
amily in e ac ion om 12 o
17yea s o age
a Fac o sco es based on wo 1- ac o models
Addi i e gene ic ac o s Sha ed en i onmen al
ac o s
Unique en i onmen al
ac o s
a295% CI c295% CI e295% CI
Rela ional suppo a
Boys
12yea s o age 0.30 0.14, 0.47 0.34 0.19, 0.47 0.36 0.31, 0.42
14yea s o age 0.21 0.02, 0.41 0.36 0.19, 0.51 0.43 0.37, 0.50
17yea s o age 0.53 0.31, 0.65 0.06 0.00, 0.25 0.41 0.35, 0.48
Gi ls
12yea s o age 0.18 0.02, 0.34 0.46 0.31, 0.59 0.36 0.32, 0.42
14yea s o age 0.29 0.13, 0.47 0.38 0.21, 0.51 0.33 0.29, 0.39
17yea s o age 0.49 0.29, 0.68 0.16 0.00, 0.33 0.35 0.30, 0.41
Rela ional ensionsa
Boys
12yea s o age 0.13 0.01, 0.32 0.39 0.23, 0.50 0.48 0.41, 0.55
14yea s o age 0.20 0.01, 0.43 0.27 0.08, 0.44 0.52 0.45, 0.61
17yea s o age 0.35 0.20, 0.48 0.05 0.00, 0.18 0.60 0.52, 0.68
Gi ls
12yea s o age 0.14 0.01, 0.28 0.53 0.40, 0.64 0.33 0.29, 0.38
14yea s o age 0.26 0.07, 0.46 0.33 0.15, 0.49 0.41 0.35, 0.47
17yea s o age 0.33 0.05, 0.53 0.23 0.06, 0.46 0.43 0.37, 0.50
372 Beha io Gene ics (2019) 49:366–375
1 3
Table 3 T ai co ela ions o amily in e ac ion om 12 o 17yea s o age and co ela ions be ween addi i e gene ic, sha ed en i onmen al and unique en i onmen al a iance componen s
explaining hese ai co ela ions wi h 95% con idence in e als (CI)
T ai co ela ion Addi i e gene ic co ela ion Sha ed en i onmen al co ela ion Unique en i onmen al co ela ion
T ai 1 T ai 2 95% CI A95% CI % o he ai co e-
la ion explained
C95% CI % o he ai co e-
la ion explained
E95% CI % o he ai
co ela ion
explained
C oss-age co ela ions
Boys
Suppo 12 Suppo 14 0.42 0.38, 0.45 0.14 − 0.61, 0.53 9 0.96 0.71, 1.00 77 0.15 0.05, 0.26 14
Suppo 12 Suppo 17 0.25 0.21, 0.29 0.06 − 0.25, 0.30 9 1.00 0.64, 1.00 85 0.04 − 0.06, 0.15 6
Suppo 14 Suppo 17 0.41 0.37, 0.44 0.68 0.38, 1.00 56 0.82 0.23, 1.00 41 0.03 − 0.09, 0.14 3
Tensions12 Tensions14 0.33 0.29, 0.36 0.64 0.22, 1.00 40 0.63 0.36, 1.00 57 0.02 − 0.07, 0.12 3
Tensions12 Tensions17 0.17 0.13, 0.22 − 0.30 − 1.00, 0.07 − 24 0.52 0.30, 1.00 81 0.14 0.05, 0.22 43
Tensions14 Tensions17 0.32 0.28, 0.36 0.30 − 1.00, 1.00 16 0.82 0.49, 1.00 58 0.15 0.04, 0.25 26
Gi ls
Suppo 12 Suppo 14 0.39 0.35, 0.43 0.43 0.00, 0.91 29 0.67 0.46, 0.92 66 0.06 − 0.05, 0.16 5
Suppo 12 Suppo 17 0.28 0.24, 0.32 0.09 − 0.45, 0.94 9 0.78 0.38, 1.00 78 0.10 − 0.01, 0.21 13
Suppo 14 Suppo 17 0.42 0.38, 0.45 0.34 0.09, 0.59 34 0.97 0.52, 1.00 52 0.17 0.06, 0.26 14
Tensions12 Tensions14 0.31 0.27, 0.34 0.43 0.00, 1.00 28 0.54 0.26, 0.79 74 − 0.02 − 0.13, 0.09 − 2
Tensions12 Tensions17 0.19 0.15, 0.23 0.41 0.14, 0.92 38 0.35 0.17, 0.65 75 − 0.06 − 0.16, 0.03 − 13
Tensions14 Tensions17 0.32 0.28, 0.36 0.14 − 0.77, 0.44 13 0.71 0.45, 1.00 64 0.17 0.07, 0.28 23
C oss- ai co ela ions
Boys
Suppo 12 Tensions12 0.41 0.38, 0.45 0.64 0.29, 0.96 37 0.62 0.46, 0.82 52 0.12 0.02, 0.21 11
Suppo 14 Tensions14 0.46 0.42, 0.49 0.59 0.10, 1.00 28 0.78 0.53, 1.00 51 0.20 0.10, 0.30 21
Suppo 17 Tensions17 0.54 0.50, 0.57 1.00 0.71, 1.00 62 0.38 − 0.42, 0.96 8 0.31 0.22, 0.40 30
Gi ls
Suppo 12 Tensions12 0.44 0.41, 0.47 0.98 0.70, 1.00 45 0.51 0.38, 0.62 53 0.02 − 0.07, 0.11 2
Suppo 14 Tensions14 0.61 0.58, 0.63 0.79 0.49, 1.00 35 0.76 0.59, 0.97 44 0.35 0.26, 0.44 21
Suppo 17 Tensions17 0.65 0.63, 0.68 0.90 0.68, 1.00 51 0.90 0.56, 1.00 27 0.36 0.28, 0.45 22
373Beha io Gene ics (2019) 49:366–375
1 3
di e om a p e ious e iew on gene ic s udies o beha io-
al p oblems inding ha he s abili y is mainly in luenced
by gene ic ac o s (Hannigan e al. 2017b). Na u ally, amily
in e ac ion is no independen o sha ed genes, bu is in lu-
enced by pa en ing which also has a gene ic backg ound
(Mile a-Sei z e al. 2016). We ound modes co ela ions
be ween pa en al and o sp ing a ings o amily in e ac ion,
which also includes he passi e gene–en i onmen co ela-
ion. Sha ed en i onmen al e ec s become smalle om 12
o 17yea s o age when gene ic ac o s become mo e impo -
an . This esul is simila o ha ound o many psychologi-
cal ai s, such as in elligence and men al heal h indica o s
(Be gen e al. 2007), and e en o BMI (Sil en oinen e al.
2016). Since adolescence is cha ac e ized by dec easing
dependence on pa en s and inc easing in luence o pee s
(Ahmed e al. 2015; Kil o d e al. 2016), we could specula e
ha his inc easing gene ic e ec e lec s he ole o an ac i e
gene–en i onmen co ela ion when child en ac i ely shape
hei en i onmen pa ly based on hei geno ype. Inc eas-
ing independence may also lead child en o in e p e amily
in e ac ions mo e h ough hei own cha ac e is ics, such as
pe sonali y, which a e a ec ed by gene ic ac o s (Spengle
e al. 2012).
Unique en i onmen al ac o s also explained a sha e o
a ia ion o amily in e ac ion, and a some ages, hey we e
mo e impo an han gene ic o sha ed en i onmen al ac-
o s. Howe e , in con as o gene ic and sha ed en i on-
men al ac o s, he unique en i onmen al co ela ions we e
small in size especially when conside ing he measu emen s
be ween ages. Mode a e unique en i onmen al co ela ions
we e, howe e , ound be ween he wo dimensions o amily
in e ac ion measu ed a he same ages. This sugges s ha
unique expe iences ela ed o amily in e ac ion a e ime-
speci ic. This small e ec o unique en i onmen al ac-
o s on he s abili y o amily in e ac ion cha ac e is ics is
suppo ed by a p e ious win s udy which ound e y low
unique en i onmen al co ela ions o pa en –child in e ac-
ion, e en when measu ed on consecu i e days (Bu e al.
2015). This may sugges ha pa en s do no sys ema ically
a o o disc imina e agains he same child o e ime, and
hus unique en i onmen al ac o s e lec ansien e ec s o
p obably e y mino en i onmen al in luences, changes in
mood o possible co ela ed measu emen e o s since ela-
ional suppo and ela ional ensions we e measu ed using
he same ques ionnai e.
In addi ion o he gene ic a chi ec u e o he amily in e -
ac ion, ou da a allowed us o s udy how he pe cei ed am-
ily in e ac ion changes om ea ly o la e adolescence as well
as di e be ween pa en s and child en. P e ious s udies ha e
sugges ed ha pa en –child ela ionships de e io a e om
childhood o adolescence (Hadiwijaya e al. 2017; Kim e al.
2001; Loebe e al. 2000). Ou esul s only pa ly suppo ed
his because we ound de e io a ion in ela ional suppo
om 12 o 17yea s o age, bu when s udying ela ional
ensions, he only di e ence was less ela ional ensions
a 12yea s o age in gi ls. Howe e , he age pa e n may
depend on how pa en ing and amily in e ac ion ha e been
assessed. In his s udy, he amily-in e ac ion ques ionnai e
was used (Na usk and Pulkkinen 1994), and based on his
ques ionnai e, he wo dimensions we e calcula ed such as
also in he p e ious s udies using his same measu emen
ins umen (La end esse e al. 2010; Sil en oinen e al.
2014). The decision o use wo dimensions was ini ially
based on he esul s o he explo a i e ac o analyses sys-
ema ically sugges ing he wo- ac o solu ion a all ages, in
boys and gi ls as well as in pa en s and hei o sp ing bu
was u he suppo ed by ou empi ical esul s. The dec eas-
ing sco es o ela ional suppo may be ela ed o he inc eas-
ing ac i i ies o child en ou side home when some child en
hink ha hey do no anymo e ge , o e en need, suppo
om hei pa en s. This may also explain why he a ia-
ion o ela ional suppo inc eases a he same ime. On he
o he hand, he inc easing independence does no inc ease
ensions in he amily and seems ac ually o le el o di -
e ences be ween child en as indica ed by he dec easing
a ia ion o ela ional ensions. The p esence o wo dimen-
sions is also suppo ed by compa isons be ween pa en al
and o sp ing a ings when he o sp ing we e a he age
o 12. Pa en s a ed less ela ional ensions bu lowe ela-
ional suppo han did o sp ing. This may e lec pa en s’
sel -c i ical a i udes owa d amily in e ac ion while ha ing
mo e posi i e a i udes owa d hei child en, a he han ice
e sa. Thus, ou esul s sugges ha ela ional-suppo and
ela ional- ensions a e co ela ed bu s ill pa ly independen
dimensions o amily-in e ac ion.
Ou s udy has bo h s eng hs and weaknesses. The main
s eng h is he longi udinal measu es o amily in e ac ion
using he same ques ions a h ee ages co e ing he c i ical
phase o li e om ea ly o la e adolescence in a la ge se
o wins, allowing us o s udy he ole o gene ic and en i-
onmen al ac o s o e ime. Using he Finnish popula ion
egis e , we we e able o iden i y all wins in he selec ed
bi h coho s. Though he esponse a es in ou win su eys
we e e y high (88–95%), he epea ed su eys dec eased
e en ion o e ime, such ha by 17yea s o age 64% o all
pai s we e s ill in he s udy. None heless, ou s udy coho
can be ega ded as ep esen a i e. Fu he , he pa en s o
wins also independen ly a ed amily in e ac ion using he
same ques ions as hei o sp ing allowing us o s udy he
associa ions be ween he a ings o pa en s and o sp ing.
The main limi a ion o ou da a is ha amily in e ac ion
was assessed wi h a limi ed numbe o ques ions. A la ge
numbe and g ea e b ead h o ques ions would ha e p ob-
ably educed he measu emen e o .
In conclusion, gene ic ac o s play an impo an ole in
pe cei ed amily in e ac ion in la e adolescence, whe eas