Parent and Child Psychopathology and Suicide Attempts among Children of Parents with Alcohol Use Disorder

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Parent and Child Psychopathology andSuicide Attempts among Children ofParents with Alcohol Use DisorderKenneth R. Conner a b , Robert M. Bossarte a b , Naiji Lu a , KimberlyKaukeinen a , Grace Chan c , Peter Wyman a , Xin M. Tu a , David B.Goldston d , Rebecca J. Houston e , Kathleen K. Bucholz f & Victor M.Hesselbrock ca University of Rochester Medical Center , Rochester , New York ,USAb VA VISN 2 Center of Excellence for Suicide Prevention ,Canandaigua , New York , USAc University of Connecticut , Mansfield , Connecticut , USAd Duke University , Durham , North Carolina , USAe State University of New York at Buffalo Research Institute onAddictions , Buffalo , New York , USAf Washington University , St. Louis , Missouri , USAAccepted author version posted online: 09 Apr 2014.Publishedonline: 08 May 2014.

To cite this article: Kenneth R. Conner , Robert M. Bossarte , Naiji Lu , Kimberly Kaukeinen , GraceChan , Peter Wyman , Xin M. Tu , David B. Goldston , Rebecca J. Houston , Kathleen K. Bucholz& Victor M. Hesselbrock (2014) Parent and Child Psychopathology and Suicide Attempts amongChildren of Parents with Alcohol Use Disorder, Archives of Suicide Research, 18:2, 117-130, DOI:10.1080/13811118.2013.826154

To link to this article: http://dx.doi.org/10.1080/13811118.2013.826154

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Parent and ChildPsychopathology andSuicide Attempts amongChildren of Parents withAlcohol Use Disorder

Kenneth R. Conner, Robert M. Bossarte, Naiji Lu,Kimberly Kaukeinen, Grace Chan, Peter Wyman, Xin M. Tu,David B. Goldston, Rebecca J. Houston, Kathleen K. Bucholz, andVictor M. Hesselbrock

Parents with psychopathology such as alcohol use disorder (AUD) that confers risk forsuicide attempt (SA)may have children who are more likely to develop such psychopathologyand to attempt suicide, suggesting that risk may be ‘‘transmitted’’ from parents to children.We examined this phenomenon during the transition from childhood to adolescence, whenrisk for SA increases dramatically. A cohort of 418 children were examined at average age9.4 (range 7–14) years at enrollment (Time 1, childhood) and approximately 5 years later,prior to reaching age 18 (Time 2, adolescence). One or both biological parents, oversampledfor AUD, were also interviewed. Structural equation models (SEM) examinedfather-child, mother-child, and either=both parent-child associations. The primary outcomewas SA over follow-up among offspring, assessed at Time 2. As hypothesized, parentalantisocial personality disorder predicted conduct disorder symptoms in offspring both duringchildhood and adolescence (parent-child model, father-child model) and maternal AUDpredicted conduct disorder symptoms during childhood (mother-child model). However,we did not find evidence to support transmission of depression from parents to offspring eitherduring childhood or adolescence, and parent psychopathology did not show statisticallysignificant associations with SA during adolescence. In conclusion, we conducted a rare studyof parent-to-child ‘‘transmission’’ of risk for SA that used a prospective research design,included diagnostic interviews with both parents and offspring, and examined the transitionfrom childhood to adolescence, and the first such study in children of parents with AUD.Results provided mixed support for hypothesized parent-child associations.

Keywords adolescent, alcohol use disorder, parent, risk factor, suicide attempt

INTRODUCTION

A suicide attempt (SA) is more likely to occurduring adolescence than at any other time in

the life course (Kessler, Borges, & Walters,1999). SA during youth is a potent risk factorfor eventual suicide (Hawton & Harriss,2007) and indeed some experts regard it as

Archives of Suicide Research, 18:117–130, 2014Copyright # International Academy for Suicide ResearchISSN: 1381-1118 print=1543-6136 onlineDOI: 10.1080/13811118.2013.826154

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‘‘the single most potent risk factor for youthsuicide,’’ p. 375 (Bridge, Goldstein, & Brent,2006). Accordingly, the prevention of suicidein youth demands a focus on the understand-ing and prevention of SA.

Prior suicidal behavior, depression, andexternalizing psychopathology (e.g., impul-sive aggression, alcohol and drug usedisorders, conduct problems) confer riskfor SA and suicide during adolescence (Brent,Johnson, Perper et al., 1994; Fergusson,Woodward, & Horwood, 2000; Gould, King,Greenwald et al., 1998; Shaffer, Gould,Fisher et al., 1996). It has been argued thatmodels of suicidal behavior during youthmust account for the potential transmissionof such risk factors from parents to offspring(Brent & Mann, 2006). In support of thisargument, parents with histories of suicidalbehavior have children that are at increasedrisk for SA (Kim, Seguin, Therrien et al.,2005; Lieb, Bronisch, Hofler et al., 2005;Melhem, Brent, Ziegler et al., 2007) and par-ents displaying key risk factors for suicidalbehavior including depressive disorders andvarious forms of externalizing psychopath-ology have children that are at increased riskfor these difficulties (Brent, Oquendo,Birmaher et al., 2002; Harold, Rice, Hayet al., 2010; Kim, Seguin, Therrien et al.,2005; van Goozen, Fairchild, Snoek et al.,2007). Integrating such data, Brent and Mann(2006) proposed that parental psychopath-ology including depression and impulsiveaggression, respectively, are key influenceson these difficulties in offspring which in turnpromote risk for SA during youth.

Attempted suicide is rare duringchildhood and prevalence increases dramati-cally in adolescence (Lewinsohn, Rohde,Seeley et al., 2001). Therefore, prospectivestudies of SA etiology that span the periodfrom childhood to adolescence when riskemerges may be especially informative,particularly if data are gathered from bothparents and youth, yet few published studieshave met these standards (Fergusson,Woodward, & Horwood, 2000; King, Kerr,

Passarelli et al., 2010; Lieb, Bronisch, Hofleret al., 2005; Melhem, Brent, Ziegler et al.,2007). These rigorous prospective studieswere an important step forward althoughthey were limited to the use of low-risk com-munity samples (Fergusson, Woodward, &Horwood, 2000; Lieb, Bronisch, Hofler et al.,2005) or very high risk clinical, psychiatricsamples (King, Kerr, Passarelli et al., 2010;Melhem, Brent, Ziegler et al., 2007), with un-clear generalizability to other populations.

Although Brent and Mann (2006) pre-sented their ideas to explain the influenceof a parent who has attempted suicide ontheir adolescent child’s risk for SA, theirideas have wider implications. For example,individuals with alcohol use disorder(AUD) are at elevated risk for suicidalbehavior (Kessler, Borges, Walters et al.,1999; Wilcox, Conner, & Caine, 2004) aswell as major risk factors for suicidal beha-vior including depression and externalizingpsychopathology (Hasin, Stinson, Ogburnet al., 2007), with increased potential thattheir children will develop such difficulties(Glowinski, Jacob, Bucholz et al., 2004),yet there is a meager database on the influ-ences of parents with AUD on offspringSA. Indeed, we were only able to identifyone investigation of SA among children ofparents with AUD that contained detaileddiagnostic interviews with both parents andchildren (Glowinski, Jacob, Bucholz et al.,2004). The study was limited to a cross-sectional design. Interestingly, it showed thatpaternal psychopathology may be especiallyinfluential on offspring SA.

The purpose of the current investi-gation was to add to the small databaseof prospective studies of SA in youth thatspan childhood and adolescence andinclude detailed interviews from parentsand children (Fergusson, Woodward,Horwood et al., 2000; King, Kerr, Passarelliet al., 2010; Lieb, Bronisch, Hofler et al.,2005; Melhem, Brent, Ziegler et al., 2007),and to conduct the first such study inchildren of parents with AUD. Informed

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by Brent and Mann’s (2006) ideas, weexamined the influences of parent SA,depression, and externalizing psychopath-ology on these behaviors in youth assessedduring childhood and approximately 5years later, during adolescence. Wehypothesized that parent depression andexternalizing psychopathology would showdirect associations with these behaviors inyouth which would, in turn, be directlyassociated with SA in youth. We alsohypothesized that a history of parent SAwould show a direct association with SAin offspring. As discussed above, parent(s)with AUD and their offspring are animportant population to test these hypoth-eses due to elevated rates of psychopath-ology and suicidal behavior. Along withan analysis of parental influences generally,we analyzed mother-child and father-childrelationships in separate models becausematernal and paternal influences onoffspring psychopathology often differ(Connell & Goodman, 2002), a pattern thatmay extend to the study of SA amongchildren of parents with AUD (Glowinski,Jacob, Bucholz et al., 2004).

METHOD

Procedure

Data were gathered for the Collabora-tive Study on the Genetics of Alcoholism(COGA), a multicenter family study inthe U.S. COGA examines individuals withalcohol dependence recruited from treat-ment centers (probands), first degreerelatives of these individuals, as well asnon-alcohol dependent comparison famil-ies recruited through various populationsources (e.g., motor vehicle registration).COGA investigators have created severaldatasets from various studies. For thecurrent analysis, we examined a cohort ofchildren who were on average age 9.4 yearsat enrollment (range 7–14 years) and who

were reassessed approximately 5 years later,with all reassessments occurring prior toreaching age 18. Individuals who were notreassessed at 5 years, approximately 22%,were excluded from analyses. At least onebiological parent to the children (i.e., adultCOGA participant) was also interviewedaround the time of the baseline assessment.The cohort was assembled between 1991and 1998 and the follow-ups were com-pleted between 1997 and 2004. An exemp-tion from the University of Rochester IRBwas granted to perform these secondaryanalyses of de-identified COGA data.

Measures

Information about the presence=absence of alcohol use disorders, drug usedisorders, mood disorders, SA, andconduct disorder and antisocial personalitydisorder among parents were obtained withthe adult version of the Semi-StructuredAssessment for the Genetics of Alcohol-ism, SSAGA (Bucholz, Cadoret, Cloningeret al., 1994). Diagnostic sections of theSSAGA have been intensively studiedand show solid reliability (Bucholz,Cadoret, Cloninger et al., 1994; Bucholz,Hesselbrock, Shayka et al., 1995; Kramer,Chan, Kuperman et al., 2009) and validity(Hesselbrock, Easton, Bucholz et al.,1999). A child=adolescent version of theSSAGA was administered to children ages17 and younger (Kuperman, Schlosser,Kramer et al., 2001). This youth versionwas primarily based on the adult SSAGA,but used age-appropriate language. Thevarious diagnostic sections of the child=adolescent version are reliable, with kappacoefficients averaging 0.72 (Kuperman,Schlosser, Kramer et al., 2001). An abbrevi-ated version of the SSAGA, the FamilyHistory Module (Rice, Reich, Bucholz et al.,1995), was administered to obtain data fromone parent about the other when one of theparents was not available for interview. Thisabbreviated interview has demonstrated

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reliability (Rice, Reich, Bucholz et al., 1995)and includes assessments of substance usedisorders, mood disorders, conduct=antisocial personality disorder, and SA. Forthe current analyses diagnoses were basedon criteria described in Diagnostic and Stat-istical Manual, 3rd edition, revised (AmericanPsychiatric Association, 1987).

Time 1 (T1) Assessments in Children. T1 datawere assessed during the baseline assess-ment and covered lifetime history up tothe time of the T1 assessment. We createda continuous measure of T1 suicidalitywith range 0–2: 0) no history of suicidalthoughts or attempt; 1) history of suicidalthoughts only; 2) history of suicide attempt(SA). The latter was assessed with the item‘‘Have you ever tried to kill yourself?’’(Preuss, Schuckit, Smith et al., 2002). Con-duct disorder symptoms were used toassess the externalizing domain (Dick,2007; Krueger & Markon, 2006). Conductdisorder symptoms were selected to assessexternal symptoms in youth because theyare in evidence at an early age, prior tothe onset of other externalizing variablesthat confer risk for SA in youth assessedby the SSAGA, for example substanceuse disorders (Lahey, Miller, Gordon et al.,1999; Wagner & Anthony, 2002). We cre-ated a continuous variable with range 0–2:0) no conduct disorder symptoms, 1)1-plus symptoms but no diagnosis, 2)conduct disorder diagnosis. To assessdepression we also created a continuousvariable with range 0–2: 0) no history ofdepressed mood or anhedonia, 1) historyof depressed mood and=or anhedonialasting at least 2 weeks but no majordepressive episode, and 2) major depressiveepisode. Depressive symptoms were codedif they were substance-induced or occurredindependent of substance use. We usedsymptoms of conduct disorder anddepression, as opposed to diagnosesalone, to increase sensitivity to detectpsychopathology in youth.

T1 Assessment in Parents. T1 data in parentswere generally obtained near the time of thechildren’s baseline assessment and coveredlifetime history up to T1. History of SAwas assessed with the same SA item usedwith children (described above). Externaliz-ing psychopathology was assessed withpresence or absence, respectively, of alco-hol use disorder including alcohol abuseor dependence, drug use disorder includingany non-alcohol abuse or dependence diag-nosis, and antisocial personality disorder.Depression was based on presence orabsence of major depressive disorderepisode including substance-induceddepression and depression independent ofsubstance use.

Time 2 (T2) Assessments (Children Only). T2data were based on the time period sincethe T1 assessment. SA at T2 was assessedwith the aforementioned SA item. Forchildren who reported a history of SA atT1, we examined the date of the last SAto confirm that the attempt occurred overfollow-up. Conduct disorder symptomsand depressive symptoms were assessed atT2 in offspring using the same measuresdescribed for T1.

Analyses

SA at T2 among children was theoutcome in all analyses. For descriptivepurposes, unadjusted comparisons betweenchildren with a suicide attempt at T2 vs.non-attempters at T2 were made on allpredictors. For these comparisons Fisher’sExact Test for categorical predictors wereused to handle cells with small numbersof observations (Fisher, 1954).

Three structural equation (SEM) mod-els (Kaplan, 2000) were used to examine 1)mother-child, 2) father-child, and 3) parent-child relationships, respectively. The lattermodel was run if data from either parent(or both) were available, and a parent

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exposure (e.g., depression) was codedpresent if it were observed in either parent(or both). SEM is an extension of regressionmodels to address limitations of the latterwhen applied to relationships involving mul-tiple variables over time (Kaplan, 2000). In aregression model, there exists a clear distinc-tion between dependent and independent

variables and the model relates the depen-dent to a set of independent variables.SEM is designed to handle the fact that avariable may serve as both an independentand a dependent variable in an analysis; SAat T1 is an example in our study (seeFigure 1). In all models, parents wereassumed to influence their children rather

FIGURE 1. Models of parent and child influences on adolescent suicide attempts. (Color figure available online.)

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than vice-versa and, among children, the pro-spective influences of T1 variables on T2were also examined. For each SEM model,we assessed model fit using the Chi-squareand Root Mean Square Error of Approxi-mation (RMSEA) goodness of fit statistics(MacCallum, Browne, & Sugawara, 1996).We used probit link function and reportedstandardized coefficients in all the models.The unit of analysis when fitting SEM forthe data was the family, rather than individualsubjects as in standard regression, to accountfor the non-independence of data withinfamilies. All SEM analyses were performedusing Mplus (Muthen & Muthen, 2006).The contribution of variables in statisticalmodels were tested using two-sided tests atthe p< .05 level.

RESULTS

Descriptive Data

Three hundred seven families partici-pated and 7 families were excluded fromanalyses due to missing data. Abouttwo-thirds of families (N¼ 203, 67.7%)had a single child participant, with mean1.4� 0.6 children per family (range 1–4).

Descriptive results are provided inTable 1. The data are presented for thesample in the father-child SEM analysis(N¼ 290 children of 199 fathers), themother-child analysis (N¼ 394 childrenof 269 mothers), and the parent-childanalysis (N¼ 418 children of 300 parentsconsisting of mother, father, or both). Ineach sample the data are stratified by theoutcome, showing a comparison of chil-dren who made a suicide attempt at T2 tonon-attempters at T2. Seventeen childrenof 12 fathers had a T2 suicide attempt(father-child sample), 18 children of 12mothers had a T2 attempt (mother-childsample), and 19 children of 13 parentshad a T2 attempt (parent-child sample). Alarge number of parents had a lifetime

history of SA including 24 (12.1%) fathers,39 (14.5%) mothers, and 60 (20.0%) eitherparent. Most parents had a history of alco-hol use disorder including 162 (81.4%)fathers, 120 (44.6%) mothers, and 247(82.3%) either parent.

Univariate comparisons on all predic-tors between children with a suicideattempt at T2 and non-attempters are pre-sented in Table 1. None of the parentalpsychopathology variables includingparent, father, or mother history of SA,AUD, drug use disorder, or antisocial per-sonality disorder were associated with aT2 suicide attempt in offspring at a statisti-cally significant level, with the lone excep-tion of maternal drug use disorderhistory. With the exception of conduct dis-order at T1, the other child predictors wereassociated with a suicide attempt at T2including depressive symptoms at T1 andT2, conduct disorder symptoms at T2,and SA at T1. Among the child covariates(age, sex, race-ethnicity), only sex was stat-istically significant, with girls being morelikely to make an attempt at T2.

SEM Results

The SEM results are presented inFigure 1 including results for the father-childmodel (A), mother-child model (B), andparent-child model (C). Tests of model fitindicated the Chi-square test was significant( p< 0.001) and the RMSEA value wasbetween 0.05 and 0.1 for each model, indica-tive of adequate fit: father-child model,v2(30)¼ 83.2, p� 0.001 and RMSEA¼0.076; mother-child model, v2(30)¼ 103.1,p� 0.001 and RMSEA¼ 0.071; parent-child model, v2(30)¼ 99.5, p� 0.001 andRMSEA¼ 0.073. In each SEM model,female sex was associated with increased riskfor SA in youth at T2; the other covariates(age, race) were not associated with SA at astatistically significant level (bottom ofFigure 1).

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TABLE1.UnadjustedComparisonsofChildSuicideAttempters

andNon-Attempters

atTim

e2

Child

Predictors

Father-childSample

Mother-childSample

Parent-childSample

Suicide

Attempters

(T2),N

(%)

Non-

Attempters

(T2),N

(%)

p-value�

Suicide

Attempters

(T2),N

(%)

Non-

Attempters

(T2),N

(%)

p-value�

Suicide

Attempters

(T2),N

(%)

Non-

Attempters

(T2),N

(%)

p-value�

T1Depression

0.0048

0.0168

0.0105

0,none

10(58.8%)

353(87.2%)

12(66.7%)

329(87.5%)

12(63.2%)

347(87.0%)

1,symptoms

5(29.4%)

43(10.6%)

4(22.2%)

39(10.4%)

5(26.3%)

43(10.8%)

2,disorder

2(11.8%)

9(2.2%)

2(11.1%)

8(2.1%)

2(10.5%)

9(2.3%)

T2Depression

0.0026

0.0217

0.0020

0,none

13(76.5%)

260(95.2%)

15(83.3%)

356(94.7%)

15(79.0%)

378(94.7%)

1,symptoms

0(0.0%)

7(2.6%)

0(0.0%)

12(3.2%)

0(0.0%)

13(3.3%)

2,disorder

4(23.5%)

6(2.2%)

3(16.7%)

8(2.1%)

4(21.1%)

8(2.0%)

T1Conduct

Sxs

0.1264

0.2349

0.1305

0,none

9(52.9%)

201(73.6%)

10(55.6%)

270(71.8%)

10(52.6%)

284(71.2%)

1,symptoms

7(41.2%)

65(23.8%)

7(38.9%)

91(24.2%)

8(42.1%)

100(25.1%)

2,disorder

1(5.9%)

7(2.6%)

1(5.6%)

15(4.0%)

1(5.3%)

15(3.8%)

T2Conduct

D=o

0.0211

0.0255

0.0098

0,none

3(17.7%)

108(39.6%)

4(22.2%)

146(38.8%)

4(21.1%)

160(40.1%)

1,symptoms

6(35.3%)

114(41.8%)

6(33.3%)

164(43.6%)

6(31.6%)

170(42.6%)

2,disorder

8(47.1%)

51(18.7%)

8(44.4%)

66(17.6%)

9(47.4%)

69(17.3%)

T1Suicidality-Continuous

<.0001

<.0001

<.0001

0,none

10(58.8%)

232(85.0%)

11(61.1%)

317(84.3%)

11(57.9%)

336(84.2%)

1,ideation

4(23.5%)

40(14.7%)

4(22.2%)

56(14.9%)

5(26.3%)

60(15.0%)

2,attempt

3(17.7%)

1(0.4%)

3(16.7%)

3(0.8%)

3(15.8%)

3(0.8%)

(Continued)

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TABLE1.Continued

Parent

Predictors

Father-child

Mother-child

Parent(s)-child

Suicide

Attempters

(T2),N

(%)

Non-

Attempters

(T2),N

(%)

p-value�

Suicide

Attempters

(T2),N

(%)

Non-

Attempters

(T2),N

(%)

p-value�

Suicide

Attempters

(T2),N

(%)

Non-

Attempters

(T2),N

(%)

p-value�

T1SuicideAttem

pt

0.1258

0.2548

0.0889

No

9(75.0%)

178(89.5%)

9(75.0%)

233(86.6%)

8(61.5%)

232(80.8%)

Yes

3(25.0%)

21(10.5%)

3(25.0%)

36(13.4%)

5(38.5%)

55(19.2%)

T1DepressiveD=o

0.5478

0.8021

0.6125

No

11(91.7%)

170(85.4%)

9(75.0%)

210(78.1%)

10(76.9%)

202(70.1%)

Yes

1(8.3%)

29(14.6%)

3(25.0%)

59(21.9%)

3(23.1%)

85(29.6%)

T1AlcoholUse

D=o

0.5797

0.5024

0.8254

No

2(16.7%)

47(23.6%)

8(66.7%)

153(56.9%)

2(15.4%)

51(17.8%)

Yes

10(83.3%)

152(76.4%)

4(33.3%)

116(43.1%)

11(84.6%)

236(82.2%)

T1DrugUse

D=o

0.7213

0.0395

0.2395

No

6(50.0%)

89(44.7%)

11(91.7%)

168(62.5%)

7(53.9%)

108(37.6%)

Yes

6(50.0%)

110(55.3%)

1(8.3%)

101(37.6%)

6(46.2%)

179(62.4%)

T1AntisocialPD

0.1735

0.7805

0.2381

No

7(58.3%)

151(75.9%)

11(91.7%)

252(93.7%)

8(61.5%)

218(76.0%)

Yes

5(41.7%)

48(24.1%)

1(8.3%)

17(6.3%)

5(38.5%)

69(24.0%)

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TABLE1.Continued

Covariates(child

variables)

Father-child

Mother-child

Parent(s)-child

Suicide

Attempters

N(%

)

Non-

Attempters

N(%

)p-value�

Suicide

Attempters

N(%

)

Non-

Attempters

N(%

)p-value�

Suicide

Attempters

N(%

)

Non-

Attempters

N(%

)p-value�

T1Age,M�SD

9.9�2.1

9.3�1.8

0.1648

9.9�2.1

9.3�1.8

0.1599

9.9�2.0

9.4�1.8

0.1567

Sex

0.0052

0.0063

0.0166

Fem

ale

14(82.4%)

128(46.9%)

15(79.0%)

184(48.9%)

15(79.0%)

194(48.6%)

Male

3(17.7%)

145(53.1%)

3(16.7%)

192(51.1%)

4(21.1%)

205(51.4%)

Race-ethnicity

0.3834

0.8004

1.0000

Whitenon-

Hispanic

11(64.7%)

207(75.8%)

13(72.2%)

254(67.7%)

13(68.4%)

268(67.3%)

Non-W

hite

6(35.3%)

66(24.2%)

5(27.8%)

121(32.3%)

6(31.6%)

130(32.7%)

Notes.Sam

plesizes:father-child

sampleincludes

190fathersand299children;mother-child

sampleincludes

269mothersand394children;parent-child

sample

includes

300parent(s)and418children.

T2suicideattempt(outcome):17childrenof12fathershad

aT2suicideattempt(father-child

sample);18childrenof12mothershad

aT2attempt(m

other-child

sample);19childrenof13parent(s)had

aT2attempt(parent-child

sample).

T!¼

time1,T2¼time2,sxs¼symptoms,hx¼history.

� P-values

based

oncomparisonsusingFisher’sExact

Test.

��Oneparentallowed

amissingvalue.

ARCHIVES OF SUICIDE RESEARCH 125

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Father-Child SEM Model Results (A). Theseresults show statistically significant paths tothe outcome from child symptoms ofdepression at T2, conduct disorder at T2,and suicidality at T1 (bottom of Figure 1).Moving distally from the outcome (andup the model), father antisocial personalitydisorder (ASPD) at T1 was associated withchild conduct disorder symptoms at T1 andT2, symptoms of child conduct disorderand child depression at T1 were associatedwith child suicidality at T1, and symptomsof conduct disorder at T1 were associatedwith conduct disorder symptoms at T2.Finally, as depicted at the top of the model,father drug use disorder (DUD) at T1 wasassociated with father SA history at T1.

Mother-Child SEM Model Results (B). Theseresults show, in the bottom half of the fig-ure, paths to the outcome that are similarto those obtained in the father-child model.In the upper half of the model, thereare some noteworthy differences from thefather-child model; namely, in themother-child model, maternal alcohol usedisorder (AUD) was associated with childconduct disorder at T1 and maternal his-tory of SA at T1 (whereas in thefather-child model, there were no statisti-cally significant paths from paternal AUD).

Parent-Child SEM Model Results (C). Theseresults show, in the bottom half of the fig-ure, paths to the outcome that are similarto those obtained in the other models. Inthe upper half of the parent-child model,parental ASPD at T1 was associated withchild conduct disorder symptoms at T1and T2 (similar to the father-child model).Several variables were associated with par-ent history of SA at T1 including parentalAUD (similar to the mother-child model)and parental depression and ASPD (whichwere not associated with SA in mothers orfathers in the other models). Finally, thepath coefficients from child depression atT1 to child depression at T2 were nearly

identical in the three models although itdid not reach statistical significance in thefather-child model.

DISCUSSION

Summary

The current analyses showed that childdepressive symptoms and conduct disordersymptoms, an externalizing variable, wereassociated with suicide attempt (SA) duringchildhood and again when assessedapproximately 5 years later, during ado-lescence, consistent with the theoreticalideas presented by Brent and Mann(2006). Depressive symptoms, conduct dis-order symptoms, and suicidality assessed inchildhood also predicted these symptomslater, during adolescence, illustrating conti-nuity of psychopathology during develop-ment. We also found evidence of‘‘transmission’’ of vulnerability from par-ents to offspring as predicted by Brentand Mann. In particular, parental antisocialpersonality disorder predicted conduct dis-order symptoms in offspring both duringchildhood (T1) and adolescence (T2)(parent-child model, father-child model)and maternal alcohol use disorder predictedconduct disorder symptoms during child-hood (mother-child model). However, wedid not find evidence to support trans-mission of depression from parents to off-spring either during childhood (T1) oradolescence (T2). Interestingly, none ofthe father, mother, or parent variablesshowed a statistically significant associationwith SA during adolescence (see compari-sons in Table 1). Moreover, father, mother,and parent SA were not associated withchild suicidality at T1 in any of the SEMmodels, inconsistent with our hypothesisof more or less direct transmission of sui-cidality from parents to offspring. Finally,consistent with Brent and Mann’s ideasand the general literature, lifetime parental

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psychopathology including depression (i.e.,major depressive episode) and externalizingvariables (i.e., AUD, drug use disorder, andantisocial personality disorder) were asso-ciated with a history of parent SA in oneor more SEM models (i.e., father, mother,parent).

Limitations and Strengths

There were limitations of the study.We did not examine the role of genetic fac-tors. The high prevalence of father AUDhistory (81.4%) in the cohort may havecontributed to the nonsignificant associ-ation between parent AUD and parentSA in analyses of fathers but not motherswhere there was a more optimal distri-bution of AUD history (44.6% of mothers)for detecting associations. The limitednumber of suicide attempts over follow-upamong youth warrant cautious interpret-ation of nonsignificant results. For examplewe did not identify a statistically significantrelationship between parent- and offspringsuicidal behavior, an association shown inprior studies (Kim, Seguin, Therrien et al.,2005; Lieb, Bronisch, Hofler et al., 2005;Melhem, Brent, Ziegler et al., 2007). Thelimited number of suicide attempters alsoruled out more detailed analyses of sex dif-ferences, for example through separateanalyses of male- and female youth.Although a limitation, all of the hypothe-sized paths to youth suicide attempts testedin our conceptual model were statisticallysignificant with the lone exception of thepath from parent SA to offspring SA (seeFigure 1). Therefore, the relatively smallnumber of SA in youth was generally nota limiting factor in testing our conceptualmodel. Moreover, there is precedence forprospective analyses of a limited numbersof suicide attempts over time, attributableto the low incidence rate of suicidal beha-vior. For example, a prior test of severalpredictors emphasized by Brent and Mann

(2006) contained 11 suicide attempts overfollow-up (Melhem, Brent, Ziegler et al.,2007). Although it is true that researchershave analyzed some large and informativelongitudinal community surveys such asthe National Longitudinal Study of Ado-lescent Health that contained large num-bers of suicide attempts (Borowsky,Ireland, & Resnick, 2001; Kidd, Henrich,Brookmeyer et al., 2006), such studies havenot contained detailed interviews with par-ents and offspring. A large and informativeScandinavian registry analysis of suicideattempts in offspring contained data onparents and offspring (Stenager & Qin,2008), although a limitation is the relianceon clinical records’ data. We also did notexamine important relational variables(e.g., suboptimal family environment) andnegative life experiences (e.g., child abuse)that were discussed by Brent and Mann(2006). The sample is not populationrepresentative.

There were several strengths of theanalyses. The current study featured aprospective design, detailed diagnosticassessments, and interviews with bothparents and offspring, representing thefirst such study in an AUD sample. Wetested a theoretical model that examinedinterrelationships among predictorsincluding potential parent-to-child path-ways in addition to tests of relationshipsbetween predictors and the SA outcome.A history of SA was common amongparents in the sample, underscoring theimportance of examining intergenerationalpathways to suicidal behavior in familieswith AUD. The direct and clear phrasingof the SA item in the current study,‘‘Have you ever tried to kill yourself?’’,likely elicited reports about suicidal actscontaining at least some intent to die asopposed to more ubiquitous non-suicidalself-injury (Silverman, Berman, Sanddalet al., 2007), acknowledging that thephrasing of the SA item likely came ata cost to sensitivity.

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CONCLUSIONS

Results of the current study reaffirm thatdepressive symptoms and externalizingbehaviors (i.e., conduct disorder symptoms)confer risk for SA among adolescentchildren of parents with AUD, a vulnerablepopulation. Moreover, the results suggestthat when these risk factors present duringchildhood they are predictive of futuredifficulties during adolescence, when riskfor SA peaks. Results also indicate thatsome forms of externalizing parental psy-chopathology (i.e., antisocial personalitydisorder in fathers, alcohol use disordersin mothers) predict offspring conduct dis-order symptoms which, in turn, promoterisk for SA, consistent with the idea thatparental risk for suicidal behavior is trans-mitted to children through externalizingbehaviors, among other factors. The dataalso suggest that child risk factors (i.e.,depressive symptoms, conduct disordersymptoms, prior suicidality) more so thanparental risk factors reliably foretell SAduring adolescence, suggesting that riskidentification and intervention efforts maybe best served by focusing on youth fromhigh-risk families who themselves manifestsymptoms suggestive of risk. Depressivesymptoms as well as suicidality during child-hood predict SA 5 years later, suggestingtheir importance in risk recognition andprevention efforts. Finally, future studiesof SA among children of parents withAUD and other vulnerable families willbe maximally informative if they containadditional contextual information aboutfamily environment and child abuse.

AUTHOR NOTE

Kenneth R. Conner, University ofRochester Medical Center, Rochester,New York, USA, and VA VISN 2 Centerof Excellence for Suicide Prevention,Canandaigua, New York, USA.

Robert M. Bossarte, University ofRochester Medical Center, Rochester,New York, USA, and VA VISN 2 Centerof Excellence for Suicide Prevention,Canandaigua, New York, USA.

Naiji Lu, University of Rochester Medi-cal Center, Rochester, New York, USA.

Kimberly Kaukeinen, University ofRochester Medical Center, Rochester,New York, USA.

Grace Chan, University of Connecticut,Mansfield, Connecticut, USA.

Peter Wyman, University of RochesterMedical Center, Rochester, New York, USA.

Xin M. Tu, University of RochesterMedical Center, Rochester, New York, USA.

David B. Goldston, Duke University,Durham, North Carolina, USA.

Rebecca J. Houston, State Universityof New York at Buffalo Research Instituteon Addictions, Buffalo, New York, USA.

Kathleen K. Bucholz, WashingtonUniversity, St. Louis, Missouri, USA

Victor M. Hesselbrock, University ofConnecticut, Mansfield, Connecticut, USA.

Correspondence concerning this articleshould be addressed to Kenneth R. Conner,University of Rochester Medical Center,Department of Psychiatry, 300 CrittendenBlvd, Rochester, NY 14642. E-mail:[email protected]

FUNDING

Funding for the study was provided by agrant from the Centers for Disease Controland Prevention, R01 CE001882-01 (Con-ner, PI). The Collaborative Study on theGenetics of Alcoholism (COGA) providedthe data for the analyses. COGA is sup-ported by NIH grant U10AA08401 fromNIAAA and NIDA.

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