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For this assignment you will complete the Introduction portion of your paper.  The Introduction should be about one page in length and will respond to two critical questions asked by ALL researchers in ALL research efforts.  Those questions are:

     1.   WHY did the authors of your article – the researchers – decide to do this research?  WHAT was the research question (or questions) they asked (their HYPOTHESIS)?  You must be VERY SPECIFIC in responding to this first question because the rest of your paper will hinge on it.

     2.  HOW did the researchers approach their research …what METHOD of research did they use?  Did they conduct a true experiment?  A correlational research design?  A longitudinal design?  WHAT?  More often than not, these two questions will be answered in the Abstract of your article.  If they are not, read their Introduction and Methods sections and the answers will be there.  Tell me WHY the authors decided to use this particular method of research.  If you have truly tried and still cannot figure out the answers, see me NOW.

ORIGINAL ARTICLE

Social phobia, depression and eating disorders during middle adolescence: longitudinal associations and treatment seeking

Klaus Rantaa, Juha V€a€an€anenb, Sari Fr€ojdc, Rasmus Isomaad, Riittakerttu Kaltiala-Heinob,e and Mauri Marttunena,f,g

aDepartment of Adolescent Psychiatry, Helsinki University Central Hospital, Helsinki, Finland; bDepartment of Adolescent Psychiatry, Tampere University Hospital, Tampere, Finland; cSchool of Health Sciences, University of Tampere, Tampere, Finland; dCity of Jakobstad, Department of Social Services and Health Care, Jakobstad, Finland; eMedical School, University of Tampere, Tampere, Finland; fDepartment of Adolescent Psychiatry, University of Helsinki, Helsinki, Finland; gDepartment of Mental Health and Substance Use Services, National Institute for Health and Welfare, Helsinki, Finland

ABSTRACT Background: Longitudinal associations between social phobia (SP), depression and eating disorders (EDs), and the impact of antecedent SP and depression on subsequent treatment seeking for EDs have rarely been explored in prospective adolescent population studies. Aim: We aimed to examine these associations in a large-scale follow-up study among middle adolescents. Method: We surveyed 3278 Finnish adolescents with a mean age of 15 years for these disorders. Two years later, 2070 were reached and again surveyed for psychopathology and treatment seeking. Longitudinal associations between the self-reported disorders and treatment-seeking patterns for self- acknowledged ED symptoms were examined in multivariate analyses, controlling for SP/depression comorbidity and relevant socioeconomic covariates. Results: Self-reported anorexia nervosa (AN) at age 15 years predicted self-reported depression at age 17 years. Furthermore, self-reported SP at age 15 years predicted not seeking treatment for bulimia nervosa (BN) symptoms, while self-reported depression at age 15 years predicted not seeking treat- ment for AN symptoms during the follow-up period. Conclusions: Adolescents with AN should be monitored for subsequent depression. Barriers caused by SP to help seeking for BN, and by depression for AN, should be acknowledged by healthcare professio- nals who encounter socially anxious and depressive adolescents, especially when they present with eating problems.

ARTICLE HISTORY Received 13 September 2016 Revised 1 June 2017 Accepted 7 August 2017

KEYWORDS Social phobia; depression; eating disorders; adolescents; comorbidity; treatment seeking

The mean onset of eating disorders (EDs) in the population is during adolescence. The peak of incidence for both bulimia nervosa (BN) and anorexia nervosa (AN) is between 15 and 19 years [1–3]. Both population [1,2] and clinical studies [4,5] indicate that BN is associated with a range of anxiety, mood, disruptive and substance use disorders in both adolescents and adults. Of the anxiety disorders, social phobia (SP) may be especially comorbid with adolescent BN [6]. Adolescent AN, as identified in the community, seems less strongly asso- ciated with other disorders [2], but clinical studies indicate that mood disorders are frequently involved [7]. In young adult populations, AN seems broadly comorbid with anxiety, mood and alcohol use disorders [1,8].

Longitudinal studies suggest that the onset of comorbid anxiety disorders generally occurs prior to that of EDs. In clin- ical studies, this order is found in �60–90% of cases [4,6,8,9], offering support for the notion of an anxiety pathway in the genesis of EDs. The association between SP and EDs in par- ticular has been found to be largely of this type [6].

With regard to depression, there is evidence of bidirec- tional connections, depression elevating the risk for EDs [10],

as well as of a heightened risk for subsequent depression in adolescents with AN and BN [11,12]. Studies with long fol- low-up spans indicate that depression may both precede and follow AN [13]. Thus, although not entirely consistent, research does indicate somewhat different types of longitu- dinal associations between SP, depression and EDs.

The mechanisms by which SP, depression and EDs are lon- gitudinally linked are not well-known [14]. Social anxiety may predispose an adolescent to subsequent EDs by participants’ preoccupation with the fear of being negatively evaluated, high performance standards, dependence on others’ opinions or negative beliefs about the public self [15,16]. In girls, a preoccupation with appearance [15] while pubertal physical changes progress may lead to ‘social appearance anxiety’ and symptoms of EDs, such as the strict pursuit of ideal body weight [17].

Regarding associations between depression and EDs, such factors as a self-deprecating thinking style, linked with both [18], may mediate bidirectional links. Moreover, biological and psychological consequences of malnutrition (e.g. apathy and numbness) could lead to the development of depression

CONTACT Klaus Ranta [email protected] Department of Adolescent Psychiatry, Helsinki University Hospital, P.O. Box 590, FI-00029 HUS, Helsinki, Finland � 2017 The Nordic Psychiatric Association

NORDIC JOURNAL OF PSYCHIATRY, 2017 VOL. 71, NO. 8, 605–613 https://doi.org/10.1080/08039488.2017.1366548

following AN [19]. Antecedent disorders may also affect treat- ment seeking for EDs. It remains unknown whether comor- bidity in fact increases or decreases treatment seeking or engagement in treatment [20,21]. Treatment seeking may vary according to the type of comorbidity.

SP could act as a barrier to seeking treatment for EDs because only very few, �9% of adolescents with SP, seek help for their anxiety [22]; furthermore, SP is typically associated with feelings of shame that may inhibit treatment- seeking behavior [21]. Indeed, some evidence suggests that high social anxiety prevents participants from engaging in treatment for EDs [23], but no studies addressing this issue in general population samples or among adolescents have been conducted [21,24].

Associated with depression, decreased activity or apathy [25], pessimism about the possibility of being helped [21,26] or negative self-evaluations and internalized feelings of shame [21] may prevent treatment seeking. Indeed, the find- ings of one large-scale adolescent population study indicated that the higher the level of depression symptoms, the lower the possibility that the adolescent will seek help [27]. The available research on treatment seeking for EDs suggests that emotional suffering or disorders may even facilitate treatment seeking. However, all studies do not report such an effect [21]. As this research is conducted mainly among adults with EDs using retrospective analyses, they likely miss a significant part of the disorders in the population. Overall, a mixed and contradictory picture emerges from this field. Studies examining treatment seeking for EDs in adolescents, in prospective designs and large population samples, are lacking.

In sum, gaps exist in knowledge on independent pro- spective associations between specific EDs (AN/BN) with SP and depression. Moreover, little is known about the possible impact of antecedent SP and depression on treatment seek- ing for EDs in adolescence. There is a need for longitudinal, controlled studies.

Aims

To address the knowledge gaps in prior research, we aimed to answer two research questions. First: Are there independ- ent, longitudinal associations between self-reported SP and depression at age 15 years and BN/AN at age 17 years, or conversely, do self-reported BN and AN symptoms at age 15 years predict self-reported SP and depression at age 17 years? Second: Are self-reported SP or depression at age 15 years associated with a reduced rate of seeking help for self-acknowledged symptoms of BN/AN at a two-year follow-up?

Three hypotheses based on the literature search were tested. 1. SP at age 15 years will increase the risk of BN and AN at age 17 years. 2. Depression at age 15 years will increase the risk of BN and AN at age 17 years, but BN and AN at age 15 years will also increase the risk for depression at age 17 years. 3. SP at age 15 years will be associated with a heightened risk of not seeking help for BN and AN during the follow-up period. We made no specific hypothesis

concerning the role of depression as affecting help-seeking behavior because the research is inconclusive and contradictory.

Material and methods

Design, procedure and sampling

The data came from the Finnish Adolescent Mental Health Cohort Study [28]. At baseline (T1), ninth-grade students aged 15–16 years from all secondary schools in the Finnish cities of Tampere and Vantaa completed a person-identifiable questionnaire containing measures on mental health (i.e. depression, anxiety, conduct disorder, EDs and substance use), health behavior and associated psychosocial variables in their schools. The survey assessment tool took one lesson (i.e. 30–45 min) to complete.

The T1 sample consisted of 3278 adolescents (1609 girls, 1669 boys) with a mean age of 15.5 (SD ¼0.39) years. The response rate for the baseline survey was 94.4%. Participants were contacted after a 2-year follow-up period (T2) by mul- tiple methods: surveys in high/vocational schools, surface mail and finally by email. In all, 2082 responses were received. Ten responses were excluded due to obvious facetiousness and due to double responding. The study was approved by the Ethics Committee of Tampere University Hospital (Study Approval No. 9924).

The 2070 adolescents who responded both times (repre- senting 63.1% of those who responded at T1) comprise the participants of the present study. At T2, their mean age was 17.6 (SD ¼ 0.41) years, and 56.4% (1167) were girls. Of the participants studying at T2, 62% were in high school and 38% in vocational school. The sample represents the Finnish general adolescent population, as in Finland more than 90% of children and adolescents attend Grades 1–9 in public schools.

Instruments

Self-reported SP: SP was assessed with a 17-item self-report instrument, the Social Phobia Inventory (SPIN) [29], which covers all DSM-IV symptom clusters for SP. The reliability and validity of this instrument to detect symptoms of SP in the adolescent age group have been demonstrated in several studies across many countries, such as USA, Canada, Germany, Finland, Spain and Brazil [30]. Using a cutoff score of 24 points, a sensitivity of 81% and a specificity of 85% relative to a diagnosis of SP has been demonstrated for the SPIN in a large Finnish adolescent population sample com- parable to the present sample [31]. Scores of 0–23 represent no self-reported SP, and scores �24 represent self-reported SP in the present study.

Self-reported depression: The 13-item Beck Depression Inventory (short version) (BDI) [32] was used as the measure of depression. The BDI has been examined in several adoles- cent samples [33]. A recent meta-analysis found 17 psycho- metric studies in this age range. A pooled estimate of internal consistency was 0.86, and the pooled estimates for both sensitivity and specificity for detecting depression

606 K. RANTA ET AL.

against a clinical interview were 0.81 [34]. Bennett et al. [35] have also reported acceptable sensitivity and specificity indi- ces for the 13-item version in adolescents. The Finnish ver- sion [36] has been found to possess good internal consistency in this age group [37]. A cutoff score of �8 points suggested by Beck et al. [38] was used to identify ado- lescents with self-reported depression, and scores of 0–7 rep- resented no self-reported depression. This cutoff has resulted in a sensitivity of 0.93 and specificity of 0.88 in detecting depression, as established through a structured psychiatric interview [39].

Self-reported EDs: We assessed self-reported BN and AN with questionnaires formulated according to the DSM-IV-TR [40] criteria, which have been extensively used in prior Finnish ED research. BN was recorded if the respondent: (i) reported having had frequent binge-eating episodes; (ii) while binge-eating had a feeling that his/her eating was out of control; (iii) reported binge-eating episodes at least twice per week over a 3-month period; (iv) reported compensatory behaviors to prevent weight gain (strict diet or fasting, heavy exercise, vomiting, misuse of laxatives or diuretics); and (v) as a consequence of binge-eating, felt bad or unsuccessful as a person unless one was thin or fit.

AN was recorded if the respondent reported: (i) an inten- tional dieting episode to lose weight; (ii) during that episode a significant fear of weight gain; (iii) had felt fat despite the obviously low weight noted and commented on by family and peers; and (iv) during the episode reported amenorrhea. Furthermore, participants’ height and weight at T1 were available, from which the body mass index (BMI) at T1 was calculated.

To exclude participants who were at T1 normal weight or recovered from an earlier AN episode, we used the standard definition for normal weight (BMI of �20) proposed by British Royal College of Psychiatrists [41]. This conservative approach for setting the cutoff is consistent with findings on the weight at the return of menstruation in adolescent girls who have recovered from AN [42]. Thus, T1 AN was recorded when the participant fulfilled all DSM-IV-TR criteria 1–4 and had a BMI of <20. The DSM-IV-derived AN items have been found to possess acceptable properties to detect a lifetime episode of AN in the Finnish adolescent population [43]. At T2, no records of height and thus BMI were available; thus, AN was recorded for those fulfilling criteria 1–4.

Treatment seeking: We assessed treatment seeking for self- acknowledged BN/AN during the follow-up period at T2 with two separate questions: ‘Have you suffered from bulimia nerv- osa (AN) during the past 2 years without seeking help for the symptoms?’. The participants were asked to respond with either ‘yes’ or ‘no’ to each question. All participants who answered the BN/AN questions were included in the respective analyses, regardless of whether they met criteria for AN or BN at T1 or T2. See the ‘Statistical analysis’ section below as well.

Covariate measures: The residential stability of the adoles- cents was assessed with an item from the Life Events Checklist (LEC) [44]. At T2, adolescents reported whether they had moved during the past year with response alternatives: no (¼0), yes (¼1). Parental unemployment was assessed at T2 with an LEC item eliciting whether their parents had been

unemployed during the past year, with response alternatives: neither (¼0), or one/both (¼1) had been unemployed. These two covariates were included because of their disruptive effect on the socioeconomic conditions of adolescents and their associations with internalizing psychopathology, EDs and treatment seeking in adolescence [26,45,46].

Statistical analysis

Associations between baseline and drop-out key variables were studied using Chi-square statistics or Fisher’s exact test when appropriate. The percentages and numbers of cases for self-reported SP, depression, BN, and AN at T1 and T2 were calculated, and for those who reported not having sought treatment for BN and AN during the past 2 years at T2. The incidence (the proportion of those with a given disorder at T2 who did not have the same disorder at T1 out of all those without the condition at T1) of SP, depression, BN and AN was calculated as the percentages and the number of cases. The change in frequency for SP, depression, BN and AN in repeated measures between T1 and T2 was tested using McNemar’s test.

Longitudinal associations between the self-reported disor- ders: These were examined in logistic regression analyses (LRAs). The simple cross-tabulated frequencies, as well as unadjusted odds ratios (ORs) and adjusted odds ratios (AORs) with 95% confidence intervals (CIs) are reported for bivariate and controlled, respectively. First, the unadjusted bivariate associations between T1 SP/depression and T2 BN/AN were calculated, then associations between T1 BN/AN and T2 SP/ depression. The multivariate LRAs were constructed to con- trol for (i) the SP/depression comorbidity (at either T1 or T2,

Table 1. Cross-tabulated frequencies and bivariate associations between self- reported SP, depression and EDs at ages 15 and 17 years.

% (n/N) OR (95% CI) p

Predicting BN at age 17 years Age 15 SP -> age 17 BN

Yes 5.3 (10/188) 3.3 (1.6–6.9) .001 No 1.7 (31/1877)

Age 15 depression -> age 17 BN Yes 6.9 (13/188) 4.9 (2.5–9.6) <.001 No 1.7 (31/1877)

Predicting AN at age 17 years Age 15 SP -> age 17 AN

Yes 1.1 (2/185) 1.2 (0.3–5.1) .827 No 0.9 (17/1850)

Age 15 depression -> age 17 AN Yes 2.7 (5/187) 3.6 (1.3–10.1) .015 No 0.8 (14/1841)

Predicting SP at age 17 years Age 15 BN -> age 17 SP

Yes 20.0 (5/25) 2.0 (0.8–5.5) .161 No 11.0 (223/2032)

Age 15 AN -> age 17 SP Yes 15.8 (3/19) 1.5 (0.4–5.2) .517 No 11.0 (223/2032)

Predicting depression at age 17 years Age 15 BN -> age 17 depression

Yes 32.0 (8/25) 5.2 (2.2–12.2) <.001 No 8.3 (169/2035)

Age 15 AN -> age 17 depression Yes 31.6 (6/19) 5.1 (1.9–13.6) .001 No 8.3 (161/1936)

Note: OR (95% CI) unadjusted OR with 95% CI. Group with no disorder (No) is treated as the reference group in each LR analysis.

NORDIC JOURNAL OF PSYCHIATRY 607

depending on the respective analysis), (ii) the effect of T1 EDs in the two LRAs where the outcome variables were T2 EDs, and (iii) for the effects of confounding socioeconomic covariates. In these LRAs, T2 BN, T2 AN, T2 SP and T2 depres- sion were each treated as the dependent outcome variables. See the footnotes of Tables 2 and 3 for the description of how each variable was entered in each sequential step of the LRAs (Model 1, Model 2 and Model 3).

Treatment seeking for self-reported BN and AN: Next, we examined predictors of not seeking treatment for self- acknowledged symptoms of BN/AN during the follow-up period. These were calculated as follows. (i) Bivariate LRAs were performed with T1 SP and T1 depression each in turn as predictors. (ii) Multivariate LRAs were performed by entering T1 SP and T1 depression in the first step (Model 1), T1 BN/AN in the second step (Model 2) and T2 family relocation and par- ental unemployment in the third step (Model 3). All analyses were performed using SPSS 19.0. (SPSS Inc., Chicago, IL).

Attrition

Of the participants, 37% who had responded to the baseline survey dropped out by follow-up. Attrition was influenced by participants’ gender (girls 28% versus boys 46%, p < .001), the family structure (intact 27% versus divorced parents 33%, p < .001) and parents’ educational level (low 23% versus high 29%, p < .001). Of the main target variables, T1 SP was not more frequent among the dropouts than among those who completed the study (8 versus 9%, p ¼ .51), neither was T1 AN (1% in both groups, non-significant) nor T1 BN (1.1 versus 1.6%, non-significant). However, T1 depression was more fre- quent among dropouts (12 versus 9%, p ¼ .020).

Results

Frequency and incidence of self-reported SP, depression and EDs

Of the participants, 9.1% (187) at T1 and 11.1% (221) at T2 had SP (change in frequency, p ¼ .014), the incidence of SP

being 7.9% (147/1865). In total, 9.2% (188) had depression at T1, while 8.6% (176) had depression at T2 (change in fre- quency, non-significant), and the incidence of depression was 5.3% (99/1861). With regard to BN, 1.2% (25) adolescents at T1 and 2.0% (41) adolescents at T2 reported BN (change in frequency, p ¼ .033); the incidence for BN was 1.6% (33/ 2045). Finally, 1.0% (19) adolescents at T1 and 0.9% (19) ado- lescents at T2 reported AN (change in frequency, non-signifi- cant), the incidence for AN being 0.7% (14/1919).

Longitudinal associations between self-reported EDs, depression and SP

Predictors of BN at age 17 years: In the bivariate analyses, SP at age 15 years alone and depression at age 15 years alone each predicted BN at age 17 years (Table 1). In the final multivariate LRA model, no independent predictive role for either SP or depression at age 15 years for BN at age 17 years was found; however, BN at age 15 years was associated with an elevated risk for this outcome (p < .001), as was recent relocation (p < .05) (Table 2).

Predictors of AN at age 17 years: In bivariate analyses, depression at age 15 years predicted AN at age 17 years (Table 1). However, in the multivariate LRA, only AN at age 15 years was associated with AN at age 17 years in the final model (p < .001).

Predictors of SP at age 17 years: In the bivariate analyses, neither BN at age 15 years nor AN at age 15 years was associated alone with SP at age 17 years (Table 1). Predicting SP at age 17 years by BN at age 15 years in the multivariate LRA showed a non-significant result. Only SP at age 15 years and depression at age 17 years were associ- ated with SP at age 17 years (p < .001). The multivariate LRA regarding AN at age 15 years as a predictor of SP at age 17 years resulted similarly in non-significant findings: the final model only showed persistent associations of SP at age 15 years and depression at age 17 years (p < .001) with SP at age 17 years (Table 3).

Predictors of depression at age 17 years. In the bivariate LRAs, both BN at age 15 years and AN at age 15 years

Table 2. Risk (AOR with 95% CIs) for age 17 years self-reported BN and AN by age 15 years self-reported SP and depression in multivariate LRAs.

Model 1, AOR (95% CI) Model 2, AOR (95% CI) Model 3, AOR (95% CI)

Outcome variable: age 17 years BN

Predictor variables T1 SP 1.8 (0.8–8.3) 1.5 (0.6–3.9) 1.5 (0.6–4.0) T1 Depression 3.8 (1.8–8.3)�� 2.4 (1.0–5.8) 1.9 (0.7–4.9) T1 BN # 15.4 (5.5–43.3)��� 16.5 (5.8–46.8)��� T2 family moved within last 12 months # # 2.6 (1.0–6.3)� T2 parental unemployment during last 12 months # # 1.0 (0.3–3.6)

Outcome variable: age 17 years AN

T1 SP 0.6 (0.1–2.9) 0.6 (0.1–3.4) 0.5 (0.1–3.1) T1 depression 4.2 (1.4–12.9)� 2.7 (0.8–9.3) 3.1 (0.9–11.0) T1 AN # 38.3 (11.5–127.9)��� 41.6 (12.2–141.2)��� T2 family moved within last 12 months # # 0.0 (0.0–)a

T2 parental unemployment during last 12 months # # 0.9 (0.1–7.5)

In the first models, SP and depression at age 15 years were entered. In the second models, baseline homotypic ED (i.e. BN/AN, depending on the analysis) was controlled for. In the third models, family relocation and parental unemployment during last year were additionally controlled for. T1: first assessment point at age 15 years. T2: second assessment point at age 17 years. �p < .05, ��p < .01, ���p < .001. #Not entered in the model. aUpper limit of CI not estimable. None of those whose family had moved had AN at age 17. The stability of Model 3 was additionally tested by dropping T2 family relocation from it. This modification did not change the significance of any one association found in Model 3.

608 K. RANTA ET AL.

predicted depression at age 17 years (Table 1). Predicting depression at age 17 years by BN at age 15 years in the multivariate LRA showed that depression at age 15 years, SP at age 17 years (p < .001) and parental unemployment during the last year (p < .01) were each associated with depression at age 17 years. Finally, predicting depression at age 17 years by AN at age 15 years in the multivariate LRA resulted in AN at age 15 years retaining an independent association with depression at age 17 years [AOR 3.6 (95% CI 1.1–11.6); p < .05], along with depression at age 15 years, SP at age 17 years (p < .001) and parental unemployment during the past year (p < .05).

Treatment seeking for self-reported symptoms of BN and an

Predictors for not seeking treatment for BN during the follow- up. In the bivariate LRAs, both SP and depression at age 15 years predicted a participant having not sought help for BN during the past 2 years (Table 4). In the multivariate LRA, the final model showed that SP at age 15 years independ- ently predicted a subject not having sought treatment for BN during the follow-up period [AOR 2.4 (95% CI 1.0–5.6), p < .05], as did relocation during the previous year (p < .01) (Table 5).

Predictors for not seeking treatment for AN during the fol- low-up. In bivariate LRAs, SP at age 15 years did not, but depression at age 15 years did predict a subject not having sought help for AN during the follow-up period (Table 4).

In the multivariate LRA, the final model revealed that depression at age 15 years [AOR 4.8 (95% CI 1.9–11.9), p < .001] and AN at age 15 years (p < .001) predicted a sub- ject not having sought help for AN during the follow-up period (Table 5).

Discussion

The first aim of this study was to examine longitudinal asso- ciations between SP, depression and EDs in adolescents fol- lowed-up from 15 to 17 years of age. The second aim was to examine whether SP and depression at age 15 years would be associated with a heightened risk of not seeking help for self-reported BN and AN symptoms during the follow-up period. We found an independent predictive association only for AN at age 15 years as a predictor of depression at age 17 years. Second, SP and depression at age 15 years had dif- ferent effects on adolescents’ treatment seeking for ED symp- toms during the follow-up period. SP was associated with not seeking help for symptoms of BN, and depression was associated with not seeking help for symptoms of AN. Our findings extend the existing knowledge of the longitudinal associations between emotional disorders and EDs as well as patterns of treatment seeking for ED symptoms by introduc- ing results from a large study in a general adolescent popula- tion sample.

Temporal order of SP, depression and EDs. Results from the uncontrolled bivariate analyses hinted at bidirectional longi- tudinal associations between depression and both AN and

Table 3. Risk (AOR with 95% CIs) for age 17 years self-reported SP and depression by age 15 years self-reported BN and AN in multivariate LRAs.

Model 1, AOR (95% CI) Model 2, AOR (95% CI) Model 3, AOR (95% CI)

Outcome variable: age 17 years SP

Predictor variables/by BN T1 BN 2.0 (0.8–5.5) 0.4 (0.1–1.4) 0.4 (0.1–1.5) T1 SP # 7.8 (5.3–11.4)

��� 7.4 (5.0–11.0)���

T2 depression # 14.5 (10.0–21.1)��� 14.7 (10.1–21.4)��� T2 family moved within last 12 months # # 1.2 (0.7–2.2) T2 parental unemployment during last 12 months # # 0.8 (0.4–1.5)

Outcome variable: age 17 years SP

Predictor variables/by AN T1 AN 1.5 (0.4-5.2) 0.4 (0.1–2.2) 0.5 (0.1–2.2) T1 SP # 8.2 (5.5–12.1)��� 7.9 (5.3–11.7)��� T2 depression # 14.7 (10.0–21.5)��� 14.8 (10.0–21.8)��� T2 family moved within last 12 months # # 1.2 (0.6–2.2) T2 parental unemployment during last 12 months # # 0.8 (0.4–1.6)

Outcome variable: age 17 years depression

Predictor variables/by BN T1 BN 5.2 (2.2–12.2)��� 1.7 (0.6–5.2) 1.7 (0.6–5.1) T1 depression # 7.7 (5.1–11.8)��� 7.6 (5.0–11.6)��� T2 SP # 12.0 (8.3–17.5)��� 12.4 (8.5–18.1)��� T2 family moved within last 12 months # # 1.6 (0.9–3.0) T2 parental unemployment during last 12 months # # 2.3 (1.2–4.1)��

Outcome variable: age 17 years depression

Predictor variables/by AN T1 AN 5.1 (1.9–13.6)�� 3.6 (1.1–11.5)� 3.6 (1.1–11.6)� T1 Depression # 8.0 (5.3–12.2)��� 7.8 (5.1–12.0)��� T2 SP # 11.8 (8.0–17.4)��� 12.2 (8.2–17.9)��� T2 family moved within last 12 months # # 1.7 (0.9–3.1) T2 parental unemployment during last 12 months # # 2.1 (1.1–3.9)�

In the first models, BN/AN at age 15 years was entered. In the second models, T2 SP/depression comorbidity was controlled for. In the third models, family relocation and parental unemployment during last year were additionally controlled for. T1: first assessment point at age 15 years. T2: second assessment point at age 17 years. �p < .05, ��p < .01, ���p < .001. #Not entered in the model.

NORDIC JOURNAL OF PSYCHIATRY 609

BN. The more robust, controlled multivariate analyses yielded a different picture. In these analyses, only the predictive asso- ciation of AN at age 15 years with depression at age 17 years persisted. This was contrary to our study hypothesis, but con- sistent with some earlier findings in adolescents [11] and the malnutrition account for depression following AN [19].

In their critical review, Mattar et al. [19] concluded that the malnutrition—depression …

,

1 3

Eur Child Adolesc Psychiatry (2018) 27:1123–1132 https://doi.org/10.1007/s00787-017-1014-y

ORIGINAL CONTRIBUTION

Genetic and environmental influences on conduct and antisocial personality problems in childhood, adolescence, and adulthood

Laura W. Wesseldijk1,2 · Meike Bartels1,2,3 · Jacqueline M. Vink4 · Catharina E. M. van Beijsterveldt1 · Lannie Ligthart1,2 · Dorret I. Boomsma1,2,3 · Christel M. Middeldorp1,3,5

Received: 10 January 2017 / Accepted: 3 June 2017 / Published online: 21 June 2017 © The Author(s) 2017. This article is an open access publication

Based Assessment, were available for 9783 9–10-year-old, 6839 13–18-year-old, and 7909 19–65-year-old twin pairs, respectively; 5114 twins have two or more assessments. At all ages, men scored higher than women. There were no sex differences in the estimates of the genetic and envi- ronmental influences. During childhood, genetic and envi- ronmental factors shared by children in families explained 43 and 44% of the variance of conduct problems, with the remaining variance due to unique environment. During adolescence and adulthood, genetic and unique environ- mental factors equally explained the variation. Longitudi- nal correlations across age varied between 0.20 and 0.38 and were mainly due to stable genetic factors. We conclude that shared environment is mainly of importance during childhood, while genetic factors contribute to variation in conduct and antisocial per