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. Author manuscript; available in PMC: 2016 Apr 1.
Published in final edited form as: J Fam Psychol. 2015 Apr;29(2):283–289. doi: 10.1037/fam0000065

Parental Criticism is an Environmental Influence on Adolescent Somatic Symptoms

BN Horwitz 1, K Marceau 2, J Narusyte 3, J Ganiban 4, EL Spotts 5, D Reiss 6, P Lichtenstein 7, JM Neiderhiser 8
PMCID: PMC4432933  NIHMSID: NIHMS685133  PMID: 25844495

Abstract

Previous studies have suggested that parental criticism leads to more somatic symptoms in adolescent children. Yet this research has not assessed the direction of causation or whether genetic and/or environmental influences explain the association between parental criticism and adolescent somatic symptoms. As such, it is impossible to understand the mechanisms that underlie this association. The current study uses the Extended Children of Twins design to examine whether parents’ genes, adolescents’ genes, and/or environmental factors explain the relationship between parental criticism and adolescent somatic symptoms. Participants came from two twin samples, including the Twin and Offspring Study in Sweden (N = 868 pairs of adult twins and each twin’s adolescent child) and from the Twin Study of Child and Adolescent Development (N = 690 pairs of twin children and their parents). Findings showed that environmental influences account for the association between parental criticism and adolescent somatic symptoms. This suggests that parents’ critical behaviors exert a direct environmental effect on somatic symptoms in adolescent children. Results support the use of intervention programs focused on parental criticism to help reduce adolescents’ somatic symptoms.

Keywords: extended children of twins, gene-environment correlation, parental criticism, somatic symptoms

Somatic symptoms refer to physical problems (e.g., vomiting, nausea, and headaches) without a definable diagnosis (Achenbach, 1987). The prevalence of somatic symptoms increases in adolescence (e.g., Campo, 2012), which is highly problematic because somatic symptoms are common causes of absence from school and health problems, including psychological problems (Haugland & Wold, 2001). Higher levels of parental criticism (i.e., dislike, disapproval, or irritability directed towards the child; Hooley, 2007) are linked to more somatic symptoms in adolescents (Repetti, Taylor, & Seeman, 2002). This link has primarily been explained as an environmental association; parents’ critical behaviors cause elevated somatic symptoms in adolescents (Repetti et al., 2002). Yet previous research has not examined reciprocal associations between parental criticism and adolescent somatic symptoms (i.e., whether parents cause adolescents’ somatic symptoms or adolescents cause parental criticism). Thus, the direction of causation cannot be inferred. Further, previous research has not assessed whether genetic and/or environmental influences explain this association. Without estimating parents’ genes, children’s genes, and environmental influences from parent to child, effects that appear environmental may be overestimated, spurious, or reflect genotype-environment correlation (McAdams et al., 2014). The Extended Children of Twins design (ECOT) is the only model that is currently capable of disambiguating the environmental impact of parenting on adolescents from parent-based and child-based genetic influences (Marceau et al., 2013, 2014; Narusyte et al., 2008, 2011). This study uses the ECOT model to examine how parental criticism is linked to somatic symptoms in adolescent children.

The risky families model has been proposed to explain the relationship between parents’ criticism and adolescents’ somatic symptoms (Repetti et al., 2002). That is, the cumulative effects of children’s exposure to hostile family environments, including parental criticism, leads to their disrupted stress responses and, in turn, more somatic symptoms in adolescence (Repetti et al., 2002). Accordingly, exposure to parental criticism is correlated with concurrent and later somatic symptoms in adolescents (e.g., Claar, Simons, & Logan, 2008; Wickrama, Lorenz, & Conger, 1997). Yet previous research has not established causality (i.e., via the examination of reciprocal associations between parental criticism and adolescent somatic symptoms) or potential contributions from genetic and environmental factors.

The role of parental criticism as an influence on adolescent somatic symptoms may be confounded by an untested alternative explanation, whereby parental criticism is the result of adolescent-driven effects, including adolescents’ genes (e.g., Neiderhiser et al., 2004). The influence of adolescents’ genes on parenting suggests evocative genotype-environment correlation (rGE), in which children’s heritable characteristics elicit particular behaviors from parents (e.g., Horwitz & Neiderhiser, 2011). For example, children with more somatic symptoms may evoke critical responses from parents. Studies of children who are twins (i.e., child-based twin designs) can disambiguate evocative rGE and environmental effects (e.g., Neiderhiser et al., 2004). Some evidence from child-based twin studies shows that genetic factors contribute to associations between negative parenting behaviors, including parental criticism, and adolescent adjustment (e.g., externalizing problems) (Reiss, Neiderhiser, Hetherington, & Plomin, 2000). These genetic influences suggest that adolescents’ adjustment problems elicit negative parenting behaviors. Conversely, there is evidence from longitudinal child-based twin research that parental criticism exerts direct environmental influences on later externalizing problems in adolescents (Burt, McGue, Iacono, & Kruger, 2006). Considered together, research that has used child-based twin designs suggests both evocative rGE and the direct effects of parenting on adolescent adjustment problems. Yet a limitation of child-based twin designs is the inability to detect potential influences from parents’ genes.

Indeed another unexamined explanation is that the link between parental criticism and adolescent somatic symptoms is an artifact of parents’ and adolescents’ shared genes. The influence of shared genes between parents and adolescents indicates passive rGE, which refers to a correlation between genes and environments that is due to parents providing both to the child (e.g., Horwitz & Neiderhiser, 2011). To illustrate, parents’ heritable somatic symptoms may be genetically transmitted to the child and demonstrated as parental criticism. Parent-based twin designs (i.e., samples of parents who are twins and each twin’s child) can distinguish between passive rGE and environmental influences from parent to child, but not evocative rGE (e.g., Neiderhiser et al., 2004). To date, studies have not used parent-based or child-based twin designs to understand how parental criticism is associated with adolescent somatic symptoms. A design that assesses the effects of parents’ genes, adolescents’ genes, and environmental influences is crucial for advancing our understanding of what mechanisms give rise to this association.

The ECOT model allows for a stringent assessment of the environmental impact of parents’ criticism on adolescents’ somatic symptoms (Narusyte et al., 2008, 2011; Marceau et al., 2013, 2014). This is because the ECOT model combines a parent-based twin sample and a child-based twin sample into a single nested model. The combined sources of information from the parents who are twins with offspring the same age as the second sample of children who are twins affords an investigation of three key mechanisms. These mechanisms include parent-based genetic effects, suggesting passive rGE, child-based genetic effects, suggesting evocative rGE, and environmental influences, suggesting the direct environmental impact of parenting on adolescents (e.g., Narusyte et al., 2008). Using the ECOT model, the current study examined how parental criticism is correlated with adolescents’ somatic symptoms.

Method

Participants

This study used two samples, including the parent-based sample from the Twin/Offspring Study in Sweden (TOSS) and the child-based twin sample from the Twin Study of Child and Adolescent Development (TCHAD). The TOSS and TCHAD samples are comparable in several key ways (see Narusyte et al., 2008). The Institutional Review Boards (IRB) of collaborating institutions approved all procedures and assessments, and all participants provided written informed consent before participating.

TOSS includes 909 same-sex MZ and DZ twin pairs who are parents and each twin’s spouse and adolescent child (Neiderhiser & Lichtenstein, 2008). The current study included 868 twin pairs for whom data were complete, comprised of 322 male pairs (n = 123 MZ pairs; n = 199 DZ pairs) and 546 female pairs (n = 262 MZ pairs; n = 284 DZ pairs). Parent twins ranged in age from 32 to 60 (M = 44.86, ± 4.89) years old. Specific criteria were used to select the children of the twins. To maximize the comparability of the cousin offspring, each twin’s child had to be of adolescent age, no more than 4 years apart in age from the co-twin’s child, and the same-sex as the co-twin’s child. As a result, the children of the twins were 51% girls and 49% boys who ranged in age from 11 to 22 (M = 15.74, ± 2.41) years old.

TCHAD is a Swedish study of adolescent children who are MZ and DZ twins and their parents (Lichtenstein, Tuvblad, Larsson, & Carlstrom, 2007). The present study included 690 same-sex twin pairs, comprised of 338 male pairs (n = 194 MZ pairs; n = 144 DZ pairs) and 352 female pairs (n = 204 MZ pairs, n = 148 DZ pairs). Adolescent twins ranged in age from 16 to 17 (M = 16.7, + 0.42) years old. Parents of the twins participated (86% mothers) and ranged in age from 30 to 75 (M = 47.5, + 5.3) years old.

Measures

The parental criticism and somatic symptoms measures were the same in TOSS and TCHAD. To minimize skewness for model fitting, raw scores were normalized and standardized to unit variance for each measure. Rank ordering scores changes the meaning of the metric to some extent, in that each normalized score indicates rank. Yet the rank of the sample remains the same and removes many of the non-additive effects required to account for variation in untransformed measures (e.g., Eaves et al., 1997). Moreover, all analyses were conducted after controlling for participant age and sex and age differences for the cousin offspring in TOSS (McGue & Bouchard, 1984).

Parental criticism

Parental criticism was measured using parent reports on the Expressed Emotion (EE) scale (10 items, α = 86 to .90 parents in both samples; Hansson & Jarbin, 1997). Parental criticism assesses critical or irritable behaviors directed towards the child (Hansson & Jarbin, 1997; Narusyte et al., 2011). Higher scores indicated higher levels of parental criticism.

Somatic symptoms

Somatic symptoms were assessed via parents’ and adolescents’ combined scores on the Child Behavior Checklist (9 items, α = .62 to .73 across parent and youth in both samples; Achenbach, 1987). Higher scores indicated more somatic symptoms. As in previous research (e.g., Garber, VanSlyke, & Walker, 1998), correlations indicated agreement between parent and youth report on adolescent somatic symptoms across samples (i.e., TOSS: r = .38; TCHAD: r = .40).

Analytic Approach

Twin Designs

Twin designs examine whether genetic, shared environmental, and nonshared environmental factors explain variance in a variable (or associations between variables). Shared environmental influences refer to non-genetic factors that make twins similar to one another. Nonshared environmental influences refer to non-genetic factors that account twin differences.

ECOT model

The ECOT model, an extension of the twin design, incorporates a parent-based and a child-based twin design in a single nested model (Figure 1). The inclusion of both components affords an investigation of the effects of parents’ genes (i.e., passive rGE), children’s genes (i.e., evocative rGE), and environmental effects (i.e., from parent to child). For assumptions of the ECOT model, see Narusyte and colleagues (2008)

Figure 1.

Figure 1

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Representation of the path diagram used to fit the ECOT model. The lower left-hand box represents the child-based sample. The larger right-hand box represents the parent-based sample. A1 and E1 = genetic and nonshared environmental influences of parents on their critical parenting, respectively. A2, C2, and E2 = genetic, shared environmental, and nonshared environmental influences of adolescents on their somatic symptoms, respectively. A1’ = the effect of genes shared by parents and adolescents on adolescents’ somatic symptoms. Path m = direct environmental effects of critical parenting on adolescents’ somatic symptoms, whereas path n = adolescent evocative effects of adolescents’ somatic symptoms on critical parenting. Path s = the influence of shared genes of parents and adolescents. Finally, ε = e error term.

In Figure 1, the parent-based component of the model estimates parent-based genetic and environmental influences. This part of the model includes MZ and DZ twin parents and one child of each twin parent. Parents’ genetic and nonshared environmental effects on their own parental criticism are denoted by A1 and E1, respectively. The correlation between parents’ genetic effects (A1) is fixed at 1.0 for MZ twins and 0.5 for DZ twins because they share 100% and 50% (on average) of their respective segregating genes. Parents’ nonshared environmental effects (E1) are uncorrelated because nonshared environmental influences account for twin differences. Parents’ shared environmental influences were excluded based on previous research (see Narusyte et al., 2008). The path leading from A1 (parent’s genetic influences on parenting) to A1’ (child’s genetic influences on somatic symptoms due to parents’ genetic influences on parenting) is fixed at 0.5 because parents share 50% of their genes with their children.

The child-based component of the model includes MZ and DZ twin children and their parents and the adolescent offspring of the MZ and DZ twin parents (see Figure 1). The cousin pairs (children of twin parents) share 25% and 12.5% of their genes with their cousins for children of MZ twins and DZ twins, respectively. The correlation between the adolescents’ genetic effects (A2) is fixed at 1.0 MZ for twins, 0.5 for DZ twins, 0.25 for the offspring of the MZ twin parents, and 0.125 for the offspring of the DZ twin parents. The influence of genetic, shared environmental, and nonshared environmental effects on adolescent somatic symptoms is denoted by A2, C2, and E2, respectively.

In Figure 1, the paths m and n represent reciprocity in the association between parental criticism and adolescent somatic symptoms. Specifically, path m represents the effect of parental criticism on adolescent somatic symptoms (i.e., the parent-based effect), whereas path n represents the effect of adolescent somatic symptoms on critical parenting (i.e., the child-based effect). Path s represents genes shared by parents and adolescents that influence both parental criticism and adolescent somatic symptoms. If the m, a1, and s paths are significant, this suggest that parents’ genes are influencing the association between parental criticism and adolescent somatic symptoms, via passive rGE. If paths n, a2, and/or s are significant, this suggests the influence of adolescents’ genes on this association, via evocative rGE. If path m is significant but path s is not significant, this suggests that parental criticism exerts an environmental influence on adolescent somatic symptoms. Measurement error was modeled as a separate parameter; otherwise, parameter estimates can be biased in a reciprocal causation model (Heath et al., 1993).

The ECOT model was fit to the raw data using maximum likelihood estimation in Mx (Neale, 1997). We tested a full model, where all of the genetic and environmental paths described above were estimated. We then systematically dropped path m (i.e., the parent-based effect) and n (i.e., the child-based effect) in order to confirm the significance of each of these paths. If paths m or n could not dropped without a significant decrement in model fit, as indicated by a significant increase in the χ2 value, the path was determined to be significant. Finally, we systematically dropped all paths that were not significant according to 95% confidence intervals in order to verify that there was not a significant decrement in model fit, thus confirming the non-significance of the paths.

Results

Phenotypic correlations among the study variables were modest but significant and in the expected directions across both samples. Higher levels of parental criticism were associated with more somatic symptoms in the adolescent children (r = .24 for TOSS and r = .22 for TCHAD).

Figure 2 depicts the model fitting results for the full model. There were parent-based genetic effects on parental criticism and adolescent-based genetic effects on adolescent somatic symptoms. The path m (i.e., environmental effect of parental criticism) was significant, whereas the paths s (i.e., passive rGE) and n (i.e., evocative rGE) were both nonsignificant. Thus, results from the full model suggest that environmental influences explain the association between parental criticism and adolescent somatic symptoms, with no evidence of contributions from passive or evocative rGE.

Figure 2.

Figure 2

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This figure is reduced from Figure 1 in order to more succinctly present results. Unstandardized path estimates and 95% confidence intervals (in brackets) are provided for each estimated path. Model fit statistics are provided in the lower left. The significant m path suggests that critical parenting exerts environmental influences on adolescent somatic symptoms. The paths s and n estimated at 0 suggests that passive rGE and evocative rGE, respectively, are not present in this association.

Nested model fitting results confirmed results from the full model. Path n could be dropped without a decrement in model fit (Full model: -2Lnl = 16486.97, df = 6175, AIC = 4136.97; without path n: -2Lnl = 16486.97, df = 6176, AIC = 4134.97, Δχ2 (1) = 0.00, p > .05). However, dropping path m resulted in a significant decrement in model fit (without path m: -2Lnl = 16640.22, df = 6176, AIC = 4288.22, Δχ2 (1) = 153.25, p < .05). This suggests that parental criticism exerts an environmental effect on adolescent symptoms.

Discussion

Using the ECOT model, the current investigation stringently assessed the extent to which environmental influences account for the association between parental criticism and adolescent somatic symptoms. Findings demonstrated that parent-driven environmental influences explained this association, independent of passive and evocative rGE. Thus, findings indicate that parental criticism contributes to somatic symptoms in adolescent children. Consistent with the risky families model (e.g., Repetti et al., 2002), the cumulative effects of adolescents’ exposure to parental criticism may give rise to their disrupted stress responses and somatic symptoms, in turn.

Our findings support the use of intervention programs that focus on parental criticism in order to cause reductions in adolescents’ somatic symptoms. Although such interventions should not be cast as a replacement for those that directly target adolescents’ somatic symptoms, training programs focused on teaching parents to regulate the expression of critical behaviors may lead to a further decrease in somatic symptoms. Accordingly, a recent study found that changes in parents’ emotion regulation predicted reduced somatic symptoms in adolescents (Kehoe, Havighurst, & Harley, 2014). Moreover, our findings may also have implications for the reduction of adolescents’ psychological problems (i.e., anxiety and depression), which are strongly correlated with somatic symptoms (Campo, 2012). Indeed, researchers have purported that adolescents may describe concurrent psychological and somatic problems as only somatic symptoms (Petanidou et al., 2014). In households where parents are highly critical, adolescents may be more likely to express psychological problems as somatic symptoms. Thus, interventions focused on reducing parental criticism may have the added benefit of reducing related psychological problems in adolescents.

In light of these results, it will be important for future studies to examine which environmental factors shape critical parenting behaviors. Perhaps the emotional strain of financial or work stress spills over and causes parents to direct more criticism towards their adolescent children (e.g. Chih-Yuan, Lee, & August, 2011; Margolin, Christensen, & John, 1996). Additionally, future studies are needed to investigate how assortative mating for characteristics that have negative repercussions for parenting (e.g., depression, Lovejoy, Graczyk, O’Hare, & Neauman, 2000) may impact adolescents’ somatic symptoms. For example, depression in both parents may augment criticism within their marriage, which may spill over to their parenting behaviors (Feinberg & Kan, 2011; Margolin et al., 1996) and cause further elevation in the adolescents’ somatic symptoms.

Study limitations must be addressed. First, the ECOT model has limited power to assess child sex differences. Though we adjusted for the adolescents’ age and sex, separate analyses between parents and sons or daughters would elucidate whether findings vary by child sex. Second, it was not possible to account for assortative mating because the ECOT model only incorporates one parent at a time. Third, there is no agreed upon clinical cutoff score for high parental criticism on the EE, so it was not possible to identify those parents at risk of expressing extreme criticism towards their adolescents. At the same time, the focus of this study was on understanding total variance rather than high or extreme scores. Fourth, the parental criticism measure included an item that may tap parental disengagement. However, the strengths of the parental criticism subscale of the EE questionnaire are that it has been well validated, used successfully in prior research, and is conceptually closest to the commonly used parental criticism subscale of the EE observational measure (Butzlaff & Hooley, 1998; Hansson & Jarbin, 1997; Narusyte et al., 2011).

The current study is a rigorous test of the environmental impact of parental criticism on adolescent somatic symptoms, free from rGE effects. Findings suggest that parents’ critical behaviors exert a direct environmental influence on somatic symptoms in adolescent children. As such, our findings support the use of interventions focused on reducing parents’ critical behaviors directed towards their adolescent children as effective strategies for reducing somatic symptoms in the adolescents.

References

  1. Achenbach TM, McConaughy SH, Howell CT. Child/adolescent behavioral and emotional problems: implications of cross-informant correlations for situational specificity. Psychological Bulletin. 1987;101:213–232. doi: 10.1037/0033-2909.101.2.213. [DOI] [PubMed] [Google Scholar]
  2. Burt AS, McGue M, Iacono WG, Krueger RF. Differential parent-child relationships and adolescent externalizing symptoms: Cross-lagged analyses within a monozygotic twin differences design. Developmental Psychology. 2006;42:1289–1298. doi: 10.1037/0012-1649.42.6.1289. [DOI] [PMC free article] [PubMed] [Google Scholar]
  3. Butzlaff RL, Hooley JM. Expressed emotion and psychiatric relapse: A meta-analysis. Archives of General Psychiatry. 1998;55:547–552. doi: 10.1001/archpsyc.55.6.547. [DOI] [PubMed] [Google Scholar]
  4. Campo JV. Annual research review: functional somatic symptoms and associated anxiety and depression--developmental psychopathology in pediatric practice. Journal of Child Psychology and Psychiatry. 2012;53:575–592. doi: 10.1111/j.1469-7610.2012.02535.x. [DOI] [PubMed] [Google Scholar]
  5. Chih-Yuan SL, Lee J, August GJ. Financial stress, parental depressive symptoms, parenting practices, and children’s externalizing problem behaviors: Underlying processes. Family Relations. 2011;60:476–490. doi: 10.1111/j.1741-3729.2011.00656.x. [DOI] [Google Scholar]
  6. Claar RL, Simons LE, Logan DE. Parental response to children’s pain: The moderating inpact of children’s emotional distress on symptoms and disability. Pain. 2008;138:172–179. doi: 10.1016/j.pain.2007.12.005. [DOI] [PubMed] [Google Scholar]
  7. Garber J, Van Slyke DA, Walker LS. Concordance between mothers’ and children’s reports of somatic and emotional symptoms in patients with recurrent abdominal pain or emotional disorders. Journal of Abnormal Child Psychology. 1998;26:381–391. doi: 10.1023/A:1021955907190. [DOI] [PMC free article] [PubMed] [Google Scholar]
  8. Eaves LJ, Silberg JL, Maes HH, Simonoff E, Pickles A, Rutter M, et al. Genetics and developmental psychopathology: 2. The main effects of genes and environment on behavioral problems in the Virginia Twin Study of Adolescent Behavioral Development. Journal of Child Psychology and Psychiatry and Allied Disciplines. 1997;38:965–980. doi: 10.1111/j.1469-7610.1997.tb01614.x. [DOI] [PubMed] [Google Scholar]
  9. Feinberg ME, Kan ML. Establishing family foundations: Intervention effects on coparenting, parent/infant well-being, and parent-child relations. Journal of Family Psychology. 2011;22:253–263. doi: 10.1037/0893-3200.22.2.253. [DOI] [PMC free article] [PubMed] [Google Scholar]
  10. Hansson K, Jarbin G. A new self-rating questionnaire in Swedish for measuring expressed emotion. Nordic Journal of Psychiatry. 1997;5:287–297. doi: 10.3109/08039489709090721. [DOI] [Google Scholar]
  11. Haugland S, Wold B. Subjective health complaints: Reliability and validity of survey methods. Journal of Adolescence. 2001;64:611–624. doi: 10.1006/jado.2000.0393. [DOI] [PubMed] [Google Scholar]
  12. Heath AC, Kessler RC, Neale MC, Hewitt JK, Eaves LJ, Kendler KS. Testing hypotheses about direction of causation using cross-sectional family data. Behavior Genetics. 1993;23:29–50. doi: 10.1007/BF01067552. [DOI] [PubMed] [Google Scholar]
  13. Henningsen P, Zimmerman T, Sattel H. Medically unexplained physical symptoms, anxiety, and depression: A meta-analytic review. Psychosomatic Medicine. 2003;65:528–533. doi: 10.1097/01.PSY.0000075977.90337.E7. [DOI] [PubMed] [Google Scholar]
  14. Horwitz BN, Neiderhiser JM. Gene-environment interplay, family relationships, and child adjustment. Journal of Marriage and Family. 2011;73:804–816. doi: 10.1111/j.1741-3737.2011.00846.x. [DOI] [PMC free article] [PubMed] [Google Scholar]
  15. Hooley JM. Expressed emotion and relapse of psychopathology. Annual Review of Clinical Psychology. 2007;3:329–352. doi: 10.1146/annurev.clinpsy.2.022305.095236. [DOI] [PubMed] [Google Scholar]
  16. Kehoe CE, Havighurst SS, Harley AE. Somatic complaints in adolescence: The role of parents’ emotion socialization. The Journal of Early Adolescence. 2014 doi: 10.1177/0272431614547052. [DOI] [Google Scholar]
  17. Lichtenstein P, Tuvblad C, Larsson H, Carlstrom E. The Swedish Twin study of Child and Adolescent Development study. Twin Research and Human Genetics. 2007;10:67–73. doi: 10.1375/twin.10.1.67. http://dx.doi.org/10.1375/twin.10.1.67. [DOI] [PubMed] [Google Scholar]
  18. Lovejoy CM, Graczyk PA, O’Hare E, Neuman G. Maternal depression and parenting behavior: A meta-analytic review. Clinical Psychology Review. 2000;20:561–592. doi: 10.1016/S0272-7358(98)00100-7. [DOI] [PubMed] [Google Scholar]
  19. Margolin G, Christensen A, John RS. The continuance and spillover of everyday tensions in distressed and nondistressed families. Journal of Family Psychology. 1996;10:304–321. doi: 10.1037/0893-3200.10.3.304. [DOI] [Google Scholar]
  20. Marceau K, Horwitz BN, Narusyte J, Ganiban JM, Spotts EL, Reiss D, Neiderhiser JM. Gene-Environment Correlation Underlying the Association Between Parental Negativity and Adolescent Externalizing Problems. Child Development. 2013;84:2031–2046. doi: 10.1111/cdev.12094. [DOI] [PMC free article] [PubMed] [Google Scholar]
  21. Marceau K, Narusyte J, Lichtenstein P, Ganiban JM, Spotts EL, Reiss D, Neiderhiser JM. Parental knowledge is an environmental influence on adolescent externalizing. The Journal of Child Psychology and Psychiatry. 2014 doi: 10.1111/cdev.12094. [DOI] [PMC free article] [PubMed] [Google Scholar]
  22. McAdams TA, Neiderhiser JM, Rijsdijk FV, Narusyte J, Lichtenstein P, Eley TC. Accounting for genetic and environmental confounds in associations between parent and child characteristics: A systematic review of children-of-twins studies. Psychological Bulletin. 2014 doi: 10.1037/a0036416. [DOI] [PubMed] [Google Scholar]
  23. McGue M, Bouchard TJ., Jr Adjustment of twin data for the effects of age and sex. Behavior Genetics. 1984;14:325–343. doi: 10.1007/BF01080045. [DOI] [PubMed] [Google Scholar]
  24. Narusyte J, Neiderhiser JM, Andershed, Karin A, D’Onofrio BM, Reiss D, Spotts E, Ganiban J, Lichtenstein P. Parental criticism and externalizing behavior problems in adolescents: the role of environment and genotype-environment correlation. Journal of Abnormal Psychology. 2011;120:365–376. doi: 10.1037/a0021815. [DOI] [PMC free article] [PubMed] [Google Scholar]
  25. Narusyte J, Neiderhiser JM, D’Onofrio BM, Reiss D, Spotts EL, Ganiban J, Lichtenstein P. Testing different types of genotype-environment correlation: an extended children-of-twins model. Developmental Psychology. 2008;44:1591–1603. doi: 10.1037/a0013911. [DOI] [PMC free article] [PubMed] [Google Scholar]
  26. Neale MC. Mx: Statistical modeling. 3. Richmond, VA: Virginia Commonwealth University; 1997. [Google Scholar]
  27. Neiderhiser JM, Lichtenstein P. The Twin and Offspring Study in Sweden: Advancing our understanding of genotype-environment interplay by studying twins and their families. Acta Psychologica Sinica. 2008;40:1116–1123. [Google Scholar]
  28. Neiderhiser JM, Reiss D, Pedersen NL, Lichtenstein P, Spotts EL, Hansson K, Cederblad M, Ellhammer O. Genetic and environmental influences on mothering of adolescents: a comparison of two samples. Developmental Psychology. 2004;40:335–351. doi: 10.1037/0012-1649.40.3.335. 0012-1649.40.3.335. [DOI] [PMC free article] [PubMed] [Google Scholar]
  29. Petanidou D, Giannakopoulos G, Tzavara C, Dimitrikaki C, Kolaitis G, Tountas K. Adolescents’ multiple recurrent subjective health complaints: Investigation associations with emotional/behavioral difficulties in a cross-sectional, school-based study. Child and Adolescent Mental Health. 2014;8:2–8. doi: 10.1186/1753-2000-8-3. http://dx.doi.org/10.1186/1753-2000-8-3. [DOI] [PMC free article] [PubMed] [Google Scholar]
  30. Reiss D, Neiderhiser JM, Hetherington E, Plomin R. The relationship code: Deciphering genetic and social influences on adolescent development. Cambridge, MA: Harvard University Press; 2000. [Google Scholar]
  31. Repetti RL, Taylor SE, Seeman TE. Risky families: family social environments and the mental and physical health of offspring. Psychological Bulletin. 2002;128:330–366. doi: 10.1037/0033-2909.128.2.330. [DOI] [PubMed] [Google Scholar]
  32. Wickrama KA, Lorenz FO, Conger RD. Parental support and adolescent physical health status: a latent growth-curve analysis. Journal of Health and Social Behavior. 1997;38:149–163. doi: 10.2307/2955422. [DOI] [PubMed] [Google Scholar]

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