@article{BuchmannSchmidBlomeyeretal.2009,
  author    = {Buchmann, Arlette F. and Schmid, Brigitte and Blomeyer, Dorothea and Becker, Katja and Treutlein, Jens and Zimmermann, Ulrich S. and Jennen-Steinmetz, Christine and Schmidt, Martin H. and Esser, G{\"u}nter and Banaschewski, Tobias and Rietschel, Marcella and Schumann, Gunter and Laucht, Manfred},
  title     = {Impact of age at first drink on vulnerability to alcohol-related problems : testing the marker hypothesis in a prospective study of young adults},
  issn      = {0022-3956},
  doi       = {10.1016/j.jpsychires.2009.02.006},
  year      = {2009},
  abstract  = {There is ample evidence that the early initiation of alcohol use is a risk factor for the development of later alcohol-related problems. The purpose of the current study was to examine whether this association can be explained by indicators of a common underlying susceptibility or whether age at drinking onset may be considered as an independent predictor of later drinking behavior, suggesting a potential causal relationship. Participants were drawn from a prospective cohort study of the long-term outcomes of early risk factors followed up from birth onwards. Structured interviews were administered to 304 participants to assess age at first drink and current drinking behavior. Data on risk factors, including early family adversity, parental alcohol use, childhood psychopathology and stressful life events, were repeatedly collected during childhood using standardized parent interviews. In addition, information on genotype was considered. Results confirmed previous work demonstrating that hazardous alcohol consumption is related to early-adolescent drinking onset. A younger age of first drink was significantly predicted by 5-HTTLPR genotype and the degree of preceding externalizing symptoms, and both factors were related to increased consumption or harmful alcohol use at age 19. However, even after controlling for these potential explanatory factors, earlier age at drinking onset remained a strong predictor of heavy alcohol consumption in young adulthood. The present longitudinal study adds to the current literature indicating that the early onset - adult hazardous drinking association cannot solely be attributed to shared genetic and psychopathologic risk factors as examined in this study.},
  language  = {en}
}
@article{HolzBoeckerSchlierBuchmannetal.2017,
  author    = {Holz, Nathalie E. and Boecker-Schlier, Regina and Buchmann, Arlette F. and Blomeyer, Dorothea and Jennen-Steinmetz, Christine and Baumeister, Sarah and Plichta, Michael M. and Cattrell, Anna and Schumann, Gunter and Esser, G{\"u}nter and Schmidt, Martin and Buitelaar, Jan and Meyer-Lindenberg, Andreas and Banaschewski, Tobias and Brandeis, Daniel and Laucht, Manfred},
  title     = {Ventral striatum and amygdala activity as convergence sites for early adversity and conduct disorder},
  series = {Frontiers in human neuroscience},
  volume    = {12},
  journal   = {Frontiers in human neuroscience},
  number    = {2},
  publisher = {Oxford Univ. Press},
  address   = {Oxford},
  issn      = {1749-5016},
  doi       = {10.1093/scan/nsw120},
  pages     = {261 -- 272},
  year      = {2017},
  abstract  = {Childhood family adversity (CFA) increases the risk for conduct disorder (CD) and has been associated with alterations in regions of affective processing like ventral striatum (VS) and amygdala. However, no study so far has demonstrated neural converging effects of CFA and CD in the same sample. At age 25 years, functional MRI data during two affective tasks, i.e. a reward (N = 171) and a face-matching paradigm (N = 181) and anatomical scans (N = 181) were acquired in right-handed currently healthy participants of an epidemiological study followed since birth. CFA during childhood was determined using a standardized parent interview. Disruptive behaviors and CD diagnoses during childhood and adolescence were obtained by diagnostic interview (2-19 years), temperamental reward dependence was assessed by questionnaire (15 and 19 years). CFA predicted increased CD and amygdala volume. Both exposure to CFA and CD were associated with a decreased VS response during reward anticipation and blunted amygdala activity during face-matching. CD mediated the effect of CFA on brain activity. Temperamental reward dependence was negatively correlated with CFA and CD and positively with VS activity. These findings underline the detrimental effects of CFA on the offspring's affective processing and support the importance of early postnatal intervention programs aiming to reduce childhood adversity factors.},
  language  = {en}
}
@article{BlomeyerBuchmannLascorzetal.2013,
  author    = {Blomeyer, Dorothea and Buchmann, Arlette F. and Lascorz, Jesus and Zimmermann, Ulrich S. and Esser, G{\"u}nter and Desrivieres, Sylvane and Schmidt, Martin H. and Banaschewski, Tobias and Schumann, Gunter and Laucht, Manfred},
  title     = {Association of PER2 genotype and stressful life events with alcohol drinking in young adults},
  series = {PLoS one},
  volume    = {8},
  journal   = {PLoS one},
  number    = {3},
  publisher = {PLoS},
  address   = {San Fransisco},
  issn      = {1932-6203},
  doi       = {10.1371/journal.pone.0059136},
  pages     = {7},
  year      = {2013},
  abstract  = {Background: Clock genes govern circadian rhythms and shape the effect of alcohol use on the physiological system. Exposure to severe negative life events is related to both heavy drinking and disturbed circadian rhythmicity. The aim of this study was 1) to extend previous findings suggesting an association of a haplotype tagging single nucleotide polymorphism of PER2 gene with drinking patterns, and 2) to examine a possible role for an interaction of this gene with life stress in hazardous drinking. Methods: Data were collected as part of an epidemiological cohort study on the outcome of early risk factors followed since birth. At age 19 years, 268 young adults (126 males, 142 females) were genotyped for PER2 rs56013859 and were administered a 45-day alcohol timeline follow-back interview and the Alcohol Use Disorders Identification Test (AUDIT). Life stress was assessed as the number of severe negative life events during the past four years reported in a questionnaire and validated by interview. Results: Individuals with the minor G allele of rs56013859 were found to be less engaged in alcohol use, drinking at only 72\% of the days compared to homozygotes for the major A allele. Moreover, among regular drinkers, a gene x environment interaction emerged (p = .020). While no effects of genotype appeared under conditions of low stress, carriers of the G allele exhibited less hazardous drinking than those homozygous for the A allele when exposed to high stress. Conclusions: These findings may suggest a role of the circadian rhythm gene PER2 in both the drinking patterns of young adults and in moderating the impact of severe life stress on hazardous drinking in experienced alcohol users. However, in light of the likely burden of multiple tests, the nature of the measures used and the nominal evidence of interaction, replication is needed before drawing firm conclusions.},
  language  = {en}
}
@article{HolzBoeckerSchlierJennenSteinmetzetal.2018,
  author    = {Holz, Nathalie E. and Boecker-Schlier, Regina and Jennen-Steinmetz, Christine and Hohm, Erika and Buchmann, Arlette F. and Blomeyer, Dorothea and Baumeister, Sarah and Plichta, Michael M. and Esser, G{\"u}nter and Schmidt, Martin and Meyer-Lindenberg, Andreas and Banaschewski, Tobias and Brandeis, Daniel and Laucht, Manfred},
  title     = {Early maternal care may counteract familial liability for psychopathology in the reward circuitry},
  series = {Social Cognitive and Affective Neuroscience},
  volume    = {13},
  journal   = {Social Cognitive and Affective Neuroscience},
  number    = {11},
  publisher = {Oxford Univ. Press},
  address   = {Oxford},
  issn      = {1749-5016},
  doi       = {10.1093/scan/nsy087},
  pages     = {1191 -- 1201},
  year      = {2018},
  abstract  = {Reward processing is altered in various psychopathologies and has been shown to be susceptible to genetic and environmental influences. Here, we examined whether maternal care may buffer familial risk for psychiatric disorders in terms of reward processing. Functional magnetic resonance imaging during a monetary incentive delay task was acquired in participants of an epidemiological cohort study followed since birth (N = 172, 25 years). Early maternal stimulation was assessed during a standardized nursing/playing setting at the age of 3 months. Parental psychiatric disorders (familial risk) during childhood and the participants' previous psychopathology were assessed by diagnostic interview. With high familial risk, higher maternal stimulation was related to increasing activation in the caudate head, the supplementary motor area, the cingulum and the middle frontal gyrus during reward anticipation, with the opposite pattern found in individuals with no familial risk. In contrast, higher maternal stimulation was associated with decreasing caudate head activity during reward delivery and reduced levels of attention deficit hyperactivity disorder (ADHD) in the high-risk group. Decreased caudate head activity during reward anticipation and increased activity during delivery were linked to ADHD. These findings provide evidence of a long-term association of early maternal stimulation on both adult neurobiological systems of reward underlying externalizing behavior and ADHD during development.},
  language  = {en}
}
@article{BoeckerSchlierHolzHohmetal.2017,
  author    = {Boecker-Schlier, Regina and Holz, Nathalie E. and Hohm, Erika and Zohsel, Katrin and Blomeyer, Dorothea and Buchmann, Arlette F. and Baumeister, Sarah and Wolf, Isabella and Esser, G{\"u}nter and Schmidt, Martin H. and Meyer-Lindenberg, Andreas and Banaschewski, Tobias and Brandeis, Daniel and Laucht, Manfred},
  title     = {Association between pubertal stage at first drink and neural reward processing in early adulthood},
  series = {Addiction biology},
  volume    = {22},
  journal   = {Addiction biology},
  publisher = {Wiley},
  address   = {Hoboken},
  issn      = {1355-6215},
  doi       = {10.1111/adb.12413},
  pages     = {1402 -- 1415},
  year      = {2017},
  abstract  = {Puberty is a critical time period during human development. It is characterized by high levels of risk-taking behavior, such as increased alcohol consumption, and is accompanied by various neurobiological changes. Recent studies in animals and humans have revealed that the pubertal stage at first drink (PSFD) significantly impacts drinking behavior in adulthood. Moreover, neuronal alterations of the dopaminergic reward system have been associated with alcohol abuse or addiction. This study aimed to clarify the impact of PSFD on neuronal characteristics of reward processing linked to alcohol-related problems. One hundred sixty-eight healthy young adults from a prospective study covering 25 years participated in a monetary incentive delay task measured with simultaneous EEG-fMRI. PSFD was determined according to the age at menarche or Tanner stage of pubertal development, respectively. Alcohol-related problems in early adulthood were assessed with the Alcohol Use Disorder Identification Test (AUDIT). During reward anticipation, decreased fMRI activation of the frontal cortex and increased preparatory EEG activity (contingent negative variation) occurred with pubertal compared to postpubertal first alcohol intake. Moreover, alcohol-related problems during early adulthood were increased in pubertal compared to postpubertal beginners, which was mediated by neuronal activation of the right medial frontal gyrus. At reward delivery, increased fMRI activation of the left caudate and higher feedback-related EEG negativity were detected in pubertal compared to postpubertal beginners. Together with animal findings, these results implicate PSFD as a potential modulator of psychopathology, involving altered reward anticipation. Both PSFD timing and reward processing might thus be potential targets for early prevention and intervention.},
  language  = {en}
}
@article{LauchtTreutleinBlomeyeretal.2009,
  author    = {Laucht, Manfred and Treutlein, Jens and Blomeyer, Dorothea and Buchmann, Arlette F. and Schmid, Brigitte and Becker, Katja and Zimmermann, Ulrich S. and Schmidt, Martin H. and Esser, G{\"u}nter and Rietschel, Marcella and Banaschewski, Tobias},
  title     = {Interaction between the 5-HTTLPR serotonin transporter polymorphism and environmental adversity for mood and anxiety psychopathology : evidence from a high-risk community sample of young adults},
  issn      = {1461-1457},
  doi       = {10.1017/S1461145708009875},
  year      = {2009},
  abstract  = {Previous research examining gene-environment interaction (G x E) with regard to vulnerability to depression and anxiety has yielded conflicting results. The present study was designed to further investigate G x F between 5-HTTLPR and exposure to environmental adversity, using different phenotypic and genotypic characterizations as well as different types of adversity within a prospective study design. Data were available from an ongoing epidemiological cohort Study following the outcome of early risk factors from birth to adulthood. At age 19 yr, 309 participants (142 males, 167 females) were characterized on measures of depression and anxiety through interview and questionnaire (DSM-IV diagnosis, Beck Depression Inventory, Harm Avoidance). Environmental adversity was assessed at birth (family adversity), and at age 19 yr (stressful life events). Bi- and tri-allelic 5-HTTLPR genotypes were obtained from genomic DNA. Results indicated that depression and anxiety in 19-yr-olds were strongly associated with both family adversity and stressful life events. Individuals with the LL genotype of 5-HTTLPR who were exposed to high family adversity displayed significantly higher rates of depressive or anxiety disorders and had more depressive symptoms than those without either condition. This G x E replicates recent findings from an epidemiological cohort study of adolescents but is in contrast to many previous reports suggesting an interaction with the S allele. No evidence for G x E was obtained with regard to current stressful life events and trait anxiety. One possible source for the conflicting findings might be attributed to heterogeneity in depression phenotypes and environmental adversity.},
  language  = {en}
}
@article{LauchtTreutleinSchmidetal.2009,
  author    = {Laucht, Manfred and Treutlein, Jens and Schmid, Brigitte and Blomeyer, Dorothea and Becker, Katja and Buchmann, Arlette F. and Schmidt, Martin H. and Esser, G{\"u}nter and Jennen-Steinmetz, Christine and Rietschel, Marcella and Zimmermann, Ulrich S. and Banaschewski, Tobias},
  title     = {Impact of psychosocial adversity on alcohol intake in young adults : moderation by the LL genotype of the serotonin transporter polymorphism},
  issn      = {0006-3223},
  doi       = {10.1016/j.biopsych.2009.02.010},
  year      = {2009},
  abstract  = {Background: Evidence from animal studies supports a role for serotonin transporter gene promoter polymorphism (5-HTTLPR) gene-environment interaction (G X E) in the development of excessive alcohol intake. Few studies in humans have been conducted on this topic, yielding inconsistent results. The present study aims to further explore G x E between 5-HTTLPR and exposure to psychosocial adversity on alcohol consumption in a high-risk community sample of young adults. Methods: Data were collected as part of the Mannheim Study of Children at Risk, an ongoing epidemiological cohort study following the outcome of early risk factors from birth into young adulthood. At age 19 years, 309 participants (142 male participants, 167 female participants) were genotyped for the biallelic and triallelic 5-HTTLPR and were administered a 45-day alcohol timeline follow-back interview, providing measures of the total number of drinks and the number of binge drinking days. Psychosocial adversity was assessed at birth (family adversity) and at age 19 (negative life events). Results: In contrast to various previous reports, a significant G x E emerged, indicating that, when exposed to high psychosocial adversity, individuals with the LL genotype of 5-HTTLPR exhibited more hazardous drinking than those carrying the S allele or those without exposure to adversity. This effect, which was confined to male participants, held both for different classifications of 5-HTTLPR and different types of adversity. Conclusions: One explanation for the discrepant results might be heterogeneity in alcohol phenotypes. While the L allele relates more strongly to early-onset alcoholism, the S allele may be linked more closely to alcohol use associated with anxiety and depression.},
  language  = {en}
}
@article{HoltmannBuchmannEsseretal.2011,
  author    = {Holtmann, Martin and Buchmann, Arlette F. and Esser, G{\"u}nter and Schmidt, Martin H. and Banaschewski, Tobias and Laucht, Manfred},
  title     = {The child behavior checklist-dysregulation profile predicts substance use, suicidality, and functional impairment : a longitudinal analysis},
  year      = {2011},
  abstract  = {Recent studies have identified a Child Behavior Checklist profile that characterizes children with severe affective and behavioral dysregulation (CBCL-dysregulation profile, CBCL-DP). In two recent longitudinal studies the CBCL-DP in childhood was associated with heightened rates of comorbid psychiatric disorders, among them bipolar disorder, an increased risk for suicidality, and marked psychosocial impairment at young-adult follow-up. This is the first study outside the US that examines the longitudinal course of the CBCL-DP. Methods: We studied the diagnostic and functional trajectories and the predictive utility of the CBCL-DP in the Mannheim Study of Children at Risk, an epidemiological cohort study on the outcome of early risk factors from birth into adulthood. A total of 325 young adults (151 males, 174 females) participated in the 19-year assessment. Results: Young adults with a higher CBCL-DP score in childhood were at increased risk for substance use disorders, suicidality and poorer overall functioning at age 19, even after adjustment for parental education, family income, impairment and psychiatric disorders at baseline. Childhood dysregulation was not related to bipolar disorder in young adulthood. The CBCL-DP was neither a precursor of a specific pattern of comorbidity nor of comorbidity in general. Conclusions: Children with high CBCL-DP values are at risk for later severe, psychiatric symptomatology. The different developmental trajectories suggest that the CBCL-DP is not simply an early manifestation of a single disease process but might rather be an early developmental risk marker of a persisting deficit of self-regulation of affect and behavior.},
  language  = {en}
}
@article{SchmidBlomeyerBeckeretal.2009,
  author    = {Schmid, Brigitte and Blomeyer, Dorothea and Becker, Katja and Treutlein, Jens and Zimmermann, Ulrich S. and Buchmann, Arlette F. and Schmidt, Martin H. and Esser, G{\"u}nter and Banaschewski, Tobias and Rietschel, Marcella and Laucht, Manfred},
  title     = {The interaction between the dopamine transporter gene and age at onset in relation to tobacco and alcohol use among 19-year-olds},
  issn      = {1355-6215},
  doi       = {10.1111/j.1369-1600.2009.00171.x},
  year      = {2009},
  abstract  = {Recent evidence suggests that heterogeneity in the age at onset could explain the inconsistent findings of association studies relating the dopamine transporter (DAT1) gene with alcohol and nicotine consumption. The aim of this study was to examine interactions between two DAT1 polymorphisms and different initiation ages with regard to alcohol and tobacco consumption levels and dependence. Two hundred and ninety-one young adults (135 males, 156 females) participating in the Mannheim Study of Children at Risk were genotyped for the 40-bp variable number of tandem repeats (VNTR) and rs27072 polymorphisms of DAT1. Age at initiation was assessed at age 15 and 19 years. Information about current alcohol and tobacco consumption was obtained at age 19 years using self-report measures and structured interviews. Results suggest that age at onset of intensive consumption moderated the association of the DAT1 gene with early adult substance use and dependence, revealing a DAT1 effect only among individuals homozygous for the 10r allele of the 40-bp VNTR who had started daily smoking or being intoxicated early in life. Equally, carriers of the T allele of the rs27072 polymorphism reporting an early age at first intoxication showed higher current alcohol consumption at age 19 years. In contrast, no interaction between rs27072 and the age at first cigarette with regard to later smoking was observed. These findings provide evidence that the DAT1 gene interacts with an early heavy or regular drug exposure of the maturing adolescent brain to predict substance (ab)use in young adulthood. Further studies are required to confirm these findings.},
  language  = {en}
}
@article{BuchmannBlomeyerJennenSteinmetzetal.2013,
  author    = {Buchmann, Arlette F. and Blomeyer, Dorothea and Jennen-Steinmetz, Christine and Schmidt, Martin H. and Esser, G{\"u}nter and Banaschewski, Tobias and Laucht, Manfred},
  title     = {Early smoking onset may promise initial pleasurable sensations and later addiction},
  series = {Addiction biology},
  volume    = {18},
  journal   = {Addiction biology},
  number    = {6},
  publisher = {Wiley-Blackwell},
  address   = {Hoboken},
  issn      = {1369-1600},
  doi       = {10.1111/j.1369-1600.2011.00377.x},
  pages     = {947 -- 954},
  year      = {2013},
  abstract  = {There is converging evidence suggesting a particular susceptibility to the addictive properties of nicotine among adolescents. The aim of the current study was to prospectively ascertain the relationship between age at first cigarette and initial smoking experiences, and to examine the combined effects of these characteristics of adolescent smoking behavior on adult smoking. It was hypothesized that the association between earlier age at first cigarette and later development of nicotine dependence may, at least in part, be attributable to differences in experiencing pleasurable early smoking sensations. Data were drawn from the participants of the Mannheim Study of Children at Risk, an ongoing epidemiological cohort study from birth to adulthood. Structured interviews at age 15, 19 and 22 years were conducted to assess the age at first cigarette, early smoking experiences and current smoking behavior in 213 young adults. In addition, the participants completed the Fagerstrom Test for Nicotine Dependence. Adolescents who smoked their first cigarette at an earlier age reported more pleasurable sensations from the cigarette, and they were more likely to be regular smokers at age 22. The age at first cigarette also predicted the number of cigarettes smoked and dependence at age 22. Thus, both the age of first cigarette and the pleasure experienced from the cigarette independently predicted aspects of smoking at age 22.},
  language  = {en}
}
@article{BuchmannKopfWestphaletal.2010,
  author    = {Buchmann, Arlette F. and Kopf, Daniel and Westphal, Sabine and Lederbogen, Florian and Banaschewski, Tobias and Esser, G{\"u}nter and Schmidt, Martin H. and Zimmermann, Ulrich S. and Laucht, Manfred and Deuschle, Michael},
  title     = {Impact of early parental child-rearing behavior on young adults' cardiometabolic risk profile : a prospective study},
  issn      = {0033-3174},
  doi       = {10.1097/Psy.0b013e3181c88343},
  year      = {2010},
  abstract  = {Objective: To examine prospectively whether early parental child-rearing behavior is a predictor of cardiometabolic outcome in young adulthood when other potential risk factors are controlled. Metabolic factors associated with increased risk for cardiovascular disease have been found to vary, depending on lifestyle as well as genetic predisposition. Moreover, there is evidence suggesting that environmental conditions, such as stress in pre- and postnatal life, may have a sustained impact on an individual's metabolic risk profile. Methods: Participants were drawn from a prospective, epidemiological, cohort study followed up from birth into young adulthood. Parent interviews and behavioral observations at the age of 3 months were conducted to assess child-rearing practices and mother-infant interaction in the home setting and in the laboratory. In 279 participants, anthropometric characteristics, low-density lipoprotein and high-density lipoprotein cholesterol, apolipoproteins, and triglycerides were recorded at age 19 years. In addition, structured interviews were administered to the young adults to assess indicators of current lifestyle and education. Results: Adverse early-life interaction experiences were significantly associated with lower levels of high- density lipoprotein cholesterol and apolipoprotein A1 in young adulthood. Current lifestyle variables and level of education did not account for this effect, although habitual smoking and alcohol consumption also contributed significantly to cardiometabolic outcomes. Conclusions: These findings suggest that early parental child-rearing behavior may predict health outcome in later life through its impact on metabolic parameters in adulthood.},
  language  = {en}
}
@article{BuchmannSchmidBlomeyeretal.2010,
  author    = {Buchmann, Arlette F. and Schmid, Brigitte and Blomeyer, Dorothea and Zimmermann, Ulrich S. and Jennen-Steinmetz, Christine and Schmidt, Martin H. and Esser, G{\"u}nter and Banaschewski, Tobias and Mann, Karl F. and Laucht, Manfred},
  title     = {Drinking against unpleasant emotions : possible outcome of early onset of alcohol use?},
  issn      = {0145-6008},
  doi       = {10.1111/j.1530-0277.2010.01180.x},
  year      = {2010},
  abstract  = {Background: Recent animal and human studies indicate that the exposure to alcohol during early adolescence increases the risk for heavy alcohol use in response to stress. The purpose of this study was to examine whether this effect may be the consequence of a higher susceptibility to develop "drinking to cope" motives among early initiators. Methods: Data from 320 participants were collected as part of the Mannheim Study of Children at Risk, an ongoing epidemiological cohort study. Structured interviews at age 15 and 19 were used to assess age at first alcohol experience and drunkenness. The young adults completed questionnaires to obtain information about the occurrence of stressful life events during the past 4 years and current drinking habits. In addition, alcohol use under conditions of negative states was assessed with the Inventory of Drinking Situations. Results: The probability of young adults' alcohol use in situations characterized by unpleasant emotions was significantly increased the earlier they had initiated the use of alcohol, even when controlling for current drinking habits and stressful life events. Similar results were obtained for the age at first drunkenness. Conclusions: The findings strengthen the hypothesis that alcohol experiences during early adolescence facilitate drinking to regulate negative affect as an adverse coping strategy which may represent the starting point of a vicious circle comprising drinking to relieve stress and increased stress as a consequence of drinking.},
  language  = {en}
}
@article{SchmidBuchmannTrautmannVillalbaetal.2013,
  author    = {Schmid, Brigitte and Buchmann, Arlette F. and Trautmann-Villalba, Patricia and Blomeyer, Dorothea and Zimmermann, Ulrich S. and Schmidt, Martin H. and Esser, G{\"u}nter and Banaschewski, Tobias and Laucht, Manfred},
  title     = {Maternal stimulation in infancy predicts hypothalamic-pituitary-adrenal axis reactivity in young men},
  series = {Journal of neural transmission},
  volume    = {120},
  journal   = {Journal of neural transmission},
  number    = {8},
  publisher = {Springer},
  address   = {Wien},
  issn      = {0300-9564},
  doi       = {10.1007/s00702-013-0970-8},
  pages     = {1247 -- 1257},
  year      = {2013},
  abstract  = {Evidence from animal research has demonstrated the effect of early maternal care on the offspring's endocrine and behavioral stress response in adulthood. The present prospective study investigates, in humans, the long-term impact of maternal responsiveness and stimulation during early mother-child interaction on adrenocorticotropic hormone (ACTH) and cortisol response to a psychosocial laboratory stressor in adulthood. The data are from an epidemiological cohort study of the long-term outcome of early risk factors assessed at birth. At age 3 months, mothers and infants were videotaped during a 10-min standardized nursing and playing situation and evaluated by trained raters for maternal stimulation and infant and maternal responsiveness. At age 19 years, 270 participants (146 females, 124 males) completed the Trier Social Stress Test. The results indicated that less maternal stimulation during early interaction at age 3 months predicted diminished plasma ACTH and cortisol increase in response to acute psychosocial stress in male, but not female offspring. In contrast, maternal responsiveness was found to be unrelated to hypothalamic-pituitary-adrenal (HPA) reactivity. In accordance with the findings from animal research, the present study provides prospective evidence in humans of a long-term association between early maternal interaction behavior and the offspring's hormonal stress response in young adulthood, suggesting that poor maternal stimulation in early infancy may result in reduced HPA axis reactivity to an acute psychosocial stressor in males.},
  language  = {en}
}
@article{BuchmannHellwegRietscheletal.2013,
  author    = {Buchmann, Arlette F. and Hellweg, Rainer and Rietschel, Marcella and Treutlein, Jens and Witt, Stephanie H. and Zimmermann, Ulrich S. and Schmidt, Martin H. and Esser, G{\"u}nter and Banaschewski, Tobias and Laucht, Manfred and Deuschle, Michael},
  title     = {BDNF Val 66 Met and 5-HTTLPR genotype moderate the impact of early psychosocial adversity on plasma brain-derived neurotrophic factor and depressive symptoms - a prospective study},
  series = {European neuropsychopharmacology : the journal of the European College of Neuropsychopharmacology},
  volume    = {23},
  journal   = {European neuropsychopharmacology : the journal of the European College of Neuropsychopharmacology},
  number    = {8},
  publisher = {Elsevier},
  address   = {Amsterdam},
  issn      = {0924-977X},
  doi       = {10.1016/j.euroneuro.2012.09.003},
  pages     = {902 -- 909},
  year      = {2013},
  abstract  = {Recent studies have emphasized an important role for neurotrophins, such as brain-derived neurotrophic factor (BDNF), in regulating the plasticity of neural circuits involved in the pathophysiology of stress-related diseases. The aim of the present study was to examine the interplay of the BDNF Val(66)Met and the serotonin transporter promoter (5-HTTLPR) polymorphisms in moderating the impact of early-life adversity on BDNF plasma concentration and depressive symptoms. Participants were taken from an epidemiological cohort study following the long-term outcome of early risk factors from birth into young adulthood. In 259 individuals (119 males, 140 females), genotyped for the BDNF Val(66)Met and the 5-HTTLPR polymorphisms, plasma BDNF was assessed at the age of 19 years. In addition, participants completed the Beck Depression Inventory (BDI). Early adversity was determined according to a family adversity index assessed at 3 months of age. Results indicated that individuals homozygous for both the BDNF Val and the 5-HTTLPR L allele showed significantly reduced BDNF levels following exposure to high adversity. In contrast, BDNF levels appeared to be unaffected by early psychosocial adversity in carriers of the BDNF Met or the 5-HTTLPR S allele. While the former group appeared to be most susceptible to depressive symptoms, the impact of early adversity was less pronounced in the latter group. This is the first preliminary evidence indicating that early-life adverse experiences may have lasting sequelae for plasma BDNF levels in humans, highlighting that the susceptibility to this effect is moderated by BDNF Val(66)Met and 5-HTTLPR genotype.},
  language  = {en}
}
@misc{LauchtBlomeyerBuchmannetal.2012,
  author    = {Laucht, Manfred and Blomeyer, Dorothea and Buchmann, Arlette F. and Treutlein, Jens and Shmidt, Martin H. and Esser, G{\"u}nter and Jennen-Steinmetz, Christine and Rietschel, Marcella and Zimmermann, Ulrich S. and Banaschewski, Tobias},
  title     = {Catechol-O-methyltransferase Val158Met genotype, parenting practices and adolescent alcohol use: testing the differential susceptibility hypothesis},
  year      = {2012},
  language  = {en}
}
@article{LauchtTreutleinBlomeyeretal.2012,
  author    = {Laucht, Manfred and Treutlein, Jens and Blomeyer, Dorothea and Buchmann, Arlette F. and Schmidt, Martin and Esser, G{\"u}nter and Jennen-Steinmetz, Christine and Reitschelb, Marcel and Banaschewski, Tobias},
  title     = {Interactive effects of corticotropin-releasing hormone receptor 1 gene and childhood adversity on depressive symptoms in young adults: Findings from a longitudinal study},
  year      = {2012},
  language  = {en}
}
@article{LauchtTreutleinBlomeyeretal.2013,
  author    = {Laucht, Manfred and Treutlein, Jens and Blomeyer, Dorothea and Buchmann, Arlette F. and Schmidt, Martin H. and Esser, G{\"u}nter and Jennen-Steinmetz, Christine and Rietschel, Marcella and Banaschewski, Tobias},
  title     = {Interactive effects of corticotropin-releasing hormone receptor 1 gene and childhood adversity on depressive symptoms in young adults findings from a longitudinal study},
  series = {European neuropsychopharmacology : the journal of the European College of Neuropsychopharmacology},
  volume    = {23},
  journal   = {European neuropsychopharmacology : the journal of the European College of Neuropsychopharmacology},
  number    = {5},
  publisher = {Elsevier},
  address   = {Amsterdam},
  issn      = {0924-977X},
  doi       = {10.1016/j.euroneuro.2012.06.002},
  pages     = {358 -- 367},
  year      = {2013},
  abstract  = {Accumulating research suggests a moderating role for the corticotropin-releasing hormone receptor 1 gene (CRHR1) in the association between childhood adversity and adult depression. The present study aims to replicate recent findings using different genetic variants and measures of early adversity assessed both prospectively and retrospectively. Data were collected in the context of an ongoing epidemiological cohort study following the outcome of early risk factors from birth into adulthood. 300 participants (137 males, 163 females) were genotyped for four CRHR1 SNPs (rs7209436, rs110402, rs242924, and rs17689882) and completed the Beck Depression Inventory at ages 19, 22 and 23 years. Childhood adversity was assessed using the Childhood Trauma Questionnaire and by a standardized parent interview yielding an index of family adversity. Our results indicate that CRHR1 and childhood adversity interacted to predict depressive symptoms in young adults. Specifically, we found that the impact of childhood maltreatment on adult depressive symptoms was significantly higher in individuals (i) with two copies of the CRHR1 TAT haplotype, and (ii) homozygous for the G allele of rs17689882. The interaction was demonstrated for exposure to childhood maltreatment as assessed by retrospective self-report, but not to prospectively ascertain objective family adversity. The present study partially replicates recent findings of a CRHR1 by childhood adversity interaction with regard to adult depression highlighting the subjective characteristics of the environmental pathogen that is operative in this interaction.},
  language  = {en}
}
@article{LauchtBlomeyerBuchmannetal.2012,
  author    = {Laucht, Manfred and Blomeyer, Dorothea and Buchmann, Arlette F. and Treutlein, Jens and Schmidt, Martin H. and Esser, G{\"u}nter and Jennen-Steinmetz, Christine and Rietschel, Marcella and Zimmermann, Ulrich S. and Banaschewski, Tobias},
  title     = {Catechol-O-methyltransferase Val158Met genotype, parenting practices and adolescent alcohol use: testing the differential susceptibility hypothesis},
  series = {The journal of child psychology and psychiatry},
  volume    = {53},
  journal   = {The journal of child psychology and psychiatry},
  number    = {4},
  publisher = {Wiley-Blackwell},
  address   = {Malden},
  issn      = {0021-9630},
  doi       = {10.1111/j.1469-7610.2011.02408.x},
  pages     = {351 -- 359},
  year      = {2012},
  abstract  = {Background: Recently, first evidence has been reported for a geneparenting interaction (G x E) with regard to adolescent alcohol use. The present investigation set out to extend this research using the catechol-O-methyltransferase (COMT) Val158Met polymorphism as a genetic susceptibility factor. Moreover, the current study examined whether a potential G x E would be consistent with one of two models of geneenvironment interplay (genetic vulnerability vs. differential susceptibility). Methods: Data were collected as part of an ongoing epidemiological cohort study following the outcome of early risk factors from birth into adulthood. Two hundred and eighty-five participants (130 males, 155 females) were genotyped for the COMT Val(158) Met polymorphism and were administered an alcohol interview, providing measures of current frequency and amount of drinking at ages 15 and 19 years. Information on three dimensions of perceived parenting behavior was obtained from the 15-year-olds. Results: Adolescents homozygous for the Met allele showed higher drinking activity at age 19 years when their parents had engaged in less supervision or were less involved, while their drinking activity was reduced under conditions of favorable parenting. No such relationship was found in individuals carrying the Val allele. Conclusions: The present findings correspond with the pattern of results predicted by the differential susceptibility hypothesis, suggesting that environmental variation would have a greater impact in individuals carrying a genetic susceptibility such that, in this group, exposure to negative environmental conditions would result in more adverse outcomes and the experience of favorable conditions would lead to more positive outcomes.},
  language  = {en}
}
@article{WittBuchmannBlomeyeretal.2011,
  author    = {Witt, Stephanie H. and Buchmann, Arlette F. and Blomeyer, Dorothea and Nieratschker, Vanessa and Treutlein, Jens and Esser, G{\"u}nter and Schmidt, Martin H. and Bidlingmaier, Martin and Wiedemann, Klaus and Rietschel, Marcella and Laucht, Manfred and Wuest, Stefan and Zimmermann, Ulrich S.},
  title     = {An interaction between a neuropeptide Y gene polymorphism and early adversity modulates endocrine stress responses},
  series = {Psychoneuroendocrinology},
  volume    = {36},
  journal   = {Psychoneuroendocrinology},
  number    = {7},
  publisher = {Elsevier},
  address   = {Oxford},
  issn      = {0306-4530},
  doi       = {10.1016/j.psyneuen.2010.12.015},
  pages     = {1010 -- 1020},
  year      = {2011},
  abstract  = {Interindividual variability in the regulation of the human stress system accounts for a part of the individual's liability to stress-related diseases. These differences are influenced by environmental and genetic factors. Early childhood adversity is a well-studied environmental factor affecting an individual's stress response which has been shown to be modulated by gene environment interaction (GxE). Neuropeptide Y (NPY) plays a role in stress regulation and genetic variation in NPY may influence stress responses. In this study, we analyzed the association of a common variant in the NPY gene promoter, rs16147, with cortisol and ACTH responses to acute psychosocial stress in young adults from the Mannheim Study of Children at Risk (MARS), an ongoing epidemiological cohort study following the outcome of early adversity from birth into adulthood. We found evidence of a GxE interaction between rs16147 and early adversity significantly affecting HPA axis responses to acute psychosocial stress. These findings suggest that the neurobiological mechanisms linking early adverse experience and later neuroendocrine stress regulation are modulated by a gene variant whose functional relevance is documented by increasing convergent evidence from in vitro, animal and human studies.},
  language  = {en}
}
@article{NikitopoulosZohselBlomeyeretal.2014,
  author    = {Nikitopoulos, Joerg and Zohsel, Katrin and Blomeyer, Dorothea and Buchmann, Arlette F. and Schmid, Brigitte and Jennen-Steinmetz, Christine and Becker, Katja and Schmidt, Martin H. and Esser, G{\"u}nter and Brandeis, Daniel and Banaschewski, Tobias and Laucht, Manfred},
  title     = {Are infants differentially sensitive to parenting? Early maternal care, DRD4 genotype and externalizing behavior during adolescence},
  series = {Journal of psychiatric research},
  volume    = {59},
  journal   = {Journal of psychiatric research},
  publisher = {Elsevier},
  address   = {Oxford},
  issn      = {0022-3956},
  doi       = {10.1016/j.jpsychires.2014.08.012},
  pages     = {53 -- 59},
  year      = {2014},
  language  = {en}
}
@article{HeinrichBuchmannZohseletal.2015,
  author    = {Heinrich, Angela and Buchmann, Arlette F. and Zohsel, Katrin and Dukal, Helene and Frank, Josef and Treutlein, Jens and Nieratschker, Vanessa and Witt, Stephanie H. and Brandeis, Daniel and Schmidt, Martin H. and Esser, G{\"u}nter and Banaschewski, Tobias and Laucht, Manfred and Rietschel, Marcella},
  title     = {Alterations of Glucocorticoid Receptor Gene Methylation in Externalizing Disorders During Childhood and Adolescence},
  series = {Behavior genetics : an international journal devoted to research in the inheritance of behavior in animals and man},
  volume    = {45},
  journal   = {Behavior genetics : an international journal devoted to research in the inheritance of behavior in animals and man},
  number    = {5},
  publisher = {Springer},
  address   = {New York},
  issn      = {0001-8244},
  doi       = {10.1007/s10519-015-9721-y},
  pages     = {529 -- 536},
  year      = {2015},
  abstract  = {Epigenetic modulations are a hypothesized link between environmental factors and the development of psychiatric disorders. Research has suggested that patients with depression or bipolar disorder exhibit higher methylation levels in the glucocorticoid receptor gene NR3C1. We aimed to investigate whether NR3C1 methylation changes are similarly associated with externalizing disorders such as aggressive behavior and conduct disorder. NR3C1 exon 1F methylation was analyzed in young adults with a lifetime diagnosis of an externalizing disorder (N = 68) or a depressive disorder (N = 27) and healthy controls (N = 124) from the Mannheim Study of Children at Risk. The externalizing disorders group had significantly lower NR3C1 methylation levels than the lifetime depressive disorder group (p = 0.009) and healthy controls (p = 0.001) This report of lower methylation levels in NR3C1 in externalizing disorders may indicate a mechanism through which the differential development of externalizing disorders as opposed to depressive disorders might occur.},
  language  = {en}
}
@article{HohmannBuchmannWittetal.2012,
  author    = {Hohmann, S. and Buchmann, Arlette F. and Witt, S. H. and Rietschel, M. and Jennen-Steinmetz, Christine and Schmidt, M. H. and Esser, G{\"u}nter and Banaschewski, Tobias and Laucht, Manfred},
  title     = {Increasing association between a neuropeptide Y promoter polymorphism and body mass index during the course of development},
  series = {Pediatric obesity},
  volume    = {7},
  journal   = {Pediatric obesity},
  number    = {6},
  publisher = {Wiley-Blackwell},
  address   = {Hoboken},
  issn      = {2047-6310},
  doi       = {10.1111/j.2047-6310.2012.00069.x},
  pages     = {453 -- 460},
  year      = {2012},
  abstract  = {Objective: To investigate the association of the neuropeptide Y (NPY) promoter polymorphism rs16147 with body mass index (BMI) during the course of development from infancy to adulthood. Design: Longitudinal, prospective study of a German community sample. Subjects: n = 306 young adults (139 males, 167 females). Measurements: Participants' body weight and height were assessed at the ages of 3 months and 2, 4.5, 8, 11, 15 and 19 years. NPY rs16147 was genotyped. Results: Controlling for a number of possible confounders, homozygote carriers of the rs16147 C allele exhibited significantly lower BMI scores when compared with individuals carrying the T allele. In addition, a significant genotype by age interaction emerged, indicating that the genotype effect increased during the course of development. Conclusions: This is the first longitudinal study to report an association between rs16147 and BMI during childhood and adolescence. The finding that this effect increased during the course of development may either be due to age-dependent alterations in gene expression or to maturation processes within the weight regulation circuits of the central nervous system.},
  language  = {en}
}
@article{BuchmannHolzBoeckerSchlieretal.2014,
  author    = {Buchmann, Arlette F. and Holz, Nathalie and Boecker-Schlier, Regina and Blomeyer, Dorothea and Rietschel, Marcella and Witt, Stephanie H. and Schmidt, Martin H. and Esser, G{\"u}nter and Banaschewski, Tobias and Brandeis, Daniel and Zimmermann, Ulrich S. and Laucht, Manfred},
  title     = {Moderating role of FKBP5 genotype in the impact of childhood adversity on cortisol stress response during adulthood},
  series = {European neuropsychopharmacology : the journal of the European College of Neuropsychopharmacology},
  volume    = {24},
  journal   = {European neuropsychopharmacology : the journal of the European College of Neuropsychopharmacology},
  number    = {6},
  publisher = {Elsevier},
  address   = {Amsterdam},
  issn      = {0924-977X},
  doi       = {10.1016/j.euroneuro.2013.12.001},
  pages     = {837 -- 845},
  year      = {2014},
  abstract  = {Recent research suggests an important role of FKBP5, a glucocorticoid receptor regulating co-chaperone, in the development of stress-related diseases such as depression and anxiety disorders. The present study aimed to replicate and extend previous evidence indicating that FKBP5 polymorphisms moderate hypothalamus-pituitary-adrenal (HPA) function by examining whether FKBP5 rs1360780 genotype and different measures of childhood adversity interact to predict stress-induced cortisol secretion. At age 19 years, 195 young adults (90 males, 105 females) participating in an epidemiological cohort study completed the Trier Social Stress Test (TSST) to assess cortisol stress responsiveness and were genotyped for the FKBP5 rs1360780. Childhood adversity was assessed using the Childhood Trauma Questionnaire (CTQ) and by a standardized parent interview yielding an index of family adversity. A significant interaction between genotype and childhood adversity on cortisol response to stress was demonstrated for exposure to childhood maltreatment as assessed by retrospective self-report (CTQ), but not for prospectively ascertained objective family adversity. Severity of childhood maltreatment was significantly associated with attenuated cortisol levels among carriers of the rs1360780 CC genotype, while no such effect emerged in carriers of the T allele. These findings point towards the functional involvement of FKBP5 in long-term alterations of neuroendocrine stress regulation related to childhood maltreatment, which have been suggested to represent a premorbid risk or resilience factor in the context of stress-related disorders. (C) 2013 Elsevier B.V. and ECNR This is an open access article under the CC BY-NC-ND license.},
  language  = {en}
}
@article{SchmidBlomeyerBuchmannetal.2011,
  author    = {Schmid, Brigitte and Blomeyer, Dorothea and Buchmann, Arlette F. and Trautmann-Villalba, Patricia and Zimmermann, Ulrich S. and Schmidt, Martin H. and Esser, G{\"u}nter and Banaschewski, Tobias and Laucht, Manfred},
  title     = {Quality of early mother-child interaction associated with depressive psychopathology in the offspring - a prospective study from infancy to adulthood},
  series = {Journal of psychiatric research},
  volume    = {45},
  journal   = {Journal of psychiatric research},
  number    = {10},
  publisher = {Elsevier},
  address   = {Oxford},
  issn      = {0022-3956},
  doi       = {10.1016/j.jpsychires.2011.05.010},
  pages     = {1387 -- 1394},
  year      = {2011},
  abstract  = {Evidence from animal research has revealed that less maternal care results in disturbed emotionality in the offspring. In the present study, the long-term impact of maternal responsiveness and stimulation during early mother child interaction on depressive psychopathology was examined until adulthood. Data are from an epidemiological cohort study of the long-term outcome of early risk factors assessed at birth. At age 3 months, mothers and infants were videotaped during a nursing and playing situation. Maternal responsiveness and stimulation as well as infant responsiveness were evaluated by trained raters. At age 19 years, 314 participants (145 males, 169 females) were characterized on measures of depression through interview and questionnaire. In addition, measures of depression and anxiety were available from assessments in childhood. Results indicated that less maternal stimulation during early interaction was associated with a higher risk of depression in the offspring until the age of 19 years. In addition, children of less stimulating mothers showed more depressive symptoms at age 19 years and displayed more anxiety and depressive symptoms between the ages of 4.5 and 15 years. In contrast, maternal responsiveness was unrelated to children's outcome. In accordance with findings from animal research, the present study provides first longitudinal evidence in humans of a continuous and long-term influence of early maternal interaction behavior on the offspring's psychological adjustment until adulthood. The results suggest that the amount of maternally initiated contact behavior in a very early developmental stage may be crucial for children's mental health, regardless of child and maternal responsiveness.},
  language  = {en}
}
@article{HoltmannBuchmannEsseretal.2011,
  author    = {Holtmann, Martin and Buchmann, Arlette F. and Esser, G{\"u}nter and Schmidt, Martin H. and Banaschewski, Tobias and Laucht, Manfred},
  title     = {The child behavior checklist-dysregulation profile predicts substance use, suicidality, and functional impairment a longitudinal analysis},
  series = {The journal of child psychology and psychiatry},
  volume    = {52},
  journal   = {The journal of child psychology and psychiatry},
  number    = {2},
  publisher = {Wiley-Blackwell},
  address   = {Malden},
  issn      = {0021-9630},
  doi       = {10.1111/j.1469-7610.2010.02309.x},
  pages     = {139 -- 147},
  year      = {2011},
  abstract  = {Background: Recent studies have identified a Child Behavior Checklist profile that characterizes children with severe affective and behavioral dysregulation (CBCL-dysregulation profile, CBCL-DP). In two recent longitudinal studies the CBCL-DP in childhood was associated with heightened rates of comorbid psychiatric disorders, among them bipolar disorder, an increased risk for suicidality, and marked psychosocial impairment at young-adult follow-up. This is the first study outside the US that examines the longitudinal course of the CBCL-DP. Methods: We studied the diagnostic and functional trajectories and the predictive utility of the CBCL-DP in the Mannheim Study of Children at Risk, an epidemiological cohort study on the outcome of early risk factors from birth into adulthood. A total of 325 young adults (151 males, 174 females) participated in the 19-year assessment. Results: Young adults with a higher CBCL-DP score in childhood were at increased risk for substance use disorders, suicidality and poorer overall functioning at age 19, even after adjustment for parental education, family income, impairment and psychiatric disorders at baseline. Childhood dysregulation was not related to bipolar disorder in young adulthood. The CBCL-DP was neither a precursor of a specific pattern of comorbidity nor of comorbidity in general. Conclusions: Children with high CBCL-DP values are at risk for later severe, psychiatric symptomatology. The different developmental trajectories suggest that the CBCL-DP is not simply an early manifestation of a single disease process but might rather be an early developmental risk marker of a persisting deficit of self-regulation of affect and behavior.},
  language  = {en}
}
@article{BuchmannZohselBlomeyeretal.2014,
  author    = {Buchmann, Arlette F. and Zohsel, Katrin and Blomeyer, Dorothea and Hohm, Erika and Hohmann, Sarah and Jennen-Steinmetz, Christine and Treutlein, Jens and Becker, Katja and Banaschewski, Tobias and Schmidt, Martin H. and Esser, G{\"u}nter and Brandeis, Daniel and Poustka, Luise and Zimmermann, Ulrich S. and Laucht, Manfred},
  title     = {Interaction between prenatal stress and dopamine D4 receptor genotype in predicting aggression and cortisol levels in young adults},
  series = {Psychopharmacology},
  volume    = {231},
  journal   = {Psychopharmacology},
  number    = {16},
  publisher = {Springer},
  address   = {New York},
  issn      = {0033-3158},
  doi       = {10.1007/s00213-014-3484-7},
  pages     = {3089 -- 3097},
  year      = {2014},
  abstract  = {Considerable evidence suggests that genetic factors combine with environmental influences to impact on the development of aggressive behavior. A genetic variant that has repeatedly been reported to render individuals more sensitive to the presence of adverse experiences, including stress exposure during fetal life, is the seven-repeat allele of the dopamine D4 receptor (DRD4) gene. The present investigation concentrated on the interplay of prenatal maternal stress and DRD4 genotype in predicting self-reported aggression in young adults. As disruption of the hypothalamic-pituitary-adrenal system has been discussed as a pathophysiological pathway to aggression, cortisol stress reactivity was additionally examined. As part of an epidemiological cohort study, prenatal maternal stress was assessed by maternal interview 3 months after childbirth. Between the ages of 19 and 23 years, 298 offspring (140 males, 158 females) completed the Young Adult Self-Report to measure aggressive behavior and were genotyped for the DRD4 gene. At 19 years, 219 participants additionally underwent the Trier Social Stress Test to determine cortisol reactivity. Extending earlier findings with respect to childhood antisocial behavior, the results revealed that, under conditions of higher prenatal maternal stress, carriers of the DRD4 seven-repeat allele displayed more aggression in adulthood (p = 0.032). Moreover, the same conditions which seemed to promote aggression were found to predict attenuated cortisol secretion (p = 0.028). This is the first study to indicate a long-term impact of prenatal stress exposure on the cortisol stress response depending on DRD4 genotype.},
  language  = {en}
}
@article{ZohselBuchmannBlomeyeretal.2014,
  author    = {Zohsel, Katrin and Buchmann, Arlette F. and Blomeyer, Dorothea and Hohm, Erika and Schmidt, Martin H. and Esser, G{\"u}nter and Brandeis, Daniel and Banaschewski, Tobias and Laucht, Manfred},
  title     = {Mothers' prenatal stress and their children's antisocial outcomes - a moderating role for the dopamine receptor D4 (DRD4) gene},
  series = {The journal of child psychology and psychiatry},
  volume    = {55},
  journal   = {The journal of child psychology and psychiatry},
  number    = {1},
  publisher = {Wiley-Blackwell},
  address   = {Hoboken},
  issn      = {0021-9630},
  doi       = {10.1111/jcpp.12138},
  pages     = {69 -- 76},
  year      = {2014},
  abstract  = {ResultsUnder conditions of elevated prenatal maternal stress, children carrying one or two DRD4 7r alleles were at increased risk of a diagnosis of CD/ODD. Moreover, homozygous carriers of the DRD4 7r allele displayed more externalizing behavior following exposure to higher levels of prenatal maternal stress, while homozygous carriers of the DRD4 4r allele turned out to be insensitive to the effects of prenatal stress. ConclusionsThis study is the first to report a gene-environment interaction related to DRD4 and prenatal maternal stress using data from a prospective study, which extends earlier findings on the impact of prenatal maternal stress with respect to childhood antisocial behavior.},
  language  = {en}
}
@article{HolzBoeckerSchlierJennenSteinmetzetal.2016,
  author    = {Holz, Nathalie E. and Boecker-Schlier, Regina and Jennen-Steinmetz, Christine and Buchmann, Arlette F. and Blomeyer, Dorothea and Baumeister, Sarah and Plichta, Michael M. and Esser, G{\"u}nter and Schmidt, Martin and Meyer-Lindenberg, Andreas and Banaschewski, Tobias and Brandeis, Daniel and Laucht, Manfred},
  title     = {Positive coping styles and perigenual ACC volume: two related mechanisms for conferring resilience?},
  series = {Frontiers in human neuroscience},
  volume    = {11},
  journal   = {Frontiers in human neuroscience},
  publisher = {Oxford Univ. Press},
  address   = {Oxford},
  issn      = {1749-5016},
  doi       = {10.1093/scan/nsw005},
  pages     = {813 -- 820},
  year      = {2016},
  abstract  = {Stress exposure has been linked to increased rates of depression and anxiety in adults, particularly in females, and has been associated with maladaptive changes in the anterior cingulate cortex (ACC), which is an important brain structure involved in internalizing disorders. Coping styles are important mediators of the stress reaction by establishing homeostasis, and may thus confer resilience to stress-related psychopathology. Anatomical scans were acquired in 181 healthy participants at age 25 years. Positive coping styles were determined using a self-report questionnaire (German Stress Coping Questionnaire, SVF78) at age 22 years. Adult anxiety and depression symptoms were assessed at ages 22, 23 and 25 years with the Young Adult Self-Report. Information on previous internalizing diagnoses was obtained by diagnostic interview (2-19 years). Positive coping styles were associated with increased ACC volume. ACC volume and positive coping styles predicted anxiety and depression in a sex-dependent manner with increased positive coping and ACC volume being related to lower levels of psychopathology in females, but not in males. These results remained significant when controlled for previous internalizing diagnoses. These findings indicate that positive coping styles and ACC volume are two linked mechanisms, which may serve as protective factors against internalizing disorders.},
  language  = {en}
}
@article{HolzBoeckerSchlierBuchmannetal.2016,
  author    = {Holz, Nathalie and Boecker-Schlier, Regina and Buchmann, Arlette F. and Blomeyer, Dorothea and Baumeister, Sarah and Hohmann, Sarah and Jennen-Steinmetz, Christine and Wolf, Isabella and Rietschel, Marcella and Witt, Stephanie H. and Plichta, Michael M. and Meyer-Lindenberg, Andreas and Schmidt, Martin H. and Esser, G{\"u}nter and Banaschewski, Tobias and Brandeis, Daniel and Laucht, Manfred},
  title     = {Evidence for a Sex-Dependent MAOAx Childhood Stress Interaction in the Neural Circuitry of Aggression},
  series = {Cerebral cortex},
  volume    = {26},
  journal   = {Cerebral cortex},
  publisher = {Oxford Univ. Press},
  address   = {Cary},
  issn      = {1047-3211},
  doi       = {10.1093/cercor/bhu249},
  pages     = {904 -- 914},
  year      = {2016},
  abstract  = {Converging evidence emphasizes the role of an interaction between monoamine oxidase A (MAOA) genotype, environmental adversity, and sex in the pathophysiology of aggression. The present study aimed to clarify the impact of this interaction on neural activity in aggression-related brain systems. Functional magnetic resonance imaging was performed in 125 healthy adults from a high-risk community sample followed since birth. DNA was genotyped for the MAOA-VNTR (variable number of tandem repeats). Exposure to childhood life stress (CLS) between the ages of 4 and 11 years was assessed using a standardized parent interview, aggression by the Youth/Young Adult Self-Report between the ages of 15 and 25 years, and the VIRA-R (Vragenlijst Instrumentele En Reactieve Agressie) at the age of 15 years. Significant interactions were obtained between MAOA genotype, CLS, and sex relating to amygdala, hippocampus, and anterior cingulate cortex (ACC) response, respectively. Activity in the amygdala and hippocampus during emotional face-matching increased with the level of CLS in male MAOA-L, while decreasing in male MAOA-H, with the reverse pattern present in females. Findings in the opposite direction in the ACC during a flanker NoGo task suggested that increased emotional activity coincided with decreased inhibitory control. Moreover, increasing amygdala activity was associated with higher Y(A)SR aggression in male MAOA-L and female MAOA-H carriers. Likewise, a significant association between amygdala activity and reactive aggression was detected in female MAOA-H carriers. The results point to a moderating role of sex in the MAOAx CLS interaction for intermediate phenotypes of emotional and inhibitory processing, suggesting a possible mechanism in conferring susceptibility to violence-related disorders.},
  language  = {en}
}
@article{HohmannZohselBuchmannetal.2016,
  author    = {Hohmann, Sarah and Zohsel, Katrin and Buchmann, Arlette F. and Blomeyer, Dorothea and Holz, Nathalie and Boecker-Schlier, Regina and Jennen-Steinmetz, Christine and Rietschel, Marcella and Witt, Stephanie H. and Schmidt, Martin H. and Esser, G{\"u}nter and Meyer-Lindenberg, Andreas and Banaschewski, Tobias and Brandeis, Daniel and Hohm, Erika and Laucht, Manfred},
  title     = {Interacting effect of MAOA genotype and maternal prenatal smoking on aggressive behavior in young adulthood},
  series = {Journal of neural transmission},
  volume    = {123},
  journal   = {Journal of neural transmission},
  publisher = {Springer},
  address   = {Wien},
  issn      = {0300-9564},
  doi       = {10.1007/s00702-016-1582-x},
  pages     = {885 -- 894},
  year      = {2016},
  abstract  = {Findings on the etiology of aggressive behavior have provided evidence for an effect both of genetic factors, such as variation in the monoamine oxidase A (MAOA) gene, and adverse environmental factors. Recent studies have supported the existence of gene × environment interactions, with early experiences playing a key role. In the present study, the effects of prenatal nicotine exposure, MAOA genotype and their interaction on aggressive behavior during young adulthood were examined. In a sample of 272 young adults (129 males, 143 females) from an epidemiological cohort study, smoking during pregnancy was measured with a standardized parent interview at the offspring's age of 3 months. Aggressive behavior was assessed between the ages of 19 and 25 years using the Young Adult Self-Report. DNA was genotyped for the MAOA 5\&\#8242; untranslated region variable number of tandem repeats polymorphism (VNTR). Results revealed a significant interaction between MAOA and smoking during pregnancy, indicating higher levels of aggressive behavior in young adults carrying the MAOA low-expressing genotype who had experienced prenatal nicotine exposure (n = 8, p = .025). In contrast, in carriers of the MAOA high-expressing genotype, maternal smoking during pregnancy had no effect on aggressive behavior during young adulthood (n = 20, p = .145). This study extends earlier findings demonstrating an interaction between MAOA genotype and prenatal nicotine exposure on aggressive behavior into young adulthood. The results point to the long-term adverse effects of smoking during pregnancy on the offspring's mental health, possibly underlining the importance of smoking cessation during pregnancy. According to the nature of the study (particularly sample size and power), analyses are exploratory and results need to be interpreted cautiously.},
  language  = {en}
}
@article{BuchmannHohmWittetal.2015,
  author    = {Buchmann, Arlette F. and Hohm, Erika and Witt, Stephanie H. and Blomeyer, Dorothea and Jennen-Steinmetz, Christine and Schmidt, Martin H. and Esser, G{\"u}nter and Banaschewski, Tobias and Brandeis, Daniel and Laucht, Manfred},
  title     = {Role of CNR1 polymorphisms in moderating the effects of psychosocial adversity on impulsivity in adolescents},
  series = {Journal of neural transmission},
  volume    = {122},
  journal   = {Journal of neural transmission},
  number    = {3},
  publisher = {Springer},
  address   = {Wien},
  issn      = {0300-9564},
  doi       = {10.1007/s00702-014-1266-3},
  pages     = {455 -- 463},
  year      = {2015},
  abstract  = {Enhanced endocannabinoid signaling has been implicated in typically adolescent behavioral features such as increased risk-taking, impulsivity and novelty seeking. Research investigating the impact of genetic variants in the cannabinoid receptor 1 gene (CNR1) and of early rearing conditions has demonstrated that both factors contribute to the prediction of impulsivity-related phenotypes. The present study aimed to test the hypothesis of an interaction of the two most studied CNR1 polymorphisms rs806379 and rs1049353 with early psychosocial adversity in terms of affecting impulsivity in 15-year-olds from an epidemiological cohort sample followed since birth. In 323 adolescents (170 girls, 153 boys), problems of impulse control and novelty seeking were assessed using parent-report and self-report, respectively. Exposure to early psychosocial adversity was determined in a parent interview conducted at the age of 3 months. The results indicated that impulsivity increased following exposure to early psychosocial adversity, with this increase being dependent on CNR1 genotype. In contrast, while individuals exposed to early adversity scored higher on novelty seeking, no significant impact of genotype or the interaction thereof was detected. This is the first evidence to suggest that the interaction of CNR1 gene variants with the experience of early life adversity may play a role in determining adolescent impulsive behavior. However, given that the reported findings are obtained in a high-risk community sample, results are restricted in terms of interpretation and generalization. Future research is needed to replicate these findings and to identify the mediating mechanisms underlying this effect.},
  language  = {en}
}
@article{HolzBoeckerSchlierHohmetal.2015,
  author    = {Holz, Nathalie E. and Boecker-Schlier, Regina and Hohm, Erika and Zohsel, Katrin and Buchmann, Arlette F. and Blomeyer, Dorothea and Jennen-Steinmetz, Christine and Baumeister, Sarah and Hohmann, Sarah and Wolf, Isabella and Plichta, Michael M. and Esser, G{\"u}nter and Schmidt, Martin and Meyer-Lindenberg, Andreas and Banaschewski, Tobias and Brandeis, Daniel and Laucht, Manfred},
  title     = {The Long-Term Impact of Early Life Poverty on Orbitofrontal Cortex Volume in Adulthood: Results from a Prospective Study Over 25 Years},
  series = {Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology},
  volume    = {40},
  journal   = {Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology},
  number    = {4},
  publisher = {Nature Publ. Group},
  address   = {London},
  issn      = {0893-133X},
  doi       = {10.1038/npp.2014.277},
  pages     = {996 -- 1004},
  year      = {2015},
  abstract  = {Converging evidence has highlighted the association between poverty and conduct disorder (CD) without specifying neurobiological pathways. Neuroimaging research has emphasized structural and functional alterations in the orbitofrontal cortex (OFC) as one key mechanism underlying this disorder. The present study aimed to clarify the long-term influence of early poverty on OFC volume and its association with CD symptoms in healthy participants of an epidemiological cohort study followed since birth. At age 25 years, voxel-based morphometry was applied to study brain volume differences. Poverty (0 = non-exposed (N = 134), I = exposed (N = 33)) and smoking during pregnancy were determined using a standardized parent interview, and information on maternal responsiveness was derived from videotaped mother infant interactions at the age of 3 months. CD symptoms were assessed by diagnostic interview from 8 to 19 years of age. Information on life stress was acquired at each assessment and childhood maltreatment was measured using retrospective self-report at the age of 23 years. Analyses were adjusted for sex, parental psychopathology and delinquency, obstetric adversity, parental education, and current poverty. Individuals exposed to early life poverty exhibited a lower OFC volume. Moreover, we replicated previous findings of increased CD symptoms as a consequence of childhood poverty. This effect proved statistically mediated by OFC volume and exposure to life stress and smoking during pregnancy, but not by childhood maltreatment and maternal responsiveness. These findings underline the importance of studying the impact of early life adversity on brain alterations and highlight the need for programs to decrease income-related disparities.},
  language  = {en}
}