TY - JOUR A1 - Boecker-Schlier, Regina A1 - Holz, Nathalie E. A1 - Hohm, Erika A1 - Zohsel, Katrin A1 - Blomeyer, Dorothea A1 - Buchmann, Arlette F. A1 - Baumeister, Sarah A1 - Wolf, Isabella A1 - Esser, Günter A1 - Schmidt, Martin H. A1 - Meyer-Lindenberg, Andreas A1 - Banaschewski, Tobias A1 - Brandeis, Daniel A1 - Laucht, Manfred T1 - Association between pubertal stage at first drink and neural reward processing in early adulthood JF - Addiction biology N2 - 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. KW - alcohol-related problems KW - electroencephalography KW - functional magnetic resonance imaging KW - puberty KW - reward processing Y1 - 2017 U6 - https://doi.org/10.1111/adb.12413 SN - 1355-6215 SN - 1369-1600 VL - 22 SP - 1402 EP - 1415 PB - Wiley CY - Hoboken ER - TY - JOUR A1 - Buchmann, Arlette F. A1 - Zohsel, Katrin A1 - Blomeyer, Dorothea A1 - Hohm, Erika A1 - Hohmann, Sarah A1 - Jennen-Steinmetz, Christine A1 - Treutlein, Jens A1 - Becker, Katja A1 - Banaschewski, Tobias A1 - Schmidt, Martin H. A1 - Esser, Günter A1 - Brandeis, Daniel A1 - Poustka, Luise A1 - Zimmermann, Ulrich S. A1 - Laucht, Manfred T1 - Interaction between prenatal stress and dopamine D4 receptor genotype in predicting aggression and cortisol levels in young adults JF - Psychopharmacology N2 - 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. KW - Prenatal stress KW - Aggression KW - Cortisol KW - DRD4 KW - Gene-environment interaction Y1 - 2014 U6 - https://doi.org/10.1007/s00213-014-3484-7 SN - 0033-3158 SN - 1432-2072 VL - 231 IS - 16 SP - 3089 EP - 3097 PB - Springer CY - New York ER - TY - JOUR A1 - Heinrich, Angela A1 - Buchmann, Arlette F. A1 - Zohsel, Katrin A1 - Dukal, Helene A1 - Frank, Josef A1 - Treutlein, Jens A1 - Nieratschker, Vanessa A1 - Witt, Stephanie H. A1 - Brandeis, Daniel A1 - Schmidt, Martin H. A1 - Esser, Günter A1 - Banaschewski, Tobias A1 - Laucht, Manfred A1 - Rietschel, Marcella T1 - Alterations of Glucocorticoid Receptor Gene Methylation in Externalizing Disorders During Childhood and Adolescence JF - Behavior genetics : an international journal devoted to research in the inheritance of behavior in animals and man N2 - 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. KW - Epigenetic KW - Glucocorticoid receptor KW - Methylation KW - Externalizing disorders KW - Adolescents Y1 - 2015 U6 - https://doi.org/10.1007/s10519-015-9721-y SN - 0001-8244 SN - 1573-3297 VL - 45 IS - 5 SP - 529 EP - 536 PB - Springer CY - New York ER - TY - JOUR A1 - Hohm, Erika A1 - Laucht, Manfred A1 - Zohsel, Katrin A1 - Schmidt, Martin H. A1 - Esser, Günter A1 - Brandeis, Daniel A1 - Banaschewski, Tobias T1 - Resilienz und Ressourcen im Verlauf der Entwicklung T1 - Resilience and Resources During Development BT - Von der frühen Kindheit bis zum Erwachsenenalter BT - From Early Childhood to Adulthood JF - Kindheit und Entwicklung N2 - Anhand von Daten der Mannheimer Risikokinderstudie, die sich mit der langfristigen Entwicklung von Kindern mit unterschiedlichen Risikobelastungen beschäftigt, wird gezeigt, wie Schutzfaktoren aufseiten des Kindes und seines familiären Umfelds im Verlauf der Entwicklung wirksam werden und zur Entstehung von Resilienz beitragen können. Eine besondere Rolle kommt dabei positiven frühen Eltern-Kind-Beziehungen zu (sowohl Mutter- als auch Vater-Kind-Interaktionen). Daneben spielen auch Interaktionserfahrungen im Alter von zwei Jahren des Kindes eine bedeutsame Rolle; diese schützen Risikokinder davor, eine ungünstige Entwicklung zu nehmen und tragen dazu bei, dass sich Kinder, die in psychosozialen Hochrisikofamilien aufwachsen, trotz ungünstiger „Startbedingungen“ positiv entwickeln. Neben Merkmalen der sozialen Umwelt nehmen auch sprachliche, sozial-emotionale und internale Kompetenzen des Kindes im Entwicklungsverlauf eine wichtige Rolle ein. Diese Kompetenzen ermöglichen es Risikokindern auch unter widrigen Lebensumständen (psychosoziale Hochrisikofamilien, Aufwachsen in Armutsverhältnissen) erfolgreich zu bestehen. Darüber hinaus zeigt die Arbeit, dass Resilienz ein Persönlichkeitsmerkmal ist, das ab dem frühen Erwachsenenalter eine hohe Stabilität besitzt. Mit diesen Befunden verweist die Arbeit auf die große Bedeutung der Resilienz bei der Vorhersage der langfristigen Entwicklung von Risikokindern. N2 - Resilience refers to the ability to successfully deal with stressful life circumstances and experiences and to cope with them. Based on data from the Mannheim Study of Children at Risk, which follows a sample of children at risk from birth to adulthood, the present paper provides convincing evidence demonstrating how protective factors in the child and his/her family environment operate during the course of development to contribute to the development of resilience. As shown, a major role is assigned to positive early parent–child relationships (both mother– and father–child interactions). Moreover, positive interactive experiences at the child’s age of 2 years play a significant role. These experiences consistently contribute to a positive child development in the face of adversity. In addition to characteristics of the social environment of the child, cognitive, social–emotional, and internal competencies during childhood, youth, and young adulthood play a major role in the development of resilience. These competencies enable children at risk who are growing up in psychosocial high-risk families or in poverty to successfully cope with conditions of high adversity. Moreover, the findings presented here demonstrate that resilience may be conceived as a personal characteristic that exhibits high stability since young adulthood. With these findings, the present study points to the significance of resilience in predicting the long-term outcome of children at risk. KW - protective factors KW - risk factors KW - longitudinal study KW - Mannheim Study of Children at Risk KW - early parent-child relationship KW - Schutzfaktoren KW - Risikofaktoren KW - Längsschnittstudie KW - Mannheimer Risikokinderstudie KW - frühe Eltern-Kind-Beziehung Y1 - 2018 U6 - https://doi.org/10.1026/0942-5403/a000236 SN - 0942-5403 SN - 2190-6246 VL - 26 SP - 230 EP - 239 PB - Hogrefe CY - Göttingen ER - TY - JOUR A1 - Hohm, Erika A1 - Zohsel, Katrin A1 - Schmidt, Martin H. A1 - Esser, Günter A1 - Brandeis, Daniel A1 - Banaschewski, Tobias A1 - Laucht, Manfred T1 - Beeinträchtigter Start ins Leben T1 - Impaired Start into Life BT - Langfristige Auswirkungen der postpartalen Depression und der Einfluss des mütterlichen Interaktionsverhaltens BT - Long-Term Effects of Postpartum Depression and the Role of Maternal Interactional Behavior JF - Kindheit und Entwicklung N2 - Postpartale Depressionen sind häufige und schwerwiegende psychische Erkrankungen mit ungünstigem Einfluss auf die kindliche Entwicklung. Als Haupttransmissionsweg gilt die frühe Mutter-Kind-Interaktion. Über die langfristigen Auswirkungen auf die Kinder im Erwachsenenalter und die Rolle der Interaktion liegen kaum Ergebnisse vor. Im Rahmen der Mannheimer Risikokinderstudie wurden postpartale Depressionen bis zwei Jahre nach der Geburt erfasst. Die kindliche Entwicklung wurde fortlaufend und die Mutter-Kind-Interaktion im Alter von 3 Monaten standardisiert erhoben. 28 Kinder postpartal depressiver und 107 Kinder gesunder Mütter konnten mit 25 Jahren untersucht werden. Beeinträchtigungen der kognitiven und psychischen Entwicklung bei Kindern postpartal depressiver Mütter waren bis ins Erwachsenenalter nachweisbar. Responsives bzw. sensitives mütterliches Verhalten wirkte der negativen Entwicklung entgegen. Dies betont die Bedeutung einer hohen Qualität der Mutter-Kind-Interaktion für die Entwicklung von Risikokindern. N2 - Postpartum depression (PPD) is a common and serious mental health problem with prevalence rates ranging from 13% to 19%, and is associated with an increased risk of adverse child development. PPD is characterized by symptoms common of depression, particularly by impairments of maternity, parenting, and mother-infant interactions. Several reviews suggest an impact on attachment, cognitive, behavioral, and health-related outcome in the offspring. However, the long-term effects of PPD regarding cognitive and mental development into adulthood and the underlying mechanisms, especially the role of maternal interactional behavior, are not yet well understood. In the Mannheim Study of Children at Risk, maternal depression was assessed when the child was 3 months and 2 years old. Development from infancy to young adulthood (25 years) was assessed at regular intervals in 28 children of postnatally depressed mothers and 107 children born to mentally healthy mothers. Cognitive outcome up to age 11 was measured using standardized instruments; in adulthood, school outcome was used approximately. Psychiatric diagnosis as well as symptom scores served as psychological outcome. At age 3 months, mothers and infants were videotaped during a nursing and a playing situation. Videotapes of the 10-min session were recorded and evaluated by trained raters (kappa > .83) using the Category System for Microanalysis of Early Mother Child Interaction (Esser, Scheven, et al., 1989). The cognitive as well as social-emotional outcome of children of mothers suffering from PPD was significantly poorer than in the children of mentally healthy mothers. The adverse effects were more pronounced during childhood. The offspring of postnatally depressed mothers who interacted in a responsive manner with their infant exhibited a better prognosis in contrast to those with mothers interacting less sensitively. This effect was observed with regard to cognitive development and symptoms of externalizing behavior at age 19 years. Regarding internalizing behavior, no impact of maternal behavior was detected. These findings emphasize the importance of high-quality early mother-child interaction in the development of children at risk. Furthermore, convincing arguments are given for very early specialized treatment of impaired mother-child interactions in mothers suffering from PPD. The PPD treatment should always comprise treatment of depression as well as treatment of the disturbed mother-child interaction. KW - postpartum depression KW - development KW - longitudinal study KW - Mannheim Study of Children at Risk KW - mother-child interaction KW - Postpartale+Depression KW - Entwicklung KW - Längsschnittstudie KW - Mannheimer+Risikokinderstudie KW - Mutter-Kind-Interaktion Y1 - 2017 U6 - https://doi.org/10.1026/0942-5403/a000234 SN - 0942-5403 SN - 2190-6246 VL - 26 SP - 210 EP - 220 PB - Hogrefe CY - Göttingen ER - TY - JOUR A1 - Hohmann, Sarah A1 - Zohsel, Katrin A1 - Buchmann, Arlette F. A1 - Blomeyer, Dorothea A1 - Holz, Nathalie A1 - Boecker-Schlier, Regina A1 - Jennen-Steinmetz, Christine A1 - Rietschel, Marcella A1 - Witt, Stephanie H. A1 - Schmidt, Martin H. A1 - Esser, Günter A1 - Meyer-Lindenberg, Andreas A1 - Banaschewski, Tobias A1 - Brandeis, Daniel A1 - Hohm, Erika A1 - Laucht, Manfred T1 - Interacting effect of MAOA genotype and maternal prenatal smoking on aggressive behavior in young adulthood JF - Journal of neural transmission N2 - 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′ 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. KW - MAOA KW - Smoking during pregnancy KW - Interaction KW - Aggression KW - Longitudinal KW - Young adulthood Y1 - 2016 U6 - https://doi.org/10.1007/s00702-016-1582-x SN - 0300-9564 SN - 1435-1463 VL - 123 SP - 885 EP - 894 PB - Springer CY - Wien ER - TY - JOUR A1 - Holz, Nathalie E. A1 - Boecker-Schlier, Regina A1 - Baumeister, Sarah A1 - Hohm, Erika A1 - Zohsel, Katrin A1 - Buchmann, Arlette F. A1 - Blomeyer, Dorothea A1 - Jennen-Steinmetz, Christine A1 - Hohmann, Sarah A1 - Wolf, Isabella A1 - Plichta, Michael M. A1 - Meyer-Lindenberg, Andreas A1 - Banaschewski, Tobias A1 - Brandeis, Daniel A1 - Laucht, Manfred T1 - Effect of prenatal exposure to tobacco smoke on inhibitory control neuroimaging results from a 25-Year prospective study JF - JAMA psychiatry N2 - IMPORTANCE: There is accumulating evidence relating maternal smoking during pregnancy to attention-deficit/hyperactivity disorder (ADHD) without elucidating specific mechanisms. Research investigating the neurobiological underpinnings of this disorder has implicated deficits during response inhibition. Attempts to uncover the effect of prenatal exposure to nicotine on inhibitory control may thus be of high clinical importance. MAIN OUTCOMES AND MEASURES: Functional magnetic resonance imaging response, morphometric data, lifetime ADHD symptoms, and novelty seeking. RESULTS: Participants prenatally exposed to nicotine exhibited a weaker response in the anterior cingulate cortex (t(168) = 4.46; peak Montreal Neurological Institute [MNI] coordinates x = -2, y = 20, z = 30; familywise error [FWE]-corrected P = .003), the right inferior frontal gyrus (t(168) = 3.65; peak MNI coordinates x = 44, y = 38, z = 12; FWE-corrected P = .04), the left inferior frontal gyrus (t(168) = 4.09; peak MNI coordinates x = -38, y = 36, z = 8; FWE-corrected P = .009), and the supramarginal gyrus (t(168) = 5.03; peak MNI coordinates x = 64, y = -28, z = 22; FWE-corrected P = .02) during the processing of the NoGo compared to neutral stimuli, while presenting a decreased volume in the right inferior frontal gyrus. These findings were obtained irrespective of the adjustment of confounders, ADHD symptoms, and novelty seeking. There was an inverse relationship between inferior frontal gyrus activity and ADHD symptoms and between anterior cingulate cortex activity and novelty seeking. CONCLUSIONS AND RELEVANCE: These findings point to a functional involvement of prenatal exposure to tobacco smoke in neural alterations similar to ADHD, which underlines the importance of smoking prevention treatments. Y1 - 2014 U6 - https://doi.org/10.1001/jamapsychiatry.2014.786 SN - 2168-622X SN - 2168-6238 VL - 71 IS - 7 SP - 786 EP - 796 PB - American Veterinary Medical Association CY - Chicago ER - TY - JOUR A1 - Holz, Nathalie E. A1 - Boecker-Schlier, Regina A1 - Hohm, Erika A1 - Zohsel, Katrin A1 - Buchmann, Arlette F. A1 - Blomeyer, Dorothea A1 - Jennen-Steinmetz, Christine A1 - Baumeister, Sarah A1 - Hohmann, Sarah A1 - Wolf, Isabella A1 - Plichta, Michael M. A1 - Esser, Günter A1 - Schmidt, Martin A1 - Meyer-Lindenberg, Andreas A1 - Banaschewski, Tobias A1 - Brandeis, Daniel A1 - Laucht, Manfred T1 - The Long-Term Impact of Early Life Poverty on Orbitofrontal Cortex Volume in Adulthood: Results from a Prospective Study Over 25 Years JF - Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology N2 - 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. Y1 - 2015 U6 - https://doi.org/10.1038/npp.2014.277 SN - 0893-133X SN - 1740-634X VL - 40 IS - 4 SP - 996 EP - 1004 PB - Nature Publ. Group CY - London ER - TY - JOUR A1 - Holz, Nathalie E. A1 - Zohsel, Katrin A1 - Laucht, Manfred A1 - Banaschewski, Tobias A1 - Hohmann, Sarah A1 - Brandeis, Daniel T1 - Gene x environment interactions in conduct disorder BT - Implications for future treatments JF - Neuroscience & biobehavioral reviews : official journal of the International Behavioral Neuroscience Society N2 - Conduct disorder (CD) causes high financial and social costs, not only in affected families but across society, with only moderately effective treatments so far. There is consensus that CD is likely caused by the convergence of many different factors, including genetic and adverse environmental factors. There is ample evidence of gene-environment interactions in the etiology of CD on a behavioral level regarding genetically sensitive designs and candidate gene-driven approaches, most prominently and consistently represented by MAOA. However, conclusive indications of causal GxE patterns are largely lacking. Inconsistent findings, lack of replication and methodological limitations remain a major challenge. Likewise, research addressing the identification of affected brain pathways which reflect plausible biological mechanisms underlying GxE is still very sparse. Future research will have to take multilevel approaches into account, which combine genetic, environmental, epigenetic, personality, neural and hormone perspectives. A better understanding of relevant GxE patterns in the etiology of CD might enable researchers to design customized treatment options (e.g. biofeedback interventions) for specific subgroups of patients. KW - Gene-environment interaction KW - Conduct disorder KW - Aggression KW - Externalizing behavior KW - fMRI Y1 - 2016 U6 - https://doi.org/10.1016/j.neubiorev.2016.08.017 SN - 0149-7634 SN - 1873-7528 VL - 91 SP - 239 EP - 258 PB - Elsevier CY - Oxford ER - TY - JOUR A1 - Millenet, Sabina A1 - Laucht, Manfred A1 - Hohm, Erika A1 - Jennen-Steinmetz, Christine A1 - Hohmann, Sarah A1 - Schmidt, Martin H. A1 - Esser, Günter A1 - Banaschewski, Tobias A1 - Brandeis, Daniel A1 - Zohsel, Katrin T1 - Sex-specific trajectories of ADHD symptoms from adolescence to young adulthood JF - European child and adolescent psychiatry : offical journal of the European Society for Child and Adolescent Psychiatry N2 - Reports of current ADHD symptoms in adults with a childhood diagnosis of ADHD are often discrepant: While one subgroup reports a particularly high level of current ADHD symptoms, another reports—in contrast—a very low level. The reasons for this difference remain unclear. Although sex might play a moderating role, it has not yet been examined in this regard. In an epidemiological cohort study from birth to young adulthood, childhood ADHD diagnoses were assessed at the ages of 4.5, 8, and 11 years based on parent ratings. Sex-specific development of ADHD symptoms was analyzed from the age of 15 to 25 years via self-reported ADHD symptoms in participants with (n = 47) and without childhood ADHD (n = 289) using a random coefficient regression model. The congruence between parent reports and adolescents’ self-ratings was examined, and the role of childhood ADHD diagnosis, childhood OCC/CD, and childhood internalizing disorder as possible sex-specific predictors of self-reported ADHD symptoms at age 25 years was investigated. With regard to self-reported ADHD symptoms, females with a childhood ADHD diagnosis reported significantly more ADHD symptoms compared to females without childhood ADHD and males with and without ADHD throughout adolescence and young adulthood. In contrast, males with childhood ADHD did not differ from control males either at age 15 or at age 25 years. Only in females did a childhood diagnosis of an externalizing disorder (ADHD and CD/ODD) predict self-reported ADHD symptoms by age 25 years. Our findings suggest that self-reports of young adults with a childhood diagnosis of ADHD are influenced by sex. Specifically, females with childhood ADHD report increased levels of ADHD symptoms upon reaching adulthood. To correctly evaluate symptoms and impairment in this subgroup, other, more objective, sources of information may be advisable, such as neurophysiological measures. KW - ADHD KW - Sex KW - Self-report KW - Longitudinal study Y1 - 2018 U6 - https://doi.org/10.1007/s00787-018-1129-9 SN - 1018-8827 SN - 1435-165X VL - 27 IS - 8 SP - 1067 EP - 1075 PB - Springer CY - New York ER -