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Objective To demonstrate that children homozygous for the 10-repeat allele of the common dopamine transporter (DAT1) polymorphism who were exposed to maternal prenatal smoke exhibited significantly higher hyperactivity-impulsivity than children without these environmental or genetic risks. Study design We performed a prospective longitudinal study from birth into early adulthood monitoring the long-term outcome of early risk factors. Maternal prenatal smoking was determined during a standardized interview with the mother when the child was 3 months old. At age 15 years, 305 adolescents participated in genotyping for the DAT1 40 base pair variable number of tandem repeats polymorphism and assessment of inattention, hyperactivity-impulsivity, and oppositional defiant/conduct disorder symptoms with die Kiddie- Sads-Present and Lifetime Version. Results There was no bivariate association between DAT1 genotype, prenatal smoke exposure and symptoms of attention deficit hyperactivity disorder. However, a significant interaction between DAT1 genotype and prenatal smoke exposure emerged (P =.012), indicating that males with prenatal smoke exposure who were homozygous for the DAT1 10r allele had higher hyperactivity-impulsivity than males from all other groups. In females, no significant main effects of DAT1 genotype or prenatal smoke exposure or interaction effects on any symptoms were evident (all P >.25). Conclusions This study provides further evidence for the multifactorial nature of attention deficit hyperactivity disorder and the importance of studying both genetic and environmental factors and their interaction.
The present study aimed to clarify the functional role of genes in the dopamine and serotonin systems by examining whether polymorphisms in these genes are related to adolescent externalizing behavior either alone or in interaction with each other. Participants were selected from an ongoing prospective study of the outcome of early risk factors. At age 15 years, 298 adolescents (144 males, 154 females) completed the Youth Self Report, 296 primary caregivers the Child Behavior Checklist and 253 teachers the Teacher Report Form. DNA was genotyped for the DRD4 exon III VNTR and the 5-HTTLPR polymorphisms. Results revealed that individuals with the DRD4 7r allele reported significantly more externalizing behavior than carriers of other variants. In addition, a significant interaction emerged, indicating that adolescents carrying two copies of the 5-HTTLPR short allele and the DRD4 7r variant scored highest on aggressive and/or delinquent behavior compared to other genotypes. This result suggests an effect of 5-HTTLPR on externalizing behavior in the presence of DRD4 7r but no effect in its absence.
Aims: To investigate whether concurrent alcohol and tobacco use during early adolescence characterizes a subgroup that differs from users of one substance only regarding several risk factors for later substance use problems. Methods: Participants were from a prospective longitudinal cohort study of 384 children at risk for later psychopathology, with the majority being born with obstetric complications and psychosocial adversities. Assessments of adolescent drug consumption and related intrapersonal characteristics were obtained at age 15. Results: Compared to consumers of alcohol only, 15-year-olds drinking and smoking during the same time period (past 4 weeks) had significantly higher levels of consumption and more excessive use of alcohol, started drinking at an earlier age, had higher scores on the Fagerstrom Test for Nicotine Dependence, and more cannabis use. This group could be distinguished from users of alcohol only by higher novelty seeking and more positive alcohol effect expectancies. Compared to consumers of tobacco only, concurrent users reported higher nicotine dependence and more cannabis use. No significant differences were observed regarding frequency and age at initiation of tobacco use, tobacco-related sensitivity, self- efficacy and instrumentality as well as novelty seeking. Conclusions: Concurrent alcohol and tobacco use during early adolescence is associated with characteristics that are well known as risk factors for later alcohol use problems and dependence and that should be targeted by prevention programs.
Teilleistungsstörungen
(1997)
Entspannungsverfahren
(2008)
Epidemiological studies have reported elevated rates of legal drug consumption among adolescents in Germany. The aim of this study was to ascertain patterns and parameters of smoking and drinking in early-users as well as to examine possible determinants of risky patterns of use. Participants were from a longitudinal study of a birth cohort of 384 children at risk. Assessments of adolescent drug consumption as well as of individual and social determinants were obtained at age 15. Adolescents drinking and smoking during the same period (past four weeks) were characterized by more excessive and impulsive consumption and by higher rates of cannabis use. No specific determinants of concurrent use could be found. These findings suggest that adolescents displaying early concurrent tobacco and alcohol use may be at higher risk for substance use problems and should be targeted by prevention programs.
Es werden Befunde aus einer prospektiven Laengsschnittstudie praesentiert, in der 321 Probanden im Alter von 8, 13, 18 und 25 Jahren untersucht werden konnten; ihre Dunkelfelddelinquenz wurde mit 18 und 25 Jahren erfasst. Wir suchten nach Assoziationen zur Delinquenzentwicklung und erwarteten Unterschiede zwischen auf das Jugendalter beschraenkter gegenueber ins fruehe Erwachsenenalter fortgesetzter sowie spaet, d.h. nach dem Alter von 18 Jahren, beginnender Delinquenz. Wir fanden gemeinsame Risikofaktoren und fuer die drei Verlaufstypen spezifische Risikokonstellationen, die eher im Jugendalter als in der Kindheit identifiziert wurden. Widrige familiaere Bedingungen, Entwicklungsverzoegerungen und psychische Stoerungen scheinen mit Delinquenz als eher persistentem Verhalten assoziiert.
In a high-risk community sample, we examined the role of regulative temperament and emotionality as well as the extent of gender specificity in the development of externalizing problems. 151 boys and 157 girls born at differing degrees of obstetric and psychosocial risk were followed from birth into adolescence. In infancy and childhood, NYLS- derived temperamental characteristics were assessed by a highly structured parent interview and standardized behavioral observations. At age 15 years, externalizing problems were measured by the Child Behavior Checklist. As revealed by multiple linear regression and logistic regression, low regulative abilities predicted adolescent behavioral and attentional problems over and above obstetric and psychosocial risks. Gender specificity was found in the strength of the association rather than in the kind with a stronger long-term prediction from infant and toddler temperament in girls. Compared to regulative abilities, temperament factors describing aspects of mood and fear/withdrawal versus approach tendencies played a minor role in the development of externalizing problems. Findings are discussed in terms of gender-specific risk factors and possible differential developmental trajectories to subtypes of disruptive behavior.
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.
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.
Dichte und Struktur von Lebensereignissen in Mannheim und Rostock in der Nachwendezeit 1989 - 1995
(1996)
Enuresis
(2008)
Die meisten Kinder werden mit 2 bis 4 Jahren am Tage und in der Nacht trocken. Gemäß den klinisch- diagnostischen Leitlinien der ICD-10 (WHO 1993) spricht man von einer Enuresis, wenn es am Tag oder in der Nacht zu einem Entleeren der Blase in die Kleidung bzw. das Bett kommt, die relativ zum geistigen Entwicklungsstand der Person abnorm ist und nicht auf organische Ursachen zurückgeführt werden kann. Die Störungen der Blasenkontrolle dürfen nicht als Folge einer neurologischen Erkrankung, epileptischer Anfälle oder einer strukturellen Anomalie der ableitenden Harnwege auftreten. Gemäß den Forschungskriterien der ICD-10 (WHO 1994) muss das einnässende Kind nach seinem Lebens- und geistigen Alter mindestens 5 Jahre alt sein, um von einer nichtorganischen Enuresis (F 98.0) zu sprechen (in den klinisch-diagnostischen Leitlinien wird ein geistiger Entwicklungsstand gefordert, der mindestens dem eines Vierjährigen entspricht). Um die Diagnose zu erhalten, müssen Kinder unter 7 Jahren zumindest 2mal monatlich, 7-jährige oder ältere Kinder wenigstens einmal im Monat einnässen. Die Symptomdauer sollte mindestens 3 Monate betragen. In der Literatur wird synonym zum Begriff der "nichtorganischen Enuresis" häufig die Bezeichnung "funktionelle Enuresis" verwendet. Auch nach dem DSM-IV (Saß et al. 1996) sollten die Kinder für die Diagnose einer Enuresis (307.6) zumindest ein Entwicklungsalter von 5 Jahren aufweisen und die Symptomatik muss wenigstens seit 3 Monaten bestehen. Im Unterschied zur ICD-10 wird das Einnässen erst dann als klinisch bedeutsam beurteilt, wenn es mindestens 2mal wöchentlich auftritt. Ist dies nicht gegeben, kann die Diagnose dennoch gestellt werden, wenn durch das Einnässen klinisch bedeutsames Leiden hervorgerufen wird oder Beeintraechtigungen in sozialen, schulischen (beruflichen) oder anderen wichtigen Funktionsbereichen entstehen. Die Forderung eines 2mal wöchentlichen Einnässens erscheint deutlich zu streng, während das ein- bzw. 2malige Einnässen pro Monat ein sehr weiches Kriterium darstellt. V. Gontard (1998b) empfiehlt, Einnässen dann als klinisch bedeutsam einzuschätzen, wenn dies mindestens einmal wöchentlich auftritt.
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.
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.
To examine whether the dopamine receptor D4 gene (DRD4) exon III VNTR moderates the risk of infants with regulatory disorders for developing attention-deficit/hyperactivity disorder (ADHD) later in childhood. In a prospective longitudinal study of children at risk for later psychopathology, 300 participants were assessed for regulatory problems in infancy, DRD4 genotype, and ADHD symptoms and diagnoses from childhood to adolescence. To examine a potential moderating effect on ADHD measures, linear and logistic regressions were computed. Models were fit for the main effects of the DRD4 genotype (presence or absence of the 7r allele) and regulatory problems (presence or absence), with the addition of the interaction term. All models were controlled for sex, family adversity, and obstetric risk status. In children without the DRD4-7r allele, a history of regulatory problems in infancy was unrelated to later ADHD. But in children with regulatory problems in infancy, the additional presence of the DRD4-7r allele increased the risk for ADHD in childhood. The DRD4 genotype seems to moderate the association between regulatory problems in infancy and later ADHD. A replication study is needed before further conclusions can be drawn, however.
Maternal stimulation in infancy predicts hypothalamic-pituitary-adrenal axis reactivity in young men
(2013)
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.
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.
Entwicklungspsychopathologie
(1998)
Context: Recent evidence suggests that gene X environment interactions could explain the inconsistent findings of association studies relating the dopamine transporter (DAT1) gene with attention-deficit/hyperactivity disorder (ADHD). 1bjective: To examine whether psychosocial adversity moderated the effect of genetic variation in DAT1 on ADHD symptoms in. adolescents from a high-risk community sample. Design: Prospective cohort study. Setting: Data were taken from the Mannheim Study of Children at Risk, an ongoing longitudinal study of the long-term outcomes of early risk factors followed up from birth on. Participants: Three hundred five adolescents (146 boys, 159 girls) participated in a follow-up assessment at age 15 years. Main Outcome Measures: Measures of ADHD symptoms according to DSM-IV were obtained using standardized structural interviews with adolescents and their parents. Psychosocial adversity was determined according to an "enriched" family adversity index as proposed by Rutter and Quinton. DNA was genotyped for the common DAT1 40-base pair (bp) variable number of tandem repeats (VNTR) polymorphism in the 3' untranslated region; 3 previously described single nucleotide polymorphisms in exon 15, intron 9, and exon 9; and a novel 30-bp VNTR polymorphism in intron 8. Results: Adolescents homozygous for the 10-repeat allele of the 40-bp VNTR polymorphism who grew up in greater psychosocial adversity exhibited significantly more inattention and hyperactivity-impulsivity than adolescents with other genotypes or who lived in less adverse family conditions (significant interaction, P=.013-017). This gene X environment interaction was also observed in individuals homozygous for the 6-repeat allele of the 30-bp VNTR polymorphism and the haplotype comprising both markers. Conclusions: These findings provide initial evidence that environmental risks as described by the Rutter Family Adversity Index moderate the impact of the DAT1 gene on ADHD symptoms, suggesting a DAT1 effect only in those individuals exposed to psychosocial adversity.
Objective: We investigated in a high-risk sample the differential impact of biological and psychosocial risk factors on antisocial behaviour pathways. Method: One hundred and thirty-eight boys and 155 girls born at differing degrees of obstetric and psychosocial risk were examined from birth until adolescence. Childhood temperament was assessed by a highly-structured parent-interview and standardized behavioural observations, adolescent temperament was measured by self-report. Neurodevelopmental variables were assessed by age-specific developmental tests. Emotional and behaviour problems were measured at the ages of 8 and 15 by the Achenbach scales. Results: In both genders, psychosocial adversity and early self-control temperament were strongly associated with early-onset persistent (EOP) antisocial behaviour. Psychosocial adversity and more severe externalizing problems differentiated the EOP from childhood-limited (CL) pathway. In girls, adolescent-onset (AO) antisocial behaviour was strongly associated with novelty seeking at 15 years. Conclusion: Our findings emphasize the need for early support and intervention in psychosocially disadvantaged families.
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.
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.
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.
We examined face memory deficits in patients with Idiopathic Parkinson's disease (IPD) with specific regard to the moderating role of sex and the different memory processes involved. We tested short- and long-term face recognition memory in 18 nonclinical participants and 18 IPD-patients matched for sex, education and age. We varied the duration of item presentation (1, 5, 10s), the time of testing (immediately, 1hr, 24hrs) and the possibility to re-encode items. In accordance with earlier studies, we report face memory deficits in IPD. Moreover, our findings indicate that sex and encoding conditions may be important moderator variables. In contrast to healthy individuals, IPD-patients cannot gain from increasing duration of presentation. Furthermore, our results suggest that I PD leads to face memory deficits in women, only.
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.
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.
Neurofeedback treatment has been demonstrated to reduce inattention, impulsivity and hyperactivity in children with attention deficit/hyperactivity disorder (ADHD). However, previous studies did not adequately control confounding variables or did not employ a randomized reinforcer-controlled design. This study addresses those methodological shortcomings by comparing the effects of the following two matched biofeedback training variants on the primary symptoms of ADHD: EEG neurofeedback (NF) aiming at theta/beta ratio reduction and EMG biofeedback (BF) aiming at forehead muscle relaxation. Thirty-five children with ADHD (26 boys, 9 girls; 6-14 years old) were randomly assigned to either the therapy group (NF; n = 18) or the control group (BF; n = 17). Treatment for both groups consisted of 30 sessions. Pre- and post-treatment assessment consisted of psychophysiological measures, behavioural rating scales completed by parents and teachers, as well as psychometric measures. Training effectively reduced theta/beta ratios and EMG levels in the NF and BF groups, respectively. Parents reported significant reductions in primary ADHD symptoms, and inattention improvements in the NF group were higher compared to the control intervention (BF, d(corr) = -.94). NF training also improved attention and reaction times on the psychometric measures. The results indicate that NF effectively reduced inattention symptoms on parent rating scales and reaction time in neuropsychological tests. However, regarding hyperactivity and impulsivity symptoms, the results imply that non-specific factors, such as behavioural contingencies, self-efficacy, structured learning environment and feed-forward processes, may also contribute to the positive behavioural effects induced by neurofeedback training.
Objective: The delineation of developmental pathways to juvenile depressive symptoms is of major clinical interest because these are known to be predictive for adult mood disorders and for a range of other mental health problems. This study investigates the impact of child temperament and early maternal distress, both of which are known to influence children's emotional development, on preadolescent depression. Methods: In a prospective, longitudinal at-risk sample (163 boys, 178 girls), we assessed temperament at the age of 3 months and at 2 years, 4.5 years, and 8 years, respectively, and chronic maternal distress during infancy. Hierarchical linear regression analysis was used to investigate the prediction of depressive symptoms at the age of 11 years measured by the Child Depression Inventory. In addition, we controlled for psychosocial and obstetric perinatal risks and gender. Results: Psychosocial risks and self-control temperament made significant independent contributions to preadolescent depression, whereas fearful, difficult temperament and obstetric risks were unrelated to depressive outcome. Interestingly, a clear gender difference emerged with a significant prediction from maternal distress only in girls. Conclusions: Our data extend previous findings of a concurrent association between regulative temperament and juvenile depression to a predictive view. Furthermore, the results point toward gender-specific pathways to preadolescent depression and support earlier findings indicating that subclinical maternal distress may exert as detrimental effects on child development as clinical depression.
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.
Objective: A difficult or undercontrolled temperament, as well as harsh parental discipline or a lack of warmth, has long been regarded as risk factors for the development of externalizing problems. In addition, it has been suggested that children with difficult temperament are especially susceptible to rearing influences. We investigated the impact of early temperament and parenting and their interactions on externalizing behavior at school age.
Methods: Participants were 148 boys and 160 girls from a prospective longitudinal study on a high-risk sample. At ages 3 months and 2 years, temperament was assessed by a highly structured parent interview and standardized behavioral observations. Maternal parenting was assessed by videotaped behavioral observation and a parent questionnaire. Externalizing problems at age 8 years were measured by the Child Behavior Checklist.
Results: Using hierarchical linear regression analyses, we found that externalizing problems were predicted by psychosocial adversity and poor self-control, whereas no main effect for restrictive parenting or maternal empathy was found. Fearful-inhibited boys were positively affected by empathic and sensitive parenting, whereas girls who were low in self-control and/or fearful developed less externalizing problems with restrictive parenting.
Conclusion: Our results partly support the differential susceptibility hypothesis. In addition, they point toward gender-specific pathways in the development of externalizing problems.
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.
Recent longitudinal studies have indicated that affective and behavioral dysregulation in childhood is associated with an increased risk for various negative outcomes in later life. However, few studies to date have examined early mechanisms preceding dysregulation during early childhood. Aim of this study was to elucidate early mechanisms relating to dysregulation in later life using data from an epidemiological cohort study on the long-term outcome of early risk factors from birth to adulthood. At age 3 months, mothers and infants were videotaped during a nursing and playing situation. Maternal responsiveness was evaluated by trained raters. Infant regulatory problems were assessed on the basis of a parent interview and direct observation by trained raters. At age 8 and 11 years, 290 children (139 males) were rated on the Child Behavior Checklist (CBCL). Additionally, participants were genotyped for the dopamine D4 receptor (DRD4) exon 3 VNTR polymorphism. A significant three-way interaction between maternal responsiveness, DRD4 genotype and infant regulatory problems was detected predicting the CBCL-dysregulation profile (CBCL-DP). Carriers of the DRD4 7r allele with regulatory problems at age 3 months showed significantly more behavior problems associated with the CBCL-DP during childhood when exposed to less maternal responsiveness. In contrast, no effect of maternal responsiveness was observed in DRD4 7r carriers without infant regulatory problems and in non-carriers of the DRD4 7r allele. This prospective longitudinal study extends earlier findings regarding the association of the CBCL-DP with early parenting and later psychopathology, introducing both DRD4 genotype and infant regulatory problems as important moderators. (C) 2015 Elsevier Ltd. All rights reserved.
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.
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.
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.
Positive coping styles and perigenual ACC volume: two related mechanisms for conferring resilience?
(2016)
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.
Background: Cannabis is the most commonly used illegal substance among adolescents and young adults. Problematic cannabis use is often associated with comorbid psychopathological problems. The purpose of the current study was to elucidate the underlying developmental processes connecting externalizing and internalizing psychopathology in childhood and adolescence with problematic cannabis use in young adulthood. Methods: Data were drawn from the Mannheim Study of Children at Risk, an ongoing epidemiological cohort study from birth to adulthood. For n = 307 participants, symptom scores of conduct/oppositional defiant disorder, attention problems, hyperactivity/impulsivity, and internalizing disorders were available for the periods of childhood (4.5-11 years) and adolescence (15 years). At age 25 years, problematic cannabis use was assessed via clinical interview and a self-rating questionnaire. Results: At age 25 years, problematic cannabis use was identified in n = 28 participants (9.1%). Childhood conduct/oppositional behavior problems were predictive of problematic cannabis use during young adulthood when comorbid symptoms were controlled for. No such effect was found for childhood attention, hyperactivity/impulsivity or internalizing problems. With respect to psychopathological symptoms during adolescence, only attention problems were significantly related to later problematic cannabis use when controlling for comorbidity. Conclusions: The current study highlights the role of conduct/oppositional behavior problems during childhood and attention problems during adolescence in later problematic cannabis use. It sheds more light on the developmental sequence of childhood and adolescence psychopathology and young adult cannabis use, which is a prerequisite for effective prevention approaches. (C) 2016 Elsevier Ireland Ltd. All rights reserved.
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.
Objective: This study assesses the short-term and intermediate effects of preschool training stimulating phonological awareness and letter-sound correspondence for children at risk of developing dyslexia. Moreover, we examined whether training reduced the frequency of subsequent dyslexic problems. Method: 25 children at risk of developing dyslexia were trained with Horen, Lauschen, Lernen 1 und 2 (Kuspert & Schneider, 2008; Plume & Schneider, 2004) by their kindergarten teachers and were compared with 60 untrained at-risk children. Results:The training revealed a significant short-term effect: The phonological awareness of trained at-risk children increased significantly over that of untrained at-risk children. However, there were no differences in phonological awareness, spelling, and reading ability between the first-graders in the training and control group. Furthermore, reading problems were reduced in the training group. Conclusions: In the future, phonological awareness as well as additional predictors should be included when identifying children vulnerable to developing dyslexia. Moreover, in order to prevent dyslexia, additional prerequisite deficits need to be identified, alleviated, and their effects evaluated.
Calcularis is a computer-based training program which focuses on basic numerical skills, spatial representation of numbers and arithmetic operations. The program includes a user model allowing flexible adaptation to the child's individual knowledge and learning profile. The study design to evaluate the training comprises three conditions (Calcularis group, waiting control group, spelling training group). One hundred and thirty-eight children from second to fifth grade participated in the study. Training duration comprised a minimum of 24 training sessions of 20 min within a time period of 6–8 weeks. Compared to the group without training (waiting control group) and the group with an alternative training (spelling training group), the children of the Calcularis group demonstrated a higher benefit in subtraction and number line estimation with medium to large effect sizes. Therefore, Calcularis can be used effectively to support children in arithmetic performance and spatial number representation.
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.
Research has shown that learning disabilities are associated with internalizing problems in (pre) adolescents. In order to examine this relationship for math disability (MD), math achievement and internalizing problem scores were measured in a representative group of 1,436 (pre) adolescents. MD was defined by a discrepancy between math achievement and IQ. Internalizing problems were measured through a multi-informant (parents, teachers, self-report) approach. The results revealed that MD puts (pre) adolescents at a higher risk for internalizing problems. External and self-ratings differed between boys and girls, indicating that either they show distinct internalizing symptoms or they are being perceived differently by parents and teachers. Results emphasize the importance of both a multi-informant approach and the consideration of gender differences when measuring internalizing symptomatology of children with MD. For an optimal treatment of MD, depressive and anxious symptoms need to be considered.
Variation in the gene encoding for the norepinephrine transporter (NET, SLC6A2) has repeatedly been linked with ADHD, although there is some inconsistency regarding the association with specific genes. The variants for which most consistent association has been found are the NET variants rs3785157 and rs28386840. Here, we tested for their association with ADHD diagnosis and ADHD-related phenotypes during development in a longitudinal German community sample. Children were followed from age 4 to age 15, using diagnostic interviews to assess ADHD. Between the ages of 8 and 15 years, the Child Behavior Checklist (CBCL) was administered to the primary caregivers. The continuous performance task (CPT) was performed at age 15. Controlling for possible confounders, we found that homozygous carriers of the major A allele of the functional promoter variant rs28386840 displayed a higher rate of ADHD lifetime diagnosis. Moreover, homozygous carriers of the minor T allele of rs3785157 were more likely to develop ADHD and showed higher scores on the CBCL externalizing behavior scales. Additionally, we found that individuals heterozygous for rs3785157 made fewer omission errors in the CPT than homozygotes. This is the first longitudinal study to report associations between specific NET variants and ADHD-related phenotypes during the course of development. (C) 2015 Elsevier Ireland Ltd. All rights reserved.
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.
Background: Medical training is very demanding and associated with a high prevalence of psychological distress. Compared to the general population, medical students are at a greater risk of developing a psychological disorder. Various attempts of stress management training in medical school have achieved positive results on minimizing psychological distress; however, there are often limitations. Therefore, the use of a rigorous scientific method is needed. The present study protocol describes a randomized controlled trial to examine the effectiveness of a specifically developed mindfulness-based stress prevention training for medical students that includes selected elements of cognitive behavioral strategies (MediMind).
Methods/Design: This study protocol presents a prospective randomized controlled trial, involving four assessment time points: baseline, post-intervention, one-year follow-up and five-year follow-up. The aims include evaluating the effect on stress, coping, psychological morbidity and personality traits with validated measures. Participants are allocated randomly to one of three conditions: MediMind, Autogenic Training or control group. Eligible participants are medical or dental students in the second or eighth semester of a German university. They form a population of approximately 420 students in each academic term. A final total sample size of 126 (at five-year follow-up) is targeted. The trainings (MediMind and Autogenic Training) comprise five weekly sessions lasting 90 minutes each. MediMind will be offered to participants of the control group once the five-year follow-up is completed. The allotment is randomized with a stratified allocation ratio by course of studies, semester, and gender. After descriptive statistics have been evaluated, inferential statistical analysis will be carried out with a repeated measures ANOVA-design with interactions between time and group. Effect sizes will be calculated using partial.-square values.
Discussion: Potential limitations of this study are voluntary participation and the risk of attrition, especially concerning participants that are allocated to the control group. Strengths are the study design, namely random allocation, follow-up assessment, the use of control groups and inclusion of participants at different stages of medical training with the possibility of differential analysis.
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.
Entwicklung und Persistenz von Hell- und Dunkelfelddelinquenz im Jugend- und frühen Erwachsenenalter
(2002)
Ziel der Untersuchung war die Bedeutung der Dunkelfelddelinquenz für die Prognose der Delinquenzentwicklung und die Bedeutung psychiatrischer Auffälligkeiten für Entstehen und Verlauf psychischer Störungen zu klären. Die Stichprobe bestand aus 281 25-Jährigen, die im Alter von 8, 13 und 18 Jahren psychiatrisch untersucht, und die mit 18 und 25 Jahren bezüglich ihrer Dunkelfelddelinquenz befragt worden waren. Es ergab sich ein klarer Zusammenhang erhöhter Dunkelfelddelinquenzraten mit gerichtlich bestrafter Delinquenz im Jugendalter. Bei Einbeziehung der Dunkelfelddelinquenz in die Prognose mußte die Wahrscheinlichkeit für den Ausblick auf delinquenten Karrieren von 76 % auf 44 % nach unten korrigiert werden, entsprechend stieg der Anteil von erwachsener als auch fortgesetzter Delinquenz. Die Mehrheit der später gerichtlich bestraften Jugendlichen und jungen Erwachsenen war im Alter von 8 und 13 Jahren psychiatrisch unauffällig gewesen. Als überlegene Prädiktoren stellten sich umschriebene Entwicklungsstörungen und widrige familiäre Bedingungen im Grund- und Hauptschulalter heraus. Als Konsequenz muß die Dunkelfelddelinquenz bei der Verlaufsprognose delinquenten Verhaltens im Jugendalter berücksichtigt werden. Präventive Überlegungen müssen sich auf Kinder mit umschriebenen Entwicklungsstörungen und solche, die in widrigen familiären Verhältnissen leben, mehr konzentrieren als auf Kinder mit hyperkinetischen und dissozialen Störungen. Schlüsselwörter: Delinquenz, Dunkelfelddelinquenz, Entwicklung und Verlauf
The ralationship between early mother-infant interaction at 3 mo old, biological and psychosocial risks, and later social withdrawal was examined using a hierarchical logistics regression approach. A group of childeren (N=20; aged 4.5-8 yrs old) who were stabily socially withdrawn and a control group of healthy children (N=143) were formed. Variables were entered into the regression models in the follwing order: At first, biological and psychosocial risks and sex, followed by mother and child variables separately, while in a final regression model all of the variables were entered at once. The results show that child behaviors (smilling and gazing) as well as maternal behaviors (facial and motor responsiveness) significantly predict social withdrawal in middle childhood. Among the risks only biolgical risks significantly contribute to later child outcome. These results suggest that a dysfunctional interaction pattern between mother and infant may be a precursor of childhood social withdrawal.
Risikofaktoren für Delinquenz bei Jugendlichen und deren Fortsetzung bis in das Erwachsenenalter
(2001)
The psycho-social development of both preterm and term children (n=347) whose mothers reported tocolytic treatment was assessed at the ages of 2, 4.5, 8 years. Term children exposed to tocolysis showed a higher rate of psychiatric disorders as well as poorer cognitive and motor performance than controls. In the preterm children no adverse impact of tocolysis could be found. The results are discussed concerning possible ways in which tocolytic treatment may influence child development. Restrictions because of the preliminary character of this study and the need of further prospective studies to clarify the developmental impact of tocolysis are also considered.
Vor- und Nachteile von Longitudinalstudien in der Klinischen Psychologie und Jugendpsychiatrie
(2000)
Entwicklung von Risikokindern im Schulalter : die langfristigen Folgen frühkindlicher Belastungen
(2000)
Theoretischer Hintergrund: Zur Erforschung der Entwicklungsepidemiologie psychischer Störungen gilt die prospektive Untersuchung von Risikogruppen als Königsweg. Fragestellung: Beschreibung der Entwicklungsmuster von Kindern mit frühen Belastungen, Ermittlung von Risiko- und Schutzfaktoren für unterschiedliche Entwicklungsresultate und Identifikation von Mechanismen, die differentiellen Verläufen zugrunde liegen. Methode: In einer prospektiven Längsschnittstudie (mit Erhebungswellen im Alter von 0;3, 2, 4 , 8 und 11 Jahren) wurden die Entstehung und der Verlauf von Entwicklungs- und Verhaltensstörungen bei 384 Kindern untersucht. Organische (prä- und perinatale Komplikationen) und psychosoziale Risiken (familiäre Belastungen) wurden in einem zwei- faktoriellen Design variiert. Ergebnisse: Die negativen Folgen früher Risiken waren bis zum Schulalter nachweisbar. Während organische Risiken vor allem die motorische und kognitive Entwicklung beeinträchtigten, konzentrierten sich die Auswirkungen psychosozialer Belastungen auf kognitive und sozial-emotionale Funktionen. Beide Risiken addierten sich in ihren negativen Konsequenzen. Schlussfolgerungen: Frühkindliche Risiken haben spezifische und langfristige Auswirkungen. Kinder mit multiplen Risikobelastungen sind in ihrer Entwicklung am stärksten gefährdet.