青少年内向性行为与遗传和环境因素相关性

目的探讨青少年内向性行为与遗传因素及环境因素的相关性。方法采用Achenbach青少年自评量表(youth self-report,YSR)对重庆市12~18岁74对双生子的内向行为进行评定。采用一般情况问卷、父母的养育方式和维度问卷(the parenting styles and dimensions questionaire,PSDQ)、家庭亲密度与适应性量表(family adaptability and cohesion evaluationscale,2nd edition,Chinese version,FACESⅡ-CV)、家庭压力问卷(family stresses questionnaire,FSQ)、应激生活事件(stressful life event,SLE)等调查环境因素;采用简易应对方式问卷(simplified coping style questionnaire,SCSQ)调查应对方式;采集双生子静脉血提取DNA进行卵型鉴定。通过OPEN-MX软件构建单因素结构方程模型,分析加性遗传因素、共享环境因素、个体特异性环境因素与双生子内向行为的相关程度。结果不同卵型双生子间父母养育方式、家庭压力、家庭亲密度及应对方式分值差异无统计学意义(P0.05);双生子内向行为与家庭亲密度(r=-0.223,P=0.011)呈负相关,与家庭压力(r=0.232,P=0.008)、专制型养育方式(r=0.206,P=0.018)、消极应对(r=0.409,P=0.001)呈正相关;与应激生活事件、父母的教育程度、职业等相关性无统计学意义(P0.05);结构方程显示,在内向行为总变异方差中加性遗传效应占0.51(95%CI:0.27~0.69)、个体特异性环境因素占0.49(95%CI:0.31~0.73)。结论青少年内向性行为与遗传及环境因素相关程度基本接近;与父母专制型养育方式、家庭压力、家庭亲密度等家庭因素及消极应对有关。     

青少年抑郁情绪影响因素的双生子研究

目的探讨遗传及环境因素对青少年抑郁情绪的影响。方法采用贝克抑郁量表(Beck depression inventory,BDI)对重庆市107对11~18岁双生子的抑郁情绪进行评定,采用一般情况问卷、父母的养育方式和维度问卷(parenting styles and dimensions questionaire,PSDQ)、家庭压力问卷(family stresses questionnaire,FSQ)、家庭亲密度与适应性量表(family adaptability and cohesion evaluation scale 2nd edition Chinese version,FACES II-CV)、应激生活事件(stressful life event,SLE)等量表调查环境因素,采集双生子静脉血标本提取DNA以进行卵型鉴定。构建单因素结构方程模型,分析加性遗传因素(A)、共享环境因素(C)、特殊环境因素(E)对双生子抑郁情绪的影响。结果双生子的抑郁情绪与父亲受教育程度(r=-0.15,P=0.03)、母亲受教育程度(r=-0.17,P=0.01)、权威型养育方式(r=-0.18,P0.01)、家庭适应性(r=-0.27,P0.01)及亲密度(r=-0.20,P0.01)呈负相关,与家庭压力呈正相关(r=0.12,P=0.04),与应激生活事件无统计学相关性(P0.05)。结构方程示,在抑郁情绪总变异方差中加性遗传效应占0.37(95%CI:0.14~0.57),个体特殊环境因素占0.63(95%CI:0.43~0.86)。结论抑郁情绪与父母权威型养育方式、家庭适应性负性相关,与家庭压力正性相关;青少年抑郁情绪受加性遗传和特殊环境因素的共同影响,但受特殊环境的影响更大。     

儿童青少年品行障碍的双生子研究进展

本文综述了近期儿童青少年品行障碍及其相关行为的病因学的双生子研究进展。品行障碍及其相关行为的发生在很大程度上受遗传因素和环境因素的影响,几乎各种危险因素与品行障碍的联系都同时受到遗传因素和环境因素的共同介导。     

遗传和环境因素对青少年脑灰质容积和皮层厚度影响的双生子研究北大核心CSCD

目的通过双生子法探索遗传和环境因素对青少年脑灰质容积、皮层厚度的影响。方法采用横断面研究设计,募集12~18岁双生子。采血液标本提取DNA进行卵型鉴定;采用韦氏儿童智力量表中国修订版进行智商测定;用3.0 T MRI进行头颅结构扫描,采集全脑166层矢状位图像并处理计算个体脑皮层分区灰质容积、皮层厚度;使用双生子结构方程分析遗传和环境对脑灰质容积、皮层厚度的影响。结果纳入57对双生子,其中同卵双生子30对,异卵双生子27对。灰质容积的最佳模型为AE模型,其中各脑区遗传度均有统计学意义(P<0.01);皮层厚度的最佳模型为ACE模型,各脑区中仅双侧扣带回及右侧额叶遗传度有统计学意义(P<0.05),其他脑区遗传度无统计学意义(P>0.05)。相比较影响各脑区皮层厚度的遗传度(A)、共享环境因素贡献度(C)与特异性环境因素(E),特异性环境因素(E)贡献度明显上升。结论在灰质容积和皮层厚度中,青少年脑的可塑性变化可能主要体现在皮层厚度改变上;遗传因素对灰质容积的影响主要驱动因素为皮层面积扩张,而非皮层厚度。     

遗传和环境因素对青少年脑灰质容积和皮层厚度影响的双生子研究

目的通过双生子法探索遗传和环境因素对青少年脑灰质容积、皮层厚度的影响。方法采用横断面研究设计,募集12~18岁双生子。采血液标本提取DNA进行卵型鉴定;采用韦氏儿童智力量表中国修订版进行智商测定;用3.0 T MRI进行头颅结构扫描,采集全脑166层矢状位图像并处理计算个体脑皮层分区灰质容积、皮层厚度;使用双生子结构方程分析遗传和环境对脑灰质容积、皮层厚度的影响。结果纳入57对双生子,其中同卵双生子30对,异卵双生子27对。灰质容积的最佳模型为AE模型,其中各脑区遗传度均有统计学意义(P0.01);皮层厚度的最佳模型为ACE模型,各脑区中仅双侧扣带回及右侧额叶遗传度有统计学意义(P0.05),其他脑区遗传度无统计学意义(P0.05)。相比较影响各脑区皮层厚度的遗传度(A)、共享环境因素贡献度(C)与特异性环境因素(E),特异性环境因素(E)贡献度明显上升。结论在灰质容积和皮层厚度中,青少年脑的可塑性变化可能主要体现在皮层厚度改变上;遗传因素对灰质容积的影响主要驱动因素为皮层面积扩张,而非皮层厚度。     

注意缺陷多动障碍与单胺类神经递质基因

近年来研究表明注意缺陷多动障碍的发生和发展与单胺类神经递质系统密切相关 ,而大量家系研究、双生子及寄养子研究已表明遗传因素起重要作用。本文综述了单胺类神经递质合成、释放、消除等过程有关的基因与儿童注意缺陷多动障碍的关系     

注意缺陷多动障碍与单胺类神经递质基因

近年来研究表明注意缺陷多动障碍的发生和发展与单胺类神经递质系统密切相关，而大量家系研究、双生子及寄养子研究已表明遗传因素起重要作用。本文综述了单胺类神经递质合成、释放、消除等过程有关的基因与儿童注意缺陷多动障碍的关系。     

精神分裂症的分子遗传学研究进展

精神分裂症在一般人群中的患病率约1%.在同卵双生子或父母双方均为精神分裂症的子女中患病率上升到40%～50%.较一般人群高40多倍;推算该病的遗传度约为80%,即遗传因素(80%)比环境因素(20%)在疾病发生过程中起更大作用[1].     

注意缺陷多动障碍核心症状对ADHD倾向儿童行为问题的影响

目的 探讨注意缺陷多动障碍（ADHD）核心症状对ADHD倾向儿童行为问题的影响,为早期识别ADHD患儿并进行有针对性的干预提供参考。方法 于2021年7月-8月,在广州市某小学筛选25名ADHD倾向儿童作为ADHD倾向组,纳入年龄、性别和年级相匹配的25名儿童作为正常组。采用中文版ADHD斯诺佩评估量表第4版（SNAP-IV）父母版评定ADHD核心症状,采用儿童困难问卷（QCD）和Conners父母症状问卷（PSQ）评定行为问题。采用Spearman相关分析考察ADHD核心症状与QCD和PSQ评分的相关性,采用分层线性回归分析探讨ADHD核心症状对行为问题的影响。结果 (1)组间差异显示,ADHD倾向组的注意缺陷和多动-冲动因子评分均高于正常组（t=7.771、6.726,P均<0.01）。(2)相关分析显示,注意缺陷因子评分与QCD总评分呈负相关（r=-0.440,P<0.05）,与PSQ的学习问题因子评分呈正相关（r=0.457,P<0.05）;多动-冲动因子评分与PSQ的焦虑因子评分呈负相关（r=-0.457,P<0.05）,与PSQ的冲动-多动因子评分呈...     

注意缺陷多动障碍与家庭因素

近年来,儿童注意缺陷多动障碍（ADHD）的研究在国内外受到广泛关注.美国儿科协会临床指南指出学龄儿童ADHD的患病率为4％～12％,是一种最常见的儿童心理行为疾病[1].我国选用DSM-Ⅳ的注意缺陷多动障碍诊断标准,近年调查学龄儿童检出率为3.94％～6.3％[2-4],调查数据普遍低于国外的数据,但总体呈上升趋势.儿童ADHD核心症状为注意力不集中、多动与冲动,它的病因目前仍不清楚,一般认为是由遗传和环境因素引起的一种心理行为性疾病.近年经许多回顾研究表明,ADHD儿童的不良行为与家庭环境因素和养育方式等具有一定的相关性,现在对此作一综述.关键词：注意缺陷多动障碍;家庭环境;教养方式;依恋     

Chernobyl exposure as stressor during pregnancy and behaviour in adolescent offspring

Objective: Research in animals has shown that exposure to stressors during pregnancy is associated with offspring behavioural disorders. We aimed to study the effect of in utero exposure to the Chernobyl disaster in 1986, and maternal anxiety presumably associated with that exposure, on behaviour disorder observed at age 14. Method: Exposed (n = 232) and non‐exposed Finnish twins (n = 572) were compared. A semi‐structured interview was used to assess lifetime symptoms of depression, generalized anxiety disorder, attention deficit hyperactivity disorder, conduct disorder and oppositional defiant disorder symptoms. Results: Adolescents who were exposed from the second trimester in pregnancy onwards, had a 2.32‐fold risk (95% CI: 1.13–4.72) of having lifetime depression symptoms, an increased risk of fulfilling DSM‐III‐R criteria of a major depressive disorder (OR = 2.48, 95% CI: 1.06–5.7), and a 2.01‐fold risk (95% CI: 1.14–3.52) of having attention deficit hyperactivity disorder symptoms. Conclusion: Perturbations in fetal brain development during the second trimester may be associated with the increased prevalence of depressive and attention deficit hyperactivity disorder symptoms.     

Impaired habituation in children with attention deficit hyperactivity disorder.

OBJECTIVE: To investigate whether children with attention deficit hyperactivity disorder show impaired habituation to peripheral stimuli. METHOD: We compared the Troxler effect (the ability to habituate to a peripheral visual stimulus when presented with a competing central visual stimulus) in groups of 23 children with attention deficit hyperactivity disorder and 15 controls matched for age, gender, and IQ. RESULTS: Regression analyses revealed a statistically significant effect of diagnosis on fading (P = 0.03), with attention deficit hyperactivity disorder subjects taking longer to fade to a peripheral stimulus than controls. Additional analyses revealed a significant interaction between diagnosis and visual field; control subjects showed similar fading times to stimuli presented in the right and left visual fields (13.25 vs. 12.96 seconds), while the attention deficit hyperactivity disorder group showed much slower fading in the right than in the left visual field (18.64 vs. 15.00 seconds). CONCLUSIONS: Our results suggest that children with attention deficit hyperactivity disorder have impaired visual habituation. The findings provide evidence of frontal dysfunction in attention deficit hyperactivity disorder and suggest that impaired habituation contributes to off-task behavior in children with the disorder.     

Comorbidity of attention deficit hyperactivity disorder with conduct, depressive, anxiety, and other disorders

OBJECTIVE: Attention deficit hyperactivity disorder is a heterogeneous disorder of unknown etiology. Little is known about the comorbidity of this disorder with disorders other than conduct. Therefore, the authors made a systematic search of the psychiatric and psychological literature for empirical studies dealing with the comorbidity of attention deficit hyperactivity disorder with other disorders. DATA COLLECTION: The search terms included hyperactivity, hyperkinesis, attention deficit disorder, and attention deficit hyperactivity disorder, cross-referenced with antisocial disorder (aggression, conduct disorder, antisocial disorder), depression (depression, mania, depressive disorder, bipolar), anxiety (anxiety disorder, anxiety), learning problems (learning, learning disability, academic achievement), substance abuse (alcoholism, drug abuse), mental retardation, and Tourette's disorder. FINDINGS: The literature supports considerable comorbidity of attention deficit hyperactivity disorder with conduct disorder, oppositional defiant disorder, mood disorders, anxiety disorders, learning disabilities, and other disorders, such as mental retardation, Tourette's syndrome, and borderline personality disorder. CONCLUSIONS: Subgroups of children with attention deficit hyperactivity disorder might be delineated on the basis of the disorder's comorbidity with other disorders. These subgroups may have differing risk factors, clinical courses, and pharmacological responses. Thus, their proper identification may lead to refinements in preventive and treatment strategies. Investigation of these issues should help to clarify the etiology, course, and outcome of attention deficit hyperactivity disorder.     

Maternal smoking during pregnancy and attention deficit hyperactivity disorder symptoms in offspring

OBJECTIVE: The aim of this study was to examine whether smoking during pregnancy is associated with symptoms of attention deficit hyperactivity disorder (ADHD) in offspring and whether these effects are additional to genetic influences. METHOD: Children's ADHD symptoms (parent- and teacher-rated), maternal smoking during pregnancy, conduct disorder symptoms, and family adversity were assessed with questionnaires for a population-based sample of twins (1,452 twin pairs 5-16 years of age). RESULTS: Although genetic influences accounted for most of the variance in offspring ADHD, maternal smoking during pregnancy was still found to show a significant environmentally mediated association. Maternal smoking remained a significant influence when other potential confounds were taken into account. CONCLUSIONS: Maternal smoking during pregnancy appears to show an association with offspring ADHD symptoms that is additional to the effects of genes and not attributable to shared rater effects, clinical referral biases, or covariation with antisocial behavior.     

Differences in the association between childhood trauma history and borderline personality disorder or attention deficit/hyperactivity disorder diagnoses in adulthood

European Archives of Psychiatry and Clinical Neuroscience - Common environmental etiological factors between borderline personality disorder (BPD) and attention deficit/hyperactivity disorder...     

Further evidence for family-genetic risk factors in attention deficit hyperactivity disorder. Patterns of comorbidity in probands and relatives psychiatrically and pediatrically referred samples.

We examined 140 probands with attention deficit hyperactivity disorder, 120 normal controls, and their 822 first-degree relatives using "blind" raters and structured diagnostic interviews. Compared with controls, probands with attention deficit hyperactivity disorder were more likely to have conduct, mood, and anxiety disorders. Compared with relatives of controls, relatives of probands with attention deficit hyperactivity disorder had a higher risk for attention deficit hyperactivity disorder, antisocial disorders, major depressive disorder, substance dependence, and anxiety disorders. Patterns of comorbidity indicate that attention deficit hyperactivity disorder and major depressive disorders may share common familial vulnerabilities, that attention deficit hyperactivity disorder plus conduct disorder may be a distinct subtype, and that attention deficit hyperactivity disorder and anxiety disorders are transmitted independently in families. These results extend previous findings indicating family-genetic influences in attention deficit hyperactivity disorder by using both pediatrically and psychiatrically referred proband samples. The distributions of comorbid illnesses in families provide further validation for subgrouping probands with attention deficit hyperactivity disorder by comorbidity.     

Neurobiology of attention deficit hyperactivity disorder

This article addresses the current understanding of the neurobiological bases of attention deficit hyperactivity disorder (ADHD), focusing on empiric research findings that connect genetic and environmental factors to structural and functional brain abnormalities, ultimately leading to a set of age-dependent behavioral manifestations. Section one presents evidence for genetic risk factors for ADHD and discusses the role of potential environmental factors in the etiology of the disorder. Section two focuses on brain imaging studies and how they have helped generate different hypotheses regarding the pathophysiology of ADHD. Finally, the article addresses the longitudinal course of symptoms in ADHD from infancy to adulthood in an attempt to place biological findings for this complex brain disorder in the context of maturation and development.     

Associations of the serotonin transporter promoter polymorphism with aggressivity,attention deficit,and conduct disorder in an adoptee population

Prior studies of the Iowa Adoption cohorts have demonstrated that the degree of adoptee aggressiveness and conduct disorder has a significant genetic component. Other studies have implicated the neurotransmitter serotonin or polymorphisms in the serotonin transporter gene (5HTT) as an important source of variability in "externalizing" behaviors such as aggressivity, conduct disorder, and attention deficit-hyperactivity disorders (ADHD). Following this lead, we genotyped a subgroup of adoptees (n = 87) at high risk for these kinds of disorders with respect to the serotonin-transporter-linked promoter region (5HTTLPR) polymorphism, and used ordinal logistic regression to conduct an association study. Primary analysis failed to detect a main effect between 5HTTLPR status and subscales of aggressivity, conduct disorder, or attention deficit. However, when biologic parent status and sex of proband were considered, certain interactions between 5HTTLPR and other genetic risk factors were evident. One type of interaction with the LL variant of 5HTTLPR increased externalizing behavior in individuals with antisocial biologic parentage; a second interaction with one or more 5HTTLPR short variants (SS or SL) appeared to increase externalizing behaviors in conjunction with a genetic diathesis for alcoholism. Gender of adoptee also appeared to interact with 5HTTLPR. Male individuals with the short variant were more likely to have higher symptom counts for conduct disorder, aggressivity, and ADHD. In contrast, among females, the short variant (SS, SL) was associated with lower levels of such behavior. The results support the hypothesis that gene-biological family history interactions are involved in the externalizing behaviors studied and constitute interesting findings for future replication.     

Response to emotional stimuli in boys with conduct disorder

OBJECTIVE: Boys with conduct disorder are at risk of persistently showing antisocial behavior in adult life, particularly if they have an additional diagnosis of attention deficit hyperactivity disorder (ADHD). In the search for biological risk factors that predispose children to the development of antisocial personality disorder, research has provided substantial data suggesting that autonomic hyporesponsiveness indicates a greater likelihood of future antisocial behavior. The purpose of this study was to examine autonomic arousal in boys with conduct disorder, comorbid conduct disorder and ADHD, and ADHD only. METHOD: In addition to self-ratings, electrodermal responses to pleasant, neutral, and unpleasant slides were obtained for 21 boys with conduct disorder and 54 boys with ADHD plus conduct disorder. Forty-three boys with a diagnosis of ADHD only were recruited as a clinical comparison group, and 43 boys with no conduct disorder or ADHD were included as a healthy comparison group. All subjects were ages 8-13 years. RESULTS: Compared to the healthy subjects and the subjects with ADHD only, the boys with conduct disorder and with ADHD plus conduct disorder reported lower levels of emotional response to aversive stimuli and lower autonomic responses to all slides independent of valence. CONCLUSIONS: Although the self-report data supported a deficit in reactivity to explicit fear cues, the psychophysiological data indicated that boys with conduct disorder both with and without a comorbid condition of ADHD are characterized by a generalized deficit in autonomic responsivity in an experimental situation in which children were exposed to complex visual stimuli of unpredictable affective quality. Psychophysiological findings may point to a deficit in associative information processing systems that normally produce adaptive cognitive-emotional reactions.     

Familial links between attention deficit hyperactivity disorder, conduct disorder, and bipolar disorder

Although family, twin, and adoption studies indicate that attention deficit hyperactivity disorder (ADHD) is a familial condition with a robust genetic component, molecular genetic studies of candidate genes have produced inconsistent findings. One of the challenges to elucidating the genetic architecture of ADHD is its potential genetic heterogeneity. Therefore, efforts are needed to identify etiologically homogenous subgroups of subjects with ADHD for use in genetic studies. The current article reviews evidence suggesting that parsing ADHD subjects based on comorbidity with conduct and bipolar disorders may yield familial subtypes that are suitable for genetic analyses.