The Role of Environmental Factors in Etiology of Attention- Deficit Hyperactivity Disorder

Environmental factors in etiology of ADHD Attention deficit and hyperactivity disorder (ADHD) is one of the most common developmental disorders of childhood. It was reported that it is a disease that affects 5.29% of children and adolescents in the entire world. Although ADHD is a disorder with high inheritability, genetic factors are not the only explanation to ADHD etiology. ADHD is a disorder etiology which has genetic and environmental components and gene-environment interaction. In spite of the fact that many environmental factors are linked to ADHD, the number of environmental factors that are proven to be in significant cause-effect relation is too small. In other words, in presence of proper genetic basis, disease appears in presence of many environmental factors each of which have a slight effect, its severity or prognosis is variable. Environmental factors that are most commonly linked to ADHD pathophysiology are; complications during pregnancy, natal and postnatal period, several toxins and food substances. It has been considered that exposure to risk factors that may affect development of the brain in any of these periods will have long-term effects on behavior. Along with mother’s cigarette or alcohol use during pregnancy, emotional difficulties, medical diseases and complications of pregnancy; natal complications, low birth weight, premature birth, post mature birth, physical traumas that may affect brain development in early childhood, psychosocial difficulties are also found to be related to ADHD. Studies of gene-environment interaction also note the importance of environmental factors. For example, a study showed that in cases which carry 7 repeated alleles of DRD4, exposure to prenatal cigarettes causes more severe symptoms of ADHD. The purpose of this paper is to evaluate the role of environmental factors in etiology of ADHD, review these factors in the light of related literature and, lastly, to mention gene-environment interaction

Dikkat Eksikliği Hiperaktivite Bozukluğu ve Genetik

Attention Deficit Hyperactivity Disorder (ADHD) is a neurodevelopmental disorder of which three basic symptoms are lack of attention, over-activity that is improper to the age and impulsivity, all of which appear in childhood. Its incidence is 5-12% in children and 4.4% in adults throughout the world. ADHD provides a basis for important problems for both patient, family and society and thus it is important to diagnose the disorder early and understand the factors that create predisposition to the disorder. ADHD is a multifactorial disorder with an etiology of genetic and environmental com-ponents. The importance of genetic factors first implied by Cantwell and Morrison is supported by many studies ever since. All these studies showed that inheritance rate of ADHD is as high as 76%. The aim of this article is to explain ADHD genetics in categorization of twin studies, adoption studies, family studies, segregation analyzes and molecular genetic researches and to review the genetic component of ADHD

Attention deficit hyperactivity disorder and anti-Purkinje autoantibodies: no link?

OBJECTIVES: Attention Deficit Hyperactivity Disorder (ADHD) is a neurobehavioral disorder that begins in early childhood, and many factors play role in its etiology. Many studies have been conducted to identify the causes of ADHD, but the exact factors are still unknown. Although cerebellar dysfunction in the etiology of ADHD was shown in different studies, the possible causes of dysfunction and the role of neuroinflammation among these causes has not been clarified yet. Anti-Yo is an antibody against the antigens in the cytoplasm of purkinje cells and indicates cerebellar degeneration, and Anti-Hu and Anti-Ri are antibodies against cellular nuclear antigens of purkinje cells. This study aimed to evaluate the role of neuroinflammation that is a potential cause of cerebellar dysfunction, which is thought to be an important factor in the development of ADHD. METHODS: This is a cross-sectional and descriptive study that aimed to evaluate the potential association between ADHD and cerebellar neuroinflammation by comparing the serum anti-purkinje cell antibody measurements between case and control groups. The cases were recruited at the Gazi University Child Psychiatry Department, and laboratory analyses were performed at the Ankara Numune Research and Training Hospital Medical Microbiology Department. Sixty children and adolescents with ADHD, and 60 healthy controls were planned to be included in the study. Cases that admitted with ADHD symptoms were given Conners teacher forms according to routine procedure; then the cases with scores over the cut-off of Conners teacher form were evaluated clinically for a diagnosis of ADHD, and after clinical evaluations they were asked to participate the study if they met the eligibility criteria. If they accept to participate the study, informed consents were given to cases and parents, and meanwhile, Turkish version of Schedule for Affective Disorders and Schizophrenia for School Age Children-Present and Lifetime Version (K-SADS-PL) was also applied to cases. A 5-ml serum was spared from the blood samples that obtained for routine test during diagnosis. Control group was planned to be formed from the blood samples of 60 healthy children that admitted to child psychiatry clinic for counselling. At the time of analyses, diluted according to the directions of manufacturers, incubated with fluorescent staining including antibodies (Anti-Hu, Anti-Yo, and Anti-Ri), and evaluated under immunofluorescent microscope by three specialists. RESULTS: Sixty healthy volunteers and 60 cases with ADHD were included in the study. Some of the samples were excluded from the study due to the damage to laboratory tubes during transport. Assessments were conducted with 52 ADHD and 52 healthy control samples. The male/female ratio was 41/11(78.8%/21.2%) in the patient group and 35/17 (67.3%/32.7%) in the control group (p = 0.185). Average age was 9.81 ± 2.41 in the patient group and 9.46 ± 2.14 in the control group (p = 0.442). No positive results were obtained for anti-Purkinje antibody in ADHD or control groups. CONCLUSIONS: No evidence regarding the potential role of cerebellar neuroinflammation in the etiology of ADHD was determined in this study. But these results need replication in larger samples and different methods

Attention deficit hyperactivity disorder and anti-Purkinje autoantibodies: no link?

OBJECTIVES: Attention Deficit Hyperactivity Disorder (ADHD) is a neurobehavioral disorder that begins in early childhood, and many factors play role in its etiology. Many studies have been conducted to identify the causes of ADHD, but the exact factors are still unknown. Although cerebellar dysfunction in the etiology of ADHD was shown in different studies, the possible causes of dysfunction and the role of neuroinflammation among these causes has not been clarified yet. Anti-Yo is an antibody against the antigens in the cytoplasm of purkinje cells and indicates cerebellar degeneration, and Anti-Hu and Anti-Ri are antibodies against cellular nuclear antigens of purkinje cells. This study aimed to evaluate the role of neuroinflammation that is a potential cause of cerebellar dysfunction, which is thought to be an important factor in the development of ADHD. METHODS: This is a cross-sectional and descriptive study that aimed to evaluate the potential association between ADHD and cerebellar neuroinflammation by comparing the serum anti-purkinje cell antibody measurements between case and control groups. The cases were recruited at the Gazi University Child Psychiatry Department, and laboratory analyses were performed at the Ankara Numune Research and Training Hospital Medical Microbiology Department. Sixty children and adolescents with ADHD, and 60 healthy controls were planned to be included in the study. Cases that admitted with ADHD symptoms were given Conners teacher forms according to routine procedure; then the cases with scores over the cut-off of Conners teacher form were evaluated clinically for a diagnosis of ADHD, and after clinical evaluations they were asked to participate the study if they met the eligibility criteria. If they accept to participate the study, informed consents were given to cases and parents, and meanwhile, Turkish version of Schedule for Affective Disorders and Schizophrenia for School Age Children-Present and Lifetime Version (K-SADS-PL) was also applied to cases. A 5-ml serum was spared from the blood samples that obtained for routine test during diagnosis. Control group was planned to be formed from the blood samples of 60 healthy children that admitted to child psychiatry clinic for counselling. At the time of analyses, diluted according to the directions of manufacturers, incubated with fluorescent staining including antibodies (Anti-Hu, Anti-Yo, and Anti-Ri), and evaluated under immunofluorescent microscope by three specialists. RESULTS: Sixty healthy volunteers and 60 cases with ADHD were included in the study. Some of the samples were excluded from the study due to the damage to laboratory tubes during transport. Assessments were conducted with 52 ADHD and 52 healthy control samples. The male/female ratio was 41/11(78.8\%/21.2\%) in the patient group and 35/17 (67.3\%/32.7\%) in the control group (p = 0.185). Average age was 9.812.41 in the patient group and 9.46 +/- 2.14 in the control group (p = 0.442). No positive results were obtained for anti-Purkinje antibody in ADHD or control groups. CONCLUSIONS: No evidence regarding the potential role of cerebellar neuroinflammation in the etiology of ADHD was determined in this study. But these results need replication in larger samples and different methods

Carboxylesterase1, alpha 2a adrenergic receptor and noradrenalin transporter gene polymorphisms and their clinical effects in attention deficit hyperactivity disorder in Turkish children

tas torun, yasemin/0000-0002-4922-7594WOS: 000433193600010The objective of this study was to examine the association between ADHD and G1287A polymorphism in the NET1 gene, C1291G polymorphism in the ADRA2A gene on the adrenergic pathway and Gly143Glu polymorphism in the CES1 gene on the metabolic pathway, and their clinical effects. The study population included 114 children with ADHD and 83 healthy controls. 103 patients are followed for 6 months, their scale points are recorded and side effects are questioned in each interview. Every patient in both control and ADHD group are found to have GG genotype when Gly143Glu polymorphism in the CES1 gene is examined, thus we came to a conclusion that Turkish population is homozygote in the mentioned polymorphism. No significant association between NET1 gene G1287A polymorphism genotypes and ADHD was found. It was found that ADRA2A C1291G polymorphism C allele and CC genotype is a risk factor for ADHD (p= 0.003, OR: 2.17, CI: 12.8-37.0) and the risk is higher in males (p= 0.013, OR: 2.43, CI: 12.0-49.5). There was no significant relation between ADRA2A C1291G polymorphism and clinical parameters but it was found that individuals with NET1 G1287A polymorphism AA genotype have less concurrent Oppositional Defiant Disorder diagnosis (18.8% vs. 81.2%, p= 0.039), their initial CTRS-attention deficit points are higher (17.47 +/- 3.73 vs. 16.15 +/- 4.58, p= 0.045). In conclusion, our study showed that the ADRA2A C1291G polymorphism C allele and CC genotype is associated with ADHD. NET1 G1287A polymorphism AA genotype is mainly associated with attention deficit cluster.Turkish Psychiatry Society's Ankara branch office [11/2014]This research has been supported by Turkish Psychiatry Society's (grant number: 11/2014, grant date: 20.01.2014) Ankara branch office