This summary provides an overview of the key findings from a review on what we have learned about the causes of attention deficit hyperactivity disorder (ADHD).
The review finds that no single risk factor explains ADHD, and both inherited and non-inherited factors contribute to its development in an interdependent way. ADHD shows high heritability in twin studies, and adoption studies demonstrate an important inherited contribution, though they do not rule out prenatal and early life environmental influences. Having a close family member with ADHD, rare genetic variants, some candidate genes, extreme early adversity, prenatal exposure to lead, and low birth weight/prematurity have been most consistently associated with ADHD risk. However, none are definitively
1) According to research, genetics play an important role in ADHD, with heritability estimates between 60-90% from twin and adoption studies. However, genome-wide association studies have not found significant genetic associations, suggesting the genetic factors are complex.
2) Prenatal factors like maternal smoking and stress during pregnancy increase the risk of ADHD in children. Perinatal risks like low birth weight and preterm birth are also associated with higher ADHD risk.
3) Various environmental exposures have been linked to ADHD, including lead, PCBs, pesticides, and certain food dyes and additives which some studies have found can exacerbate ADHD symptoms.
4) However
This study examined the relationship between autism symptoms, victimization by peers, and aggression in youth with Autism Spectrum Disorder (ASD). One hundred and twenty youth with ASD and their caregivers completed questionnaires assessing these variables. Results showed that greater autism symptoms predicted higher rates of victimization by peers and proactive aggression. Victimization by peers also predicted higher proactive aggression. Mediation analyses found that victimization by peers partially mediated the relationship between autism symptoms and proactive aggression. However, autism symptoms and victimization did not predict reactive aggression. This suggests that social factors like peer victimization may influence proactive but not reactive aggression in youth with ASD.
Objectives: The goal of this intervention study was to examine the influence of an individualized evidence based psycho educational intervention on appraisal of caregivers (CGs).
Method: This pre-post longitudinal study (baseline, six, twelve and 18 months follow-up) was based on a psychoeducational
intervention (Progressively Lowered Stress Threshold (PLST) model) and a NYU caregiver intervention with 125 informal caregivers of community dwelling people with dementia (PWD). Statistical analysis consisted of T-test, repeated measures Anova and Linear Mixed Models.
This document discusses ADHD in youth. It describes ADHD as a disorder characterized by inattention, hyperactivity, and impulsiveness. While the causes are debated, research suggests it has both genetic and environmental factors. One study found maternal hostility was associated with higher ADHD symptoms in children, even after controlling for genetics. Other research has found certain genetic variants can increase risk and severity of ADHD. Diet may also impact ADHD symptoms, as one study found rats on a "Western-style" diet displayed more hyperactive and impulsive behaviors. Treatment approaches for ADHD, like stimulant medications, are controversial but some research has found medications can significantly reduce ADHD symptoms for many patients.
There is evidence that certain mental illnesses like bipolar disorder are correlated with increased artistic and creative abilities. However, leaving these illnesses untreated can worsen over time and impair creativity. While medication may diminish creative output for some, it is usually necessary for treatment to prevent worsening of symptoms that could become catastrophic. Further research is still needed to better understand the links between specific illnesses and creativity.
Parent-infant interactions in families with women diagnosed with postnatal depression: a longitudinal study on the effects of a psychodynamic treatment
This document reviews literature on the impact of adverse childhood experiences (ACEs). It finds that ACEs are linked to negative health outcomes later in life through their effects on stress response systems and brain development. ACEs are common, affecting up to 67% of the population, and disproportionately impact low-income communities. The impacts of ACEs are cyclical as they increase risks for future generations. While ACEs have lasting biological and behavioral effects, perception of stress may influence outcomes. More research is needed to understand impacts, develop treatments, and engage communities to address this major public health issue.
1) According to research, genetics play an important role in ADHD, with heritability estimates between 60-90% from twin and adoption studies. However, genome-wide association studies have not found significant genetic associations, suggesting the genetic factors are complex.
2) Prenatal factors like maternal smoking and stress during pregnancy increase the risk of ADHD in children. Perinatal risks like low birth weight and preterm birth are also associated with higher ADHD risk.
3) Various environmental exposures have been linked to ADHD, including lead, PCBs, pesticides, and certain food dyes and additives which some studies have found can exacerbate ADHD symptoms.
4) However
This study examined the relationship between autism symptoms, victimization by peers, and aggression in youth with Autism Spectrum Disorder (ASD). One hundred and twenty youth with ASD and their caregivers completed questionnaires assessing these variables. Results showed that greater autism symptoms predicted higher rates of victimization by peers and proactive aggression. Victimization by peers also predicted higher proactive aggression. Mediation analyses found that victimization by peers partially mediated the relationship between autism symptoms and proactive aggression. However, autism symptoms and victimization did not predict reactive aggression. This suggests that social factors like peer victimization may influence proactive but not reactive aggression in youth with ASD.
Objectives: The goal of this intervention study was to examine the influence of an individualized evidence based psycho educational intervention on appraisal of caregivers (CGs).
Method: This pre-post longitudinal study (baseline, six, twelve and 18 months follow-up) was based on a psychoeducational
intervention (Progressively Lowered Stress Threshold (PLST) model) and a NYU caregiver intervention with 125 informal caregivers of community dwelling people with dementia (PWD). Statistical analysis consisted of T-test, repeated measures Anova and Linear Mixed Models.
This document discusses ADHD in youth. It describes ADHD as a disorder characterized by inattention, hyperactivity, and impulsiveness. While the causes are debated, research suggests it has both genetic and environmental factors. One study found maternal hostility was associated with higher ADHD symptoms in children, even after controlling for genetics. Other research has found certain genetic variants can increase risk and severity of ADHD. Diet may also impact ADHD symptoms, as one study found rats on a "Western-style" diet displayed more hyperactive and impulsive behaviors. Treatment approaches for ADHD, like stimulant medications, are controversial but some research has found medications can significantly reduce ADHD symptoms for many patients.
There is evidence that certain mental illnesses like bipolar disorder are correlated with increased artistic and creative abilities. However, leaving these illnesses untreated can worsen over time and impair creativity. While medication may diminish creative output for some, it is usually necessary for treatment to prevent worsening of symptoms that could become catastrophic. Further research is still needed to better understand the links between specific illnesses and creativity.
Parent-infant interactions in families with women diagnosed with postnatal depression: a longitudinal study on the effects of a psychodynamic treatment
This document reviews literature on the impact of adverse childhood experiences (ACEs). It finds that ACEs are linked to negative health outcomes later in life through their effects on stress response systems and brain development. ACEs are common, affecting up to 67% of the population, and disproportionately impact low-income communities. The impacts of ACEs are cyclical as they increase risks for future generations. While ACEs have lasting biological and behavioral effects, perception of stress may influence outcomes. More research is needed to understand impacts, develop treatments, and engage communities to address this major public health issue.
The document provides a literature review and methodology for a study examining the non-medical information needs of parents with newly diagnosed sick children. The literature review identifies key challenges faced by parental caregivers like stress, informational barriers, and needs. A quantitative survey was conducted with parents in oncology and haematology units to understand their awareness and satisfaction with supportive information provided. The results found that length of care, timing of information, and availability of financial support information most impacted parental satisfaction.
This study examined the influence of peers and parents on the sexual attitudes of male undergraduate students. Questionnaire data was collected from 97 male undergraduates assessing their resistance to peer influence, sexual attitudes, and relationship with parents. The results found that higher resistance to peer influence was marginally correlated with reporting less permissive sexual attitudes. No significant relationship was found between perceived parental warmth and attitudes about birth control responsibility.
This document provides an overview and update on autism spectrum disorder (ASD) research. It summarizes several studies on various topics:
- Genetic factors are strongly implicated in ASD risk, though hundreds of genes may be involved.
- Early intensive behavioral intervention shows benefits for social/communication skills but evidence is limited.
- Some treatments like risperidone and melatonin show benefits for specific symptoms but evidence is still limited overall.
- Joint attention interventions effectively improve joint attention skills in children with ASD.
- Ongoing research is exploring new drug treatments and personalized approaches.
Sydney Sexual Health Centre Journal Club presentation by Kristen McCormack on AIDS and Behaviour Volume 20 Issue 7, published in July 2016.
AIDS and Behavior provides an international venue for the scientific exchange of research and scholarly work on the contributing factors, prevention, consequences, social impact, and response to HIV/AIDS. The journal publishes original peer-reviewed papers addressing all areas of AIDS behavioral research including: individual, contextual, social, economic and geographic factors that facilitate HIV transmission; interventions aimed to reduce HIV transmission risks at all levels and in all contexts; mental health aspects of HIV/AIDS; medical and behavioral consequences of HIV infection - including health-related quality of life, coping, treatment and treatment adherence; and the impact of HIV infection on adults children, families, communities and societies. The journal publishes original research articles, brief research reports, and critical literature reviews.
The Sydney Sexual Health Centre Journal Club allows our team to stay up-to-date with what is being published in the field of sexual health. Staff members take turns to read, review and share the contents of an allocated journal. Journal Club encourages knowledge sharing and discussion about topics raised.
Although migraine treatments determined to be effective for adults are frequently adapted for use in children with little evaluation prior to implementation, existing research suggests that this approach may not be best practice. Specifically, pharmacological interventions found to be statistically significant for adults may not be as effective or safe for children. Psychological treatments such as cognitive behavioral therapy (CBT) have shown efficacy for both children and adults, but are underutilized, especially as first-line treatment options. Better evaluation of treatment efficacy across different age groups is needed to determine the most appropriate migraine interventions for children versus adults.
Freijy - ASBHM - Do interventions based on cognitive dissonance promote healt...Emily Kothe
The document reviews research on using cognitive dissonance interventions to promote health behavior change. It finds that 15 of 20 studies showed changes in behavior, attitudes or intentions. The hypocrisy paradigm was the most effective, producing positive effects in 10 of 14 studies, while induced compliance had null or mixed results. Intervention effects were not influenced by health topic but were influenced by the paradigm used. More research is needed to minimize biases and explore moderators like self-esteem and gender.
ISPCAN Jamaica 2018 - Personality-targeted Interventions for Building Resilie...Christine Wekerle
Personality-targeted Interventions for Building Resilience against Substance Use and Mental Health Problems among Adolescents Involved in Child Welfare System
Hanie Edalati, Patricia Conrod
Poster presentations.com a0-template-v5Áine Mc Kenna
This research poster summarizes a study with the following objectives:
1) Estimate the percentage of the population exposed to corporal punishment using a representative Northern Ireland sample
2) Estimate the percentage of psychiatric disorders attributable to exposure to corporal punishment during childhood
3) Estimate the percentage of Northern Ireland parents who used corporal punishment on their own children
The study analyzed data from 1,986 participants who completed a health and stress survey. Measures assessed physical and sexual abuse, neglect, domestic violence, and corporal punishment. Logistic regressions examined associations between corporal punishment and anxiety, mood, and substance disorders. Results found 31.4% of the population was exposed to corporal punishment as children. Exposures significantly increased
This study examined how activating the behavioral immune system (BEH) influences the biological immune system (BIO). Participants were randomly assigned to complete questionnaires about disgust, a computer task with sick faces, and saliva samples in different orders. Results found that sick faces drew unconscious attention better than chance. There were no group differences in disgust responses. However, those who viewed sick faces before questionnaires reported higher moral judgments of disgust. This suggests a more sensitive measure may be needed to understand how the BEH influences the BIO and that findings have social and medical implications.
Original paper parents’ experiences of home based applied bSAHIL781034
This document summarizes a study that interviewed parents of children with autism who received 2 years of early intensive behavioral intervention (EIBI) therapy. The study aimed to obtain first-hand accounts of the perceived benefits and challenges of home-based EIBI programs from the parents' perspectives. In general, parents reported positive experiences with EIBI and benefits for their children, families, and themselves. However, interviews also revealed some challenging aspects of managing intensive therapy programs at home, such as financial burdens and disruptions to family routines. The implications of these findings could help improve support for families undertaking EIBI.
Freijy - ASBHM - Do interventions based on cognitive dissonance promote healt...Emily Kothe
Freijy, T., & Kothe, E., (2013). Do interventions based on cognitive dissonance promote health behaviour?. Paper presented at the Australasian Society of Behavioural Health and Medicine (ASBHM) 10th Annual Proceedings, Newcastle, Australia
Exploring Adventure Therapy as an Early Intervention for Struggling AdolescentsWill Dobud
This paper presents an account of a research project that explored the experiences of adolescents struggling with behavioural and emotional issues, who participated in a 14-day adventure therapy program in Australia referred to by the pseudonym, ”Onward Adventures.” All participants of this program over the age of 16 who completed within the last two years were asked to complete a survey. Additionally, the parents of these participants were invited to complete a similar survey. The qualitative surveys were designed to question participants’ and parents’ perceptions of the program (pre- and post-), the relationships (therapeutic alliance) built with program therapists, follow-up support, and outcomes of the program. Both participants and parents reported strong relationships with program leaders, stressed the importance of effective follow-up services, and perceived positive outcomes when it came to self-esteem and social skills, seeing comparable improvement in self-concept, overall behaviour, and coping skills.
This document provides a primer on ADHD and its relationship to criminality. It summarizes research showing high rates of ADHD in prison populations worldwide compared to the general population. The document reviews the genetic, neurobiological, and evolutionary literature on ADHD, discussing candidate genes, brain structures and neurotransmitter systems implicated in ADHD like dopamine and serotonin. It examines theories like Reinforcement Sensitivity Theory to understand the emotional and behavioral dysregulation associated with ADHD. The goal is to inform criminologists about ADHD given its importance as a risk factor for antisocial behavior.
Parental stress, affective symptoms and marital satisfaction in parents of ch...James Cook University
Lovisotto, R., Caltabiano, N., & Hajhashemi, K. (2015). International Journal of Humanities and Social Science, 5(10), 30-38.
Abstract: Parents of children with Autism Spectrum Disorder (ASD), a life-long developmental disorder, responded to an online survey considering their stress experience, affective symptoms and marital satisfaction. As these parents sourced different programs for their children, type of program was used to assign parents to different groups in order to consider their stress, affective symptoms and marital satisfaction. The type of programs parents used included the Applied Behaviour Analysis (n=15); Early Intervention Centre (n=13) and no formal program (n=16). Parents of children with ASD in the ABA group reported significantly lower parental stress scores, lower affective symptoms scores and higher marital satisfaction scores compared to the other two groups. These results are suggestive of the beneficial effect that an ABA program can have on the family unit.
This document summarizes research on risk factors for substance use among adolescents. It finds that individual factors like impulsivity and difficulty regulating emotions are correlated with increased substance use. Environmental factors like associating with peers who use substances also increases risk. While adolescents develop logical reasoning by age 15, the parts of the brain involved in self-control and decision making are still maturing, making teens more susceptible to risky behaviors. The document concludes that a combination of individual and environmental characteristics influence adolescent substance use.
Glenthøj et al. - 2016 - Social cognition in patients at ultra-high risk for ...Tina Dam Kristensen
This study examined social cognition, social skills, and functioning in 65 patients at ultra-high risk of developing psychosis compared to 30 healthy controls. The patients performed worse on tasks of emotion recognition and social inference compared to controls. Patients also exhibited poorer social skills. Aspects of emotion recognition and social cognition were associated with measures of social and role functioning. Negative symptoms were associated with impairments in overall functioning. The study suggests social cognitive deficits and negative symptoms influence functioning and social skills in the ultra-high risk population.
The document discusses the history and current state of evidence-based practices in children's mental health. It notes that while research has identified hundreds of evidence-based therapies and interventions, many children still have unmet mental health needs. It summarizes the levels of evidence for different psychosocial and pharmacological treatments, as well as home- and community-based services. However, it states that significant challenges remain in implementing evidence-based practices into real-world mental health systems and services.
The document discusses the drug problem and treatment of drug dependence in the Philippines. It provides statistics on drug use and admissions to rehabilitation centers. It then covers the psychological dimensions of drug problems, reasons for drug use, treatment processes including discontinuation of substance use and behavioral modification, and prevention strategies.
Genetics of attention deficit hyperactivity disorder (adhd)Joy Maria Mitchell
Attention deficit hyperactivity disorder (ADHD) is a developmental disorder. ADHD is the commonly studied and
diagnosed as psychiatric disorder. Here we shall see the relation between extraversion and ADHD, neuroticism,
biological relation, Environmental factors and with diagnosis of ADHD. It is known that Genetics is one of the factors
that may contribute to, or exacerbate ADHD. Recent research probing towards the environmental and Genetic factors
causing ADHD differences is the main source for investigation
Genetic epidemiology studies the distribution and risk factors of diseases based on genetic and environmental causes. It employs study designs like family, twin, adoption, and migration studies to identify the joint contribution of genes and environment to complex diseases. Family studies examine disease patterns within families to infer genetic patterns. Twin studies estimate genetic and environmental influences on diseases by comparing identical and fraternal twin pairs. Adoption studies compare disease risk between biological and adoptive relatives to identify genetic and environmental sources. Migration studies examine disease rate changes between immigrants and their ancestral populations to identify cultural and environmental risk factors.
The document provides a literature review and methodology for a study examining the non-medical information needs of parents with newly diagnosed sick children. The literature review identifies key challenges faced by parental caregivers like stress, informational barriers, and needs. A quantitative survey was conducted with parents in oncology and haematology units to understand their awareness and satisfaction with supportive information provided. The results found that length of care, timing of information, and availability of financial support information most impacted parental satisfaction.
This study examined the influence of peers and parents on the sexual attitudes of male undergraduate students. Questionnaire data was collected from 97 male undergraduates assessing their resistance to peer influence, sexual attitudes, and relationship with parents. The results found that higher resistance to peer influence was marginally correlated with reporting less permissive sexual attitudes. No significant relationship was found between perceived parental warmth and attitudes about birth control responsibility.
This document provides an overview and update on autism spectrum disorder (ASD) research. It summarizes several studies on various topics:
- Genetic factors are strongly implicated in ASD risk, though hundreds of genes may be involved.
- Early intensive behavioral intervention shows benefits for social/communication skills but evidence is limited.
- Some treatments like risperidone and melatonin show benefits for specific symptoms but evidence is still limited overall.
- Joint attention interventions effectively improve joint attention skills in children with ASD.
- Ongoing research is exploring new drug treatments and personalized approaches.
Sydney Sexual Health Centre Journal Club presentation by Kristen McCormack on AIDS and Behaviour Volume 20 Issue 7, published in July 2016.
AIDS and Behavior provides an international venue for the scientific exchange of research and scholarly work on the contributing factors, prevention, consequences, social impact, and response to HIV/AIDS. The journal publishes original peer-reviewed papers addressing all areas of AIDS behavioral research including: individual, contextual, social, economic and geographic factors that facilitate HIV transmission; interventions aimed to reduce HIV transmission risks at all levels and in all contexts; mental health aspects of HIV/AIDS; medical and behavioral consequences of HIV infection - including health-related quality of life, coping, treatment and treatment adherence; and the impact of HIV infection on adults children, families, communities and societies. The journal publishes original research articles, brief research reports, and critical literature reviews.
The Sydney Sexual Health Centre Journal Club allows our team to stay up-to-date with what is being published in the field of sexual health. Staff members take turns to read, review and share the contents of an allocated journal. Journal Club encourages knowledge sharing and discussion about topics raised.
Although migraine treatments determined to be effective for adults are frequently adapted for use in children with little evaluation prior to implementation, existing research suggests that this approach may not be best practice. Specifically, pharmacological interventions found to be statistically significant for adults may not be as effective or safe for children. Psychological treatments such as cognitive behavioral therapy (CBT) have shown efficacy for both children and adults, but are underutilized, especially as first-line treatment options. Better evaluation of treatment efficacy across different age groups is needed to determine the most appropriate migraine interventions for children versus adults.
Freijy - ASBHM - Do interventions based on cognitive dissonance promote healt...Emily Kothe
The document reviews research on using cognitive dissonance interventions to promote health behavior change. It finds that 15 of 20 studies showed changes in behavior, attitudes or intentions. The hypocrisy paradigm was the most effective, producing positive effects in 10 of 14 studies, while induced compliance had null or mixed results. Intervention effects were not influenced by health topic but were influenced by the paradigm used. More research is needed to minimize biases and explore moderators like self-esteem and gender.
ISPCAN Jamaica 2018 - Personality-targeted Interventions for Building Resilie...Christine Wekerle
Personality-targeted Interventions for Building Resilience against Substance Use and Mental Health Problems among Adolescents Involved in Child Welfare System
Hanie Edalati, Patricia Conrod
Poster presentations.com a0-template-v5Áine Mc Kenna
This research poster summarizes a study with the following objectives:
1) Estimate the percentage of the population exposed to corporal punishment using a representative Northern Ireland sample
2) Estimate the percentage of psychiatric disorders attributable to exposure to corporal punishment during childhood
3) Estimate the percentage of Northern Ireland parents who used corporal punishment on their own children
The study analyzed data from 1,986 participants who completed a health and stress survey. Measures assessed physical and sexual abuse, neglect, domestic violence, and corporal punishment. Logistic regressions examined associations between corporal punishment and anxiety, mood, and substance disorders. Results found 31.4% of the population was exposed to corporal punishment as children. Exposures significantly increased
This study examined how activating the behavioral immune system (BEH) influences the biological immune system (BIO). Participants were randomly assigned to complete questionnaires about disgust, a computer task with sick faces, and saliva samples in different orders. Results found that sick faces drew unconscious attention better than chance. There were no group differences in disgust responses. However, those who viewed sick faces before questionnaires reported higher moral judgments of disgust. This suggests a more sensitive measure may be needed to understand how the BEH influences the BIO and that findings have social and medical implications.
Original paper parents’ experiences of home based applied bSAHIL781034
This document summarizes a study that interviewed parents of children with autism who received 2 years of early intensive behavioral intervention (EIBI) therapy. The study aimed to obtain first-hand accounts of the perceived benefits and challenges of home-based EIBI programs from the parents' perspectives. In general, parents reported positive experiences with EIBI and benefits for their children, families, and themselves. However, interviews also revealed some challenging aspects of managing intensive therapy programs at home, such as financial burdens and disruptions to family routines. The implications of these findings could help improve support for families undertaking EIBI.
Freijy - ASBHM - Do interventions based on cognitive dissonance promote healt...Emily Kothe
Freijy, T., & Kothe, E., (2013). Do interventions based on cognitive dissonance promote health behaviour?. Paper presented at the Australasian Society of Behavioural Health and Medicine (ASBHM) 10th Annual Proceedings, Newcastle, Australia
Exploring Adventure Therapy as an Early Intervention for Struggling AdolescentsWill Dobud
This paper presents an account of a research project that explored the experiences of adolescents struggling with behavioural and emotional issues, who participated in a 14-day adventure therapy program in Australia referred to by the pseudonym, ”Onward Adventures.” All participants of this program over the age of 16 who completed within the last two years were asked to complete a survey. Additionally, the parents of these participants were invited to complete a similar survey. The qualitative surveys were designed to question participants’ and parents’ perceptions of the program (pre- and post-), the relationships (therapeutic alliance) built with program therapists, follow-up support, and outcomes of the program. Both participants and parents reported strong relationships with program leaders, stressed the importance of effective follow-up services, and perceived positive outcomes when it came to self-esteem and social skills, seeing comparable improvement in self-concept, overall behaviour, and coping skills.
This document provides a primer on ADHD and its relationship to criminality. It summarizes research showing high rates of ADHD in prison populations worldwide compared to the general population. The document reviews the genetic, neurobiological, and evolutionary literature on ADHD, discussing candidate genes, brain structures and neurotransmitter systems implicated in ADHD like dopamine and serotonin. It examines theories like Reinforcement Sensitivity Theory to understand the emotional and behavioral dysregulation associated with ADHD. The goal is to inform criminologists about ADHD given its importance as a risk factor for antisocial behavior.
Parental stress, affective symptoms and marital satisfaction in parents of ch...James Cook University
Lovisotto, R., Caltabiano, N., & Hajhashemi, K. (2015). International Journal of Humanities and Social Science, 5(10), 30-38.
Abstract: Parents of children with Autism Spectrum Disorder (ASD), a life-long developmental disorder, responded to an online survey considering their stress experience, affective symptoms and marital satisfaction. As these parents sourced different programs for their children, type of program was used to assign parents to different groups in order to consider their stress, affective symptoms and marital satisfaction. The type of programs parents used included the Applied Behaviour Analysis (n=15); Early Intervention Centre (n=13) and no formal program (n=16). Parents of children with ASD in the ABA group reported significantly lower parental stress scores, lower affective symptoms scores and higher marital satisfaction scores compared to the other two groups. These results are suggestive of the beneficial effect that an ABA program can have on the family unit.
This document summarizes research on risk factors for substance use among adolescents. It finds that individual factors like impulsivity and difficulty regulating emotions are correlated with increased substance use. Environmental factors like associating with peers who use substances also increases risk. While adolescents develop logical reasoning by age 15, the parts of the brain involved in self-control and decision making are still maturing, making teens more susceptible to risky behaviors. The document concludes that a combination of individual and environmental characteristics influence adolescent substance use.
Glenthøj et al. - 2016 - Social cognition in patients at ultra-high risk for ...Tina Dam Kristensen
This study examined social cognition, social skills, and functioning in 65 patients at ultra-high risk of developing psychosis compared to 30 healthy controls. The patients performed worse on tasks of emotion recognition and social inference compared to controls. Patients also exhibited poorer social skills. Aspects of emotion recognition and social cognition were associated with measures of social and role functioning. Negative symptoms were associated with impairments in overall functioning. The study suggests social cognitive deficits and negative symptoms influence functioning and social skills in the ultra-high risk population.
The document discusses the history and current state of evidence-based practices in children's mental health. It notes that while research has identified hundreds of evidence-based therapies and interventions, many children still have unmet mental health needs. It summarizes the levels of evidence for different psychosocial and pharmacological treatments, as well as home- and community-based services. However, it states that significant challenges remain in implementing evidence-based practices into real-world mental health systems and services.
The document discusses the drug problem and treatment of drug dependence in the Philippines. It provides statistics on drug use and admissions to rehabilitation centers. It then covers the psychological dimensions of drug problems, reasons for drug use, treatment processes including discontinuation of substance use and behavioral modification, and prevention strategies.
Genetics of attention deficit hyperactivity disorder (adhd)Joy Maria Mitchell
Attention deficit hyperactivity disorder (ADHD) is a developmental disorder. ADHD is the commonly studied and
diagnosed as psychiatric disorder. Here we shall see the relation between extraversion and ADHD, neuroticism,
biological relation, Environmental factors and with diagnosis of ADHD. It is known that Genetics is one of the factors
that may contribute to, or exacerbate ADHD. Recent research probing towards the environmental and Genetic factors
causing ADHD differences is the main source for investigation
Genetic epidemiology studies the distribution and risk factors of diseases based on genetic and environmental causes. It employs study designs like family, twin, adoption, and migration studies to identify the joint contribution of genes and environment to complex diseases. Family studies examine disease patterns within families to infer genetic patterns. Twin studies estimate genetic and environmental influences on diseases by comparing identical and fraternal twin pairs. Adoption studies compare disease risk between biological and adoptive relatives to identify genetic and environmental sources. Migration studies examine disease rate changes between immigrants and their ancestral populations to identify cultural and environmental risk factors.
WRTG 3014 - Lydia Wallace - ASD Research ReviewLydia Wallace
The document analyzes potential causes of autism spectrum disorders (ASD) in Utah, specifically the Wasatch Front region which has one of the highest ASD diagnosis rates in the nation. It finds that ASD is caused by a complex combination of genetic and environmental factors. Genetic factors like single nucleotide polymorphisms and copy number variants increase risk when combined with environmental exposures during prenatal development, like air pollutants. Studies have identified ASD "hotspots" in densely populated areas along the Wasatch Front with higher pollution levels. Both the genetic characteristics of the local population from founders and current environmental exposures may contribute to elevated ASD rates in the region.
This study assessed externalizing behaviors in children prenatally exposed to methamphetamine (PME), compared to children with ADHD. Parents completed behavior ratings of 113 PME children and 113 children with ADHD. PME children showed significantly higher ratings of hyperactivity, aggression, conduct problems, and overall behavioral difficulties than children with ADHD. These differences remained even after controlling for prenatal alcohol exposure. The findings suggest prenatal methamphetamine exposure negatively impacts emotional regulation and behavioral control, independent of other substance exposures.
1) Tracking student progress over time through a shared tracking system and regularly reviewing information can help identify students experiencing academic or behavioral problems or who are at risk of adverse childhood experiences (ACEs).
2) Providing volunteers and staff with brief training on common ACEs faced by the community and strategies to support students can help strengthen relationships between students and mentors.
3) Integrating ACE prevention, early detection, and community support are recommended to interrupt the intergenerational cycle of ACEs and promote resilience among students attending the Out-of-School Time program.
Child Development, JanuaryFebruary 2002, Volume 73, Number .docxbissacr
Child Development, January/February 2002, Volume 73, Number 1, Pages 1–21
Nature, Nurture, and Development: From Evangelism through
Science toward Policy and Practice
Michael Rutter
During the second half of the 20th century there was an immense increase in both empirical findings on, and
conceptual understanding of, the effects of nature, nurture, and developmental processes on psychological
functioning—both normal and abnormal. Unfortunately, the good science has also been accompanied by ex-
cessive polarizing claims and by unwarranted extrapolations. This article provides a summary review of the
real gains in knowledge, outlines some of the misleading claims, and notes the potential for research and for
science-led improvements in policies and practice. The need to bring about a better interpretation of genetic,
psychosocial, and developmental research strategies and theoretical concepts is emphasized.
INTRODUCTION
Over the last half century, there has been an explosion
of knowledge on the effects of nature, nurture, and
developmental processes. As a result, we have a much
improved understanding of many of the mechanisms
involved in normal and abnormal development,
which carries with it a huge potential for improving
children’s lives. Unfortunately, these advances have
been accompanied by as much misleading scientific
evangelism and journalistic hype as by good science
and honest reporting. As a consequence, both the pages
of scientific journals and the media have been full of the
most absurd confrontations and polarizations. These
have given rise to an unhelpful level of misunder-
standing of the true scientific advances and, more es-
pecially, about their meaning and the implications for
policy and practice. Of course, there have also been
numerous examples of good reporting by scientists
and by journalists. There is every reason to be in-
debted to both. The need is to avoid the twin dangers
of destructive cynicism and gullible expectation.
Nature, nurture, and development are dealt with
in this article as separate topics (with the focus being
mainly on their effects on psychopathology). In each
case, the real advances in knowledge are considered
first, some of the misleading claims are outlined sec-
ond, and the potential for research and for improve-
ments in policies and practice are noted third. Al-
though these are considered as supposedly separate
influences, the truth is that they are closely inter-
twined. The separation is heuristically useful for test-
ing causal hypotheses, but it is crucial that such hy-
potheses deal with the different forms of interplay
that may be occurring. To a considerable extent, it is
the failure to do so that has led to many of the polar-
izing battles and absurd claims.
NATURE: GENETIC RISK AND
PROTECTIVE MECHANISMS
With regard to the influences that reflect nature,
quantitative genetics and molecular genetics are dis-
cussed separately, because they have rather different
patterns .
Substance abuse linked to genetic, environmental, and peer influencesAbby_Dickens
Substance abuse has been linked to several negative effects. Often, the cause of substance abuse is connected to one’s peers who hold a personal or familial influence. However, could other influences — namely genetic and environmental influences – play a role in substance abuse? Researchers from Florida Atlantic University, University of Montreal, the University of Quebec, and Laval University sought to find out.
This document discusses gene-environment interactions and their role in phenotypic expression and disease development. It explains that all traits are influenced by both genetic and environmental factors, and that variations in genetic makeup are associated with most diseases. Common diseases like diabetes and heart disease are caused by a complex interplay between multiple genetic and environmental risk factors. The effects of genes depend on the environment, and the environment's effects depend on an individual's genes. Several examples are provided to illustrate how changes in environment can influence the phenotype of genetic traits and alter disease risk.
This document summarizes a study on systems-level barriers that contribute to secondary conditions in individuals with fetal alcohol spectrum disorders (FASD). The study involved interviews and focus groups with parents of children with FASD and service providers.
The key findings were:
1) A pervasive lack of knowledge about FASD exists throughout multiple systems, including healthcare, education, and social services. This lack of knowledge contributes to barriers across different systems.
2) Systems-level barriers that interfere with preventing secondary conditions include delayed diagnosis of FASD, difficulty qualifying for and accessing services, poor implementation of services, and challenges maintaining services long-term.
3) Broad system changes are needed using a public
The document defines prevention psychiatry as reducing mental disorders and behavioral problems by identifying risk and protective factors and applying evidence-based interventions. It provides examples of different types of prevention including universal, selective, and indicated interventions. It discusses risk and protective factors and illustrates various prevention programs targeting different populations.
1
RUNNING HEAD: MILESTONE 2
Milestone 2: Outside Factors & Effective Treatment
LaChelle Prince
Southern New Hampshire University
There are many factors that can influence the treatment for autistic children. These factors include environmental, culture and family. Environmental factors concerning the onset of autism is an essential area of study. Genetic factor has been associated with the onset of autism as well. Parents who have been exposed to teratogens have substantiated factors that stimulate the chance of autism (Castro et al., 2016). Environmental factors of autism include maternal age, multiple pregnancies in a short period, inadequate prenatal care and low birth weight. Children who are associated with autism can experience a delay in brain development. There are many risk factors that are associated with autism. They include the parents age during the time of conception, maternal nutrition, inflection during pregnancy and prematurity.
In some cases individuals’ can be hereditarily prone to autism. Children can develop symptoms of autism based on their environment. Vaccines have been linked to the onset of autism. Also, an individual's genetic predisposition can cause autism (Reynolds & Dombeck, 2006).
Parents of autistic children tend to suffer from multiple factors. Parents can exhibit an increase in stress, a poor quality of marriage, depression, anxiety and increased anger (Magana & Smith, 2006). Clinicians consider how cultural values, such as religion, can influence the diagnosis, treatment and welfare of families. Religion can also influence the treatment of a child with autism. South Asian Muslim’s believe that doctors undermine their children (Ennis-Cole, Durodoye & Harris, 2013). In some culture and religion, parents believe that an autistic child is a punishment from God. Also, some cultures are less likely than others to receive regular visits to the physicians. Culture can also play a role when viewing signs and symptoms of autism. Some parents do not realize that their child is experience symptoms of autism. Parents are more likely to experience developmental delays before social issues (Mandell & Novak, 2005). Cultures conflicts in the treatment options for children who have been diagnosed with autism. Some cultures will reach out to non-professionals before seeking professional help.
Parents of individuals with ASD have also shown a willingness to persist with this strategy of using diverse treatments that include those without empirical support, or even those that are harmful, despite evidence of ineffectiveness (Offit & Jew, 2003). Parents use treatments that work at cross-purposes to each other. Having children conduct in multiple treatments make it difficult to evaluate the effectiveness of any single treatment or specific combination of treatments for a given individual (Green et al, 2006). Parents can be dissatisfied with certain treatment options.
Since cultural factors are.
Chemical Risk Assessment Traditional vs PublicHealth PerspeJinElias52
Chemical Risk Assessment: Traditional vs Public
Health Perspectives
Preventing adverse health ef-
fects of environmental chemical
exposure is fundamental to pro-
tecting individual and public he-
alth. When done efficiently and
properly, chemical risk assess-
ment enables risk management
actions that minimize the in-
cidence and effects of environ-
mentally induced diseases related
to chemical exposure. However,
traditional chemical risk assess-
ment is faced with multiple chal-
lenges with respect to predicting
and preventing disease in human
populations, and epidemiological
studies increasingly report obser-
vations of adverse health effects
at exposure levels predicted
from animal studies to be safe
for humans. This discordance
reinforces concerns about the
adequacy of contemporary risk
assessment practices for pro-
tecting public health.
It is becoming clear that to
protect public health more effec-
tively, future risk assessments will
need to use the full range of
available data, draw on innovative
methods to integrate diverse data
streams, and consider health
endpoints that also reflect the
range of subtle effects and mor-
bidities observed in human pop-
ulations.
Considering these factors,
there is a need to reframe
chemical risk assessment to be
more clearly aligned with the
public health goal of minimizing
environmental exposures asso-
ciated with disease. (Am J Public
Health. 2017;107:1032–1039.
doi:10.2105/AJPH.2017.303771)
Maureen R. Gwinn, PhD, Daniel A. Axelrad, MPP, Tina Bahadori, ScD, David Bussard, BA, Wayne E.
Cascio, MD, Kacee Deener, MPH, David Dix, PhD, Russell S. Thomas, PhD, Robert J. Kavlock, PhD, and
Thomas A. Burke, PhD, MPH
See also Greenberg, p. 1020.
For the past several decades,human health risk assessment
has been a pillar of environmental
health protection. In general,
the products of risk assessment
have been numerical risk values
derived from animal toxicology
studies of observable effects at
high doses of individual chem-
icals. Although this approach has
contributed to our understanding
of overt health outcomes from
chemical exposures, it does not
always match our understanding
from epidemiology studies of the
consequences of real-world ex-
posures in human populations,
which are characterized by expo-
sure to multiple pollutants, often
chronically, at concentrations that
can fluctuate over wide ranges;
susceptible populations and life
stages; potential interactions be-
tween chemicals and nonchemical
stressors and background disease
states; and lifestyle factors that
modify exposures (e.g., airtight
houses).1 Theseandotherissuesare
particularly important when de-
termining risk of complex diseases,
such as cardiovascular disease.
Ten years ago, the National
Research Council offered a new
paradigm for evaluating the safety
of chemicals on the basis of
chemical characterization, testing
using a toxicity pathway ap-
proach, and modeling and ex-
trapolating the ...
Running Head Critique 1Critique2CritiqueAma.docxjoellemurphey
Running Head: Critique 1
Critique 2
Critique
Amanda Kroeger
PSY 326
Prof. Luker
June 30, 2014
Critique
The purpose regarding this paper is to discuss the health and social challenges as a result of drug addiction globally. Particularly it brings to the attention of the reader the complexities that arise with the combined forces by diverse organizations, families, governments, and individuals in striving to counteract the abuse of drugs within traditional families whereby jeopardizing significant social virtues and values creating room for deviant behavior such as crime. The study at hand, “Familial Risk Factors Favoring Drug Addiction Onset” by Zimi & Jukic aim at the identification of the familial factors that favor the onset of drug addiction in the community. The paper further evaluates and critiques the various scholarly articles on drug addiction and their effects socially, economically, and culturally.
From this study’s 146 addicts and around 134 fundamental subjects, the authors discovered that “the families the addicts were born into, familial risk factors capable of influencing their psychosocial progress and favoring drug addiction onset had been statistically more encountered during childhood and youth as compared to the controls” (Journal of Psychoactive Drugs, 2012). In addition, the outcomes from the study indicate the need to research further into three sections namely the structure of the drug addict families, familial interrelations of the families from which the drug addicts come from and the importance of implementing family-based approaches to address prevention and therapy for drug addiction. The hypothesis of the study is the effect of poor inter-parental relations on the psychological development of children. This showed that conflicts in marriages have were linked to the child’s social adjustment, incapacity, and harsh upbringing regiment which in turn results in risky behavior patterns including substance abuse (Journal of Psychoactive Drugs, 2012)]. It is from this understanding that Zimi ´ and Jukic’s study tries to investigate the familial factors in favor of drug addiction onset by putting into consideration social, developmental, and interaction elements as the determinants of family relations and familial features associated with drug addicts thus, causing children to turn to drug abuse.
In analyzing both the study at hand, that is, “Familial Risk Factors Favoring Drug Addiction Onset” and various articles from the bibliography such as Development: Which Way Now?, Personal Savings and Anticipated Inflation, Assessment and management of pain in infants, The capability of psychodynamic treatment and cognitive behavior therapy in the nursing of personality disorders: A meta-analysis, Macro dynamics, Regime Switching and Financial Stress: Hypothesis and Empirics for the US, the EU and Non-EU Countries, and Hunger, Human Development, and Health in Canada: Research, Practice, and ...
Returning genetic research results in neurodevelopmental disorders: report an...KBHN KT
This report originated from discussions at the Annual Brain Development Conference in
late 2013 between researchers in the Neuroethics Core and Autism Spectrum Disorders
Project of NeuroDevNet. Discussants felt that return of research results is a pertinent
issue but that researchers are missing a comprehensive picture of the recommendations,
approaches and empirical data related to the return of research results in genetics studies
in children, in neurodevelopmental disorders, and specifically in autism.
This report provides an overview of recent genetic studies of autism spectrum disorder
(ASD), and reviews the ethical guidance (policies and peer-reviewed literature) and
best practices on the return of individual research results in adult and pediatric genetic
research. We focus on this case because of the wealth of genetic research being
carried out in families and cohorts to explain the etiology of ASD and because there is a
burgeoning literature on parental perspectives on the return of results in this case. The
empirical perspectives are collected and summarized and provide context with regard to
researcher and parent perspectives on the return of genetic results in ASD studies.
We conclude by making recommendations about the return of both incidental and
ASD-related findings and highlight issues that merit further discussion, including the
role of the child or adolescent with developmental disability in decision-making, and
the importance of risk communication. We believe that the report will be of use not only
for those working in the area of ASD but more broadly in the field of pediatric genetic
research and neurodevelopmental disorder research. For example, the publication of new
evidence showing that genetic alterations play an important role in the etiology of cerebral
palsy in some children means that genetic research may becoming increasingly common
in other areas of the study of neurodevelopmental disorders.
Environmental Pollutants and Disease in American: Children: Estimates of Morbidity, Mortality, and Costs for Lead Poisoning, Asthma, Cancer, and Developmental Disabilities
Kathleen Jones wrote a literature review on the effects of parental alcoholism on children. The review examined research showing that children with antisocial or depressed alcoholic parents are at greater risk for externalizing symptoms. Parental alcoholism was also linked to increased risk of psychopathology in children, including conduct disorder and depression. However, one study found that only a minority of children of alcoholics develop alcohol problems themselves. Factors like family support and positive influences can help mitigate risks to children in alcoholic families. The review identified areas for further research on identifying the most impactful risk factors and how supportive influences may help children raised in negative environments.
This document discusses prevention psychiatry and outlines various prevention strategies. It defines prevention psychiatry as identifying risk factors and applying evidence-based interventions to reduce mental disorders. Primary prevention aims to reduce incidence, secondary prevention aims to reduce prevalence through early detection and treatment, and tertiary prevention aims to reduce disability. The document provides examples of prevention interventions targeting different populations and behaviors, such as parenting programs, counseling for new mothers, and motivational interviewing for college students. It discusses identifying risk and protective factors and implementing interventions to modify risk factors and enhance protective factors.
The Long-Term Effects of Exposure to Low Doses of Lead in Childhood - 1991Marion Sills
This document is a letter responding to an article published in the New England Journal of Medicine regarding the long-term effects of exposure to low doses of lead in childhood. The letter raises concerns about potential confounding factors like socioeconomic status that were not fully accounted for. It argues that social and medical risk factors, rather than low-level lead exposure, could better explain deficits seen. The letter calls for more studies that better control for confounding to clarify the relationship between low-level lead exposure and neurobehavioral/cognitive effects.
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Here is the updated list of Top Best Ayurvedic medicine for Gas and Indigestion and those are Gas-O-Go Syp for Dyspepsia | Lavizyme Syrup for Acidity | Yumzyme Hepatoprotective Capsules etc
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These lecture slides, by Dr Sidra Arshad, offer a quick overview of the physiological basis of a normal electrocardiogram.
Learning objectives:
1. Define an electrocardiogram (ECG) and electrocardiography
2. Describe how dipoles generated by the heart produce the waveforms of the ECG
3. Describe the components of a normal electrocardiogram of a typical bipolar lead (limb II)
4. Differentiate between intervals and segments
5. Enlist some common indications for obtaining an ECG
6. Describe the flow of current around the heart during the cardiac cycle
7. Discuss the placement and polarity of the leads of electrocardiograph
8. Describe the normal electrocardiograms recorded from the limb leads and explain the physiological basis of the different records that are obtained
9. Define mean electrical vector (axis) of the heart and give the normal range
10. Define the mean QRS vector
11. Describe the axes of leads (hexagonal reference system)
12. Comprehend the vectorial analysis of the normal ECG
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14. Explain the concepts of current of injury, J point, and their significance
Study Resources:
1. Chapter 11, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 9, Human Physiology - From Cells to Systems, Lauralee Sherwood, 9th edition
3. Chapter 29, Ganong’s Review of Medical Physiology, 26th edition
4. Electrocardiogram, StatPearls - https://www.ncbi.nlm.nih.gov/books/NBK549803/
5. ECG in Medical Practice by ABM Abdullah, 4th edition
6. Chapter 3, Cardiology Explained, https://www.ncbi.nlm.nih.gov/books/NBK2214/
7. ECG Basics, http://www.nataliescasebook.com/tag/e-c-g-basics
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Basavarajeeyam is a Sreshta Sangraha grantha (Compiled book ), written by Neelkanta kotturu Basavaraja Virachita. It contains 25 Prakaranas, First 24 Chapters related to Rogas& 25th to Rasadravyas.
- Video recording of this lecture in English language: https://youtu.be/kqbnxVAZs-0
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- Link to download the book free: https://nephrotube.blogspot.com/p/nephrotube-nephrology-books.html
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share - Lions, tigers, AI and health misinformation, oh my!.pptxTina Purnat
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Practitioner Review: What have we learnt about the causes of ADHD?
1. Journal of Child Psychology and Psychiatry 54:1 (2013), pp 3–16
doi:10.1111/j.1469-7610.2012.02611.x
Practitioner Review: What have we learnt about
the causes of ADHD?
Anita Thapar,1,2 Miriam Cooper,1,2 Olga Eyre,1,2 and Kate Langley1,2
1
Child & Adolescent Psychiatry Section, Institute of Psychological Medicine and Clinical Neurosciences, Cardiff
University School of Medicine, Cardiff; 2MRC Centre for Neuropsychiatric Genetics and Genomics, Cardiff University
School of Medicine, Cardiff, UK
Background: Attention deficit hyperactivity disorder (ADHD) and its possible causes still attract controversy. Genes, pre and perinatal risks, psychosocial factors and environmental toxins have all been
considered as potential risk factors. Method: This review (focussing on literature published since 1997,
selected from a search of PubMed) critically considers putative risk factors with a focus on genetics and
selected environmental risks, examines their relationships with ADHD and discusses the likelihood that
these risks are causal as well as some of the main implications. Results: No single risk factor explains
ADHD. Both inherited and noninherited factors contribute and their effects are interdependent. ADHD is
familial and heritable. Research into the inherited and molecular genetic contributions to ADHD suggest
an important overlap with other neurodevelopmental problems, notably, autism spectrum disorders.
Having a biological relative with ADHD, large, rare copy number variants, some small effect size candidate
gene variants, extreme early adversity, pre and postnatal exposure to lead and low birth weight/prematurity have been most consistently found as risk factors, but none are yet known to be definitely causal.
There is a large literature documenting associations between ADHD and a wide variety of putative environmental risks that can, at present, only be regarded as correlates. Findings from research designs that
go beyond simply testing for association are beginning to contest the robustness of some environmental
exposures previously thought to be ADHD risk factors. Conclusions: The genetic risks implicated in
ADHD generally tend to have small effect sizes or be rare and often increase risk of many other types of
psychopathology. Thus, they cannot be used for prediction, genetic testing or diagnostic purposes beyond
what is predicted by a family history. There is a need to consider the possibility of parents and siblings
being similarly affected and how this might impact on engagement with families, influence interventions
and require integration with adult services. Genetic contributions to disorder do not necessarily mean that
medications are the treatment of choice. We also consider how findings might influence the conceptualisation of ADHD, public health policy implications and why it is unhelpful and incorrect to dichotomise
genetic/biological and environmental explanations. It is essential that practitioners can interpret genetic
and aetiological research findings and impart informed explanations to families. Keywords: ADHD,
genetics, risk factors, perinatal, prenatal, aetiology, environmental–gene interactions.
Introduction
Despite still periodically attracting public controversy, attention deficit hyperactivity disorder (ADHD)
has long been recognised as a clinical entity (Taylor,
2011). In the last few decades, there has been an
enormous amount of research into the aetiology of
ADHD. What should we believe? How do research
findings impact on clinical practice if at all? In this
article, our aims are to critically review selected
factors that have been considered as likely contributors to ADHD risk, update practitioners on key
findings and their interpretation and provide some
‘take-home’ messages. In accordance with Kraemer
et al. (Kraemer, Stice, Kazdin, Offord, & Kupfer,
2001), we use the terms ‘risk’ to mean the probability
of developing an outcome (herein, ADHD) within a
population of subjects, ‘correlate’ where a factor is
associated with outcome, ‘risk factor’ where a factor
Re-use of this article is permitted in accordance with the Terms
and Conditions set out at http://wileyonlinelibrary.com/
online open#OnlineOpen_Terms
Conflicts of interest statement: No conflicts declared.
precedes outcome and ‘causal risk factor’ where
a factor alters the risk of outcome when manipulated.
Methods
This is a narrative review, focusing on literature in
the last 15 years, selected from a PubMed search.
The key words used were ADHD and genetic, inherited, gene-environment interaction, gene-environment interplay, aetiology, linkage, genome-wide
association study, copy number variant, twin studies, adoption studies, COMT, conduct disorder,
candidate gene, environment, toxins, lead, polychlorinated biphenyls, PCB, pesticides, diet, prenatal, perinatal, pregnancy, smoking, tobacco,
substance, stress, birth weight and prematurity. We
supplemented these with reviews and book chapters
and emphasise replicated findings.
An inherited contribution to ADHD
Attention deficit hyperactivity disorder, like other
psychiatric and developmental disorders runs in
Ó 2012 The Authors. Journal of Child Psychology and Psychiatry Ó 2012 Association for Child and Adolescent Mental Health.
Published by Blackwell Publishing, 9600 Garsington Road, Oxford OX4 2DQ, UK and 350 Main St, Malden, MA 02148, USA
2. 4
Anita Thapar et al.
families. Genetic risk when passed on from parents
is known as inherited risk/liability; not all genetic
risks are necessarily inherited (see later). First degree relatives of those with ADHD are two to eight
times more likely than relatives of unaffected individuals to also show ADHD (Faraone et al., 2005).
Twin studies in many different countries show high
heritability rates for ADHD of around 71–90%
(Faraone et al., 2005; Nikolas & Burt, 2010; Thapar,
Holmes, Poulton, & Harrington, 1999) with evidence
of shared familial/inherited risks for combined and
inattentive type symptoms (Willcutt et al., 2012).
Heritability estimates not only include genetic
influences, but also the effects of gene-environment
interplay that are very likely to be important (see
later). Thus, high heritability estimates do not rule
out the contribution of environmental risks. Although caution is needed in interpreting absolute
estimates of heritability, what is interesting is that
findings are consistent across different populations
and measures. That is not always the case. For
example, twin studies of child and adolescent
depression show widely differing heritability estimates (Thapar & Rice, 2006). Estimates will also
depend on the population studied and environmental context. For example, theoretically if everyone in
a population was equally exposed to an environmental risk factor of major effect size, most variation
in disorder would be explained by genetic differences. Thus, the consistency in heritability estimates
is surprising as it might be expected that environmental risks would differ across time and for different countries.
Adoption studies allow separation of inherited and
postnatal environmental effects by examining the
degree of concordance or similarity between individuals who have ADHD and their biologically related
and unrelated relatives. All five published adoption
studies of ADHD (Alberts-Corush, Firestone, & Goodman, 1986; Cantwell, 1975; Cunningham, Cadoret,
Loftus, & Edwards, 1975; Morrison & Stewart, 1973;
Sprich, Biederman, Crawford, Mundy, & Faraone,
2000) are consistent in showing a strong inherited
contribution. Do genetically informative designs like
adoption studies simply show this consistent pattern
of strong inherited effects for all psychopathology?
The answer is that findings are not identical across all
phenotypes. For example, genetically informative
studies of depression and antisocial behaviour (Harold et al., 2011; Lewis, Rice, Harold, Collishaw, &
Thapar, 2011; Silberg, Maes, & Eaves, 2012; Tully,
Iacono, & McGue, 2008) show the important contribution of noninherited factors to intergenerational
transmission of these problems and highlight that the
manifestation of genetic liability varies with the
environmental context (Rhee & Waldman, 2002). Although when taken with family and twin study findings, adoption studies of ADHD suggest an important
inherited contribution to ADHD, they do not remove
the influence of prenatal risks or early postnatal
J Child Psychol Psychiatry 2013; 54(1): 3–16
adversity. Future adoption studies of ADHD will be
invaluable, especially those that involve adoption at
birth and look more closely at environmental influences that modify the clinical presentation and outcomes in those at higher genetic risk.
Finally, as we will keep emphasising, the issue is
never genes or biology versus environment given that
there is overwhelming evidence that their effects are
so closely intertwined (Rutter, 2006). The most
important environmental risk factors for psychopathology, including ADHD and its secondary adverse
consequences, are likely to be affected by genetically
influenced parental and child dispositions (Rutter,
2006); for example, prenatal exposure to maternal
cigarette smoking or peer rejection (gene-environment correlation). Thus, associations of environmental risks with ADHD might arise completely or
partly through inherited confounds and genetic risks
might operate on manifest phenotypes through
environmental mechanisms (see Figure 1). Genetic
risks can also influence susceptibility by altering
individual sensitivity to environmental risks or protective factors (gene-environment interaction; Nigg,
Nikolas, & Burt, 2010).
The overlap of ADHD with other
developmental and psychiatric disorders
ADHD shows comorbidity with a wide variety of
problems (Taylor, 2011; Willcutt et al., 2012). There
are well-established strong associations with lower
IQ and intellectual disability, specific learning and
developmental problems, such as reading disability,
speech and language problems, motor co-ordination
difficulties and also autistic spectrum disorders
(ASDs). Recent twin studies suggest that shared
inherited factors contribute to the comorbidity of
ADHD and other neurodevelopmental problems,
including ASDs (Lichtenstein, Carlstrom, Rastam,
Gillberg, & Anckarsater, 2010; Ronald, Larsson,
Anckarsater, & Lichtenstein, 2011; Ronald, Simonoff, Kuntsi, Asherson, & Plomin, 2008) and reading
problems, especially with regards to the inattentive
features of ADHD (Willcutt, Pennington, & DeFries,
2000). The close clinical relationships, shared genetic
risk factors, coupled with other shared features,
notably an early age of onset and male excess, provide
a strong argument for considering ADHD as one of a
group of neurodevelopmental disorders (Rutter, 2011).
However, ADHD also shows a high level of comorbidity with other psychiatric and behavioural
disorders, notably conduct problems/antisocial
behaviour, alcohol and substance misuse and mood
disorders, that is explained by shared heritability
(Cole, Ball, Martin, Scourfield, & McGuffin, 2009;
Thapar, Harrington, & McGuffin, 2001; Willcutt et al.,
2012). Thus, there is also a view that ADHD might be
best considered as one of a cluster of externalising
disorders (Andrews, Pine, Hobbs, Anderson, & Sunderland, 2009). However, one key difference from the
Ó 2012 The Authors. Journal of Child Psychology and Psychiatry Ó 2012 Association for Child and Adolescent Mental Health.
3. doi:10.1111/j.1469-7610.2012.02611.x
Panel (A)
What have we learnt about the causes of ADHD?
5
Require methods to
manipulate this.
e.g. animal studies,
assisted conception design
‘Third variable’
Inherited and unmeasured
background environmental
factors
(confounds)
Child ADHD
Prenatal parent characteristics/behaviour
e.g. maternal smoking in pregnancy
Environmental mediation
e.g. exposure to carbon
monoxide,
nicotine,
placental dysfunction
Panel (B)
Require methods to
remove confounds e.g.
randomised control
trials, longitudinal
studies
‘Third variable’
Inherited and unmeasured
background environmental
factors
(confounds)
Parent characteristics/behaviour
after birth e.g. early parent/child
relationship
Environmental
mediators. Could be
via biological changes
Child ADHD
Reverse
causation
Figure 1 The associations of environmental risks with child attention deficit hyperactivity disorder, illustrating how environmental
mediation may operate for (A) prenatal and (B) perinatal risks
overlap with neurodevelopmental problems is that
some of these problems/disorders can present later in
development and might arise as a consequence of
having ADHD (analogous to diabetes potentially
resulting in blindness; Fergusson & Horwood, 1995;
Taylor, Chadwick, Heptinstall, & Danckaerts, 1996),
although that is not necessarily the case for early
onset conduct problems that are closely associated
with ADHD (Willcutt et al., 2012).
ADHD genetics
Identifying ADHD ‘risk genes’
Genetics is not much different from other aetiological
research, in that it involves testing for a relationship
between variation in a risk/predictor measure and
an outcome. New technologies are, however, allowing
for the more detailed capture of genetic variation. For
common, complex disorders, such as ADHD, the
predominant starting assumption has been that risk
is mainly explained by multiple common gene variants of small effect size as well as environmental
risks. Family-based linkage study findings have not
been consistent with a more simplistic ‘major gene
effect model’.
Early candidate gene studies: starting with what we
think we know
The earliest studies of ADHD involved testing for
association between disorder and variants in candidate genes selected because they were thought likely
to be involved in the pathophysiology of ADHD.
Multiple candidate gene association studies of ADHD
have been published (see Gizer, Ficks, & Waldman,
2009). There is greater confidence in findings that
have been replicated and show association in metaanalyses and pooled analyses. For ADHD, a number
of these early studies found replicated evidence for
association – see Table 1. This relatively large body
of replicated findings compared favourably to other
research into other psychiatric disorders and further
supported evidence that genetic factors were important in the aetiology of ADHD. However, the effect
size of each risk variant is small and thus there is no
Ó 2012 The Authors. Journal of Child Psychology and Psychiatry Ó 2012 Association for Child and Adolescent Mental Health.
4. 6
Anita Thapar et al.
J Child Psychol Psychiatry 2013; 54(1): 3–16
Table 1 Candidate genes with the most consistent meta-analytic evidence for association with attention deficit hyperactivity disorder
Gene name
Codes for
Dopaminergic genes
DRD4
Dopamine D4 receptor
DRD5
DAT1
Dopamine D5 receptor
Carrier protein involved
in dopamine reuptake
Serotonergic genes
5HTT
Carrier protein involved
in serotonin reuptake
HTR1B
Serotonin 1B receptor
Other
SNAP-25
Protein involved in
neurotransmitter release,
synaptic plasticity and
axonal growth
Variant
Risk allele
Pooled odds ratio
VNTR in exon 3
Polymorphism in promoter
region
Dinucleotide repeat in 5¢ flank
VNTR in intron 8
Polymorphism in 3¢UTR
VNTR in 3¢UTR
7-repeat
5-repeat
T allele
148-bp allele
3 repeat
G allele
10 repeat
1.33
1.68
1.21
1.23
1.25
1.20
1.17
5HTTLPR polymorphism in
promoter region
Polymorphism in exon 1
Long allele
1.31 (Faraone et al., 2005)
G allele
1.11 (Gizer et al., 2009)
Polymorphism in 3¢UTR
Not known
1.19 (Faraone et al., 2005)
(Smith, 2010)
(Li et al., 2006)
(Gizer et al., 2009)
(Gizer et al., 2009)
(Gizer et al., 2009)
(Gizer et al., 2009)
(Yang et al., 2007)
VNTR, variable number tandem repeat; UTR, untranslated region.
predictive value and nor do they highlight novel
biological mechanisms.
Searching the whole genome: common
and rare variants
Common DNA sequence variants
One of the rationales for undertaking genetic studies
is to discover previously unidentified risk pathways.
This has led to ‘hypothesis-free’ whole genome
searches for common genetic variants (SNPs) that
tagged much (but not all) genetic variation. Detailed
accounts of such genome-wide association studies
(GWAS) findings and methods are described elsewhere (Franke, Neale, & Faraone, 2009; Stergiakouli
& Thapar, 2010). GWAS that have been based on
testing common genetic variants (single nucleotide
polymorphisms, SNPs) of ADHD have been disappointing. No study to date, including a meta-analysis
(Neale et al., 2010), has revealed any gene variant
that passes the statistical threshold (p = 5 · 10)8)
for genome-wide significance. The statistical
threshold is set high because of the multiple testing
burden (recent published studies include testing
500,000–1 million genetic variants; p-values of .05
would therefore include 25,000–50,000 SNPs significant by chance). However, it is now apparent that
none of these studies was adequately sized. To date,
the largest meta-analysis includes fewer than 3000
ADHD cases. Studies of other disorders (e.g. diabetes, schizophrenia) have required thousands and
tens of thousands of affected individuals for associated SNPs to reach statistical significance.
There are mixed opinions on the value of such
studies. On the one hand, identifying common gene
variants that uncover novel biological risk pathways
underlying psychiatric disorder is attractive and
potentially important. The aim is for this to be
achieved by assembling much larger ADHD sample
sizes through international collaborations and by
performing exome (genetic coding regions) and whole
genome sequencing to capture all DNA sequence
variation and structural variants (e.g. chromosomal
deletions, duplications; Cirulli & Goldstein, 2010;
Lander, 2011). Others are more sceptical, suggesting that common genetic variants, at least as currently captured, might not be as important as rare
variants in psychiatric disorders (St Clair, 2009), or
are worried about the value of identifying risk
variants of small effect size (Maher, 2008). The
counterarguments, herein, are that the genetic
architecture of ADHD appears to be explained by a
complex blend of common and rare variants and
that the aims of genetic searches are to uncover
novel biological and brain risk mechanisms, rather
than focus on individual risk factors. All are agreed,
however, that better understanding of the pathogenesis of psychiatric disorders, including ADHD, is
needed.
Rare chromosomal structural variants
There has been growing interest in the contribution
of rare (traditionally defined as frequency of <1%)
rather than common genetic variants to neuropsychiatric disorders, the effects of which have needed
to be very large to be detected. It is has long been
recognised that rare chromosomal microdeletion
syndromes, such as 22q11 microdeletion syndrome
(velocardiofacial syndrome, VCFS), that involve a
deletion encompassing many genes, can lead to
increased risk of ADHD and psychosis (Antshel
et al., 2006). Even more subtle chromosomal duplications and deletions, known as structural or copy
number variants (CNVs) are becoming increasingly
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recognised as an important class of genetic variation.
All individuals carry CNVs. However, individuals
with a variety of brain and neuropsychiatric disorders, including autism (Glessner et al., 2009), intellectual disability (ID; Cooper et al., 2011) and
schizophrenia (Grozeva et al., 2012; Raychaudhuri
et al., 2010), appear to have an increased burden of
rare CNVs, both deletions and duplications, that are
of larger size (still submicroscopic, but >500 kb) and
encompass multiple different genes.
It is now frequently recommended that clinical
genetics services should screen for CNVs in individuals with idiopathic ID (Schaaf, Wiszniewska, &
Beaudet, 2011). However, working out which CNVs
are pathogenic is not always straightforward. Like
with most risk factors, in most instances, there is not
a one-to-one relationship between risk and clinical
outcome.
The earliest CNV studies of ADHD did not find an
increased burden of rare CNVs, but suggested disruption of neurodevelopmental pathways (Elia
et al., 2010; Lesch et al., 2011). More recently, the
focus has turned to large (>500 kb), rare CNVs. Our
UK study found an increased burden of large, rare
CNVs in ADHD and that the chromosomal regions
involved significantly overlapped with those previously found in autism and schizophrenia (Williams
et al., 2010). Although especially high in those with
ADHD and ID, the rate of CNVs was not restricted
to this group and all analyses were restricted to
those without ID. These findings have now been
independently replicated (Stergiakouli et al., 2012;
Williams et al., 2012). Two specific chromosomal
regions have been significantly implicated; one on
16p13.11 that was found in the UK and an
Icelandic sample (Williams et al., 2010), and the
other potentially involves a region on chromosome
15q11–13 (that contains the nicotinic a7 acetylcholine receptor gene; Stergiakouli et al., 2012;
Williams et al., 2012).
As previously highlighted, as would be expected
for any risk factor for a complex disorder (e.g.
smoking and ischaemic heart disease), the risk factor (herein a higher burden of large rare CNVs) was
not found in all children with ADHD and was present
in controls (14% vs. 7%; Williams et al., 2010) who
remained presumably unaffected (although this was
not definitely known as control phenotype data in
genotyped samples are not usually available). Large,
rare CNVs are interesting because although rare,
their effect size has had to be large to be detected
[e.g. odds ratio of 13.88 for CNVs spanning 16p13.11
(Williams et al., 2010)], (much larger than is the case
for common variants).
Given their rarity, are the children with ADHD who
carry large, rare CNVs clinically and biologically
atypical? One study found that the children with
ADHD with and without such CNVS showed similar
clinical features (Langley et al., 2011). Another
study showed that the biological pathways impacted
What have we learnt about the causes of ADHD?
7
upon by large, rare CNVs significantly overlapped
with those indexed by common genetic variants
(Stergiakouli et al., 2012). These findings suggest
that large, rare CNVs do not necessarily result in an
atypical form of ADHD. Moreover, the findings suggest that dismissing the contribution of common
variants to psychiatric disorder, as some suggest,
might be premature. Future research needs to consider models that incorporate both rare and common
variants.
Overall, the CNV findings once again suggest that
ADHD shows an overlap with other neurodevelopmental disorders, in this instance, autism and
schizophrenia. It is of interest that association
between CNVs and mood disorders has not been
consistently found suggesting that such variants
might be especially important in neurodevelopmental disorders (Grozeva et al., 2010).
Many questions remain despite replication. Which
of the associated CNVs are causal? Newer research
of autism and schizophrenia suggests that both rare
sequence and structural variants will be important
to examine and that noninherited CNVs that occur
de novo contribute to sporadic cases. Interestingly,
environmental factors might contribute to the
appearance of de novo mutations (Najmabadi et al.,
2011). This has yet to be properly investigated in
ADHD. Another critical question is how does the
same genetic variant result in a different psychiatric
or developmental phenotype? It is not unusual in
other areas of medicine for the same risk factor to
result in different disorders (e.g. cigarette smoking
leads to heightened risks for lung cancer and
ischaemic heart disease). Are there additional common and rare genetic and nongenetic factors that
shape clinical presentations?
Antisocial behaviour in ADHD and COMT
ADHD shows considerable clinical heterogeneity in
terms of symptom severity, admixture of symptoms,
developmental course and comorbidity that are
influenced by inherited and noninherited factors. So
far there have been few consistent findings that have
withstood replication and pooled analyses as to
what genetic variants might influence ADHD phenotype variation. One exception is a functional variant in the gene encoding the enzyme COMT (COMT
val158met) that is the primary mechanism for
breakdown of dopamine in the prefrontal cortex.
This gene variant modifies COMT enzyme activity
whereby those with the val/val genotype have a
higher activity version of the enzyme and breakdown
dopamine more rapidly. This gene variant has been
found to be associated with conduct disorder symptoms in two clinical studies of ADHD (Monuteaux,
Biederman, Doyle, Mick, & Faraone, 2009; Thapar
et al., 2005), three independent population-based
cohorts and a pooled analysis (Caspi et al., 2008;
Langley, Heron, O’Donovan, Owen, & Thapar, 2010);
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although as expected, nonreplications have also
been published (Sengupta et al., 2006). The effect
size is modest, but strongest for more severe conduct problems [e.g. odds ratio for association with
conduct disorder in ADHD vs. no conduct disorder
in ADHD = 3.37 (Langley, Heron, et al., 2010)]. Also,
the COMT val158met variant is only associated
with antisocial behaviour in the presence of ADHD
and not with antisocial behaviour alone (Caspi et al.,
2008; Langley, Heron, et al., 2010). These findings suggest that risk factors for antisocial behaviour in the context of ADHD are not necessarily the
same as antisocial behaviour in the general
population.
The next question is how might this gene variant
exert risk effects? There are a few clues from clinical,
cognitive and imaging studies. These studies, that
include a meta-analysis, suggest that the COMT
val158met variant in normal individuals is associated with performance on executive function measures and emotional dysfunction (Mechelli et al.,
2009; Meyer-Lindenberg & Weinberger, 2006; Mier,
Kirsch, & Meyer-Lindenberg, 2010). A recent study
suggests that the COMT val158met variant is associated with both executive function and impaired
social understanding, but the links with antisocial
behaviour in ADHD appear to be mediated through
impaired social understanding (Langley, Heron,
et al., 2010). If this finding is replicated, and different genetic and environmental risks impact on the
same pathways, it suggests alternative treatment
targets for the prevention and treatment of antisocial
behaviour in ADHD; for example, targeting the social
cognitive impairments in ADHD or undertaking pilot
studies of COMT inhibitors in those with extreme,
intractable aggression.
What do we know about environmental risks?
Many different environmental factors have been
reportedly associated with ADHD, but it has been
difficult to identify which are definitely causal (see
Lahey, D’Onofrio, & Waldman, 2009; Rutter, 2007;
Thapar & Rutter, 2009 for more detailed explanations). As correlation does not necessarily mean
causation, extreme caution is needed when interpreting association findings from epidemiological
and clinical studies. Many observed associations
could arise as a consequence of child and/or parent
psychopathology or disposition (e.g. negative
mother–child relationship). They could also represent the effects of an unmeasured ‘third variable’ (see
Figure 1). Most putative environmental factors (e.g.
maternal smoking in pregnancy) are not randomly
distributed and could arise because of individuals
and/or their parents selecting or shaping their environments. As randomised controlled trials (RCTs) of
potential environmental risks and their modification
are not always possible or ethical, other types of designs that include quasi experimental, genetically
informative and longitudinal studies are helpful in
removing some, but not all, of these confounding and
reverse causation effects. The aim is to rigorously
attempt to disprove causal hypotheses using different designs (see Lahey et al., 2009; Rutter, 2007).
There are many good examples where through
such approaches, environmental risks have been
found to be causal. For example, for antisocial behaviour, there is consistent evidence from longitudinal
(Patterson, DeGarmo, & Forgatch, 2004), randomised
control treatment trials (Scott et al., 2010), quasiexperimental research (Costello, Compton, Keeler, &
Angold, 2003) and genetically informative studies
(Jaffee et al., 2004) that negative parenting, maltreatment and poverty are causal risk factors, especially in those that are also genetically susceptible.
For ADHD, this quality of evidence is mainly lacking
– see Table 2 for a summary of the environmental
factors that have been most widely studied. To limit
the scope of this review, we do not focus on
environmental factors associated with ADHD continuity or that are manipulated as an intervention for
those who already have ADHD (notably dietary
interventions).
Table 2 Environmental risks that have been most commonly been studied in relation to attention deficit hyperactivity disorder
Pre- and perinatal
factors
Environmental toxins
Dietary factors
Psychosocial adversity
Maternal smoking,
alcohol and substance
misuse
Risk but not proven
causal risk factor
Organophosphate
pesticides
Risk but not proven
causal risk factor
Nutritional deficiencies eg zinc, magnesium,
polyunsaturated fatty acids
Correlate not yet proven risk factor
Family adversity & low
income
Correlate not yet proven
risk factor
Maternal stress
Risk but not proven
causal risk factor
Polychlorinated
biphenyls
Risk but not proven
causal risk factor
Nutritional surpluses eg sugar,
artificial food colourings
Correlate not yet proven risk factor
Conflict/parent–child hostility
Correlate not yet proven risk
factor
Low birth weight and
prematurity
Risk but not proven
causal risk factor
Lead
Risk but not proven
causal risk factor
Low/high IgG foods
Correlate not yet proven risk factor
Severe early deprivation
Risk, likely causal risk factor
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Pre and perinatal risks
Maternal smoking during pregnancy is one of the most
commonly cited prenatal risks associated with increased rates of ADHD in pooled analyses with an
estimated odds ratio of 2.36 (Langley, Rice, van den
Bree, & Thapar, 2005). Associations with both ADHD
symptoms and diagnoses have been observed using
maternal reports of cigarette smoking and objective
measures of serum cotinine, whereas a dose–
response relationship has also been seen – the more
the mother smokes, the greater the associated risk.
Similarly, maternal stress during pregnancy has also
been noted to be associated with offspring ADHD (e.g.
Glover, 2011; Grizenko, Shayan, Polotskaia, TerStepanian, & Joober, 2008). Although there are biologically plausible mechanisms through which these
risks could lead to ADHD, it remains unclear whether
or not the associations are causal (Thapar & Rutter,
2009). There is growing evidence from studies using
genetically sensitive designs, based on children who
remain unrelated to their mothers through assisted
conception and siblings where the mother has
smoked during one pregnancy and not the other
(D’Onofrio et al., 2008; Rice, Harold, Boivin, van den
Bree, & Thapar, 2009; Thapar et al., 2009), that
associations between maternal smoking, stress during pregnancy and ADHD (D’Onofrio et al., 2010; Rice
et al., 2009) are due, at least in part, to confounding
genetic or other household-level factors. Interestingly,
the same designs did not find that inherited confounds contributed to the links between maternal
stress and offspring antisocial behaviour and mood/
anxiety problems. Also, there is no evidence that as
rates of maternal smoking in pregnancy have dropped
(Office for National Statistics, 2006), population
prevalence rates of ADHD have similarly dropped
(Collishaw, Maughan, Natarajan, & Pickles, 2010).
Exposure to other substances during pregnancy
has also been found to be associated with ADHD,
although with the exception of foetal alcohol syndrome, less robustly. Moderate maternal alcohol use
during pregnancy and exposure to illicit substances
has been associated with increased risk of ADHD in
some, but not all, studies (Linnet et al., 2003).
ADHD, especially the inattentive subtype, has also
been found to be associated with low birth weight and
prematurity, with a meta-analysis suggesting significant association and an odds ratio of 2.6 for low birth
weight (Bhutta, Cleves, Casey, Cradock, & Anand,
2002). Again, it is necessary to consider whether or
not these associations are causal and additional
study in this area is required as premature birth and
low birth weight and obstetric complications might
reflect underlying foetal problems (Bailey et al.,
1995). However, some genetically informative studies
suggest low birth weight is not likely to represent an
inherited confound (Groen-Blokhuis, Middeldorp,
van Beijsterveldt, & Boomsma, 2011). As is the case
for the genetic findings on large, rare CNVs, low birth
What have we learnt about the causes of ADHD?
9
weight and prematurity are present in only a very
small proportion of individuals with ADHD.
Thus, at present, evidence of pre and perinatal
factors being causal is lacking. Nevertheless, it is
worthwhile having a higher index of suspicion about
the presence of ADHD in premature, low birth weight
children. Emerging evidence is beginning to challenge
the hypotheses that maternal stress and smoking in
pregnancy are causal risk factors for ADHD, but further quasi-experimental research is needed.
Environmental toxins
Exposures to other toxins in prenatal and/or postnatal life have also been considered as increasing the
risk of ADHD. In particular, organic pollutants and
lead may damage the neural systems implicated in
ADHD (Nigg, 2008).
Pesticides
Organophosphate pesticides have been studied in
relation with ADHD, although not widely. A crosssectional investigation of the relationship between
urinary dialkyl phosphate (DAP) metabolites of
organophosphates and ADHD diagnosis in middle
childhood and early adolescence found that those with
detectable urinary dimethyl alkylphosphate (DMAP)
metabolite concentrations above the median level had
double the odds of ADHD in contrast with those with
untraceable levels (Bouchard, Bellinger, Wright, &
Weisskopf, 2010). More stringent longitudinal research has found high prenatal organophosphate
exposure to be associated with adverse outcomes related to ADHD symptomatology in an investigation of
umbilical cord plasma chlorpyrifos levels on subsequent cognitive and motor development in infancy
and early childhood (Rauh et al., 2006). However,
findings have been inconsistent. Others find that prenatal maternal and postnatal child urinary metabolites
of a range of pesticides have no link with ADHD-like
symptoms at age 2 years (Eskenazi et al., 2007), but
subsequent follow up at 3.5 and 5 years found prenatal
DAP metabolites were associated with maternally
reported attention difficulties and ADHD symptoms at
age 3.5 and these associations became significant at
age 5 (Marks et al., 2010). Although commercial use of
organochlorine pesticides have now largely been replaced by organophosphates, they do persist in the
environment and a Spanish study (Ribas-Fito et al.,
2007) did find an association between high cord serum
levels of the organochlorine hexachlorobenzene and
teacher-rated ADHD behaviours scored by a DSM-IV
symptom checklist at age 4.
Toxic industrial products
Polychlorinated biphenyls (PCBs) are toxic manufactured organochlorine congeners, which were once
mass-produced for a variety of industrial and com-
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mercial uses and now persist as environmental contaminants. Both human and importantly, animal
studies have found that PCB exposure leads to
impairments in working memory, response inhibition
and cognitive flexibility – neurobehavioural effects,
which are comparable with those seen in ADHD (Eubig, Aguiar, & Schantz, 2010). Furthermore, a dose–
response relationship, between low level prenatal PCB
exposure (as measured by umbilical cord PCB levels)
and ADHD-type behaviours in middle childhood was
found in a prospective study of a PCB-contaminated
area (Sagiv et al., 2010).
Lead
As with PCBs, human and animal studies of lead
exposure have looked at effects on cognitive domains
relevant to ADHD; cognitive flexibility, vigilance and
alertness have been found to be most dependably affected (Eubig et al., 2010). An association between
blood lead level and an actual ADHD diagnosis has been
found in several recent studies (including Braun, Kahn,
Froehlich, Auinger, & Lanphear, 2006; Froehlich et al.,
2009; Nigg, Nikolas, Mark Knowttnerus, et al., 2010).
It is worth noting that there is evidence that both
prenatal exposure to PCBs (reviewed in Schantz,
Widholm, & Rice, 2003) and even technically ‘low’
blood lead levels (reviewed in Bellinger, 2008a) have
more general effects on cognitive function and neurodevelopment as well as on neuropsychological domains specific to ADHD. Nonetheless, due to the
neurobiological dysfunction caused by environmental
pollutants and the research also implicating them in
altered neurodevelopment specific to ADHD, it seems
biologically plausible that toxins could indeed have a
role. However, as exposure to such substances may
not be random, causality cannot yet be firmly inferred
from the evidence to date. Conversely, an exception to
nonrandom exposure seems to be lead, for which
associations with altered neurodevelopment are unlikely to be fully explicable by residual confounding in
view of the heterogeneity of settings in which associations have been found (Bellinger, 2008b), and there
is now no dietary threshold below which intake can be
considered safe (Food and Agriculture Organization of
the United Nations and World Health Organization,
2010). At the very least, there is emerging evidence,
from both cross-sectional and longitudinal research,
of the negative effect of pollutants on neurodevelopment. There needs to be more research making use of
quasi-experimental designs and multiple informant
assessments of ADHD. Nevertheless, public health
and environmental policies aimed at reducing exposure to toxins, particularly for children, is clearly a
desirable way forward.
Diet
Nutritional deficiencies have been studied as aetiological factors, modifying factors and supplementation
J Child Psychol Psychiatry 2013; 54(1): 3–16
and exclusion of dietary constituents have also been
used as interventions to try and improve outcomes (see
Nigg, Lewis, Edinger, & Falk, 2012 for a review). As with
environmental toxins, any relationship between diet
and ADHD symptoms is unlikely to be straightforward.
Although there has been research into several nutritional deficiencies as possible aetiological factors in
ADHD, (e.g. zinc (reviewed in Arnold & DiSilvestro,
2005), magnesium (Kozielec & Starobrat-Hermelin,
1997) and polyunsaturated fatty acids (Spahis et al.,
2008)), there is not strong enough evidence to conclude
that such deficiencies have a causal effect. Equally, it is
not established whether the biological processes involved in ADHD mean that affected children require an
excess of what is considered ‘normal’ ranges of dietary
constituents to ameliorate brain function, to justify supplementation in the absence of baseline deficiency. Whilst it is established that extreme nutritional
deficiency can interfere with neurodevelopment, the
biological effects of more subtle insufficiencies are less
clear (Sinn, 2008). Whilst there are also biologically
plausible hypotheses as to why diet might be implicated in the development or maintenance of ADHD
symptomatology, especially in some individuals, there
is not yet consistent enough evidence from research
into diet to wholeheartedly support the notion that
such factors play a major causal role in ADHD.
Family adversity and early care-giving
Multiple indicators of psychosocial adversity,
including family adversity and low income, have been
found to be associated with child mental health
problems, including ADHD (Pheula, Rohde, & Schmitz, 2011; Scahill et al., 1999; Taylor & SonugaBarke, 2008). Children who suffer maltreatment have
also shown a high incidence of ADHD (Famularo,
Kinscherff, & Fenton, 1992). A significant difficulty
lies in working out the direction of the relationship
between adversity and ADHD. For example, family
conflict may be seen more commonly in families of a
child with ADHD, but is this a cause or consequence
of ADHD in the child or parent? Longitudinal and twin
designs (Lifford, Harold, & Thapar, 2008, 2009), have
suggested that associations between parent–child
hostility and ADHD symptoms appear to be accounted for by confounding inherited factors with the
exception of the link between mother–son hostility
and ADHD symptoms. However, it appears that it is
the child’s ADHD symptoms that impact on mother–
son hostility, rather than the hostility having a causal
role in ADHD. Other studies have shown that treatment with stimulant medication for ADHD improves
symptoms, but also improves the mother–child relationship (Schachar, Taylor, Wieselberg, Thorley, &
Rutter, 1987). Taken together, this evidence suggests
that ADHD symptoms themselves may contribute to
family conflict. However, it is possible that family and
psychosocial adversity even if it does not play a causal
role in the onset of ADHD, may modify its presenta-
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tion and result in secondary adverse consequences,
such as antisocial behaviour (Langley, Fowler et al.,
2010). This warrants additional investigation.
ADHD is an early onset disorder. Thus, the contribution of early care-giving requires separate consideration. The impact of severe early deprivation on
development of ADHD symptoms has been seen in
the English and Romanian Adoptees study
(O’Connor & Rutter, 2000; Rutter, Beckett, et al.,
2007). This study has the unique strength of being
quasi experimental, as it involved examining adopted away children who had been exposed to extreme
early deprivation. These results suggest that extreme
forms of early deprivation can result in ADHD-type
symptoms as well as quasi-autistic symptoms (Rutter, Kreppner, et al., 2007). However, it remains to be
seen whether milder forms of early adversity have
causal risk effects that could be examined, for
example, using adoption study designs. Again,
exposures to such risks are likely to be rare and will
not account for most ADHD in the population.
At present, with the exception of rare exposure to extreme forms of early adversity, there is no clear-cut evidence that psychosocial adversity causes ADHD,
although such factors may well modify its expression and
outcomes. Noting adverse circumstances (e.g. maltreatment, poverty) is clearly clinically important with regards
to clinical management, but care is needed in ascribing
direction of effects, causality and potential blame.
Gene–environment interplay
As already highlighted, genes and environment do not
work independently of each other (see Nigg, Nikolas, &
Burt, 2010 for a comprehensive review). Inherited
risks can contribute not only directly, but are also
likely to operate by increasing the likelihood of exposure to environmental adversity and altering sensitivity to environmental risks and protective factors.
There is growing evidence that such interplay is
important; for example, gene-environment correlation and interaction play an important role in adolescent depression (Caspi, Hariri, Holmes, Uher, &
Moffitt, 2010; Caspi et al., 2003; Thapar, Collishaw,
Pine, & Thapar, 2012). Twin and molecular genetic
studies have started to test in an exploratory way for
gene-environment interaction effects in ADHD (see
Nigg, Nikolas, & Burt, 2010). However, as yet, findings
have either not been replicated or hypotheses have not
been based on neuroscience evidence in the way that
was the case for depression. Environmental factors
can also impact on early and later development in a
more dynamic fashion by influencing how genes are
expressed; this is known as epigenetics (see Mill &
Petronis, 2008 for a more detailed explanation; Weaver, Diorio, Seckl, Szyf, & Meaney, 2004). This type of
complex interplay early on in life could amplify or
modify ADHD risk and/or its later consequences and
at least in animals such epigenetic effects can be
transmitted across generations and reversed.
What have we learnt about the causes of ADHD?
11
Implications for practitioners
Genetic testing and explaining genetics to families
At present, there are no clinical impacts of the
molecular genetic findings. Identified genetic risks on
their own have small effect sizes or are very rare and
are unlikely to be useful in a predictive or diagnostic
sense beyond what can already be predicted by a
family history. One exception to where genetic testing
might be helpful in the future is for children with
intellectual disability who have ADHD and other
neurodevelopmental disorders (Cooper et al., 2011;
Williams et al., 2010). One of the key aims of molecular genetic studies is to identify underlying, as yet
unknown, biological, cognitive, brain and psychosocial risk pathways that lead to the disorder; we provided the example of the COMT association with
antisocial behaviour in ADHD as possibly being
mediated via impaired social understanding.
When families ask about genetic contributions, it is
important that they realise familial and genetic risks
only increase the probability of ADHD and do not
determine the presence of disorder. Heritability estimates refer to populations and do not mean for example
that 90% of an individual’s ADHD is caused by genes.
Like other complex disorders, ADHD is not
explained by any single risk factor alone and not all
those who are exposed to a given risk show disorder.
Its occurrence is not explained by inherited factors
alone and the pattern of results suggests the contribution of multiple inherited and noninherited
factors to its aetiology.
Conceptualisation of ADHD
In terms of associations with inherited and noninherited factors and adverse consequences, ADHD
appears to behave like a trait measure (hyperactivity-impulsiveness and inattentiveness) akin to
blood pressure/hypertension; rather than as a qualitatively discrete category. The empirical evidence in
favour of using dimensional modifiers in research
and practice has been recently highlighted (Willcutt
et al., 2012). Evidence of an inherited, molecular
genetic and clinical overlap with autism and intellectual disability might strengthen the argument to
consider ADHD as a neurodevelopmental disorder,
where all such early problems are assessed together
in an interdisciplinary health setting with careful
assessment of educational and developmental needs
and early intervention.
Considering parents and siblings of the child
and integrating services
Given ADHD is familial and heritable, for those seeing
children with ADHD, the possibility that a parent/
parents might be similarly affected and how this might
impact on parenting and the intervention plan (e.g.
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parenting, family relationships and psycho-educational interventions) needs to be considered (e.g.
Johnston, Mash, Miller, & Ninowski, 2012; Thompson et al., 2009). Also, when more than one child in a
family has ADHD, there needs to be consideration of
the impact on family and parental stress and the
practicality of how interventions are delivered.
This could require close working with adult services that will increasingly be required to deal with
adult neurodevelopmental problems.
Implications of genetic findings on treatment
choice
Identifying a genetic contribution does not necessarily
mean that only biological treatments or medication
will be effective. At present, multimodal interventions
are recommended for ADHD (NICE, 2008). Moreover,
ADHD is not explained by a simple one on one relationship between gene and disorder. Even for single
gene disorders where this is the case, for example,
phenylketonuria, environmental manipulations (PKU
is treated by diet) can be effective.
Public health implications
At present, there are no clear-cut causal environmental risks that have been identified, with the
possible exception of extreme early adversity in some
rare instances. There are a number of candidates
that require further investigation, but it is critical to
use designs that go beyond simply assessing correlations. Nevertheless, there are clear health benefits
of mothers not smoking, misusing alcohol and drugs
and reducing stress levels in pregnancy, for example,
because of causal links with birth weight and prematurity. However, the evidence so far suggests that
these risks might not play a direct causal role in
ADHD. Similarly, good prenatal and later diet, lim-
J Child Psychol Psychiatry 2013; 54(1): 3–16
iting exposure to toxins is a generally sensible approach. However, if these are not true causal risks,
exclusively focusing on them as a means of reducing
population rates of ADHD will not be sufficient and
could distract from searching for and tackling other
potentially modifiable risks.
Discarding the dichotomisation of genes/biology
versus environment in practice as well as research
Finally, a key message of this review for practitioners
and families is that there is overwhelming evidence
that the polarisation between genetic/biological and
environmental factors, perpetuated by some due
to misinterpretation of aetiological and genetics
research in relation to complex disorders, is incorrect and unhelpful. Indeed, they are complementary
rather than competing explanations.
Acknowledgements
Research supported by the Wellcome Trust, Action
Research and Baily Thomas Charitable Trust. We are
very grateful to all the families of children with ADHD,
the children themselves and the CAMHS and Community Child Health clinicians and practitioners
across the UK who have participated in our research
and been so generous in giving up their time and
supporting the research. We thank the reviewers, editors and Joanna Martin, Cardiff University for valuable
suggestions.
Correspondence
Anita Thapar, Child & Adolescent Psychiatry Section,
Institute of Psychological Medicine and Clinical Neurosciences, MRC Centre in Neuropsychiatric Genetics and
Genomics, Cardiff University School of Medicine, Heath
Park, Cardiff CF14 4XN, UK; Email: thapar@cf.ac.uk
Key points
Key practitioner message:
• There is no single risk factor that explains ADHD. Many different risks and risk pathways may all lead to the
same clinical phenotype.
• Both inherited and noninherited factors contribute to ADHD, and their effects are interdependent.
• The most consistently found risk factors for ADHD include having a relative with the disorder, large rare CNVs,
candidate gene variants, extreme early adversity, pre and postnatal exposure to lead and low birth weight/
prematurity.
• The risk factors implicated in ADHD tend to have small effect sizes or are rare. They also may increase risk of
many other types of psychopathology.
• It is important to remember that associations between ADHD and investigated risk factors may not necessarily
be due to causal effects.
• There is important overlap with other neurodevelopmental problems, including autistic spectrum disorders, as
well as comorbidity with other psychiatric and behavioural disorders.
Ó 2012 The Authors. Journal of Child Psychology and Psychiatry Ó 2012 Association for Child and Adolescent Mental Health.
11. doi:10.1111/j.1469-7610.2012.02611.x
What have we learnt about the causes of ADHD?
13
Areas for future research:
• Further genetic studies, that are adequately sized, may be useful in allowing DNA sequence variation and
structural variants for ADHD to be captured.
• Future studies into environmental risk factors associated with ADHD need to use designs that go beyond
assessing correlation and look for evidence of causal links.
• For children with ADHD, the possibility that a parent might be similarly affected needs to be considered, and
studies looking at how this may impact on the intervention and outcome for the child, could provide
important information for future management.
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Accepted for publication 20 July 2012
Published online: 11 September 2012
Ó 2012 The Authors. Journal of Child Psychology and Psychiatry Ó 2012 Association for Child and Adolescent Mental Health.