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Attention-deficit hyperactivity disorder

Affiliations.

1 Columbia University Vagelos College of Physicians and Surgeons, Columbia University, New York, NY, USA; New York State Psychiatric Institute, Columbia University, New York, NY, USA. Electronic address: [email protected].
2 Faculdade de Medicina, Universidade de São Paulo, São Paulo, Brazil.
3 Department of Child and Adolescent Psychiatry, King's College London, London, UK.
PMID: 31982036
PMCID: PMC7880081
DOI: 10.1016/S0140-6736(19)33004-1

Attention-deficit hyperactivity disorder (ADHD), like other psychiatric disorders, represents an evolving construct that has been refined and developed over the past several decades in response to research into its clinical nature and structure. The clinical presentation and course of the disorder have been extensively characterised. Efficacious medication-based treatments are available and widely used, often alongside complementary psychosocial approaches. However, their effectiveness has been questioned because they might not address the broader clinical needs of many individuals with ADHD, especially over the longer term. Non-pharmacological approaches to treatment have proven less effective than previously thought, whereas scientific and clinical studies are starting to fundamentally challenge current conceptions of the causes of ADHD in ways that might have the potential to alter clinical approaches in the future. In view of this, we first provide an account of the diagnosis, epidemiology, and treatment of ADHD from the perspective of both the fifth edition of the Diagnostic and Statistical Manual of Mental Disorders and the eleventh edition of the International Classification of Diseases. Second, we review the progress in our understanding of the causes and pathophysiology of ADHD on the basis of science over the past decade or so. Finally, using these discoveries, we explore some of the key challenges to both the current models and the treatment of ADHD, and the ways in which these findings can promote new perspectives.

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Attention-Deficit/Hyperactivity Disorder

What is adhd.

Attention-deficit/hyperactivity disorder (ADHD) is marked by an ongoing pattern of inattention and/or hyperactivity-impulsivity that interferes with functioning or development. People with ADHD experience an ongoing pattern of the following types of symptoms:

Inattention means a person may have difficulty staying on task, sustaining focus, and staying organized, and these problems are not due to defiance or lack of comprehension.
Hyperactivity means a person may seem to move about constantly, including in situations when it is not appropriate, or excessively fidgets, taps, or talks. In adults, hyperactivity may mean extreme restlessness or talking too much.
Impulsivity means a person may act without thinking or have difficulty with self-control. Impulsivity could also include a desire for immediate rewards or the inability to delay gratification. An impulsive person may interrupt others or make important decisions without considering long-term consequences.

What are the signs and symptoms of ADHD?

Some people with ADHD mainly have symptoms of inattention. Others mostly have symptoms of hyperactivity-impulsivity. Some people have both types of symptoms.

Many people experience some inattention, unfocused motor activity, and impulsivity, but for people with ADHD, these behaviors:

Are more severe
Occur more often
Interfere with or reduce the quality of how they function socially, at school, or in a job

Inattention

People with symptoms of inattention may often:

Overlook or miss details and make seemingly careless mistakes in schoolwork, at work, or during other activities
Have difficulty sustaining attention during play or tasks, such as conversations, lectures, or lengthy reading
Not seem to listen when spoken to directly
Find it hard to follow through on instructions or finish schoolwork, chores, or duties in the workplace, or may start tasks but lose focus and get easily sidetracked
Have difficulty organizing tasks and activities, doing tasks in sequence, keeping materials and belongings in order, managing time, and meeting deadlines
Avoid tasks that require sustained mental effort, such as homework, or for teens and older adults, preparing reports, completing forms, or reviewing lengthy papers
Lose things necessary for tasks or activities, such as school supplies, pencils, books, tools, wallets, keys, paperwork, eyeglasses, and cell phones
Be easily distracted by unrelated thoughts or stimuli
Be forgetful in daily activities, such as chores, errands, returning calls, and keeping appointments

Hyperactivity-impulsivity

People with symptoms of hyperactivity-impulsivity may often:

Fidget and squirm while seated
Leave their seats in situations when staying seated is expected, such as in the classroom or the office
Run, dash around, or climb at inappropriate times or, in teens and adults, often feel restless
Be unable to play or engage in hobbies quietly
Be constantly in motion or on the go, or act as if driven by a motor
Talk excessively
Answer questions before they are fully asked, finish other people’s sentences, or speak without waiting for a turn in a conversation
Have difficulty waiting one’s turn
Interrupt or intrude on others, for example in conversations, games, or activities

Primary care providers sometimes diagnose and treat ADHD. They may also refer individuals to a mental health professional, such as a psychiatrist or clinical psychologist, who can do a thorough evaluation and make an ADHD diagnosis.

For a person to receive a diagnosis of ADHD, the symptoms of inattention and/or hyperactivity-impulsivity must be chronic or long-lasting, impair the person’s functioning, and cause the person to fall behind typical development for their age. Stress, sleep disorders, anxiety, depression, and other physical conditions or illnesses can cause similar symptoms to those of ADHD. Therefore, a thorough evaluation is necessary to determine the cause of the symptoms.

Most children with ADHD receive a diagnosis during the elementary school years. For an adolescent or adult to receive a diagnosis of ADHD, the symptoms need to have been present before age 12.

ADHD symptoms can appear as early as between the ages of 3 and 6 and can continue through adolescence and adulthood. Symptoms of ADHD can be mistaken for emotional or disciplinary problems or missed entirely in children who primarily have symptoms of inattention, leading to a delay in diagnosis. Adults with undiagnosed ADHD may have a history of poor academic performance, problems at work, or difficult or failed relationships.

ADHD symptoms can change over time as a person ages. In young children with ADHD, hyperactivity-impulsivity is the most predominant symptom. As a child reaches elementary school, the symptom of inattention may become more prominent and cause the child to struggle academically. In adolescence, hyperactivity seems to lessen and symptoms may more likely include feelings of restlessness or fidgeting, but inattention and impulsivity may remain. Many adolescents with ADHD also struggle with relationships and antisocial behaviors. Inattention, restlessness, and impulsivity tend to persist into adulthood.

What are the risk factors of ADHD?

Researchers are not sure what causes ADHD, although many studies suggest that genes play a large role. Like many other disorders, ADHD probably results from a combination of factors. In addition to genetics, researchers are looking at possible environmental factors that might raise the risk of developing ADHD and are studying how brain injuries, nutrition, and social environments might play a role in ADHD.

ADHD is more common in males than females, and females with ADHD are more likely to primarily have inattention symptoms. People with ADHD often have other conditions, such as learning disabilities, anxiety disorder, conduct disorder, depression, and substance use disorder.

How is ADHD treated?

While there is no cure for ADHD, currently available treatments may reduce symptoms and improve functioning. Treatments include medication, psychotherapy, education or training, or a combination of treatments.

For many people, ADHD medications reduce hyperactivity and impulsivity and improve their ability to focus, work, and learn. Sometimes several different medications or dosages must be tried before finding the right one that works for a particular person. Anyone taking medications must be monitored closely by their prescribing doctor.

Stimulants. The most common type of medication used for treating ADHD is called a “stimulant.” Although it may seem unusual to treat ADHD with a medication that is considered a stimulant, it works by increasing the brain chemicals dopamine and norepinephrine, which play essential roles in thinking and attention.

Under medical supervision, stimulant medications are considered safe. However, like all medications, they can have side effects, especially when misused or taken in excess of the prescribed dose, and require an individual’s health care provider to monitor how they may be reacting to the medication.

Non-stimulants. A few other ADHD medications are non-stimulants. These medications take longer to start working than stimulants, but can also improve focus, attention, and impulsivity in a person with ADHD. Doctors may prescribe a non-stimulant: when a person has bothersome side effects from stimulants, when a stimulant was not effective, or in combination with a stimulant to increase effectiveness.

Although not approved by the U.S. Food and Drug Administration (FDA) specifically for the treatment of ADHD, some antidepressants are used alone or in combination with a stimulant to treat ADHD. Antidepressants may help all of the symptoms of ADHD and can be prescribed if a patient has bothersome side effects from stimulants. Antidepressants can be helpful in combination with stimulants if a patient also has another condition, such as an anxiety disorder, depression, or another mood disorder. Non-stimulant ADHD medications and antidepressants may also have side effects.

Doctors and patients can work together to find the best medication, dose, or medication combination. To find the latest information about medications, talk to a health care provider and visit the FDA website .

Psychotherapy and psychosocial interventions

Several specific psychosocial interventions have been shown to help individuals with ADHD and their families manage symptoms and improve everyday functioning.

For school-age children, frustration, blame, and anger may have built up within a family before a child is diagnosed. Parents and children may need specialized help to overcome negative feelings. Mental health professionals can educate parents about ADHD and how it affects a family. They also will help the child and his or her parents develop new skills, attitudes, and ways of relating to each other.

All types of therapy for children and teens with ADHD require parents to play an active role. Psychotherapy that includes only individual treatment sessions with the child (without parent involvement) is not effective for managing ADHD symptoms and behavior. This type of treatment is more likely to be effective for treating symptoms of anxiety or depression that may occur along with ADHD.

Behavioral therapy is a type of psychotherapy that aims to help a person change their behavior. It might involve practical assistance, such as help organizing tasks or completing schoolwork, or working through emotionally difficult events. Behavioral therapy also teaches a person how to:

Monitor their own behavior
Give oneself praise or rewards for acting in a desired way, such as controlling anger or thinking before acting

Parents, teachers, and family members also can give feedback on certain behaviors and help establish clear rules, chore lists, and structured routines to help a person control their behavior. Therapists may also teach children social skills, such as how to wait their turn, share toys, ask for help, or respond to teasing. Learning to read facial expressions and the tone of voice in others, and how to respond appropriately can also be part of social skills training.

Cognitive behavioral therapy helps a person learn how to be aware and accepting of one’s own thoughts and feelings to improve focus and concentration. The therapist also encourages the person with ADHD to adjust to the life changes that come with treatment, such as thinking before acting, or resisting the urge to take unnecessary risks.

Family and marital therapy can help family members and spouses find productive ways to handle disruptive behaviors, encourage behavior changes, and improve interactions with the person with ADHD.

Parenting skills training (behavioral parent management training) teaches parents skills for encouraging and rewarding positive behaviors in their children. Parents are taught to use a system of rewards and consequences to change a child’s behavior, to give immediate and positive feedback for behaviors they want to encourage, and to ignore or redirect behaviors they want to discourage.

Specific behavioral classroom management interventions and/or academic accommodations for children and teens have been shown to be effective for managing symptoms and improving functioning at school and with peers. Interventions may include behavior management plans or teaching organizational or study skills. Accommodations may include preferential seating in the classroom, reduced classwork load, or extended time on tests and exams. The school may provide accommodations through what is called a 504 Plan or, for children who qualify for special education services, an Individualized Education Plan (IEP).

To learn more about the Individuals with Disabilities Education Act (IDEA), visit the U.S. Department of Education’s IDEA website .

Stress management techniques can benefit parents of children with ADHD by increasing their ability to deal with frustration so that they can respond calmly to their child’s behavior.

Support groups can help parents and families connect with others who have similar problems and concerns. Groups often meet regularly to share frustrations and successes, to exchange information about recommended specialists and strategies, and to talk with experts.

The National Resource Center on ADHD, a program of Children and Adults with Attention-Deficit/Hyperactivity Disorder (CHADD®) supported by the Centers for Disease Control and Prevention (CDC), has information and many resources. You can reach this center online or by phone at 1-866-200-8098.

Learn more about psychotherapy .

Tips to help kids and adults with ADHD stay organized

Parents and teachers can help kids with ADHD stay organized and follow directions with tools such as:

Keeping a routine and a schedule. Keep the same routine every day, from wake-up time to bedtime. Include times for homework, outdoor play, and indoor activities. Keep the schedule on the refrigerator or a bulletin board. Write changes on the schedule as far in advance as possible.
Organizing everyday items. Have a place for everything, (such as clothing, backpacks, and toys), and keep everything in its place.
Using homework and notebook organizers. Use organizers for school material and supplies. Stress to your child the importance of writing down assignments and bringing home necessary books.
Being clear and consistent. Children with ADHD need consistent rules they can understand and follow.
Giving praise or rewards when rules are followed. Children with ADHD often receive and expect criticism. Look for good behavior and praise it.

For adults:

A professional counselor or therapist can help an adult with ADHD learn how to organize their life with tools such as:

Keeping routines.
Making lists for different tasks and activities.
Using a calendar for scheduling events.
Using reminder notes.
Assigning a special place for keys, bills, and paperwork.
Breaking down large tasks into more manageable, smaller steps so that completing each part of the task provides a sense of accomplishment.

How can I find a clinical trial for ADHD?

Clinical trials are research studies that look at new ways to prevent, detect, or treat diseases and conditions. The goal of clinical trials is to determine if a new test or treatment works and is safe. Although individuals may benefit from being part of a clinical trial, participants should be aware that the primary purpose of a clinical trial is to gain new scientific knowledge so that others may be better helped in the future.

Researchers at NIMH and around the country conduct many studies with patients and healthy volunteers. We have new and better treatment options today because of what clinical trials uncovered years ago. Be part of tomorrow’s medical breakthroughs. Talk to your health care provider about clinical trials, their benefits and risks, and whether one is right for you.

To learn more or find a study, visit:

NIMH’s Clinical Trials webpage : Information about participating in clinical trials
Clinicaltrials.gov: Current Studies on ADHD : List of clinical trials funded by the National Institutes of Health (NIH) being conducted across the country
Join a Study: Children - ADHD : List of studies being conducted on the NIH Campus in Bethesda, MD

Where can I learn more about ADHD?

Free brochures and shareable resources.

Attention-Deficit/Hyperactivity Disorder: What You Need to Know: This brochure provides information about attention-deficit/hyperactivity disorder (ADHD) in children, teens, and adults including symptoms, how it is diagnosed, causes, treatment options, and resources to find help for yourself or your child.
Attention-Deficit/Hyperactivity Disorder in Adults: What You Need to Know : This brochure provides information about attention-deficit/hyperactivity disorder (ADHD) in adults including symptoms, how ADHD is diagnosed, causes, treatment options, and resources to find help for yourself or someone else. Also available en español .
Shareable Resources on ADHD : These digital resources, including graphics and messages, can be used to spread the word about ADHD and help promote awareness and education in your community.
Mental Health Minute: ADHD : Take a mental health minute to learn about ADHD.
NIMH Expert Discusses Managing ADHD : Learn the signs, symptoms, and treatments of ADHD as well as tips for helping children and adolescents manage ADHD during the pandemic.

Federal resources

ADHD : CDC offers fact sheets, infographics, and other resources about the signs, symptoms, and treatment of children with ADHD.
ADHD : (MedlinePlus – also available en español .)

Research and statistics

Journal Articles : This webpage provides information on references and abstracts from MEDLINE/PubMed (National Library of Medicine).
ADHD Statistics : This web page provides statistics about the prevalence and treatment of ADHD among children, adolescents, and adults.

Last Reviewed: September 2023

Unless otherwise specified, the information on our website and in our publications is in the public domain and may be reused or copied without permission. However, you may not reuse or copy images. Please cite the National Institute of Mental Health as the source. Read our copyright policy to learn more about our guidelines for reusing NIMH content.

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ADHD Research Roundup: New Studies, Findings & Insights

Adhd research continues to reveal new insights about attention deficit — its relationship to trauma, race, emotional dysregulation, rejection sensitive dysphoria, and treatments ranging from medication to video games. we’ve curated the most significant news of the past year., adhd research continues to reveal new truths.

ADHD research has produced groundbreaking and impactful discoveries in the past year. Our understanding of the relationship between health care and race has deepened. Alternative treatments, like video games and neurofeedback, are showing encouraging promise while ADHD stimulant medication continues to demonstrate benefits for patients of all ages. The connections between comorbid conditions, gender, and ADHD are better understood than ever before. And we are encouraged by the ongoing work coming from the world’s leading research teams.

Read below to catch up on the most significant news and research from 2020, and stay updated on new findings as they are published by subscribing to ADDitude’s free monthly research digest .

General ADHD Research

Study: Long-Term Health Outcomes of Childhood ADHD are Chronic, Severe November 24, 2020 Childhood ADHD should be considered a chronic health problem that increases the likelihood of adverse long-term health outcomes, according to a population-based birth cohort study of children with ADHD and psychiatric disorders. Further research on the impact of treatment is needed.

Study: Living with ADHD Causes Significant Socioeconomic Burden October 21, 2020 Living with ADHD poses a significant economic burden, according to a new study of the Australian population that found the annual social and economic cost of ADHD was $12.76 billion, with per person costs of $15,664 over a lifetime.

Study: Unmedicated ADHD Increases the Risk of Contracting COVID-19 July 23, 2020 The COVID-19 infection rate is nearly 50% higher among individuals with unmedicated ADHD compared to individuals without ADHD , according to a study of 14,022 patients in Israel. The study found that ADHD treatment with stimulant medication significantly reduces the risk of virus exposure among individuals with ADHD symptoms like hyperactivity and impulsivity.

[ Does My Child Have ADHD? Take This Test to Find Out ]

Study: Poverty Increases Risk for ADHD and Learning Disabilities March 23, 2020 Children from families living below the poverty level, and those whose parents did not pursue education beyond high school, are more likely to be diagnosed with ADHD or learning disabilities, according to a new U.S. data brief that introduces more questions than it answers.

ADHD and Children

Study: Diagnosed and Subthreshold ADHD Equally Impair Educational Outcomes in Children December 21, 2020 Children with diagnosed and subthreshold ADHD both experienced impaired academic and non-academic performance compared to controls used in an Australian study examining the two community cohorts.

Study: Children with ADHD More Likely to Bully — and to Be Bullied November 23, 2020 Children with ADHD are more likely than their neurotypical peers to be the bully, the victim of bullying, or both, according to a new study.

Study: ADHD Symptoms in Girls Diminish with Extracurricular Sports Activity October 16, 2020 Consistent participation in organized sports reliably predicted improved behavior and attentiveness in girls with ADHD, according to a recent study of elementary school students active — and not active — in extracurricular activities. No such association was found for boys with ADHD.

[ Do I Have ADHD? Take This Test to Find Out ]

Study: ADHD in Toddlers May Be Predicted by Infant Attentional Behaviors August 12, 2020 Infants who exhibit behaviors such as “visually examining, acting on, or exploring nonsocial stimuli including objects, body parts, or sensory features” may be more likely to demonstrate symptoms of ADHD as a toddler, according to a new study that also found a correlation between this Nonsocial Sensory Attention and later symptoms of executive dysfunction.

Study Shows Gender Disparities in ADHD Symptoms of Hyperactivity and Poor Response Inhibition June 26, 2020 Girls with ADHD are less physically hyperactive than are boys with the condition, and experience fewer problems with inhibition and cognitive flexibility, according to a new meta-analysis that says more accurate screening tools are needed to recognize the subtler manifestations of ADHD in girls.

Study: Raising a Child with ADHD Negatively Impacts Caregivers’ Mental Wellbeing July 27, 2020 Caring for a child with ADHD negatively impacts caregivers’ quality of sleep, relationships, and satisfaction with free time, among other indicators of mental wellbeing, according to a recent study from the United Kingdom. The significant deficit in sleep and leisure satisfaction led researchers to conclude that caregivers may benefit from greater support — for example, coordinated health and social care — that focuses on these areas.

Study: ADHD, Diet, Exercise, Screen Time All Directly or Indirectly Impact Sleep July 27, 2020 A child with ADHD is more likely to experience sleep problems, in part because ADHD symptoms influence diet and physical activity — two factors that directly impact sleep. This finding comes from a new study that also shows how screen time impacts exercise, which in turn impacts sleep. Understanding these interwoven lifestyle factors may help caregivers and practitioners better treat children with ADHD.

ADHD and Adolescents

Teens with ADHD Should Be Regularly Screened for Substance Use Disorder: International Consensus Reached July 17, 2020 Adolescents with ADHD should be regularly screened for comorbid substance use disorder, and vice versa. This was one of 36 statements and recommendations regarding SUD and ADD recently published in the European Research Addiction Journal.

Study: Girls with ADHD Face Increased Risk for Teen Pregnancy February 12, 2020 Teenagers with ADHD face an increased risk for early pregnancy, according to a new study in Taiwan. However, long-term use of ADHD medications does reduce the risk for teen pregnancies. Researchers suggested that ADHD treatment reduces the risk of any pregnancy and early pregnancy both directly by reducing impulsivity and risky sexual behaviors and indirectly by lowering risk and severity of the associated comorbidities, such as disruptive behavior and substance use disorders.

Study: Teens with ADHD Face Increased Risk for Nicotine Addiction January 27, 2020 Young people with ADHD find nicotine use more pleasurable and reinforcing after just their first smoking or vaping experience, and this may lead to higher rates of dependence, according to findings from a new study published in the Journal of Neuropsychopharmacology .

Study: Adolescent Health Risks Associated with ADHD Go Unmonitored by Doctors February 27, 2020 The health risks facing adolescents with ADHD — teen pregnancy, unsafe driving, medication diversion, and more — are well documented. Yet, according to new research, primary care doctors still largely fail to address and monitor these urgent topics during their patients’ transition to young adulthood.

Study: Emotional Dysregulation Associated with Weak, Risky Romantic Relationships Among Teens with ADHD May 20, 2020 Severe emotional dysregulation increases the chances that an adolescent with ADHD will engage in shallow, short-lived romantic relationships and participate in unprotected sex, according to a new study that suggests negative patterns developed in adolescence may continue to harm the romantic relationships and health of adults with ADHD .

ADHD and Adults

Study: Discontinuing Stimulant Medication Negatively Impacts Pregnant Women with ADHD December 17, 2020 Women with ADHD experience negative impacts on mood and family functioning when they discontinue stimulant medication use during pregnancy, according to a new observational cohort study that suggests medical professionals should consider overall functioning and mental health when offering treatment guidance to expectant mothers.

New Study: Adult ADHD Diagnosis Criteria Should Include Emotional Symptoms April 21, 2020 The ADHD diagnosis criteria in the DSM-5 does not currently include emotional symptoms, despite research indicating their importance. Now, a new replication analysis has found that ADHD in adults presents in two subtypes: attentional and emotional. Researchers suggest that this system offers a more clinically relevant approach to diagnosing ADHD in adults than does the DSM-5 .

Study: Stimulant ADHD Medication Relatively Safe and Effective for Older Adults June 30, 2020 Older adults with ADHD largely experience symptom improvement when taking a low dose of stimulant medication, which is well tolerated and does not cause clinically significant cardiovascular changes. This is the finding of a recent study examining the effects of stimulant medication among adults aged 55 to 79 with ADHD, some of whom had a pre-existing cardiovascular risk profile.

ADHD, Race, and Culture

Study Explores Medication Decision Making for African American Children with ADHD June 23, 2020 In a synthesis of 14 existing studies, researchers have concluded that African American children with ADHD are significantly less likely than their White counterparts to treat their symptoms with medication for three main reasons: caregiver perspectives on ADHD and ADHD-like behaviors; beliefs regarding the risks and benefits associated with stimulant medications; and the belief that ADHD represents a form of social control.

Culturally Adapted Treatment Improves Understanding of ADHD In Latinx Families August 31, 2020 Latinx parents are more likely to recognize and understand ADHD after engaging in culturally adapted treatment (CAT) that includes parent management training sessions adapted to be more culturally appropriate and acceptable, plus home visits to practice skills. This recent review of ADHD knowledge among Latinx parents found that CAT outperformed evidence-based treatment (EBT) in terms of parent-reported knowledge of ADHD.

Treating ADHD

Study: New Parent Behavior Therapy Yields Longer ADHD Symptom Control in Children October 6, 2020 ADHD symptom relapse was significantly reduced in children of parents who participated in a new schema-enhanced parent behavior therapy, compared to those whose parents participated in standard PBT.

Research: Physical Exercise Is the Most Effective Natural Treatment for ADHD — and Severely Underutilized January 22, 2020 A new meta-analysis shows that physical exercise is the most effective natural treatment for controlling ADHD symptoms such as inhibition, attention, and working memory . At the same time, a comprehensive study reveals that children with ADHD are significantly less likely to engage in daily physical activity than are their neurotypical peers.

A Video Game Prescription for ADHD? FDA Approves First-Ever Game-Based Therapy for Attention June 18, 2020 Akili Interactive’s EndeavorRx is the first game-based digital therapeutic device approved by the FDA for the treatment of attention function in children with ADHD. The history-making FDA OK followed a limited-time release of the device during the coronavirus pandemic, and several years of testing the device in randomized controlled trials.

Study: Neurofeedback Effectively Treats ADHD April 9, 2020 Neurofeedback is an effective treatment for ADHD , according to a new quantitative review that used benchmark studies to measure efficacy and effectiveness against stimulant medication and behavior therapy. These findings relate to standard neurofeedback protocols, not “unconventional” ones, for which significant evidence was not found.

Study: Mindfulness-Enhanced Behavioral Parent Training More Beneficial for ADHD Families June 29, 2020 Behavioral parent training (BPT) enhanced with mindfulness meditation techniques provides additional benefits to parents of children with ADHD, such as improved discipline practices and parental behavioral regulation. This is the finding of a new randomized control trial conducted by researchers who compared mindfulness-enhanced to standard BPT.

Mapping the ADHD Brain: MRI Scans May Unlock Better Treatment and Even Symptom Prevention March 9, 2020 Brain MRI is a new and experimental tool in the world of ADHD research. Though brain scans cannot yet reliably diagnose ADHD, some scientists are using them to identify environmental and prenatal factors that affect symptoms, and to better understand how stimulant medications trigger symptom control vs. side effects.

New Clinical Guidelines: Holistic Treatment Is Best for Children with ADHD and Comorbidities February 3, 2020 The Society for Developmental and Behavioral Pediatrics (SDBP) says that children and teens with ADHD plus comorbidities should receive psychosocial treatment, such as classroom-based management tools, in addition to ADHD medication.

Study: Mindfulness Exercises Effectively Reduce Symptoms in Boys with ADHD and ODD May 19, 2020 Boys with both ADHD and ODD were less hyperactive and more attentive after attending a multi-week mindfulness training program, according to a new study that finds promise in this treatment as a viable complement or alternative to medication.

ADHD and Comorbid Conditions

Study: Risk for Diabetes 50% Higher for Adults with ADHD October 23, 2020 A diagnosis of ADHD increased the likelihood of diabetes by as much as 50% for adults with ADHD, according to a recent study from the National Health Interview Survey that found the strong correlation independent of BMI.

Study: ADHD Symptoms Associated with More Severe Gambling Disorder and Emotional Dysregulation January 28, 2020 Roughly one-fifth of individuals diagnosed with gambling disorder in the study also tested positive for ADHD symptoms. This population is more likely to experience severe or acute symptoms of gambling disorder, which is tied to higher emotional dysregulation, according to a new study of 98 Spanish men.

ADHD Research: Next Steps

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ADHD: Latest Research

Attention deficit hyperactivity disorder (ADHD) was first described in 1902, and research on it continues to this day. Here’s what some of the most recent studies say about ADHD symptoms , diagnosis, treatment, and more.

The Power of Exercise

A recent review of studies suggested that exercise was the most effective nondrug way to improve mental skills often affected by ADHD . These include things like attention span and working memory. Another study found that aerobic exercise may help children with ADHD think flexibly, or adjust to new situations more easily. Another study looked at kids 6 to 10 years old. It found that girls with ADHD who regularly took part in after-school sports had milder symptoms by age 12, compared to girls who played sports less often.

ADHD and Race

A review of studies looked at more than 150,000 Black people in the United States and found that about 15% had ADHD. The researchers who did the review said this suggests that the disorder is more common -- not less, as other estimates say -- among Black people, compared to the general U.S. population. They said their findings show a need for more ADHD testing among Black people from different social backgrounds.

Does Girls’ ADHD Look Different?

A review of studies compared the ADHD symptoms of boys and girls. The results showed that boys tended to be more hyperactive, had more trouble adjusting mentally to new situations, and found it harder to stop themselves from making certain body movements. The researchers said one of the takeaways of their review is that there needs to be more research into how ADHD can look different in girls.

Could Strep Throat Make Children’s ADHD Worse?

A recent study suggested that the bacteria that causes strep throat might make a couple of ADHD symptoms worse in kids. The researchers found that children with ADHD who’d gotten an infection from the bacteria appeared to become more hyperactive and impulsive. But the study only showed a link. It didn’t prove cause and effect.

An Alarming Trend With Teens?

A recent study found that the number of 13- to 19-year-olds that abuse stimulant drugs for ADHD was on the rise in years past. Between 1998 and 2005, the American Association of Poison Control Centers saw a 76% hike in calls about teens abusing these prescription meds. The researchers suggested that this is still a growing problem today. If you have a teenager that takes a stimulant medication for ADHD, make sure they take it exactly as prescribed.

ADHD During College

A recent study looked at how college students with ADHD did academically, compared to those without the disorder. It found that the students with ADHD had lower grade point averages. Also, more students without the disorder completed college than those with ADHD who didn’t take meds for it.

The researchers said their findings highlight the need for students with ADHD to get academic support services before they go to college. They said the support should focus on boosting mental skills like planning and organization. It should also treat any symptoms of depression .

A Tech Treatment Shows Promise

A review of research found that the alternative treatment neurofeedback seemed to lessen children’s ADHD symptoms, as rated by their parents and teachers.

During neurofeedback, a technician places small devices on your forehead called electrodes -- they’re not painful. Then the technician asks you to respond to cues, like a beep or a special video game, while they track your brain activity. The idea is that this may teach you to harness your brain’s electrical activity and boost your attention span. The researchers who did the recent study said most people need 30 to 40 sessions of neurofeedback, and it may cost $4,000 to $6,000.

ADHD Linked to Suicide Attempts

A Canadian study found that adults with ADHD were more likely to try to take their own lives than those who don’t have the disorder. The researchers also found that 1 in 4 women with ADHD had made a suicide attempt. If you’re concerned that someone you care about is thinking of taking their own life, you can call the National Suicide Prevention Lifeline at 800-273-TALK (800-273-8255) for help.

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Review Article
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Published: 11 June 2018

Genetics of attention deficit hyperactivity disorder

Stephen V. Faraone ORCID: orcid.org/0000-0002-9217-3982 1 &
Henrik Larsson 2 , 3

Molecular Psychiatry volume 24 , pages 562–575 ( 2019 ) Cite this article

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Neuroscience

Decades of research show that genes play an vital role in the etiology of attention deficit hyperactivity disorder (ADHD) and its comorbidity with other disorders. Family, twin, and adoption studies show that ADHD runs in families. ADHD’s high heritability of 74% motivated the search for ADHD susceptibility genes. Genetic linkage studies show that the effects of DNA risk variants on ADHD must, individually, be very small. Genome-wide association studies (GWAS) have implicated several genetic loci at the genome-wide level of statistical significance. These studies also show that about a third of ADHD’s heritability is due to a polygenic component comprising many common variants each having small effects. From studies of copy number variants we have also learned that the rare insertions or deletions account for part of ADHD’s heritability. These findings have implicated new biological pathways that may eventually have implications for treatment development.

Polygenic profiles define aspects of clinical heterogeneity in attention deficit hyperactivity disorder

Differences in the genetic architecture of common and rare variants in childhood, persistent and late-diagnosed attention-deficit hyperactivity disorder

Shared genetic background between children and adults with attention deficit/hyperactivity disorder

Attention deficit hyperactivity disorder (ADHD) is a childhood-onset condition with impairing symptoms of inattention, impulsivity, and hyperactivity. Decades of research have documented and replicated key facts about the disorder (for a review, see ref. [ 1 ]). It occurs in about 5% of children with little geographic or cross-cultural variation in prevalence and often co-occurs with other conditions, including mood, anxiety, conduct, learning, and substance use disorders. Longitudinal studies show that two-thirds of ADHD youth will continue to have impairing symptoms of ADHD in adulthood. People with ADHD are at risk for a wide range of functional impairments: school failure, peer rejection, injuries due to accidents, criminal behavior, occupational failure, divorce, suicide, and premature death. Although many details of ADHD’s pathophysiology are unknown, neuropsychological and neuroimaging studies implicate brain circuits regulating executive functioning, reward processing, timing, and temporal information processing.

This article reviews data about the role that genes play in the etiology of ADHD from two perspectives. Family, twin, and adoption studies provide a firm foundation for asserting that genes are involved in the etiology of ADHD. The view from molecular genetics provides a basis for understanding mechanisms whereby genes affect biological pathways that lead to ADHD.

Family, twin and adoption studies of ADHD

Evidence for heritability from family, adoption, and twin studies.

A study of 894 ADHD probands and 1135 of their siblings aged 5–17 years old found a ninefold increased risk of ADHD in siblings of ADHD probands compared with siblings of controls [ 2 ]. Adoption studies suggest that the familial factors of ADHD are attributable to genetic factors rather than shared environmental factors [ 3 , 4 ] with the most recent one reporting rates of ADHD to be greater among biological relatives of non-adopted ADHD children than adoptive relatives of adopted ADHD children. The adoptive relatives had a risk for ADHD like the risk in relatives of control children [ 4 ].

Twin studies rely on the difference between the within-pair similarities of monozygotic (MZ) twin pairs, who are genetically identical, and dizygotic (DZ) twin pairs, who share, on average, 50% of their segregating genes. The mean heritability across 37 twin studies of ADHD or measures of inattentiveness and hyperactivity is 74% (Fig. 1 ). A similar heritability estimate of around 80% was seen in a study of MZ and DZ twins, full siblings, and maternal and paternal half-siblings [ 5 ]. The heritability is similar in males and females and for the inattentive and hyperactive-impulsive components of ADHD [ 6 , 7 , 8 ].

Heritability of ADHD from twin studies of ADHD diagnoses or symptom counts [ 153 , 154 , 155 , 156 , 157 , 158 , 159 , 160 , 161 , 162 , 163 , 164 , 165 , 166 , 167 , 168 , 169 , 170 , 171 , 172 , 173 ]

Only a few of the twin studies in Fig. 1 used categorical measures of ADHD [ 9 , 10 , 11 , 12 ]. Their heritability estimates range from 77 to 88%, which is consistent with the larger number of studies using symptom count measures of ADHD. Twin studies have explored whether ADHD is best viewed as a categorical disorder or as an extreme of a continuous trait. A study of 16,366 Swedish twins found a strong genetic link between the extreme and the sub-threshold variation of DSM-IV ADHD symptoms [ 13 ]. This study confirmed an early study of 583 same-sexed twin pairs using ADHD-III-R symptoms [ 14 ]. Both studies suggest that the diagnosis of ADHD is the extreme of a continuous distribution of ADHD symptoms in the population and that the etiologic factors involved in the disorder also account for the full range of symptoms. These data are consistent with clinical studies showing the clinical implications of subthreshold ADHD [ 15 ].

ADHD’s clinical features and course

Reporter effects.

Parent and teacher ratings of ADHD symptoms result in high heritability estimates (70–80%) [ 6 ]. In contrast, studies using self-ratings in adolescence and adulthood show lower heritabilities (<50%) [ 16 , 17 , 18 , 19 ]. Two twin studies examined these rater effects [ 20 , 21 ]. They showed that self-ratings, as well as different-parent and different-teacher ratings within twin pairs, were associated with lower heritability estimates (~30–40%) compared with heritabilities based on same-parent and same-teacher ratings (~70–80%) [ 20 , 21 , 22 ]. Low reliability of self-reports may explain why heritability estimates are lower in studies of self-rated ADHD symptoms. Using different informants for ADHD symptom ratings of each twin in a pair introduces rater effects (i.e., each rater experiences and reports different ADHD symptoms) or rater bias (i.e., a rater consistently over- or underestimates ADHD symptoms or similarities between twins). These effects could explain why heritability estimates are lower in studies relying on different informants for each twin in a pair compared with studies using the same raters [ 23 ].

Developmental effects

The first twin studies of ADHD in adults used self-reports and estimated heritability at 30–40% (Fig. 2) , (e.g. [ 24 ]), which is substantially lower than the heritability among children and adolescents. In contrast, one study estimated heritability to be 80% after combining self and parent ratings into a composite index of ADHD. Another study found the heritability of clinically diagnosed ADHD in adults to be 72% [ 25 ]. These findings (Fig. 2 ) suggest that the heritability of ADHD is stable during the transition from childhood into adulthood. They explain previous reports of low heritability for ADHD symptoms in adults as due to measurement error from rater effects. The higher heritabilities for clinically diagnosed adult ADHD confirm family studies suggesting that persistent ADHD is highly familial [ 5 , 26 , 27 ].

Heritability of ADHD in adults depends on method of diagnosis

Twin studies show that both stable and dynamic genetic risk factors influence ADHD over the course of the development from childhood to early adulthood [ 7 , 28 , 29 , 30 ]. These study findings explain the developmental structure of genetic risk factors for ADHD with both stable and dynamic processes. The stable component of the genetic risk suggests that persistent ADHD and its pediatric form are genetically linked. The dynamic component suggests that the set of genetic variants accounting for the onset of ADHD differs from those accounting for the persistence and remission of the disorder. For a review of the genetics of adult ADHD, see Franke et al. [ 26 ].

Psychiatric comorbidity

Multivariate twin and sibling studies have found a general genetic factor that influences ADHD and a broad spectrum of neuropsychiatric conditions [ 31 , 32 ]. These studies have shown that a latent shared genetic factor accounts for up to 45% of co-variance across childhood externalizing, internalizing, and phobia symptoms [ 31 , 33 ] and 31% of co-variance in childhood neurodevelopmental symptoms [ 34 ]. Similar results have been reported for register-based clinical diagnoses, with one study showing that a general genetic factor explained 10–36% of disorder liability across several psychiatric diagnoses [ 32 ]. Two studies have assessed the contribution of measured genetic variants for a general psychopathology dimension. One study estimated the SNP-heritability as 18% for maternal ratings of total problems on the Child Behavior Checklist, which measures internalizing, externalizing, and attention problems [ 35 ]. Similarly, another study estimated the SNP heritability as 38% for a general psychopathology factor derived from childhood psychopathology symptoms assessed by multiple raters [ 36 ]. These studies also support spectrum-specific genetic factors, such as genetic factors that load specifically on externalizing disorders [ 31 ]. The finding of externalizing-specific genetic factors for ADHD is consistent with a large number of twin and family studies demonstrating genetic overlaps of ADHD with oppositional-defiant disorder symptoms [ 37 ], conduct disorder [ 38 ], antisocial behavior [ 39 ], and substance use problems [ 40 , 41 , 42 ].

Twin studies have tested for genetic overlap between ADHD and autism spectrum disorders (ASD) [ 43 , 44 ], which often co-occur [ 45 ]. Studies of community samples of youth, from the United States of America [ 46 ], the United Kingdom [ 47 ], and Sweden [ 11 , 48 ] show that genetic factors influence this comorbidity. Ronald et al. [ 47 ]. found genetic correlations between ADHD and ASD above 0.50. Similar results have been found in adult twin studies [ 49 ]. A register-based study in Sweden found that individuals with ASD and their relatives were at increased risk of ADHD. The pattern of association across relatives supported the existence of a genetic overlap between clinically ascertained ASD and ADHD [ 50 ]. Some features of ASD are differentially linked to either the inattentive or the hyperactive-impulsive components of ADHD [ 51 , 52 ]. For instance, Polderman et al. [ 51 ]. found that the symptoms reflecting the repetitive and restricted aspects of ASD showed the strongest genetic association with ADHD and a Swedish twin study found that the subcomponents of ADHD and ASD are influenced by specific genetic factors [ 48 ].

Fewer studies have explored how genetic factors contribute to the co-occurrence between ADHD and internalizing disorders. A large family study found an increased risk of attempted and completed suicide in first- and second-degree relatives of ADHD probands [ 53 ]. The pattern of familial risks across different levels of relatedness suggests that shared genetic factors are important for these associations [ 53 ]. Family studies that studied the association between ADHD and depression suggest that the co-occurrence is influenced by shared familial factors [ 54 , 55 ]. Twin studies of this issue suggest that shared genetic factors explain the overlap of ADHD with depression, anxiety, and internalizing symptoms [ 56 , 57 , 58 , 59 , 60 ]. For example, Cole et al. [ 59 ]. found that shared genetic factors explained most of the association between traits of ADHD and depression. Similar results were found by Spatola et al. [ 60 ]., who used a multivariate twin analysis to study the overlap between different subscales of the Child Behavior Check List (CBCL), such as affective problems, anxiety problems, and attention-deficit/hyperactivity problems.

In contrast to the wealth of information about the familial co-transmission of ADHD and many other disorders, very little is known about ADHD’s familial links to intellectual disability (ID). A meta-analysis reported that the intelligence quotient (IQ) of youth with ADHD is nine points lower than typically developing peers [ 61 ] and much evidence suggests it is valid to diagnose ADHD in the context of ID [ 62 ]. Faraone et al. [ 63 ] studied the genetic association of ADHD and ID in Swedish medical registry data. Individuals with ID were at increased risk for ADHD and relatives of ID cases had an increased risk for ADHD compared with relatives of those without ID. Model fitting analyses attributed 91% of the correlation between the liabilities of ADHD and ID to genetic factors. This work attributes nearly all the comorbidity between ADHD and ID to genetic factors. Only a few twin and family studies have explored how genetic factors contribute to non-psychiatric comorbidity. The literature suggests novel etiologic links with asthma [ 64 ], obesity [ 65 ], and epilepsy [ 66 ].

The search for common genetic variants

Genetic linkage studies.

Genetic linkage was the first genome-wide method applied to ADHD. This method searches the genome for evidence that a segment of DNA is transmitted with a disorder within families. A review of the linkage literature found substantial disagreement about which chromosomal regions are linked to ADHD [ 67 ]. Although there is some overlap in “suggestive” findings, no finding met genome-wide significance [ 68 ]. To make sense of these results, Zhou et al. [ 69 ] applied Genome Scan Meta-Analysis. They found genome-wide significant linkage for a region on chromosome 16 between 64 Mb and 83 Mb. Because the linkage method only detects genetic variants that have large effects, the paucity of significant findings for other loci suggests that common DNA variants having a large effect on ADHD are unlikely to exist. Nearly all ADHD linkage studies have selected either sibling pairs or small families from outbred populations. Another approach is to assess for linkage in multigenerational population isolates. Arcos-Burgos et al. [ 70 ] used this strategy to study 16 multi-generational families from Colombia. In some of these families, they found evidence supporting linkage to chromosomes 4q13.2, 5q33.3, 8q11.23, 11q22, and 17p11. one region implicated LPHN3 . For a review of supporting evidence, see ref. [ 71 ].

Candidate gene association studies

Early molecular genetic studies of ADHD sought to associate ADHD with genes that had some a priori plausibility as being involved in its etiology. Because the drugs that treat ADHD target dopaminergic or noradrenergic transmission, many studies examined “candidate genes” in these pathways. Results were frequently contradictory [ 26 , 67 ]. In the meta-analyses of Gizer et al. [ 72 ], eight candidate DNA variants showed a statistically significant association with ADHD across multiple studies. These variants implicated six genes: the serotonin transporter gene ( 5HTT ), the dopamine transporter gene ( DAT1 ), the D4 dopamine receptor gene ( DRD4 ), the D5 dopamine receptor gene ( DRD5 ), the serotonin 1B receptor gene ( HTR1B ) and a gene coding for a synaptic vesicle regulating protein known as SNAP25 . A meta-analysis covering all genetic association studies of adults with ADHD reported a significant association between adult ADHD and BAIAP2 (brain-specific angiogenesis inhibitor 1-associated protein 2). BAIAP2 is involved in neuronal proliferation, survival, and maturation and dendritic spine morphogenesis and may affect neuronal growth-cone guidance. These findings were significant even after Bonferroni correction [ 73 ]. For both the child and adult meta-analyses, the strength of each association, as measured by the odds ratio, is small, less than 1.5.

Many studies examined the dopamine transporter gene ( SLC6A3) , especially a 40-base pair variable number of tandem repeats regulatory polymorphism located in the 3′-untranslated region of the gene. This variant produces two common alleles with 9- and 10-repeats (9R and 10R). In humans, the 10R allele of this polymorphism has been associated with ADHD in youth [ 67 ] while the 9R allele is associated with ADHD in adults [ 74 ]. A meta-analysis showed that the 9R allele is associated with increased DAT activity in human adults as measured by positron emission tomography [ 75 ].

Genome-wide significant common variants

Genome-wide association studies (GWAS) scan the entire genome to detect common DNA variants having very small etiologic effects. By “common” we mean greater than 1% of the population. To do this, GWAS assay hundreds of thousands or even millions of single nucleotide polymorphisms (SNPs). Doing so has a statistical cost: to assert genome-wide statistical significance, an observed association must have a p value less than 0.00000005. This stringent p value needs very large samples.

The initial GWAS of ADHD [ 76 , 77 , 78 , 79 , 80 , 81 , 82 , 83 , 84 , 85 , 86 ] did not discover any DNA variants that achieved genome-wide significance, even when most of these samples were combined in meta-analysis having a sample size of 2064 trios (two parents and an ADHD child), 896 ADHD patients, and 2455 controls [ 87 ]. That study did find statistical significance for a group of candidate genes previously nominated by members of the International Multisite ADHD Genetics (IMAGE) project [ 88 ]. For a review of early GWAS studies, see Franke et al. [ 89 ]. Examination of the “molecular landscape” derived from the top findings from these initial GWAS studies along with other data concluded that genes regulating directed neurite outgrowth were strongly implicated in the etiology of ADHD [ 90 ]. Pathway and gene set analyses of GWAS data implicated pathways involved in the regulation of neurotransmitter release, neurite outgrowth and axon guidance as contributors to the etiology of ADHD [ 91 , 92 , 93 ].

A consortium of ADHD researchers completed a GWAS meta-analysis of 12 studies comprising 20,183 people with ADHD and 35,191 controls. For methodologic details about the studies contributing data to this meta-analysis, see Demontis et al. [ 94 ]. Twelve loci achieved genome-wide significance. None of the genome-wide significant SNPs showed significant heterogeneity between studies. Among the implicated genes, FOXP2 is especially notable because prior work had implicated it in adult ADHD (Ribases, 2012 #26445) and in speech and language disorders [ 95 ]. A FOXP2 knockout mouse study found that the gene regulates dopamine in ADHD-associated brain regions [ 96 ].

As described by Demontis et al. [ 94 ], other genes implicated by the genome-wide significant loci have relevant biological roles. DUSP6 regulates neurotransmitter homeostasis by affecting dopamine levels in the synapses. SEMA6D is expressed in the brain. It regulates neuronal wiring during embryonic development. ST3GAL3 harbors missense mutations associated with ID. LINC00461 is expressed in brain and includes variants associated with educational attainment. Another gene implicated at that locus is MEF2C , which has been associated with ID and several psychiatric disorders.

The consortium conducted several gene set analyses including three sets of genes regulated by FOXP2 : (1) genes enriched in wild-type versus control FOXP2 knockout mouse brains; (2) genes showing differential expression in wild-type versus FOXP2 knockout mouse brains; and (3) genes enriched in basal ganglia or inferior frontal cortex from human fetal brain samples. None of these sets were associated with ADHD. Also, non-significant was a set of candidate genes for ADHD previously proposed by a panel of ADHD experts [ 88 ]. Among these, only SLC9A9 showed a weak association with ADHD. No Gene Ontology gene sets attained statistical significance but a set of genes showing high intolerance to loss of function did associate with ADHD.

Common variant ADHD as a polygenic disorder

The GWAS analyses also showed that much of ADHD’s heritability is due to the polygenic effects of many common variants each having very small effects. The SNP heritability was 0.22, which is about one-third of ADHD’s heritability computed from twin studies [ 97 ]. The polygenic architecture for ADHD was confirmed by estimating polygenic risk scores in one subset of the sample and showing that it predicted ADHD, in a dose-dependent manner, in a validation subset. As seen for other psychiatric disorders [ 98 ], the variance explained by these risk scores was low (5.5%).

Further evidence for the validity of the ADHD’s polygenic background comes from analyses showing that the relevant SNPs were enriched for annotations implicating conserved regions of the genome (which are known to have biological significance) and for regulatory elements specific to the central nervous system. The discovery of a polygenic susceptibility to ADHD does not show which DNA variants comprise the susceptibility. It does, however, support the idea that more genome-wide significant variants will be discovered in larger samples.

Martin et al. [ 99 ] showed that ADHD’s polygenic liability derived from a clinical sample predicted ASD traits in a population sample, which confirms twin study data [ 48 , 51 ] and gene set analyses [ 100 ] showing genetic overlap between ADHD and ASDs. The polygenic liability score derived from Martin et al.’s ADHD case-control clinical sample also predicted both inattention and hyperactivity in the general population. This latter finding was replicated by Groen-Blokhuis et al. [ 101 ] who found that ADHD polygenic risk scores significantly predicted both parent and teacher ratings of attention in preschool- and school-aged children in the population. Likewise, Stergiakouli et al. [ 102 ] showed that the polygenic liability for ADHD traits in a population sample predicted ADHD clinical diagnoses in a case-control study. These results confirmed conclusions from twin studies that the liability for clinically defined ADHD is the extreme of a trait that varies continuously in the population [ 13 ].

Other polygenic score studies are confirming cross-disorder genetic associations previously predicted by family and twin studies. We have long known that ADHD co-occurs with conduct disorder. Both family and twin studies have implicated shared genes in this association [ 38 , 103 , 104 , 105 ]. Consistent with this prior work, Hamshere et al. [ 106 ] reported a high polygenic risk for ADHD among children with comorbid conduct problems. In a large population study, Larsson et al. [ 107 ] reported that the relatives of ADHD individuals had an increased risk for schizophrenia and bipolar disorder. Consistent with that report, the polygenic risk score derived from a large GWAS of schizophrenia significantly discriminated ADHD cases from controls [ 108 ]. This discrimination was strongest for alleles that were risk alleles for both adult schizophrenia and adult bipolar disorder, which confirms prior family and twin data suggesting a genetic link between ADHD and bipolar disorder [ 109 ]. Moreover, a joint GWAS of ADHD and bipolar disorder reported a significant correlation between the polygenic scores of ADHD and bipolar disorder and also identified genome-wide significant loci for the two disorders [ 110 ]. Similarly, prior reports of familial co-transmission of ADHD and depression [ 54 ] have been extended by showing shared SNP heritability between the two disorders [ 98 ]. Using a novel drug challenge paradigm, Hart et al. [ 111 ] found that the polygenic scores for both schizophrenia and ADHD were associated with the euphoric response to amphetamine, which suggests that the genetic association between these disorders may be due to variants in the neural systems regulating the euphoric response to amphetamine.

Using GWAS results from many studies, it is possible to compute genetic correlations that indicate the degree to which the polygenic architectures of two disorders or traits overlap. When Demontis et al. [ 94 ] correlated ADHD’s polygenic risk with 220 disorders and traits, many highly significant correlations emerged. Figure 3 shows some of the most significant of these correlations (each passing the Bonferroni significance threshold). Some of these genetic correlations fit with prior expectations (e.g., with neuroticism, depression and the cross disorder GWAS). Others are consistent with the clinical epidemiology of ADHD (e.g., with obesity, IQ, smoking and school achievement). In some cases, these significant correlations offer new directions for understanding comorbidity. For example, some have interpreted the comorbidity between ADHD and obesity, which has been confirmed via meta-analysis [ 112 ], as being caused by the impulsivity associated with ADHD. The genetic correlation data suggest that shared genetic risk factors, and an underlying shared pathophysiology, account for this comorbidity.

Genetic correlations of ADHD with other traits based on LD score regression

Some of the genetic correlations in Fig. 3 are entirely novel. These include ADHD’s genetic correlations with medical outcomes (lung cancer, coronary artery disease, parents’ age at death) and with demographics (number of children in the family, age first child born). There are, however, some consistent findings in the prior literature, which suggest that people with ADHD are more likely to have larger families [ 113 ] and more likely to die prematurely [ 114 ].

The search for rare genetic variants

Initially, information about rare DNA variants (<1% of the population) came from reports of syndromic chromosomal anomalies associated with multiple medical and psychiatric problems along with ADHD. Examples are velo-cardio facial syndrome fragile-X syndrome, Turner syndrome, tuberous sclerosis, neurofibromatosis, Klinefelter syndrome, and Williams syndrome (Fig. 4 ). In a single family, a peri-centric inversion of chromosome 3 co-segregating with ADHD symptoms [ 115 , 116 ] implicated SLC9A9 . Mutations of that gene lead to an animal model of ADHD [ 117 , 118 ] and have been associated with both autism [ 119 , 120 ] and ADHD [ 121 ].

Prevalence of ADHD in rare genetic syndromes

The common variant genotyping arrays used in GWAS studies can detect large copy number variants (CNVs). Because CNVs often delete or duplicate a large genomic segment spanning part of a gene or even entire genes, they often have clear implications for gene functioning. Studies of CNVs in ADHD assessed ADHD youth and controls for the presence of large (>500 kb), rare CNVs [ 77 , 122 , 123 , 124 , 125 , 126 , 127 ]. Each study, except one, found an odds ratio greater than one, indicating a greater burden of large, rare CNVs among ADHD patients compared with controls. The discrepant study used a different definition of burden [ 125 ]. Only three studies found a statistically significant burden among ADHD patients for large CNVs (for a summary, see Thapar et al. [ 128 ]). As their review shows, deletions and duplications are equally over-represented in ADHD samples although statistical significance emerged only for duplications. Thapar et al. also found enrichment for duplications (but not deletions) previously implicated in schizophrenia and, to a lesser extent, ASDs. The top biological pathways implicated by these CNV studies were: respiratory electron transport, organonitrogen compound catabolic process, transmembrane transporter activity, carbohydrate derivative catabolic process, ligand-gated ion channel activity, methyltransferase activity, transmembrane transport and ion gated channel activity.

A study of 489 ADHD patients and 1285 controls found rare CNVs in the parkinson protein two gene ( PARK2 ) [ 123 ]. The result was significant after empirical correction for genome-wide testing. PARK2 regulates the cell’s ubiquitin-proteasome system which helps dispose damaged, misshapen, and excess proteins. Two other genes involved in this pathway ( FBXO33 and RNF122 ) had been implicated in other studies [ 84 , 129 ]. A study of adult ADHD did not find a significant effect for large CNVs, but did find a significant effect for small CNVs [ 126 ].

The CNV studies have implicated several biological pathways. Williams et al. [ 127 ] found that ADHD patients harbored duplications in the alpha-7 nicotinic acetylcholine receptor gene ( CHRNA7) and showed that the finding replicated in four independent cohorts from the United Kingdom, the United States, and Canada. Another replication was reported in an Italian sample [ 130 ]. The implication of the nicotinic system is particularly interesting given that nicotinic neurons modulate dopaminergic neurons, ADHD patients have a high rate of smoking [ 131 ] and nicotine administration reduces ADHD symptoms [ 132 ]. In a sample of 99 children and adolescents with severe ADHD. Lesch et al. [ 124 ] found several CNVs, including a 3 Mb duplication on chromosome 7p15.2-15.3 harboring neuropeptide Y ( NPY ). Investigation of other family members yielded an association of this duplication with increased NPY plasma concentrations and functional magnetic imaging assessed brain abnormalities.

Thapar et al. [ 128 ] reported biological pathway studies of ADHD CNV data pooled from five studies. These CNV data were enriched for genes previously implicated in schizophrenia, Fragile X intellectual disability and, to a lesser degree, autism. Several biological pathways were significantly enriched in the ADHD CNV findings, most notably ion channel pathways, which had been implicated in cross-disorder analyses of ADHD, autism, schizophrenia, bipolar disorder, and depression [ 133 ]. The CNV analyses also pointed to pathways regulating immune functioning and oxidative stress. These pathways had previously been implicated in ADHD by non-genetic studies, (e.g. refs. [ 134 , 135 , 136 ]).

Elia et al. [ 122 ] showed that CNVs impacting metabotropic glutamate receptor genes were significantly enriched across multiple cohorts of patients. Supporting evidence came from Akutagava-Martins et al. [ 137 ] who reported that CNVs in glutamatergic genes were associated with the cognitive and clinical impairments of ADHD. In a pharmacogenomics GWAS, an SNP in glutamate receptor gene GRM7 was one of the most significant findings [ 138 ]. Glutamatergic defects have been observed in a rat model of ADHD [ 139 , 140 ] and magnetic resonance spectroscopy in humans shows dysregulation of glutamate and glutamate/glutamine concentrations in ADHD patients(e.g. ref. [ 141 ]).

An exome sequencing study of ADHD [ 121 ] reported results for 123 adults with persistent ADHD and 82 healthy controls. Significantly more cases than controls had a rare missense or disruptive variant in a set of ADHD candidate genes. In an exome sequencing study of ADHD patients without a family history of ADHD, Kim et al. [ 142 ] reported six de novo missense SNVs in brain-expressed genes: TBC1D9, DAGLA, QARS, CSMD2, TRPM2 , and WDR83 . They also sequenced 26 genes implicated in ID and ASDs but found only one potentially deleterious variant. In an exome chip study, Zayats et al. [ 143 ] assayed a sample of 1846 cases and 7519 controls to search for rare genetic variants. They detected four study-wide significant loci that implicated four genes known to be expressed in the brain during prenatal stages of development: NT5DC1 , SEC23IP , PSD , and ZCCHC4 . Hawi et al. [ 144 ] found novel rare variants in the BDNF gene by sequencing 117 genes in 152 youth with ADHD and 188 controls.

Pharmacogenetics of ADHD

Several studies have clarified the genetics of the metabolism of ADHD patients. Some patients are slow metbolizers of atomoxetine due to variants in the cytochrome P450 isoenzyme 2D6, which is regulated by the CYP2D6 gene. As a result, the half-life of atomoxetine ranges from 5.2 h in rapid metabolizers to 21.6 h in slow metabolizers [ 145 ]. Some work has looked into CES1 variants regarding the regulation of methylphenidate metabolism and CYP2D6/CYP3A4 variants and the metabolism of ADHD, but the evidence base has not generated consistent results for either children [ 146 ] or adults [ 73 ].

Myer et al. [ 147 ] used meta-analysis to evaluate pharmacogenetic studies of the efficacy response to methylphenidate for the treatment of ADHD. They found 36 studies comprising 3647 ADHD youth treated with methylphenidate. Statistically significant effects were found for: rs1800544 in ADRA2A (odds ratio (OR): 1.69; confidence interval (CI): 1.12−2.55), rs4680 COMT (OR: 1.40; CI: 1.04−1.87), rs5569 SLC6A2 (OR: 1.73; CI: 1.26−2.37), and rs28386840 SLC6A2 (OR: 2.93; CI: 1.76−4.90), and, repeat variants VNTR 4 DRD4 (OR: 1.66; CI: 1.16−2.37) and VNTR 10 SLC6A3 (OR: 0.74; CI: 0.60−0.90). The following variants did not reach statistical significance: rs1947274 LPHN3 (OR: 0.95; CI: 0.71−1.26), rs5661665 LPHN3 (OR: 1.07; CI: 0.84−1.37) and VNTR 7 DRD4 (OR: 0.68; confidence interval: 0.47−1.00). The significant findings were not due to publication biases. Although the odds ratios are small, these findings suggest that a personalized medicine approach to ADHD is a reasonable goal of future research.

Conclusions and future directions

There can be no doubt that DNA variants in genes or regulatory regions increase the risk for ADHD. In rare cases, a single genetic defect may lead to ADHD in the absence of other DNA variants. We do not know how many of these rare variants exist or if such variants require environmental triggers for ADHD to emerge. It is equally clear that no common DNA variants are necessary and sufficient causes of ADHD. Genome-wide association studies show that a genetic susceptibility to ADHD comprised of many common DNA variants accounts for about one-third of the twin study estimates of ADHD’s heritability. We do not know yet which variants or how many of them make up the polygenic component. The heritability that cannot be explained by main effects of rare or common variants is likely due to gene−gene interactions, gene−environment interactions or gene−environment correlations.

The convincing evidence for genes as risk factors for ADHD does not exclude the environment as a source of etiology. The fact that twin estimates of heritability are less than 100% asserts quite strongly that environmental factors must be involved. ADHD’s heritability is high, and that estimate encompasses gene by environment interaction. Thus, it is possible that such interactions will account for much of ADHD’s etiology. Environmental risk factors likely work through epigenetic mechanisms, which have barely been studied in ADHD [ 148 ]. The importance of the environment can also be seen in the fact that, as for other complex genetic disorders, much of ADHD’s heritability is explained by SNPs in regulatory regions rather than coding regions [ 149 ].

Another hypothesis for future research to explore is the possibility that ADHD is an omnigenic disorder. The omnigenic model of Boyle et al. [ 150 ] posits the existence of a small number of “core genes” having “biologically interpretable roles in disease” along with a much greater quantity of “peripheral genes” regulating the core genes. Because there are many more peripheral genes, they account for a greater proportion of the variability in heritability than do the core genes. Because core genes are more likely than peripheral genes to be relevant for developing biomarkers and treatment targets, separating these two classes from one another will require more research.

Gene discovery for ADHD has succeeded but has left us with unexpected results. None of the genome-wide significant findings had been predicted a priori and a set of ADHD candidate genes, implicated primarily by the disorder’s neuropharmacology, did not reach statistical significance. These findings challenge the idea that the core of ADHD’s pathophysiology rests within the machinery of catecholaminergic transmission. Instead, it is possible that the catecholaminergic dysregulation believed to underlie ADHD is a secondary compensation to ADHD’s primary etiology (see discussion by Hess et al. [ 151 ]).

In the years to come, we can expect breakthroughs in the genetics of ADHD to come from several fields of study. Our knowledge of rare variants should increase dramatically as we learn more about CNVs and as reports from exome, full genome and targeted sequencing studies unfold. With the discovery of genome-wide significant common variants, we look forward to studies that discover the functional variants responsible for these findings. With the discovery of these functional variants, we will learn more about the mechanisms whereby genetic risk variants increase the risk for ADHD.

Accumulating evidence from family, twin, and molecular genetic studies suggests that the disorder we know as ADHD is the extreme of a dimensional trait in the population. The dimensional nature of ADHD has wide-ranging implications. If we view ADHD as analogous to cholesterol levels, then diagnostic approaches should focus on defining the full continuum of “ADHD-traits” along with clinically meaningful thresholds for defining who does and does not need treatment and who has clinically subthreshold traits that call for careful monitoring. The dimensional nature of ADHD should also shift the debate about the increases in ADHD’s prevalence in recent years. Instead of assuming that misdiagnoses are the main explanation for the increased prevalence, perhaps researchers should explore to what extent the threshold for diagnosis has decreased over time and whether changes in the threshold are clinically sensible or not. A shift from categorical to dimensional constructs harmonizes with the Research Domain Criteria (RDoC) initiative of the National Institute of Mental Health [ 152 ]. RDoC seeks to define and validate dimensional constructs mediating psychopathology along with the neurobiological underpinnings of these constructs.

Unraveling the genetics of ADHD will be challenging. Technological advances are moving at a rapid pace. The next decade of work should give us more accurate measures of brain structure and function along with much more genomic, transcriptomic and epigenomic data. These advances will set the stage for breakthroughs in our understanding of the etiology of ADHD and in our ability to diagnose and treat the disorder.

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Acknowledgements

Dr. Faraone is supported by the K.G. Jebsen Centre for Research on Neuropsychiatric Disorders, University of Bergen, Bergen, Norway, the European Union’s Seventh Framework Programme for research, technological development and demonstration under grant agreement no. 602805, the European Union’s Horizon 2020 research and innovation programme under grant agreement no. 667302 and NIMH grant 5R01MH101519. Dr. Larsson is supported by the European Union’s Horizon 2020 research and innovation programme under grant agreement no. 667302 and the Swedish Research Council (2013-2280; 2014-3831).

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In the past year, SVF received income, potential income, travel expenses continuing education support and/or research support from Lundbeck, KenPharm, Rhodes, Arbor, Ironshore, Shire, Akili Interactive Labs, CogCubed, Alcobra, VAYA, Sunovion, Genomind, and NeuroLifeSciences. With his institution, he has US patent US20130217707 A1 for the use of sodium−hydrogen exchange inhibitors in the treatment of ADHD. HL has served as a speaker for Eli-Lilly and Shire and has received research grants from Shire.

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Faraone, S.V., Larsson, H. Genetics of attention deficit hyperactivity disorder. Mol Psychiatry 24 , 562–575 (2019). https://doi.org/10.1038/s41380-018-0070-0

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Brain Connectivity Breakthrough Sheds New Light on ADHD

Summary: Researchers have made a pivotal discovery in ADHD research, finding that the disorder’s symptoms are connected to unusual interactions between the brain’s frontal cortex and its deeper information processing centers. By analyzing an unprecedented dataset of over 10,000 functional brain images from youths with and without ADHD, the study uncovers heightened connectivity between key brain areas responsible for learning, emotion, and behavior control.

This research overcomes the limitations of previous smaller studies, offering new, solid evidence of the neural pathways involved in ADHD. These findings not only deepen our understanding of ADHD but also pave the way for developing more targeted and effective treatments.

The study analyzed functional brain connectivity in over 8,000 youths, identifying increased connectivity between deep brain structures and the frontal cortex in those with ADHD.
It provides robust evidence supporting the theory of atypical brain interactions underlying ADHD symptoms, a theory previously suggested but not conclusively proven due to the small scale of past studies.
The research was conducted by the NIH’s NIMH and National Human Genome Research Institute, marking a significant advancement in understanding ADHD’s neural mechanisms.

Source: NIH

Researchers at the National Institutes of Health (NIH) have discovered that symptoms of attention-deficit/hyperactivity disorder (ADHD) are tied to atypical interactions between the brain’s frontal cortex and information processing centers deep in the brain.

The researchers examined more than 10,000 functional brain images of youth with ADHD and published their results in the American Journal of Psychiatry . The study was led by researchers at NIH’s National Institute of Mental Health (NIMH) and National Human Genome Research Institute.

This shows a little girl and brain scans.

Luke Norman, Ph.D., a staff scientist in the NIMH Office of the Clinical Director, and colleagues analyzed brain images supplied by more than 8,000 youth with and without ADHD sourced from six different functional imaging datasets. Using these images, the researchers examined associations between functional brain connectivity and ADHD symptoms.

They found that youth with ADHD had heightened connectivity between structures deep in the brain involved in learning, movement, reward, and emotion (caudate, putamen, and nucleus accumbens seeds) and structures in the frontal area of the brain involved in attention and control of unwanted behaviors (superior temporal gyri, insula, inferior parietal lobe, and inferior frontal gyri).

While neuroscience researchers have long suspected that ADHD symptoms result from atypical interactions between the frontal cortex and these deep information-processing brain structures, studies testing this model have returned mixed findings, possibly due to the small nature of the studies, with only 100 or so subjects.

Researchers suggest that the smaller studies may not have been able to reliably detect the brain interactions leading to the complex behaviors seen in ADHD.

The findings from this study help further our understanding of the brain processes contributing to ADHD symptoms—information that can help inform clinically relevant research and advancements.

About this ADHD and brain connectivity research news

Author: Claire Cole Source: NIH Contact: Claire Cole – NIH Image: The image is credited to Neuroscience News

Original Research: The findings will be presented in American Journal of Psychiatry

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A systematic study of ADHD assessments in child and adolescent psychiatry

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Adequate treatment of ADHD requires a correct diagnosis. The assessment process for neurodevelopmental conditions is often more extensive than for other psychiatric disorders, and is often associated with long waiting lists, thus consuming a large proportion of psychiatric resources. The overarching aim of the present study is to gain knowledge about diagnostic processes to enable valid, reliable, and cost-effective ADHD assessments, and to increase the understanding of mechanisms underpinning ADHD that can aid the diagnostic process. To this end, we will compare a brief and a comprehensive ADHD assessment protocol.

Participants in the study are children aged 8 to 16 years who have been referred to child and adolescent psychiatric care for assessment. Participants will be randomized to either the brief or the comprehensive ADHD assessment protocol. We also aim to investigate whether biomarkers in the form of heart rate variability and pupil dilation can serve as diagnostic biomarkers for ADHD.

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College students with adhd: a selective review of qualitative studies.

1. Introduction

1.1. qualitative research methods, 1.2. the present study, 2. materials and methods, 2.1. search strategy, 2.2. study selection, 2.3. variable identification, 3.1. quantitative results, 3.2. qualitative results, 3.2.1. the college experience of students with adhd, 3.2.2. interventions, 3.2.3. cognitive and academic functioning, 3.2.4. self-functioning, 4. discussion, 5. conclusions, author contributions, conflicts of interest, appendix a. summaries of included studies, appendix a.1. the college experience of students with adhd, appendix a.1.1. college transitions, appendix a.1.2. adhd as an identity, appendix a.1.3. race, appendix a.1.4. community college, appendix a.2. interventions, appendix a.2.1. coaching, appendix a.2.2. strategies, appendix a.2.3. medication, appendix a.3. cognitive and academic functioning, appendix a.4. self-functioning.

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Share and Cite

Cohen, S.L.; Shavel, K.; Lovett, B.J. College Students with ADHD: A Selective Review of Qualitative Studies. Disabilities 2024 , 4 , 658-677. https://doi.org/10.3390/disabilities4030041

Cohen SL, Shavel K, Lovett BJ. College Students with ADHD: A Selective Review of Qualitative Studies. Disabilities . 2024; 4(3):658-677. https://doi.org/10.3390/disabilities4030041

Cohen, Shira L., Katie Shavel, and Benjamin J. Lovett. 2024. "College Students with ADHD: A Selective Review of Qualitative Studies" Disabilities 4, no. 3: 658-677. https://doi.org/10.3390/disabilities4030041

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Understanding Attention-Deficit/Hyperactivity Disorder From Childhood to Adulthood

Timothy e. wilens.

1 Clinical Research Program in Pediatric Psychopharmacology, Massachusetts General Hospital and Harvard Medical School, Boston, MA

Thomas J. Spencer

Attention deficit/hyperactivity disorder (ADHD) is among the most common neurobehavioral disorders presenting for treatment in children and adolescents. ADHD is often chronic with prominent symptoms and impairment spanning into adulthood. ADHD is often associated with co-occurring disorders including disruptive, mood, anxiety, and substance abuse. The diagnosis of ADHD is clinically established by review of symptoms and impairment. The biological underpinning of the disorder is supported by genetic, neuroimaging, neurochemistry and neuropsychological data. Consideration of all aspects of an individual’s life needs to be considered in the diagnosis and treatment of ADHD. Multimodal treatment includes educational, family, and individual support. Psychotherapy alone and in combination with medication is helpful for ADHD and comorbid problems. Pharmacotherapy including stimulants, noradrenergic agents, alpha agonists, and antidepressants plays a fundamental role in the long-term management of ADHD across the lifespan.

INTRODUCTION AND OVERVIEW

Attention-deficit/hyperactivity disorder (ADHD) is among the most common neurobehavioral disorders presenting for treatment in children 1 , 2 . It carries a high rate of comorbid psychiatric problems such as oppositional defiant disorder (ODD), conduct disorder, mood and anxiety disorders, and cigarette and substance use disorders 3 . Across the life span, the social and societal costs of untreated ADHD are considerable, including academic and occupational underachievement, delinquency, motor vehicle safety, and difficulties with personal relationships 3 - 5 , 6 .

ADHD affects an estimated 4% to 12% of school-aged children worldwide 7 with survey and epidemiologically derived data showing that 4 to 5% of college aged students and adults have ADHD 8 . In more recent years, the recognition and diagnosis of ADHD in adults have been increasing although treatment of adults with ADHD continues to lag substantially behind that of children 8 , 9 . In contrast to a disproportionate rate of boys diagnosed with ADHD relative to girls in childhood, in adults, an equal number of men and women with ADHD are presenting for diagnosis and treatment 10 .

PSYCHIATRIC COMORBIDITY

During the past decade, epidemiological studies have documented high rates of concurrent psychiatric and learning disorders among individuals with ADHD 3 , 11 , 12 , 13 . Consistent with childhood studies, studies of ADHD adults have found high rates of childhood conduct disorder as well as adult antisocial disorders in these subjects 3 .

Mood & Anxiety

Anxiety often confounds the diagnosis and treatment of ADHD 3 , 11 , 12 . High rates of the various anxiety symptoms exist in ADHD and may manifest as social, generalized or panic-like symptoms. Similarly, ADHD increases the likelihood of having a depressive disorder by at least two-fold 8 , 14 . Interestingly, recent data suggest that stimulant treatment of ADHD over time may decrease the ultimate risk for anxiety and depressive disorders 15 .

A growing literature reports the co-occurrence of bipolar disorder and ADHD. Systematic studies of children and adolescents indicate rates of ADHD ranging from 57% to 98% in bipolar children; and conversely, rates of bipolar disorder in 22% of ADHD children and adolescents 16 . There continues to be much controversy about the validity of the concurrent diagnoses of ADHD and severe mood instability or bipolar disorder. Whereas ADHD is characterized by the typical cognitive and hyperactive/impulsive features of the disorder, bipolar disorder (BPD) is characterized by mood instability, pervasive irritability/rage, grandiosity, psychosis, cyclicity, and lack of response to structure 17 . When individuals experience both sets of symptoms, they may suffer from both ADHD and BPD 17 .

Substance Use Disorders

Combined data from retrospective accounts of adults and prospective observations of youth indicate that juveniles with ADHD are at increased risk for cigarette smoking and substance abuse (SA) during adolescence 18 . ADHD adolescents and adults become addicted to cigarette smoking at twice the rate compared to non-ADHD individuals 19 , 20 . ADHD youth disproportionately become involved with cigarettes, 19 which increases the risk for subsequent alcohol and drug use 21 . Individuals with ADHD tend to have more severe substance abuse and maintain their addictions longer compared to their non-ADHD peers 19 , 22 - 24 .

Concerns of the abuse liability of stimulants and the potential kindling of substance abuse secondary to early stimulant exposure in ADHD children have been raised. 25 These concerns are based largely on data from animal studies. 25 However, the preponderance of clinical data and consensus in the field do not appear to support such a contention. For example, in a prospective study of ADHD girls followed into adolescence, a significant reduction in the risk for SA was reported in treated compared to untreated ADHD youth 26 with no increase (or decreased) SUD risk associated with stimulant treatment into adulthood 27 .

DIAGNOSING ADHD

ADHD can be reliably diagnosed in children, adolescents, and adults 28 . Using the current guidelines, the child or adult patient must meet the criteria in the Diagnostic and Statistical Manual of Mental Disorders (DSM-IV-TR) 29 . It is important to note, however, that the DSM-IV-TR criteria for ADHD symptoms were derived from youth to age 17 years and therefore were not specifically tailored to adults and hence, may not always “fit” adults with the disorder 28 , 30 . The symptoms of the disorder are categorized as follows: inattention-difficulty sustaining attention and mental effort, forgetfulness, and distractibility; hyperactivity-fidgeting, excessive talking, and restlessness; and impulsivity-difficulty waiting one’s turn and frequent interruption of others. The DSM-IV-TR criteria also include onset by age 7, impaired functioning in at least 2 settings (home, work, school, job), and more than 6 months of duration 30 . Three subtypes of the syndrome are currently recognized: predominantly inattentive, predominantly hyperactive-impulsive, and the combined type, which is the most common and typically more severe and with more comorbidity 29 , 31 , 32 . Between 90 to 95% of adolescents and adults with ADHD manifest the inattention cluster of symptoms at least as a component of their disorder 31 . Of interest, the combined subtype of ADHD may simply represent a more severe and debilitating presentation of ADHD (e.g. more symptoms) and there may be relatively more stability of the subtype with development 32 , 33 .

To meet the diagnostic criteria for the inattentive or hyperactive-impulsive subtypes, an individual must have 6 or more of the 9 symptoms from either group of criteria (18 possible traits in all) 30 . For the combined subtype, an individual must have 6 or more inattentive symptoms and 6 or more hyperactive-impulsive symptoms. To warrant the ADHD diagnosis, symptoms must cause significant impairment. Adults diagnosed with the disorder must have had childhood onset and persistent and current symptoms, although allowance is made for incomplete persistence of full criteria (ADHD-in partial remission) or lack of clear childhood symptoms (ADHD NOS).

Of interest, whereas clinicians are concerned as to the possibility of purposely misrepresenting or over-reporting of ADHD symptoms by college students or adults, data suggest the opposite may be operant. Mannuzza et al. 34 in a prospective 16-year follow-up of children with ADHD now at a mean age of 25, found that of the 176 individuals with a well characterized past history of ADHD, only 28% of the adults through direct interviews were identified as having childhood ADHD. These data further highlight issues around the relatively poor sensitivity of recalling symptoms (and establishing the diagnosis of ADHD) by adult self-report, particularly when not anchoring symptoms in childhood.

The diagnosis of ADHD is made clinically with scales used in an ancillary manner. The patient’s symptoms, severity of impairment, possible comorbidity, family history, and psychosocial stressors may be determined during the patient and/or parent interview. In pediatric evaluations, the adolescent’s behavior and parent-child interaction are observed, and the child’s school, medical, and neurological status are evaluated 2 . A number of diagnostic and follow-up scales are available (see www.schoolpsychiatry.org ) 35 . Symptom scales used with all age groups (to assess home, school, and job performance) include, but are not limited to, the ADHD Symptom Checklist, SNAP-IV Teacher and Parent Rating Scale, Conners Rating Scales-Revised,, Brown Attention-Deficit Disorder Scales for Children, and the ADHD Symptoms Rating Scale 36 . Although these tools quantify behavior deviating from norms, they should not be used alone to make or refute the diagnosis.

Diagnosing adults involves careful querying for developmentally appropriate criteria from the DSM-IV-TR concerning the childhood onset, persistence, and current presence of symptoms 29 . Diagnostic aids are available for adult ADHD 36 , 37 . For instance, the Adult Self Report Scale, Conners Adult ADHD Scales, and Brown Attention scales for adults are among instruments available to assist in the diagnosis of ADHD 36 , 37 . For a briefer screening of adults, the World Health Organization Adult ADHD self-report scale ( Figure 1 ) can be downloaded ( www.who.org ) and has been validated as a manner of identifying those at risk for ADHD who necessitate further screening 38 .

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Follow-up studies show that prominent symptoms and impairment related to the disorder persist into adulthood in approximately one-half of cases 39 , 40 . There appears to be developmental variance in the ADHD symptom profile across the life span 31 , 32 , 39 - 41 . Longitudinally derived data in ADHD youth growing up indicate that the symptom cluster of hyperactivity and impulsivity decays over time, while the symptoms of inattention largely persist 32 , 39 - 41 , 31 . In support of this notion, data derived from a group of clinically referred adults with ADHD indicate that approximately half of adults endorse clinically significant levels of hyperactivity/impulsivity, but 90% endorse prominent attentional symptoms 32 , 31 .

A substantial body of literature implicates abnormalities of brain structure and function in the pathophysiology of both childhood and adult ADHD 42 - 48 , 49 - 51 . We have known for decades that ADHD youth show impaired performance on tasks assessing vigilance, motoric inhibition, organization, planning, complex problem solving, and verbal learning and memory 52 , 53 . Prominent neuropsychologically-derived executive dysfunction is associated with learning disabilities and poorer overall prognosis over time in ADHD youth 54 . Similar findings are emerging in adults with ADHD 52 . While neuropsychological testing is not used clinically to diagnose ADHD in adults, such testing aids in identifying learning disabilities, sub average intelligence, and specific information processing deficits.

PATHOPHYSIOLOGY AND GENETICS

Neurobiology.

ADHD has been conceptualized as a disorder affecting “frontal” circuitry due to associated deficits in executive cognitive functioning. Structural imaging studies have documented diffuse abnormalities in children and adults with ADHD. A large study by Castellanos and colleagues 55 reported smaller total cerebrum, cerebellum, and the four cerebral lobes that did not change over time. A structural magnetic resonance imaging (MRI) study 56 in adults with and without ADHD also revealed a smaller anterior cingulate cortex (ACC) and dorsolateral prefrontal cortex (DLPFC). The DLPFC controls working memory that involves the ability to retain information while processing new information. These differences are thought to account for deficits in goal-directed and on task behavior in ADHD. The ACC is thought to be a key region of regulation involving the ability to focus on one task and choose between options.

Investigators have also examined the developmental pattern of cortical maturation in ADHD. Shaw and colleagues 57 reported a delay in cortical thickness among ADHD patients. The pattern of brain development, from sensorimotor to associative areas, was similar in children with and without ADHD. However, the age of peak development was delayed in those with ADHD. Using the same measure of cortical thickness data in adults, Makris and associates 58 have shown that cortical thickness is not normalized and that the areas of the brain that are affected in children with ADHD remain affected in adulthood. In this study the DLPFC, parietal areas, and ACC had thinner measures of cortical thickness in adults with ADHD than in adults without ADHD.

Functional magnetic resonance imaging (fMRI) has been used to examine brain activity during selective cognitive challenges in individuals with ADHD. One study that measures brain activity using a neuropsychological test (go/no-go) found that both youth and adults with ADHD showed attenuated activity in the frontostriatal regions of the brain that are key for inhibitory control and for attention (prefrontal cortex and caudate) 59 . Adults with ADHD also activated non-frontostriatal regions (ACC, parietal areas) moreso than controls. The amount of brain activation observed correlated closely with the degree of efficiency on the task in both children and adults with ADHD.

The results of fMRI studies were reviewed by Casey and Durston 60 who hypothesized that top-down and bottom-up control systems were affected in ADHD. They speculated that bottom-up neural systems detect the regularities and irregularities in the environment to activate the frontal brain systems to alter behavior. These systems are key regulators of maintaining sustained attention vs. shifting attention due to sensory input. Casey and Durston 60 posited that the striatum regulates what to expect (type of task), the cerebellum regulates when to expect it (timing of task), and the parietal lobe alerts one to novel or newer competing stimuli.

Interestingly, medication may normalize some of these functional deficits. Bush and colleagues published a study showing that 7 weeks of treatment with methylphenidate normalized activation in the ACC 61 . Those receiving medication showed increases in activation of the ACC and DLPFC at follow-up as compared to baseline and to those receiving placebo treatment. Hence, those areas of the brain that were underactive in adults without treatment normalized with treatment.

The neurobiology of ADHD is strongly influenced by genetic factors. As highlighted in a special issue of Science dedicated to the human genome project, ADHD is among the most recognized genetic-based disorders in psychiatry 62 . Family studies of ADHD have shown that the relatives of ADHD children are at high risk for ADHD, comorbid psychiatric disorders, school failure, learning disability and impairments in intellectual functioning 63 . Additional lines of evidence from twin, adoption and segregation analysis studies suggest that the familial aggregation of ADHD has a substantial genetic component. Twin studies find greater similarity for ADHD and components of the syndrome between monozygotic twins compared with dizygotic twins 64 , 65 . Faraone and colleagues 66 in a meta-analysis of the various studies reported on the mean heritability of ADHD. Heritability refers to the amount of genetic influence for a particular condition. A coefficient of 1 indicates an entirely genetically influenced phenomenon, while a 0 indicates no genetic influence. Depression, anxiety, panic, and even Asthma had mean heritability rates below 50%. In contrast, two of the most biologically related psychiatric disorders, schizophrenia and autism, are heritable at ~75%. ADHD falls in this higher range as well, with work by Rietveld and associates showing a mean heritability rate of 75% 67 .

As with many complex neuropsychiatric conditions, multifactorial causation is thought to be involved in ADHD; an additive effect of multiple vulnerability genes interacting with environmental influences. Pooled analyses reveal that there is not one single gene associated with ADHD 66 . The disorder is thought to result from a combination of small effects from a number of genes (polygenetic). Some of the candidate genes that have been identified thus far relate to synthesis, packaging, release, detection and recycling of dopamine or catecholamines including the post-synaptic DRD4, dopamine transporter, and SNAP 25 genes; as well as others related to other neurotransmitters such as serotonin. Clearly, more work is necessary in disentangling the relationship of candidate genes in producing specific phenocopies of ADHD, as well as response prediction to psychosocial and pharmacological intervention.

The management of ADHD includes consideration of two major areas: non-pharmacological (educational remediation, individual and family psychotherapy) and pharmacotherapy 2 . Support groups for children and adolescents and their families, as well as adults with ADHD, provide an invaluable and inexpensive environment in which individuals are able to learn about ADHD and resources available for their children or themselves. Support groups can be accessed by calling an ADHD hotline or a large support group organization (i.e. Children and adults with ADHD-CHADD, Adults with ADHD-ADDA,), or by accessing the internet.

Specialized educational planning based on the child’s difficulties is necessary in a majority of cases 68 . Since learning disorders co-occur in one-third of ADHD youth, ADHD individuals should be screened and appropriate individualized educational plans developed. Parents should be encouraged to work closely with the child’s school guidance counselor who can provide direct contact with the child as well as serve as a valuable liaison for teachers and school administrators. The school’s psychologist can be helpful in providing cognitive testing as well as assisting in the development and implementation of the individualized education plan. Educational adjustments should be considered in individuals with ADHD with difficulties in behavioral or academic performance. Increased structure, predictable routine, learning aids, resource room time, and checked homework are among typical educational considerations in these individuals. Similar modifications in the home environment should be undertaken to optimize the ability to complete homework. For youth, frequent parental communication with the school about the child’s progress is essential.

PSYCHOSOCIAL TREATMENTS

Clinicians have at their disposal a variety of psychosocial interventions for ADHD (for review see 68 , 69 ). Apart from traditional psychotherapy, which addresses underlying emotions, tutors are available to help children develop strategies for improving academic performance and interpersonal relations. Tutors can assist the child with skills in organization and prioritization, as well as act as mentors, advocates, and motivational figures.

Parent training is often conducted using the antecedent behavior consequence model, and is implemented using various methods, including small and large parent training groups, parent training with individual families, videotapes, and behavioral sessions that include children 70 . In the academic setting, virtually all children with ADHD must cope with organizational and behavioral demands and expectations. Classroom behavioral interventions often involve training the teacher in use of these methods.

Teachers can conduct individual and class-wide interventions using antecedents and/or consequence methods 71 . Antecedent interventions are based on an understanding of the range of antecedents (eg, boredom, peer provocation, unclear inconsistent rules) that precipitate behavioral problems. Antecedent/consequence interventions involve understanding antecedents to inappropriate behavior and reinforcing appropriate behavior with rewards. Consequence interventions involve the judicious use of punishment to encourage appropriate classroom behavior.

Accommodations should be considered to assist the child with ADHD. For instance, other behavioral strategies can be used in the classroom setting to facilitate attention 72 . These include placing the child with ADHD in proximity to the teacher, eliminating environmental distractions, and arranging seating in traditional rows rather than clusters. Lessons that involve novelty and stimulation in easy and repetitive tasks rather than new or difficult ones have been shown to benefit the child with ADHD. Additional interventions shown to be effective in the academic setting include peer-mediated interventions and token economies.

Exciting new work has shown that cognitive therapies 73 and cognitive behavioral therapy have been shown effective in medicated adults with ADHD who manifest residual ADHD symptoms 74 - 77 . Social skills remediation for improving interpersonal interactions and coaching for improving organization and study skills may be useful adjuncts to treatment, although there generalizeability remains debated. Little data exists for the use of neurofeedback, cerebellar training, attention or memory training, or ophthalmic manipulation for the treatment of core ADHD symptoms 71 .

PHARMACOTHERAPY

Medications remain a mainstay of treatment for children, adolescents, and adults with ADHD (see Table 1 ). In fact, NIH-funded multisite studies support that medication management of ADHD is the most important variable in outcome (for core ADHD symptoms) in context to multimodal treatment at least over the first year to two of treatment 78 - 80 . The stimulants, noradrenergic agents, and alpha agonists comprise the available agents for ADHD. The medications used in ADHD have been observed to have pharmacological responsivity across the lifespan for school-aged children, adolescents, and adult groups with ADHD.

Generic class (Brand name)	DAILY DOSE (MG/KG)	DAILY DOSAGE SCHEDULE	TYPICAL DOSING SCHEDULE	COMMON ADVERSE EFFECTS



	0.3-1.5			-Insomnia
		Twice or three times	5-30 mg BID to TID	-Decreased appetite, weight loss -Tic exacerbation
				-Depression, anxiety
		Once or twice	5-30 mg BID	-Rebound phenomena (short acting preparations)
				-Increased blood pressure/ pulse
		Once	10-70 mg QD
				-Insomnia
	0.5.0-2.0 (< 1 mg for d-MPH or patch)	Twice to four times	5-40 mg BID to QID	-Decreased appetite, weight loss -Tic exacerbation -Depression, anxiety
		Once or twice	10-60 mg QD to BID	-Rebound phenomena (short acting preparations) - Increased blood pressure/ pulse
		Once	10-90 mg QD

Agents

(Strattera)	1.0-2.0	Once or twice	25-140 mg QD	-GI Upset, nausea -Sedation, insomnia -Agitation



)	30-100 mcg/kg	Twice	0.5-1 mg TID 1-4 mg daily	-Similar to clonidine but less sedation

	3-10 mcg/kg	Twice or three times	0.05-0.1 mg TID	-Sedation, dry mouth, depression -Confusion (with high dose)
				-Bradycardias, syncope
				-Rebound hypertension

		Once or twice	100-400 mg QD	-Insomnia -Weight loss
				-Increased blood pressure/pulse



e.g., Imipramine, Desipramine, Nortriptyline (NT)	2.0-5.0 (1.0-3.0 for NT)	Once or twice	25-300 mg QD (25-150 mg QD for NT)	-Dry mouth, constipation -Weight loss -Vital sign and ECG changes

	1.0-6.0	Once to three times	75-100 mg TID 150-200 BID (SR); 150-450 XL	-Irritability, insomnia -Risk of seizures -Contraindicated in bulimics

The stimulant class medications are among first line agents for pediatric and adult groups with ADHD based on their extensive efficacy and safety data 1 . The most commonly used compounds in this class include methylphenidate-based (Ritalin, Concerta, Focalin, Metadate, Daytrana and others) and amphetamine-based (Adderall, Dexedrine, Vyvanse) formulations. Stimulants are sympathomimetic drugs which increase intrasynaptic catecholamines (mainly dopamine and norepinephrine) by inhibiting the presynaptic reuptake mechanism and releasing presynaptic catecholamines 81 . Whereas methylphenidate is specific for blockade of the dopamine and noradrenergic transporter proteins, amphetamines (in addition to blocking the dopamine and noradrenergic transporter protein) release catecholaminergic stores and cytoplasmic dopamine and noradrenaline directly into the synaptic cleft (for review see 1 , 81 ).

Given the need to additionally treat ADHD outside of academic settings (i.e. social, homework, driving) and to reduce the need for in school dosing and likelihood for diversion, there has been a shift to the extended release preparations of the stimulants. Extended release preparations diminish afternoon wear-off and rebound and appear to manifest less abuse liability compared to their immediate-release counterparts 82 , 83 . The extended release stimulants include methylphenidate (trade names: Concerta, Daytrana Patch, Focalin XR, Metadate CD, Ritalin LA) and amphetamine formulations (trade names: Adderall XR, Vyvanse). The literature suggests more similarities than differences in response to the various available stimulants 1 , 84 . However, based on different mechanisms of action and individual tolerability, some patients who lack a satisfactory response or manifest adverse effects to one stimulant may respond favorably to another. Stimulants should be initiated at the lowest available dosing once daily and increased every three to seven days until a response is noted or adverse effects emerge.

Stimulants appear to work in all age groups of individuals with ADHD. For instance, a controlled multi-site study in preschoolers showed improvement in ADHD symptoms and structured tasks; however, the response was less robust with a higher side effect burden compared to other age groups 85 . There has been a great interest in the use of stimulant treatment in adults with ADHD. There have been approximately 40 studies of stimulants demonstrating moderate efficacy 86 . Currently FDA approval is only for the extended-release preparation of stimulants in adults.

Predictable short-term adverse effects include reduced appetite, insomnia, edginess, and GI upset 87 . Elevated vital signs may emerge necessitating baseline and on-drug monitoring. Although stimulants may produce anorexia and weight loss, their effect on ultimate height remains less certain 88 , 89 . Whereas a number of studies have indicated potential growth delay earlier in treatment, normalization appears to occur with chronic treatment. Longitudinal studies suggest that the majority of ADHD youth with tics can tolerate stimulant medications 90 ; however, up to one-third of children with tics may have worsening of their tics with stimulant exposure 91 . Current consensus suggests that stimulants can be used in youth with comorbid ADHD plus tics with careful monitoring for stimulant-induced tic exacerbation.

Warnings have also highlighted potential cardiovascular adverse events. Data suggest that rates of sudden and catastrophic adverse cardiovascular effects are no higher on stimulants and nonstimulants to treat ADHD compared to the general population 92 . Based on guidelines from the American Academy of Pediatrics 93 , 94 , history and symptoms referable to structural heart disease should be queried prior to starting and during treatment with medications (see Figure 2 ) including family history of premature death, congenital heart disease, palpitations, syncopal episodes, dizziness, or chest pain 93 , 94 . Blood pressure and pulse monitoring at baseline and periodically thereafter is recommended whereas ECG monitoring is optional 93 , 94 .

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Despite lingering concerns of stimulant abuse, there is a paucity of scientific data supporting that stimulant-treated ADHD individuals systematically abuse their medication 95 and the preponderance of recent data continue to suggest reductions of cigarette smoking and substance abuse associated with treatment 19 , 26 . However, data suggest that diversion of stimulants to non-ADHD youth continues to be a concern 96 , 97 . Families should closely monitor stimulant medication, and college students receiving stimulants should be advised to carefully store their medication 96 . Two studies have shown less abuse liability associated with extended-release relative to immediate release MPH 82 , 83 .

Atomoxetine

Atomoxetine is a potent norepinephrine-specific reuptake inhibitor that has been studied in youths and adults 98 , 99 . Atomoxetine has been shown to be effective in long-term use 100 . Atomoxetine has also been shown particularly useful in comorbid ADHD. In a noninferiority study in children with ADHD and tic disorder, atomoxetine reduced tic severity while improving ADHD symptoms. Children with ADHD and clinically significant anxiety responded more favorably to atomoxetine than placebo with reductions in both anxiety and ADHD scores 101 . Likewise, data in young adults with ADHD has shown that 12 week treatment with atomoxetine in recently abstinent alcoholics (4-30 days) was associated with significant reductions in ADHD and heavy drinking (not relapse) compared to placebo 102 . In clinical trials, atomoxetine is associated with nausea, GI distress, and sedation most commonly reported. Patients may rarely experience hostility, irritability, and/or suicidality. There is currently a black box warning for rare, but potentially serious, hepatitis (see http://www.strattera.com/pages/index ) 103 . While routine liver function monitoring is not recommended, careful informed consent with patients and their families can enhance vigilance for warning signs and symptoms.

Antihypertensives/alpha agonists

The antihypertensives guanfacine and clonidine are alpha-adrenergic agonists; an extended-release preparation of guanfacine is FDA approved. Whereas clonidine affects alpha receptors more broadly, guanfacine appears to be more selective for the alpha 2a receptor. Improvements in both attention and hyperactivity/impulsivity have been demonstrated with the alpha agonists 104 . The alpha agonists have been used for the treatment of core ADHD as well as associated tics, oppositional defiant behavior, aggression, and sleep disturbances, particularly in younger children 105 .

Multisite combination studies using alpha agonists and stimulants have been conducted in youth with ADHD and ADHD plus tics. Interestingly, all studies have shown that the combination was more effective than either agent alone in improving ADHD and/or tics 106 - 109 , 110 . In these studies, no clinically meaningful adverse cardiovascular events were observed 106 , 107 . Cardiovascular monitoring by ECG remains optional. Adverse effects with the alpha agonists include sedation, fatigue, mood, and the potential for rebound hypertension with abrupt discontinuation.

Several additional medications have demonstrated benefit in controlled trials, but have not been approved by the FDA for the treatment of ADHD. The antidepressant bupropion has been shown effective for ADHD in controlled trials of children 111 and adults 112 , 113 . Additionally, open trials in adolescents with ADHD and depression 114 and adults with ADHD and bipolar disorder 115 have suggested a further utility for this agent. Given its utility in reducing cigarette smoking, improving mood, lack of monitoring requirements, and general tolerability, bupropion is often used as an agent for complex ADHD patients with substance abuse or a mood disorder. Adverse events include activation, irritability, insomnia, and in rare cases, seizures.

The tricyclic antidepressants (TCAs) such as imipramine are effective in controlling abnormal behaviors and improving cognitive impairments associated with ADHD, but less so than the majority of stimulants 116 . The TCAs are particularly useful when other FDA approved agents fail and/or when oppositionality, anxiety, tics, sleep, or depressive symptoms co-occur within ADHD. Unwanted side effects include sedation, weight gain, dry mouth, and constipation. Blood levels should be measured periodically and, since TCAs prolong the cardiac repolarization, ECG monitoring is recommended but not required to screen for arrhythmia risk. TCAs can be fatal in overdose and need to be stored carefully, particularly if toddlers are in the family.

Modafinil is currently approved as treatment for narcolepsy and has been shown effective in pediatric, but not adult, trials of ADHD 117 . Modafinil has not been approved by the FDA for the treatment of ADHD due to safety concerns (rare but potentially serious erythema multiforme).

In summary, ADHD is a prevalent world-wide, heterogeneous disorder that frequently persists through adolescence into adult years. ADHD continues to be diagnosed by careful history with an understanding of the developmental presentation of normal behavior and symptoms of the disorder. ADHD has been reconceptualized as a more chronic condition with approximately one-half of children continuing to exhibit symptoms and impairment of the disorder into adulthood 39 , 40 .. Most individuals with ADHD have a comorbid disorder: including oppositional, conduct, anxiety, or mood disorders 3 , 11 , 12 .. In addition, ADHD carries with it significant impairment in academic, occupational, social, and intrapersonal domains necessitating treatment. Converging data strongly support a neurobiological and genetic basis for ADHD with catecholaminergic dysfunction as a central finding.

Psychosocial interventions such as educational remediation, structure/routine, and cognitive-behavioral approaches should be considered in the management of ADHD. Contemporary work exhibiting improved outcomes associated with specific cognitive therapies in adults with ADHD has been demonstrated. An extensive literature supports the effectiveness of pharmacotherapy not only for the core behavioral symptoms of ADHD but also improvement in linked impairments. Similarities between pediatric and adult groups in the presentation, characteristics, neurobiology, and treatment response of ADHD support the continuity of the disorder across the lifespan.

Attention-deficit/hyperactivity disorder is a heterogenous disorder that is prevalent worldwide and frequently persists from adolescence into adult years. Attention-deficit/hyperactivity disorder continues to be diagnosed by careful history with an understanding of the developmental presentation of normal behavior and symptoms of the disorder. It has been reconceptualized as a more chronic condition, with approximately half of children continuing to exhibit symptoms and impairment into adulthood. 39 , 40 Most individuals with ADHD have a comorbid disorder, including oppositional, conduct, anxiety, or mood disorders. 3 , 11 , 12 In addition, ADHD carries with it significant impairment in academic, occupational, social, and intrapersonal domains necessitating treatment. Converging data strongly support a neurobiological and genetic basis for ADHD, with catecholaminergic dysfunction as a central finding.

Psychosocial interventions such as educational remediation, structure/routine, and cognitive behavioral approaches should be considered in the management of ADHD. Contemporary work exhibiting improved outcomes associated with specific cognitive therapies in adults with ADHD has been demonstrated. Extensive literature supports the effectiveness of pharmacotherapy not only for the core behavioral symptoms of ADHD but also improvement in linked impairments. Similarities between pediatric and adult groups in the presentation, characteristics, neurobiology, and treatment response of ADHD support the continuity of the disorder across the lifespan.

Acknowledgments

This article was in part underwritten by K24 DA016264 to Timothy Wilens, MD.

Conflict of Interest Statement

Timothy Wilens, MD discloses conflicts of interest with Abbott, AstraZeneca, Eli Lilly and Co., McNeil Pharmaceuticals, Merck, the National Institutes of Health (National Institute on Drug Abuse), Novartis, and Shire. Thomas Spencer, MD discloses conflicts of interest with Cephalon, Eli Lilly and Co., GlaxoSmithKline, Janssen Pharmaceutical, McNeil Pharmaceuticals, the National Institute of Mental Health, Novartis, Pfizer, and Shire.

Schools & departments

Dyslexia and ADHD share genetic links, study shows

Scientists have shed new light on the genetic basis of dyslexia, showing how it overlaps with that of attention deficit hyperactivity disorder (ADHD).

Dyslexia and ADHD often occur together in people and they share many genes in common – links which make them distinct from developmental and mental health diagnoses such as autism, bipolar disorder and schizophrenia, a study shows.

Genetic links

This study, led by the University of Edinburgh, is the first to explore the genetic links to dyslexia – believed to affect 10 per cent of the population – in the context of neurodevelopmental and psychiatric traits.

The findings could help in tailoring targeted educational, employment and wellbeing support systems for people with dyslexia or ADHD, experts say.

The findings aid understanding of the biology behind dyslexia – a difficulty with reading and spelling – and ADHD, a condition associated with difficulty concentrating, hyperactivity and impulsivity.

Public datasets

Researchers at the University of Edinburgh analysed large public anonymised datasets of genetic data on 10 neurodevelopmental and psychiatric conditions from the Psychiatric Genomics Consortium, along with dyslexia genetic statistics from an analysis of around one million people in collaboration with 23andMe, a genomics and biotechnology company.

They used a statistical tool to find clusters of genetically similar traits for dyslexia and 10 neurodevelopmental and psychiatric traits including ADHD, anorexia nervosa and Tourette syndrome.

Genetic regions

They conducted more detailed analyses to identify specific genetic regions that overlap between dyslexia and ADHD.

Among the 10 psychiatric traits included in the study, five genetically linked clusters known as latent genomic factors were identified.

ADHD was more strongly related to an attention and learning difficulties factor than with factors related to neurodevelopmental traits like autism and Tourette syndrome.

Follow-up analyses of the attention and learning difficulties factor identified 49 genetic regions and 174 genes shared between dyslexia and ADHD, of which 40 regions and 121 genes have not been previously identified.

This is the first time that genetic links to dyslexia have been studied in the context of psychiatric traits. In the future, other learning difficulties such as dyscalculia or dyspraxia should be included to allow for a more nuanced understanding of the relationships between them. Austėja Čiulkinytė A Translational Neuroscience PhD student at the University of Edinburgh, who led the study

By studying many related behaviours together we are able boost the statistical power for gene discovery. Professor Michelle Luciano School of Philosophy, Psychology and Language Sciences

The study is published in the Journal Molecular Psychiatry.

This study is in collaboration with 23andMe and supported by Wellcome, the Biotechnology and Biological Sciences Research Council and the Max Planck Society.

Link to study

School of Philosophy, Psychology and Language Sciences

Image credit -Izusek via Getty Images

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Dyslexia and ADHD share genetic links, study shows

by University of Edinburgh

Scientists have shed new light on the genetic basis of dyslexia, showing how it overlaps with that of attention deficit hyperactivity disorder (ADHD).

This study, led by the University of Edinburgh, is the first to explore the genetic links to dyslexia —believed to affect 10 percent of the population—in the context of neurodevelopmental and psychiatric traits.

The findings could help in tailoring targeted educational, employment and well-being support systems for people with dyslexia or ADHD, experts say.

The findings aid understanding of the biology behind dyslexia—a difficulty with reading and spelling—and ADHD, a condition associated with difficulty concentrating, hyperactivity and impulsivity.

Researchers at the University of Edinburgh analyzed large public anonymized datasets of genetic data on 10 neurodevelopmental and psychiatric conditions from the Psychiatric Genomics Consortium, along with dyslexia genetic statistics from an analysis of around one million people in collaboration with 23andMe, a genomics and biotechnology company.

They used a statistical tool to find clusters of genetically similar traits for dyslexia and 10 neurodevelopmental and psychiatric traits including ADHD, anorexia nervosa and Tourette syndrome.

They conducted more detailed analyses to identify specific genetic regions that overlap between dyslexia and ADHD.

Among the 10 psychiatric traits included in the study, five genetically linked clusters known as latent genomic factors were identified.

ADHD was more strongly related to an attention and learning difficulties factor than with factors related to neurodevelopmental traits like autism and Tourette syndrome.

"This is the first time that genetic links to dyslexia have been studied in the context of psychiatric traits. In the future, other learning difficulties such as dyscalculia or dyspraxia should be included to allow for a more nuanced understanding of the relationships between them," says Austėja Čiulkinytė, A Translational Neuroscience Ph.D. student at the University of Edinburgh, who led the study.

"By studying many related behaviors together we are able boost the statistical power for gene discovery," adds Professor Michelle Luciano of the School of Philosophy, Psychology and Language Sciences.

The work is published in the journal Molecular Psychiatry .

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