the adhd population, as have mood disorders (especially bipolar disorder and major depressive disorder). boys diagnosed with the combined adhd subtype are more likely to have a mood disorder. adults and children with adhd sometimes also have bipolar disorder, which requires careful assessment to accurately diagnose and treat both conditions. sleep disorders and adhd commonly co-exist. they can also occur as a side effect of medications used to treat adhd. in children with adhd, insomnia is the most common sleep disorder with behavioural therapy being the preferred treatment. problems with sleep initiation are common among individuals with adhd but often they will be deep sleepers and have significant difficulty getting up in the morning. melatonin is sometimes used in children who have sleep onset insomnia. specifically, the sleep disorder restless legs syndrome has been found to be more common in those with adhd and is often due to iron deficiency anemia. however, restless legs can simply be a part of adhd and requires careful assessment to differentiate between the two disorders. delayed sleep phase disorder is also a common comorbidity of those with adhd. there are other psychiatric conditions which are often co-morbid with adhd, such as substance use disorders. individuals with adhd are at increased risk of substance abuse.: 9 this is most commonly seen with alcohol or cannabis.: 9 the reason for this may be an altered reward pathway in the brains of adhd individuals, self-treatment and increased psychosocial risk factors.: 9 this makes the evaluation and treatment of adhd more difficult, with serious substance misuse problems usually treated first due to their greater risks. other psychiatric conditions include reactive attachment disorder, characterised by a severe inability to appropriately relate socially, and sluggish cognitive tempo, a cluster of symptoms that potentially comprises another attention disorder and may occur in 30–50% of adhd cases, regardless of the subtype. individuals with adhd are three times more likely to develop and be diagnosed with an eating disorder compared to those without adhd; conversely, individuals with eating disorders are two times more likely to have adhd than those without eating disorders. trauma adhd, trauma, and adverse childhood experiences are also comorbid, which could in part be potentially explained by the similarity in presentation between different diagnoses. the symptoms of adhd and ptsd can have significant behavioural overlap—in particular, motor restlessness, difficulty concentrating, distractibility, irritability/anger, emotional constriction or dysregulation, poor impulse control, and forgetfulness are common in both. this could result in trauma-related disorders or adhd being mis-identified as the other. additionally, traumatic events in childhood are a risk factor for adhd - it can lead to structural brain changes and the development of adhd behaviours. finally, the behavioural consequences of adhd symptoms cause a higher chance of the individual experiencing trauma (and therefore adhd leads to a concrete diagnosis of a trauma-related disorder). non-psychiatric some non-psychiatric conditions are also comorbidities of adhd. this includes epilepsy, a neurological condition characterised by recurrent seizures. there are well established associations between adhd and obesity, asthma and sleep disorders, and an association with celiac disease. children with adhd have a higher risk for migraine headaches, but have no increased risk of tension-type headaches. in addition, children with adhd may also experience headaches as a result of medication. a 2021 review reported that several neurometabolic disorders caused by inborn errors of metabolism converge on common neurochemical mechanisms that interfere with biological mechanisms also considered central in adhd pathophysiology and treatment. this highlights the importance of close collaboration between health services to avoid clinical overshadowing. suicide risk systematic reviews conducted in 2017 and 2020 found strong evidence that adhd is associated with increased suicide risk across all age groups, as well as growing evidence that an adhd diagnosis in childhood or adolescence represents a significant future suicidal risk factor. potential causes include adhd's association with functional impairment, negative social, educational and occupational outcomes, and financial distress. a 2019 meta-analysis indicated a significant association between adhd and suicidal spectrum behaviours (suicidal attempts, ideations, plans, and completed suicides); across the studies examined, the prevalence of suicide attempts in individuals with adhd was 18.9%, compared to 9.3% in individuals without adhd, and the findings were substantially replicated among studies which adjusted for other variables. however, the relationship between adhd and suicidal spectrum behaviours remains unclear due to mixed findings across individual studies and the complicating impact of comorbid psychiatric disorders. there is no clear data on whether there is a direct relationship between adhd and suicidality, or whether adhd increases suicide risk through comorbidities. iq test performance certain studies have found that people with adhd tend to have lower scores on intelligence quotient (iq) tests. the significance of this is controversial due to the differences between people with adhd and the difficulty determining the influence of symptoms, such as distractibility, on lower scores rather than intellectual capacity. in studies of adhd, higher iqs may be over-represented because many studies exclude individuals who have lower iqs despite those with adhd scoring on average nine points lower on standardised intelligence measures. however, other studies contradict this, saying that in individuals with high intelligence, there is an increased risk of an missed adhd diagnosis, possibly because of compensatory strategies in said individuals. studies of adults suggest that negative differences in intelligence are not meaningful and may be explained by associated health problems. causes adhd is generally claimed to be the result of neurological dysfunction in processes associated with the production or use of dopamine and norepinephrine in various brain structures, but there are no confirmed causes. it may involve interactions between genetics and the environment. genetics adhd has a high heritability of 74%, meaning that 74% of the presence of adhd in the population is due to genetic factors. there are multiple gene variants which each slightly increase the likelihood of a person having adhd; it is polygenic and arises through the combination of many gene variants which each have a small effect. the siblings of children with adhd are three to four times more likely to develop the disorder than siblings of children without the disorder. arousal is related to dopaminergic functioning, and adhd presents with low dopaminergic functioning. typically, a number of genes are involved, many of which directly affect dopamine neurotransmission. those involved with dopamine include dat, drd4, drd5, taar1, maoa, comt, and dbh. other genes associated with adhd include sert, htr1b, snap25, grin2a, adra2a, tph2, and bdnf. a common variant of a gene called latrophilin 3 is estimated to be responsible for about 9% of cases and when this variant is present, people are particularly responsive to stimulant medication. the 7 repeat variant of dopamine receptor d4 (drd4–7r) causes increased inhibitory effects induced by dopamine and is associated with adhd. the drd4 receptor is a g protein-coupled receptor that inhibits adenylyl cyclase. the drd4–7r mutation results in a wide range of behavioural phenotypes, including adhd symptoms reflecting split attention. the drd4 gene is both linked to novelty seeking and adhd. the genes gfod1 and cdh13 show strong genetic associations with adhd. chd13's association with asd, schizophrenia, bipolar disorder, and depression make it an interesting candidate causative gene. another candidate causative gene that has been identified is adgrl3. in zebrafish, knockout of this gene causes a loss of dopaminergic function in the ventral diencephalon and the fish display a hyperactive/impulsive phenotype. for genetic variation to be used as a tool for diagnosis, more validating studies need to be performed. however, smaller studies have shown that genetic polymorphisms in genes related to catecholaminergic neurotransmission or the snare complex of the synapse can reliably predict a person's response to stimulant medication. rare genetic variants show more relevant clinical significance as their penetrance (the chance of developing the disorder) tends to be much higher. however their usefulness as tools for diagnosis is limited as no single gene predicts adhd. asd shows genetic overlap with adhd at both common and rare levels of genetic variation. environment in addition to genetics, some environmental factors might play a role in causing adhd. alcohol intake during pregnancy can cause fetal alcohol spectrum disorders which can include adhd or symptoms like it. children exposed to certain toxic substances, such as lead or polychlorinated biphenyls, may develop problems which resemble adhd. exposure to the organophosphate insecticides chlorpyrifos and dialkyl phosphate is associated with an increased risk; however, the evidence is not conclusive. exposure to tobacco smoke during pregnancy can cause problems with central nervous system development and can increase the risk of adhd. nicotine exposure during pregnancy may be an environmental risk. extreme premature birth, very low birth weight, and extreme neglect, abuse, or social deprivation also increase the risk as do certain infections during pregnancy, at birth, and in early childhood. these infections include, among others, various viruses (measles, varicella zoster encephalitis, rubella, enterovirus 71). at least 30% of children with a traumatic brain injury later develop adhd and about 5% of cases are due to brain damage. some studies suggest that in a small number of children, artificial food dyes or preservatives may be associated with an increased prevalence of adhd or adhd-like symptoms, but the evidence is weak and may only apply to children with food sensitivities. the european union has put in place regulatory measures based on these concerns. in a minority of children, intolerances or allergies to certain foods may worsen adhd symptoms. individuals with hypokalemic sensory overstimulation are sometimes diagnosed as having attention deficit hyperactivity disorder (adhd), raising the possibility that a subtype of adhd has a cause that can be understood mechanistically and treated in a novel way. the sensory overload is treatable with oral potassium gluconate. research does not support popular beliefs that adhd is caused by eating too much refined sugar, watching too much television, parenting, poverty or family chaos; however, they might worsen adhd symptoms in certain people. society the youngest children in a class have been found to be more likely to be diagnosed as having adhd, possibly due to them being developmentally behind their older classmates. one study showed that the youngest children in fifth and eight grade was nearly twice as likely to use stimulant medication than their older peers. in some cases, an inappropriate diagnosis of adhd may reflect a dysfunctional family or a poor educational system, rather than any true presence of adhd in the individual. in other cases, it may be explained by increasing academic expectations, with a diagnosis being a method for parents in some countries to get extra financial and educational support for their child. behaviours typical of adhd occur more commonly in children who have experienced violence and emotional abuse. pathophysiology current models of adhd suggest that it is associated with functional impairments in some of the brain's neurotransmitter systems, particularly those involving dopamine and norepinephrine. the dopamine and norepinephrine pathways that originate in the ventral tegmental area and locus coeruleus project to diverse regions of the brain and govern a variety of cognitive processes. the dopamine pathways and norepinephrine pathways which project to the prefrontal cortex and striatum are directly responsible for modulating executive function (cognitive control of behaviour), motivation, reward perception, and motor function; these pathways are known to play a central role in the pathophysiology of adhd. larger models of adhd with additional pathways have been proposed. brain structure the left prefrontal cortex, shown here in blue, is often affected in adhd. in children with adhd, there is a general reduction of volume in certain brain structures, with a proportionally greater decrease in the volume in the left-sided prefrontal cortex. the posterior parietal cortex also shows thinning in individuals with adhd compared to controls. other brain structures in the prefrontal-striatal-cerebellar and prefrontal-striatal-thalamic circuits have also been found to differ between people with and without adhd. the subcortical volumes of the accumbens, amygdala, caudate, hippocampus, and putamen appears smaller in individuals with adhd compared with controls. structural mri studies have also revealed differences in white matter, with marked differences in inter-hemispheric asymmetry between adhd and typically developing youths. function mri (fmri) studies have revealed a number of differences between adhd and control brains. mirroring what is known from structural findings, fmri studies have showed evidence for a higher connectivity between subcortical and cortical regions, such as between the caudate and prefrontal cortex. the degree of hyperconnectivity between