Causes

In Brief

ADHD is partly caused by genes (the instructions that tell your body how to grow and work) and is partly related to things in the environment around us.

Let’s clear up some misconceptions…

Parenting styles don’t cause ADHD, but learning effective parenting skills is the most important way to help young children diagnosed with ADHD. The risk of ADHD becoming severe is lower when there are stable family relationships and a strong circle of supportive friends and relations in the community.

Giving your children too much sugar may well be an unhealthy diet choice, and many parents say it makes their children become hyper, but it absolutely doesn’t cause ADHD.

A mother smoking cigarettes during pregnancy may well be linked to a number of poor health outcomes, including a statistical correlation to increased risk for ADHD; however, that does not mean that the maternal smoking causes ADHD.

The primary cause is thought to be genetic

ADHD is inherited from one or both parents.

Environmental factors such as problems during pregnancy may also play a role.

But they aren’t usually direct causes of ADHD by themselves.

Key Takeaways

For most people with ADHD, many genetic and environmental risk factors accumulate to cause the disorder.
Genes:
- Some people have different versions of genes that make them more likely to have ADHD. These versions are called genetic risk variants. Most people with ADHD have many genetic risk variants, each having a very small effect. These genetic risk variants can also make people more likely to have other problems, like anxiety or depression. However, there are too many gene differences among people with and without ADHD for this to be useful in diagnosis or genetic screening.
- Some people with ADHD have rare changes in their genes that have a big effect. This is called a single gene defect or a chromosomal abnormality. These changes can also make people more likely to have other disorders, like autism or intellectual disability.
Environment:
- Things that happen or exist around you can also affect how your genes work and how you behave. These are called environmental risk factors. Sometimes, the same genes or environment that are related to ADHD can cause different disorders, like schizophrenia or bipolar disorder. This means that these disorders share some causes and some brain problems.
- Things in the environment themselves are not known to directly cause ADHD, but because environmental differences are often noticed when large numbers of people with ADHD are studied as a group, they are thought to be associated in some way. This association is called correlation, which is different from causation.
- It is important to stress that environmental factors associated with ADHD do not necessarily cause ADHD. It may be that ADHD causes some of these things, or that ADHD and some of these factors are both the result of some other unknown cause or causes. The exact relationship between these factors is not know. All that we know is that they seem to be related together somehow.
- Some environmental factors that have varying levels of correlation with ADHD are listed below.
  - Artificial or naturally occurring poisonous substances in the environment called toxicants, including childhood exposure to:
    - high levels of lead
    - cigarette smoke
    - some chemicals used in manufacturing and agriculture
    - some kinds of air pollution – particularly air pollution related to traffic
    - foods with artificial food colourings (only reported by parents)
  - Lower levels of some kinds of nutrients in the blood (this doesn’t mean you should take these as supplements unless a doctor advises it):
    - Serum ferritin – a protein that stores iron (youths)
    - Omega−3 fatty acids (youths)
    - Vitamin-D (mothers)
  - Problems during pregnancy and birth, such as:
    - Very preterm or extremely low birth weight (babies)
    - High blood pressure during pregnancy (mothers)
    - Obesity and severe obesity (mothers)
    - High levels of the thyroid hormone (mothers)
    - Multiple previous miscarriages (mothers)
    - Cystic ovary syndrome (mothers)
    - Type 1 diabetes (mothers)
  - Deprivation, stress, infection, poverty and trauma
    - Some viral infections (enterovirus)
    - Death of a close relative during pregnancy (mothers)
    - Exposure to maltreatment, abuse, or neglect (children)
    - Lower family income levels, poverty, parental unemployment, mental disorders, substance abuse, low educational attainment, not having a fixed place to live, and criminality (parents)
While you may observe increased energy levels among children after they have consumed sugary foods or drinks, no relationship has been found between eating sugar and ADHD. There may be a slight link with sugary drinks specifically, but not enough research has been done to be sure.

Details

The environmental risks for ADHD exert their effects very early in life, during the foetal or early postnatal period. In rare cases, however, ADHD-like symptoms can be caused by extreme deprivation early in life, a single genetic abnormality, or traumatic brain injury early in life. These findings are helpful to understand the causes of ADHD but are not useful for diagnosing the disorder.

The associations between aspects of the environment and the onset of ADHD have attained a very high level of evidential support. Some have strong evidence for a causal role but, for most, the possibility remains that these associations are due to correlated genetic and environmental effects. For this reason, we refer to features of the pre- and post-natal environments that increase risk for ADHD as correlates, rather than causes. The genetic and environmental risks described below are not necessarily specific to ADHD.

Genetic causes of ADHD

A review of 37 twin studies from the United States, Europe, Scandinavia, and Australia found that genes and their interaction with the environment must play a substantial role in causing ADHD.
In a genome-wide study, an international team analysed DNA from over 20,000 people with ADHD and over 35,000 without ADHD from the United States, Europe, Scandinavia, China, and Australia. They identified many genetic risk variants, each having a small effect on the risk for the disorder. This study confirmed a polygenic cause for most cases of ADHD, meaning that many genetic variants, each having a very small effect, combine to increase risk for the disorder. The polygenic risk for ADHD is associated with general psychopathology and several psychiatric disorders.
Additional genes have been implicated by meta-analyses, but their status as risk genes remains uncertain until validated in a genome-wide study. These genes are ANKK1, DAT1, LRP5 and LRP6, SNAP25, ADGRL3, DRD4 and BAIAP2.
The polygenic risk for ADHD predicts ADHD symptoms in the population, suggesting that the genetic causes of ADHD as a disorder also influence sub-threshold levels of ADHD symptoms in the population.
In the population, those with a high polygenic risk for ADHD are more likely to have been diagnosed with ADHD, anxiety, or depression.
ADHD can also be the result of rare single gene defects or abnormalities of the chromosomes. When the DNA of 8000+children with autism spectrum disorder (ASD) and/or ADHD and 5000 controls was analysed, those with ASD and those with ADHD had an increased rate of rare genetic mutations compared with controls.
Family, twin, and DNA studies show that genetic and environmental influences are partially shared between ADHD and many other psychiatric disorders (e.g. schizophrenia, depression, bipolar disorder, autism spectrum disorder, conduct disorder, eating disorders, and substance use disorders) and with somatic disorders (e.g. migraine and obesity). However, there is also a unique genetic risk for ADHD. Evidence of shared genetic and environmental risks among disorders suggest that these disorders also share a pathophysiology in the biological pathways that dysregulate neurodevelopment and create brain variations leading to disorder onset.
Very large studies of families suggest that ADHD shares genetic or familial causes with autoimmune diseases, hypospadias, and intellectual disability.
The Saudi ADHD Clinical Practice Guidelines recognise children and young people diagnosed with oppositional defiant disorder or conduct disorder, children and young people with mood disorders (for example, anxiety and depression), people with a close family member diagnosed with ADHD, people with epilepsy, people with neurodevelopmental disorders (for example, autism spectrum disorder, tic disorders, intellectual disability and specific learning difficulties), adults with mental health conditions, and people with a history of substance use disorders as having increased prevalence of ADHD compared with the general population.³

Environmental correlates of ADHD

Environmental correlates: exposure to toxicants

A pair of meta-analyses found small correlations between lead burden and inattention symptoms (27 studies, over 9300 youths) and hyperactivity-impulsivity symptoms (23 studies, over 7800 youths). A more recent meta-analysis of 14 studies with over 17,000 children reported that higher blood lead levels were associated with quadrupled odds of ADHD. A study of over 2500 youths from the National Health and Nutrition Examination Survey, a cross-sectional, nationally representative sample of the U.S. population, found that those with blood lead levels in the top third were 2.3 times more likely to have ADHD compared with those in the bottom third. A similar study, with over 4700 youths from the same national survey, found that those with blood lead levels in the highest fifth were four times more likely to have ADHD compared with those in the bottom fifth.
Three meta-analyses with over twenty studies covering more than three million persons have found prenatal exposure to maternal smoking associated with a greater than 50% increase in incidence of ADHD. Although this association has also been seen in large population studies, it disappears after adjusting for family history of ADHD, which indicates that the association between maternal smoking during pregnancy and ADHD is due to familial or genetic factors that increase the risk for both smoking and ADHD.
A meta-analysis of nine studies spanning three continents and over 100,000 participants found that childhood exposure to secondhand cigarette smoke was associated with a 60% greater likelihood of ADHD. It was unclear to what extent the association was causal versus due to confounders.
In a meta-analysis of 15 double-blind, placebo-controlled trials with 219 participants, artificial food dyes were associated with a small increase in hyperactivity in children. Another meta-analysis, covering 20 studies with a combined total of 794 individuals, found a very small increase in ADHD symptoms, but only when rated by parents, not by teachers or other observers.
In a Taiwanese study of over 10,000 births, maternal use of acetaminophen during pregnancy was associated with a 33% greater likelihood of ADHD in their children. Another study, examining 113,000 offspring from the Norwegian Mother and Child Cohort Study and the Norwegian Patient Registry, including 2246 with ADHD, found a dose-response relationship between maternal prenatal use of acetaminophen and ADHD.
A nationwide study using the Danish national registers looked at 913,000 children born between 1997 and 2011. Prenatal exposure to the anti-epileptic drug valproate was associated with a 50% greater risk of ADHD. No associations were found for other anti-epileptic drugs.
In a Norwegian registry study, 297 children with ADHD and 553 controls were randomly sampled from an eligible population of over 24,000. Children of mothers in the highest quintile of phthalate metabolite levels were three times more likely to have had ADHD as children compared with those in the bottom quintile, after adjusting for confounders, such as maternal age at delivery, sex of the child, maternal education, marital status, and prenatal maternal smoking.
Organophosphate pesticides are potent neurotoxins. In a sample of 1139 children from the U.S. population, a tenfold increase in the organophosphate metabolite dimethyl alkylphosphate (DMAP) was associated with 55% increase in the probability of having ADHD. Children with detectable levels of the most- commonly detected DMAP metabolite were twice as likely to have ADHD compared with those with undetectable levels.
A meta-analysis found no significant effect of two classes of air pollutants – particulate matter (six studies, over 51,000 persons) and nitrogen oxides (five studies, over 51,000 persons). A Taiwan-wide longitudinal cohort study geo-linking over 16,000 mother-infant pairs to levels of air pollutants found no association between small particulate matter levels, sulphur dioxide levels, or nitrogen dioxide levels during gestation and ADHD diagnoses in the first eight years of their offsprings’ lives. It did find 25% greater odds for having ADHD with exposures to nitric oxide, a common traffic pollutant.
A nationwide cohort study used the South Korean national health insurance registry to identify all 7200 hospital admissions of adolescents with a primary diagnosis of ADHD from 2013 to 2015, and daily readings of three air pollutants from 318 monitoring stations distributed across the country over the same period. It found that spikes in nitrogen dioxide, sulphur dioxide, and particulate matter were associated, respectively, with 47%, 27%, and 12% increases in ADHD related hospital admissions in succeeding days. There were no significant differences between male and female adolescents, or between older and younger adolescents.
A meta-analysis of nine European population studies encompassing 4826 mother-child pairs examined the relationship between exposure to Perfluoroalkyl Substances (PFAS) via breast milk in infancy and development of ADHD. No associations were found with ADHD in offspring.
A meta-analysis of seven studies encompassing a total of over 25,000 participants from six countries on three continents found no evidence of an association between sugar consumption and ADHD in youth.¹ Two studies that looked exclusively at sugar-sweetened beverages reported an 80% increase in the odds of ADHD; however there was no way to evaluate publication bias or to conduct a proper meta-analysis.²
After adjusting for age, sex, race/ethnicity, education level, family income to poverty ratio, and geographic region, youths with food allergies were found to be over 70% more likely to be diagnosed with ADHD than those without food allergies. After further mutual adjustment for other allergic conditions, they were still well over 40% more likely to be diagnosed with ADHD than their non-allergic peers.²

Environmental correlates: nutrient deficiencies

A pair of meta-analyses found no difference in serum iron levels in youths with ADHD (six studies, 617 participants) but small-to- moderate reductions in serum ferritin, a protein that stores iron (ten studies, over 2100 participants). Another pair of meta-analyses likewise found no difference in serum iron levels (six studies, over 1700 participants) but small-to-moderate reductions in serum ferritin (12 studies, over 6000 participants).
A meta-analysis of nine studies and 586 people found moderately lower overall blood levels of omega-3 PUFAs in ADHD than non- ADHD youth.
A nationwide population-based case-control study using the Finnish national registers compared 1067 patients with ADHD born between 1998 and 1999 with 1067 matched controls. Lower maternal vitamin D levels were associated with a roughly 50% greater likelihood of ADHD in their children.
Clinicians may wish to refer to the Saudi ADHD Clinical Practice Guidelines section on dietary guidance³.

Environmental correlates: events during pregnancy and birth

A meta-analysis of twelve studies with over 6000 participants found a threefold increase in the rate of ADHD among very/ extremely preterm or very/extremely low birth weight babies. Another meta-analysis, combining 85 studies with a total of over 4.6 million births, found a small-to-moderate correlation between low birth weight and ADHD. A Swedish national register study of 1.2 million children found a stepwise increase in the likelihood of ADHD with increasing prematurity. Results were not due to having an ADHD relative or socioeconomic stress. Similar results were reported from the Finnish national registers when comparing over 10,000 people with ADHD with over 38,000 controls.¹ A study conducted in Saudi Arabia by Professor Mohammed Alqahtani in 2016 found a correlation with increased risk of ADHD and additional learning needs in school aged children,⁴ and the Saudi ADHD Clinical Practice Guidelines recognise people born preterm as having increased prevalence of ADHD compared with the general population.³
A meta-analysis of six studies combining 1.4 million people found that children whose mothers had hypertensive disorders during pregnancy had a 25% increase in the rate of ADHD.
A nationwide population-based cohort study using Swedish registers and covering more than two million children, 115,000 of them with ADHD, found that maternal preeclampsia during pregnancy is associated with a 15% greater subsequent likelihood of ADHD in offspring, rising to over 40% when the foetus is small for gestational age and exposed to preeclampsia. This pattern in families showed that it is not due to genetic or other family influences.
Two meta-analyses, one with seven studies with over 28,000 participants and another with three studies and over 1.4 million participants, found that children of obese mothers were roughly 60% more likely to develop ADHD. A study of over 80,000 mother-child pairs participating in the Danish National Birth Cohort reported an almost 50% elevated risk of ADHD in children of obese mothers and a doubled risk in children of severely obese mothers.
A meta-analysis of two large cohort studies with a combined total of over 3.1 million persons found a slight but significant association between maternal hyperthyroidism during pregnancy and ADHD in offspring. A second meta-analysis of four cohort studies encompassing over 3.4 million participants likewise found a slight but significant association between maternal hypothyroidism and ADHD in offspring. No attempt was made to assess the role of confounders.
A nationwide cohort study using Danish national registers examined over a million births, comparing offspring of mothers with a single prior miscarriage and mothers with more than one prior miscarriage with mothers with no history of miscarriage. It found that after adjusting for a wide range of possible confounders which turned out to have little effect, children of mothers with a single prior miscarriage were 9% more likely to develop ADHD than those of mothers without any miscarriage. Children of mothers with two or more prior miscarriages were 22% more likely to be diagnosed with ADHD. This upward exposure-response trend was statistically significant.
A meta-analysis found that children born to mothers with polycystic ovary syndrome (PCOS) were 43% more likely to develop ADHD. The 95% confidence interval stretched from 35% to 51%, indicating a highly reliable finding. Moreover, there was between-study variation: They all produced essentially identical results. There was also no sign of publication bias.²
A Taiwanese study utilising the Taiwan National Health Insurance Research Database (NHIRD) found that persons with type 1 diabetes (T1DM) were found to be 8 times more likely to be diagnosed with ADHD than those who were not diabetic. They noted that the exact path of mechanisms between T1DM and ADHD should be elucidated in future studies.²
A Swedish nationwide cohort study finds Cesarean delivery (CD) does not appear to be a risk factor for ADHD. Findings of this study suggest that the association between CD and increased risk of neurodevelopmental disorders in the children is most likely explained by unmeasured familial confounding.²
A Chinese meta-analysis found that childhood antibiotic exposure does not appear to be a risk factor for ADHD. The meta-analysis of six studies with a combined total of over 1.5 million participants indicated that while early-life antibiotic exposure was associated with a subsequent 18% increased risk of ASD or ADHD, such association was not found in the sibling-matched analysis, indicating that genetic and familial confounding factors may largely explain the observed association.²

Environmental correlates: deprivation, stress, infection, poverty and trauma

A Taiwan-wide longitudinal cohort study based on the country’s universal coverage National Health Insurance Research Database compared over 14,000 enterovirus patients (ER71) with an equal number of controls matched by age and sex. After further adjusting for paternal occupation and urbanisation level of residence it found the enterovirus patients were 25 percent more likely to subsequently be diagnosed with ADHD.
A nationwide population-based cohort study using Danish registers compared over 29,000 children born to women who lost a close relative during pregnancy with a million other children in the same cohort and found that boys born to these women were twice as likely to have ADHD.
A U.S. population-based study of over 14,000 participants in the National Longitudinal Study of Adolescent Health found that after adjusting for demographic, socioeconomic, and familial risk factors for child maltreatment, ADHD inattentive type was associated with having been exposed to sexual abuse and physical neglect.
A nationwide population-based cohort study of over 18,000 children from the South Korean National Health Insurance database found that lower levels of family income were associated with increased rates of ADHD. A Swedish study of over 800,000 people reported similar results even after adjusting for shared familial/genetic risk factors in families.
A Danish national register longitudinal cohort study of a million people found that Rutter’s indicators of adversity were predictive of ADHD. Out-of-home care was strongly predictive; low social class, paternal criminality, maternal mental disorder, and severe marital discord were moderately predictive. Large family size had no effect.
A countrywide population study using Danish national registers looked at over 630,000 youths and found dose-response relationships between lower parental educational attainment, parental unemployment, and parental relative poverty and higher risk of ADHD in offspring. Combinations of social disadvantages had cumulative risks. For instance, parental relative income poverty plus completion of no more than compulsory education plus unemployment was associated with a roughly five percent higher risk of ADHD in their offspring.
A Swedish national register cohort study of over 540,000 people found a dose-response relationship between cumulative indicators of adversity in the family and ADHD. A death in the family increased the subsequent likelihood of ADHD by 60%. Substantial parental substance abuse, criminality, or psychiatric disorder each more than doubled the likelihood as did residential instability and household public assistance.
In a Saudi Arabian meta-analysis in 2023, children of women with psychological disorders during pregnancy, insufficient vitamin B during pregnancy, allergic reactions, and disabling symptoms of muscle pain during pregnancy were associated with an increased risk of ADHD.⁵
In a 2022 Saudi Arabian cross-sectional study conducted in Jeddah by Dr Waleed Alghamdi et al. multivariate analyses revealed that high family income, low grade in the last semester, parental divorce, diagnosis and severity of depression and anxiety, and cigarette smoking increased the likelihood of adult ADHD.⁶
In a 2021 Saudi Arabian study conducted in Jeddah by Dr Faten Al Zaben et al. among school-aged children found that early parental loss, head trauma, motor/language delay, family psychiatric problems, and high family stress were among the risk factors for ADHD. For children diagnosed with ADHD, older age, family psychiatric history, and presence of motor/language delay were identified as risk factors for psychiatric comorbidity, while high family stress, family psychiatric problems, and chronic illness were predictors of academic and behavioural impairment.⁷
In 2004, Abdulfattah et al. published the results of a 2-phase cross-sectional/case-control study examining emotional and behavioural problems among school boys in Taif, Saudi Arabia. While ADHD was not measured specifically, problems studied included hyperactivity, aggression, anxiety, and depression. It was reported that unwanted pregnancy, history of meningitis, accidents and bronchial asthma increased risk of emotional and/or behavioural disturbances.⁸
The Saudi ADHD Clinical Practice Guidelines recognise looked-after children and young people (e.g. those living in care homes such as orphanages or juvenile detention facilities), people known to the youth or adult criminal justice organisations, and people with acquired brain injury as having increased prevalence of ADHD compared with the general population.³
In a sample of 4122 U.S. youths with ADHD from the 2016 U.S. National Survey of Children’s Health, greater family cohesion and community support decreased the risk for moderate to severe ADHD.

Sources

All information is from source #1 unless specifically referenced by number in the text above.