ADHD is a relatively common disorder of children and adolescents with incidence rates of 3-6% amongst children and lowering amongst adults (Linnet et al 2003). ADHD is frequently associated with inattentiveness, hyperactivity and impulsive behaviour and is strongly linked to poor academic achievement, addiction and misdemeanours warranting disciplinary action. The three main subtypes of ADHD are inattentive, hyperactive and combined, with the latter being a combination of the former two and considered to be more serious due to greater correlation with poor academic achievement and felony.

It has been proven that ADHD is highly heritable, with twin studies showing that ADHD is genetically conserved at a range of between 60-90% (A.E. Doyle et al. 2005).

Further studies into the biological basis of the disorder indicate that children with specific versions of genes associated with ADHD have depleted brain tissue in the regions governing attention. However, the National Institute of Mental Health has clarified that this observation is transient and that children bearing this gene version displayed normal phenotype in later years, with corresponding improvement in ADHD symptoms (Shaw et al 2007).

Consumption of alcohol, drugs and cigarettes during pregnancy also corelates with higher incidence of ADHD in children. High alcohol consumption by pregnant mothers increases risk of Foetal Alcohol Spectrum Disorder which inherently displays the main symptoms of ADHD (Linnet et al 2003). Alcohol disrupts epigenetic modulation of gene expression in all three possible ways. Namely DNA methylation, histone modification and non-coding RNA. The gross effects of alcohol on Foetal brain development has been further experimentally verified in monkey test subjects, which invariably display symptoms of ADHD. Alcohol also inhibits neuroendocrine hormonal production which attenuates brain growth.

ADHD has a greater chance of occurring in individuals with a family history of depression. It also occurs with greater frequency in children possessing conduct disorder, tic disorder, learning disabilities or Tourette’s syndrome. Additionally, premature birth or low birth weight are factors increasing the risk of ADHD. These suggest a strong biological influence governs expression of ADHD with genetic heritability being the origin in an estimated 70% of cases (Faraone S.V., Larsson H. 2018).

Environmental factors which have been proven to increase ADHD risk include high levels of lead and injury to the prefrontal brain regions controlling attention. It is posited that lead can alter cognition and behaviour by facilitating hyperoxia mediated cell death. It also has epigenetic implications whereby it binds to histones in the hippocampus thus mediating gene expression in a sustained manner, which subsequently affects behaviour (Luo et al 2019).

There is some evidence that particular genes influence ADHD. These include genes for dopamine receptor and transporters, serotonin receptors and transporters, norepinephrine transporter, noradrenergic receptor, monoamine oxidase-A, catechol-O-methyltransferase and one GABA receptors. Although there is strong evidence linking the aforementioned genes with ADHD. Research has been inconsistent and inconclusive as the genes in question seem to play a small role in contributing towards the overall expression of ADHD (Luo et al 2019).

Although childhood ADHD has been commonly linked to excessive sugar intake and consumption of artificial food additives. There is inconclusive evidence to support these claims. Side effects of some drugs such as those used to treat seizure have elicited ADHD symptoms, but these are impermanent and resolve soon after cessation of administration of the drug.

Expression of ADHD bears a highly complex aetiology with no single factor alone being proven to cause it. There is clearly a very strong hereditary correlation as evidenced by twin studies and the main regions of the brain involved look to be narrowed down to prefrontal lobes and hippocampus. The environmental factors which appear to increase risk of the disorder are dominated by biological based influences. However, there seems to be little in the way of concrete determining factors and future research to further pinpoint the root causes is obligatory for furthering our understanding of this relatively common yet highly complex disorder.

 

A Review of Heterogeneity in Attention Deficit/Hyperactivity Disorder (ADHD) (2019). Yuyang Luo, Dana Weibman, Jeffrey M. Halperin and Xiaobo Li. Frontiers in Human Neuroscience 11 February 2019

 

Maternal Lifestyle Factors in Pregnancy Risk of Attention Deficit Hyperactivity Disorder and Associated Behaviors: Review of the Current Evidence (2003). Linnet K.M, Dalsgaard S, Obel C, Wisborg K, Henriksen T.B, Rodriguez A, Kotimaa A, Moilanen I, Thomsen P.H, Olsen J, Marjo-Riitta Jarvelin. American Journal of Psychiatry 160:6, June 2003

 

Understanding the Link Between Lead Toxicity and ADHD (2016). Joel T. Nigg. Psychiatric Times, September 30, 2016

 

Genetics of attention deficit hyperactivity disorder (2018). Faraone S.V., Larsson H. Molecular Psychiatry. June 2018

 

Attention-Deficit/Hyperactivity Disorder Endophenotypes (2005). Alysa E. Doyle, Erik G. Willcutt, Larry J. Seidman, Joseph Biederman, Virginie-Anne Chouinard, Julie Silva, and Stephen V. Faraone. Biological Psychiatry 2005;57:1324 –1335

 

Polymorphisms of the dopamine D4 receptor, clinical outcome and cortical structure in attention-deficit/hyperactivity disorder (2007). Shaw P, Gornick M, Lerch J, Addington A, Seal J, Greenstein D, Sharp W, Evans A, Giedd J.N, Castellanos F.X, Rapoport J.L. Archives of General Psychiatry, 2007 Aug; 64(8):921-931