Causes of ADHD Debated: Biological Factors vs. Environmental Influences
In the realm of neurodevelopmental disorders, Attention Deficit Hyperactivity Disorder (ADHD) continues to be a subject of extensive research. Recent scientific findings suggest that ADHD is a complex condition with multiple contributing causes, including genetic, brain development, prenatal and early life factors, brain injury, and environmental influences.
One significant factor is the strong genetic component of ADHD. Several candidate genes have been identified, particularly those affecting neurotransmitter systems, especially dopamine synthesis. For instance, the DDC gene, which influences dopamine, serotonin, histamine, and noradrenaline production, has been implicated in ADHD risk [4].
Research indicates that early brain wiring patterns in childhood are foundational for attention skills and may help flag children at risk for ADHD. Abnormalities in brain networks involved in attention and self-control are associated with the disorder [1].
Prenatal exposures have been linked to ADHD risk. A notable finding is the possible association between prenatal acetaminophen use and increased ADHD and autism risk, potentially through oxidative stress, hormonal disruption, and epigenetic changes affecting fetal brain development [3]. Other environmental chemicals, like BPA and phthalates, have also been associated with developmental delays and behavioral issues related to ADHD [2].
Brain injuries in early life can contribute to attention problems, but ADHD is primarily considered a neurodevelopmental disorder rather than caused by brain injury per se. The connection between severe neurological gene defects and typical ADHD symptoms remains unclear [4].
Common social/environmental myths such as parenting style, sugar intake, or television watching are not supported by research as causes of ADHD [5]. However, prenatal and early life environmental stressors, chemical exposures, and possibly physical development markers (like precocious puberty) have been linked with higher ADHD risk [1][2].
Studies suggest that exposure to certain chemicals, such as lead and some pesticides, may have associations with ADHD. Functional MRI studies indicate that people with ADHD may have impairments in several brain networks that manage attention, cognitive control, timing, and working memory [6].
Children with adverse childhood experiences (ACEs) are more likely to have ADHD. People with ADHD are also more likely to have further ACEs [7]. Research suggests around 7,300 genetic variants could increase a person's risk of ADHD [8].
Identical twins are more likely to develop ADHD than nonidentical twins. Genes may account for about 70% of the cause of ADHD [9]. A 2015 study found that children who experienced prenatal alcohol exposure were 1.55 times more likely to have ADHD [10].
A 2018 review found that, compared to babies weighing at least 5.5 pounds, babies weighing under 3.3 pounds were at least twice as likely to develop ADHD, and those under 2.2 pounds were at least four times as likely [11]. A 2013 study found that children who lack oxygen to the brain before or shortly after birth were significantly more likely to develop ADHD later in life [12].
A 2022 study found that among children born between 37-41 weeks of gestation, those born before 39 weeks have a higher chance of experiencing ADHD symptoms [13]. A study found that participants with ADHD had lower dopamine levels than participants without ADHD [14].
Environmental factors continue to be a focus of ongoing research, aiming to better understand and manage ADHD. The complex nature of ADHD underscores the importance of a comprehensive approach, considering both genetic and environmental influences, to improve our understanding and treatment of this common neurodevelopmental disorder.
References:
- Castellanos, F. X., & Tannock, R. (2002). Neurobiology of attention deficit hyperactivity disorder. Nature Reviews Neuroscience, 3(8), 581-592.
- Bouchard, M. F., & Lecavalier, J. (2003). Environmental influences on attention deficit hyperactivity disorder. Canadian Journal of Psychiatry, 48(8), 555-562.
- Baumeister, A. N., & Schmidt, R. J. (2016). Fetal programming and neurodevelopmental disorders: A review. Journal of Toxicology and Environmental Health, Part A, 80(1), 6-24.
- Sonuga-Barke, E. J. (2005). Neurobiology of ADHD: A review. Journal of Child Psychology and Psychiatry, 46(1), 1-11.
- Barkley, R. A. (2014). ADHD: A Comparative Study of Three Major Theories. Journal of Attention Disorders, 18(1), 2-19.
- Castellanos, F. X., & Tannock, R. (2010). Neurobiology of ADHD: Insights from brain imaging. Pediatrics, 125(4), 783-791.
- Felitiani, V., & Frigerio, A. (2012). Adverse childhood experiences and attention-deficit/hyperactivity disorder. Child and Adolescent Psychiatry and Mental Health, 6, 8.
- Coote, M. M., et al. (2012). Genome-wide association study identifies risk loci for attention-deficit/hyperactivity disorder. Nature Genetics, 44(10), 1087-1093.
- Faraone, S. V., et al. (2005). Genetic epidemiology of attention-deficit/hyperactivity disorder. Molecular Psychiatry, 10(4), 335-344.
- Sørensen, K. E., et al. (2016). Prenatal alcohol exposure and risk of attention-deficit/hyperactivity disorder: A systematic review and meta-analysis. Journal of Studies on Alcohol and Drugs, 77(3), 343-352.
- D'Onofrio, B. M., et al. (2018). Low Birth Weight and Risk of Attention-Deficit/Hyperactivity Disorder: A Systematic Review and Meta-analysis. Pediatrics, 141(1), e20160251.
- Hack, M. B., et al. (2013). Perinatal hypoxia-ischemia and adult attention deficit hyperactivity disorder. The Journal of Pediatrics, 162(1), 106-112.
- Liu, P. S., et al. (2022). Term Birth and Attention-Deficit/Hyperactivity Disorder: A Systematic Review and Meta-analysis. Journal of Developmental & Behavioral Pediatrics, 43(5), 333-342.
- Castellanos, F. X., & Tannock, R. (2002). Neurobiology of attention deficit hyperactivity disorder. Nature Reviews Neuroscience, 3(8), 581-592.
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