Editing Attention deficit hyperactivity disorder (section)

==Causes==
ADHD arises from brain maldevelopment especially in the prefrontal executive networks that can arise either from genetic factors (different gene variants and mutations for building and regulating such networks) or from acquired disruptions to the development of these networks and regions involved in [[executive functioning]] and self-regulation.<ref name="Faraone_2021" /><ref name="Antshel_2014" /> Their reduced size, functional connectivity, and activation contribute to the pathophysiology of ADHD, as well as imbalances in the noradrenergic and dopaminergic systems that mediate these brain regions.<ref name="Faraone_2021" /><ref name="Biederman_2005">{{cite journal |vauthors=Biederman J |title=Attention-deficit/hyperactivity disorder: a selective overview |journal=[[Biological Psychiatry (journal)|Biological Psychiatry]] |volume=57 |issue=11 |pages=1215–1220 |date=June 2005 |pmid=15949990 |doi=10.1016/j.biopsych.2004.10.020 |s2cid=23671547}}</ref>

Genetic factors play an important role; ADHD has a heritability rate of 70-80%. The remaining 20-30% of variance is mediated by de-novo mutations and non-shared environmental factors that provide for or produce brain injuries; there is no significant contribution of the rearing family and social environment.{{refn|<ref name=hl/><ref name="Faraone_2019"/><ref name="pmid20141238">{{cite journal |vauthors=Nikolas MA, Burt SA |title=Genetic and environmental influences on ADHD symptom dimensions of inattention and hyperactivity: a meta-analysis |journal=[[Journal of Abnormal Psychology]] |volume=119 |issue=1 |pages=1–17 |date=February 2010 |pmid=20141238 |doi=10.1037/a0018010}}</ref><ref>{{cite journal |vauthors=Demontis D, Walters RK, Martin J, Mattheisen M, Als TD, Agerbo E, Baldursson G, Belliveau R, Bybjerg-Grauholm J, Bækvad-Hansen M, Cerrato F, Chambert K, Churchhouse C, Dumont A, Eriksson N, Gandal M, Goldstein JI, Grasby KL, Grove J, Gudmundsson OO, Hansen CS, Hauberg ME, Hollegaard MV, Howrigan DP, Huang H, Maller JB, Martin AR, Martin NG, Moran J, Pallesen J, Palmer DS, Pedersen CB, Pedersen MG, Poterba T, Poulsen JB, Ripke S, Robinson EB, Satterstrom FK, Stefansson H, Stevens C, Turley P, Walters GB, Won H, Wright MJ, Andreassen OA, Asherson P, Burton CL, Boomsma DI, Cormand B, Dalsgaard S, Franke B, Gelernter J, Geschwind D, Hakonarson H, Haavik J, Kranzler HR, Kuntsi J, Langley K, Lesch KP, Middeldorp C, Reif A, Rohde LA, Roussos P, Schachar R, Sklar P, Sonuga-Barke EJ, Sullivan PF, Thapar A, Tung JY, Waldman ID, Medland SE, Stefansson K, Nordentoft M, Hougaard DM, Werge T, Mors O, Mortensen PB, Daly MJ, Faraone SV, Børglum AD, Neale BM |title=Discovery of the first genome-wide significant risk loci for attention deficit/hyperactivity disorder |journal=[[Nature Genetics]] |volume=51 |issue=1 |pages=63–75 |date=January 2019 |pmid=30478444 |pmc=6481311 |doi=10.1038/s41588-018-0269-7 |hdl-access=free |hdl=10023/20827}}</ref><ref name="Intergenerational" /><ref name="Grimm_2020">{{cite journal |vauthors=Grimm O, Kranz TM, Reif A |title=Genetics of ADHD: What Should the Clinician Know? |journal=[[Current Psychiatry Reports]] |volume=22 |issue=4 |page=18 |date=February 2020 |pmid=32108282 |pmc=7046577 |doi=10.1007/s11920-020-1141-x }}</ref>}} Very rarely, ADHD can also be the result of abnormalities in the chromosomes.<ref>{{cite journal |vauthors=Cederlöf M, Ohlsson Gotby A, Larsson H, Serlachius E, Boman M, Långström N, Landén M, Lichtenstein P |title=Klinefelter syndrome and risk of psychosis, autism and ADHD |journal=[[Journal of Psychiatric Research]] |volume=48 |issue=1 |pages=128–130 |date=January 2014 |pmid=24139812 |doi=10.1016/j.jpsychires.2013.10.001}}</ref>

=== Genetics ===
{{See also|Missing heritability problem}}

In November 1999, ''[[Biological Psychiatry (journal)|Biological Psychiatry]]'' published a [[literature review]] by psychiatrists [[Joseph Biederman]] and Thomas Spencer found the average [[heritability]] estimate of ADHD from [[Twin study|twin studies]] to be 0.8,<ref>{{cite journal |vauthors=Biederman J, Spencer T |title=Attention-deficit/hyperactivity disorder (ADHD) as a noradrenergic disorder |journal=[[Biological Psychiatry (journal)|Biological Psychiatry]] |volume=46 |issue=9 |pages=1234–1242 |date=November 1999 |pmid=10560028 |doi=10.1016/S0006-3223(99)00192-4 |publisher=[[Elsevier]] |s2cid=45497168 |author1-link=Joseph Biederman}}</ref> while a subsequent [[Family study|family]], twin, and [[Adoption study|adoption studies]] literature review published in ''[[Molecular Psychiatry]]'' in April 2019 by psychologists [[Stephen Faraone]] and Henrik Larsson that found an average heritability estimate of 0.74.<ref name="Faraone_2019" /> Additionally, [[Evolutionary psychiatry|evolutionary psychiatrist]] [[Randolph M. Nesse]] has argued that the 5:1 [[Sex differences in psychology|male-to-female sex ratio]] in the [[Mental disorders and gender|epidemiology of ADHD]] suggests that ADHD may be the [[Variability hypothesis|end of a continuum where males are overrepresented at the tails]], citing clinical psychologist [[Simon Baron-Cohen]]'s [[Empathising–systemising theory|suggestion]] for the [[Sex differences in autism|sex ratio in the epidemiology of autism]] as an analogue.<ref name="Baron-Cohen 2002">{{cite journal |vauthors=Baron-Cohen S |title=The extreme male brain theory of autism |journal=[[Trends in Cognitive Sciences]] |volume=6 |issue=6 |pages=248–254 |date=June 2002 |pmid=12039606 |doi=10.1016/S1364-6613(02)01904-6 |url=https://www.cell.com/trends/cognitive-sciences/fulltext/S1364-6613(02)01904-6 |access-date=9 July 2020 |publisher=[[Elsevier]] |url-status=live |s2cid=8098723 |archive-url=https://web.archive.org/web/20130703172532/http://www.cell.com/trends/cognitive-sciences/fulltext/S1364-6613(02)01904-6 |archive-date=3 July 2013 |author-link=Simon Baron-Cohen}}</ref><ref name="Nesse 2005 p. 918">{{cite book |vauthors=Nesse RM |author1-link=Randolph M. Nesse |veditors=Buss DM |editor-link=David Buss |title=The Handbook of Evolutionary Psychology |chapter=32. Evolutionary Psychology and Mental Health |page=918 |year=2005 |edition=1st |place=[[Hoboken, New Jersey|Hoboken, NJ]] |publisher=[[Wiley (publisher)|Wiley]] |isbn=978-0-471-26403-3}}</ref><ref name="Nesse 2016 p. 1019">{{cite book |vauthors=Nesse RM |author-link1=Randolph M. Nesse |veditors=Buss DM |editor1-link=David Buss |year=2016 |orig-date=2005 |title=The Handbook of Evolutionary Psychology, Volume 2: Integrations |edition=2nd |chapter=43. Evolutionary Psychology and Mental Health |page=1019 |place=[[Hoboken, New Jersey|Hoboken, NJ]] |publisher=[[Wiley (publisher)|Wiley]] |isbn=978-1-118-75580-8}}</ref>

[[Evolution by natural selection|Natural selection]] has been acting against the genetic variants for ADHD over the course of at least 45,000 years, indicating that it was not an adaptive trait in ancient times.<ref>{{cite journal |vauthors=Esteller-Cucala P, Maceda I, Børglum AD, Demontis D, Faraone SV, Cormand B, Lao O |title=Genomic analysis of the natural history of attention-deficit/hyperactivity disorder using Neanderthal and ancient Homo sapiens samples |journal=[[Scientific Reports]] |volume=10 |issue=1 |page=8622 |date=May 2020 |pmid=32451437 |pmc=7248073 |doi=10.1038/s41598-020-65322-4 |bibcode=2020NatSR..10.8622E}}</ref> The disorder may remain at a stable rate by the balance of genetic mutations and removal rate (natural selection) across generations; over thousands of years, these genetic variants become more stable, decreasing disorder prevalence.<ref>{{cite journal |vauthors=Keller MC |title=The evolutionary persistence of genes that increase mental disorders risk. |journal=[[Current Directions in Psychological Science]] |date=December 2008 |volume=17 |issue=6 |pages=395–399 |doi=10.1111/j.1467-8721.2008.00613|doi-broken-date=24 April 2025 }}</ref> Throughout human evolution, the executive functions involved in ADHD likely provide the capacity to bind contingencies across time thereby directing behaviour toward future over immediate events so as to maximise future social consequences for humans.<ref>{{cite book |vauthors=Barkley RA |date=2004 |chapter=Attention-deficit/hyperactivity disorder and self-regulation: Taking an evolutionary perspective on executive functioning. |veditors=Baumeister RF, Vohs KD |title=Handbook of self-regulation: Research, theory, and applications |pages=301–323 |publisher=[[Guilford Press]] |url=https://psycnet.apa.org/record/2004-00163-014}}</ref>

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 disease|polygenic]] and thus arises through the accumulation of many genetic risks each having a very small effect.<ref name="Faraone_2021" /><ref name="Faraone_2019" /> The siblings of children with ADHD are three to four times more likely to develop the disorder than siblings of children without the disorder.<ref>{{cite book |vauthors=Nolen-Hoeksema S |title=Abnormal Psychology |year=2013 |isbn=978-0-07-803538-8 |page=267 |publisher=[[McGraw-Hill Education]] |edition=6th}}</ref>

The association of maternal smoking observed in large population studies 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 the confluence of smoking and ADHD.<ref>{{cite journal |vauthors=Skoglund C, Chen Q, D'Onofrio BM, Lichtenstein P, Larsson H |title=Familial confounding of the association between maternal smoking during pregnancy and ADHD in offspring |journal=[[Journal of Child Psychology and Psychiatry|Journal of Child Psychology and Psychiatry, and Allied Disciplines]] |volume=55 |issue=1 |pages=61–68 |date=January 2014 |pmid=25359172 |pmc=4217138 |doi=10.1111/jcpp.12124}}</ref><ref>{{cite journal |vauthors=Obel C, Zhu JL, Olsen J, Breining S, Li J, Grønborg TK, Gissler M, Rutter M |title=The risk of attention deficit hyperactivity disorder in children exposed to maternal smoking during pregnancy - a re-examination using a sibling design |journal=[[Journal of Child Psychology and Psychiatry|Journal of Child Psychology and Psychiatry, and Allied Disciplines]] |volume=57 |issue=4 |pages=532–537 |date=April 2016 |pmid=26511313 |doi=10.1111/jcpp.12478 |url=https://kclpure.kcl.ac.uk/portal/en/publications/b67579b4-68c2-4010-86c4-0392822d2662}}</ref>

ADHD presents with reduced size, functional connectivity and activation<ref name="Faraone_2021" /> as well as low noradrenergic and dopaminergic functioning<ref name="Biederman_2005" /><ref>{{cite journal |vauthors=Hinshaw SP |title=Attention Deficit Hyperactivity Disorder (ADHD): Controversy, Developmental Mechanisms, and Multiple Levels of Analysis |journal=[[Annual Review of Clinical Psychology]] |volume=14 |issue=1 |pages=291–316 |date=May 2018 |pmid=29220204 |doi=10.1146/annurev-clinpsy-050817-084917 }}</ref> in brain regions and networks crucial for executive functioning and self-regulation.<ref name="Faraone_2021" /><ref name="Barkley_2011a" /><ref name="Antshel_2014" /> Typically, a number of genes are involved, many of which directly affect brain functioning and neurotransmission.<ref name="Faraone_2021" /> Those involved with dopamine include [[Dopamine transporter|DAT]], [[DRD4]], [[DRD5]], [[TAAR1]], [[MAOA]], [[Catechol O-methyltransferase|COMT]], and [[Dopamine-beta-hydroxylase|DBH.]]<ref name="Kebir_2011">{{cite journal |vauthors=Kebir O, Joober R |title=Neuropsychological endophenotypes in attention-deficit/hyperactivity disorder: a review of genetic association studies |journal=[[European Archives of Psychiatry and Clinical Neuroscience]] |volume=261 |issue=8 |pages=583–594 |date=December 2011 |pmid=21409419 |doi=10.1007/s00406-011-0207-5 |s2cid=21383749}}</ref><ref name="Berry_2007" /><ref>{{cite journal |vauthors=Sotnikova TD, Caron MG, Gainetdinov RR |title=Trace amine-associated receptors as emerging therapeutic targets |journal=[[Molecular Pharmacology]] |volume=76 |issue=2 |pages=229–235 |date=August 2009 |pmid=19389919 |pmc=2713119 |doi=10.1124/mol.109.055970}}</ref> Other genes associated with ADHD include [[Serotonin transporter|SERT]], [[HTR1B]], [[SNAP25]], [[GRIN2A]], [[ADRA2A]], [[TPH2]], and [[Brain-derived neurotrophic factor|BDNF]].<ref name="Gizer_2009">{{cite journal |vauthors=Gizer IR, Ficks C, Waldman ID |title=Candidate gene studies of ADHD: a meta-analytic review |journal=[[Human Genetics]] |volume=126 |issue=1 |pages=51–90 |date=July 2009 |pmid=19506906 |doi=10.1007/s00439-009-0694-x |s2cid=166017}}</ref> 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.<ref>{{cite journal |vauthors=Arcos-Burgos M, Muenke M |title=Toward a better understanding of ADHD: LPHN3 gene variants and the susceptibility to develop ADHD |journal=Attention Deficit and Hyperactivity Disorders |volume=2 |issue=3 |pages=139–147 |date=November 2010 |pmid=21432600 |pmc=3280610 |doi=10.1007/s12402-010-0030-2}}</ref> The [[DRD4–7R|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 [[phenotype]]s, including ADHD symptoms reflecting split attention.<ref>{{cite journal |vauthors=Nikolaidis A, Gray JR |title=ADHD and the DRD4 exon III 7-repeat polymorphism: an international meta-analysis |journal=[[Social Cognitive and Affective Neuroscience]] |volume=5 |issue=2–3 |pages=188–193 |date=June 2010 |pmid=20019071 |pmc=2894686 |doi=10.1093/scan/nsp049}}</ref> The DRD4 gene is both linked to novelty seeking and ADHD. The genes [[glucose-fructose oxidoreductase|GFOD1]] and [[T-cadherin|CDH13]] show strong genetic associations with ADHD. CDH13's association with ASD, [[schizophrenia]], bipolar disorder, and [[Depression (mood)|depression]] make it an interesting candidate causative gene.<ref name="Grimm_2020" /> Another candidate causative gene that has been identified is [[Latrophilin 3|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]].<ref name="Grimm_2020" />

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 polymorphism]]s in genes related to [[catecholaminergic]] neurotransmission or the [[SNARE (protein)|SNARE]] complex of the [[synapse]] can reliably predict a person's response to [[Stimulant|stimulant medication]].<ref name="Grimm_2020" /> Rare genetic variants show more relevant clinical significance as their penetrance (the chance of developing the disorder) tends to be much higher.<ref name="Zayats_2020">{{cite journal |vauthors=Zayats T, Neale BM |title=Recent advances in understanding of attention deficit hyperactivity disorder (ADHD): how genetics are shaping our conceptualization of this disorder |journal=F1000Research |volume=8 |page=2060 |date=12 February 2020 |pmid=31824658 |pmc=6896240 |doi=10.12688/f1000research.18959.2 |doi-access=free}}</ref> 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.<ref name="Zayats_2020" />

=== Environment ===

In addition to genetics, some environmental factors might play a role in causing ADHD.<ref name="Sonu_2013" /><ref name="cdc2016">{{cite web |author=CDC |title=Attention-Deficit / Hyperactivity Disorder (ADHD) |publisher=Centers for Disease Control and Prevention |url=https://www.cdc.gov/ncbddd/adhd/research.html |date=16 March 2016 |access-date=17 April 2016 |url-status=live |archive-date=14 April 2016 |archive-url=https://web.archive.org/web/20160414160548/http://www.cdc.gov/ncbddd/adhd/research.html}}</ref> Alcohol intake during pregnancy can cause [[fetal alcohol spectrum disorder]]s which can include ADHD or symptoms like it.<ref name="Burger_2011">{{cite journal |vauthors=Burger PH, Goecke TW, Fasching PA, Moll G, Heinrich H, Beckmann MW, Kornhuber J |title=[How does maternal alcohol consumption during pregnancy affect the development of attention deficit/hyperactivity syndrome in the child] |language=de |journal=Fortschritte der Neurologie-Psychiatrie |volume=79 |issue=9 |pages=500–506 |date=September 2011 |pmid=21739408 |doi=10.1055/s-0031-1273360 |trans-title=How does maternal alcohol consumption during pregnancy affect the development of attention deficit/hyperactivity syndrome in the child |type=Review |s2cid=140766296}}</ref> Children exposed to certain toxic substances, such as [[lead poisoning|lead]] or [[polychlorinated biphenyls]], may develop problems which resemble ADHD.<ref name="nimh" /><ref name="Eubig_2010">{{cite journal |vauthors=Eubig PA, Aguiar A, Schantz SL |title=Lead and PCBs as risk factors for attention deficit/hyperactivity disorder |journal=[[Environmental Health Perspectives]] |volume=118 |issue=12 |pages=1654–1667 |date=December 2010 |pmid=20829149 |pmc=3002184 |doi=10.1289/ehp.0901852 |bibcode=2010EnvHP.118.1654E |type=Review. Research Support, N.I.H., Extramural. Research Support, U.S. Gov't, Non-P.H.S.}}</ref> Exposure to the [[organophosphate]] [[insecticide]]s [[chlorpyrifos]] and [[Alkyl phosphate|dialkyl phosphate]] is associated with an increased risk; however, the evidence is not conclusive.<ref name="de_Cock_2012">{{cite journal |vauthors=de Cock M, Maas YG, van de Bor M |title=Does perinatal exposure to endocrine disruptors induce autism spectrum and attention deficit hyperactivity disorders? Review |journal=[[Acta Paediatrica]] |volume=101 |issue=8 |pages=811–818 |date=August 2012 |pmid=22458970 |doi=10.1111/j.1651-2227.2012.02693.x |type=Review. Research Support, Non-U.S. Gov't |s2cid=41748237}}</ref> Exposure to tobacco smoke during pregnancy can cause problems with central nervous system development and can increase the risk of ADHD.<ref name="nimh">{{cite web |title=Attention Deficit Hyperactivity Disorder (Easy-to-Read) |url=http://www.nimh.nih.gov/health/publications/attention-deficit-hyperactivity-disorder-easy-to-read/index.shtml |publisher=National Institute of Mental Health |year=2013 |access-date=17 April 2016 |url-status=live |archive-date=14 April 2016 |archive-url=https://web.archive.org/web/20160414031036/http://www.nimh.nih.gov/health/publications/attention-deficit-hyperactivity-disorder-easy-to-read/index.shtml}}</ref><ref name="Abbott_2012">{{cite journal |vauthors=Abbott LC, Winzer-Serhan UH |title=Smoking during pregnancy: lessons learned from epidemiological studies and experimental studies using animal models |journal=[[Critical Reviews in Toxicology]] |volume=42 |issue=4 |pages=279–303 |date=April 2012 |pmid=22394313 |doi=10.3109/10408444.2012.658506 |type=Review |s2cid=38886526}}</ref> [[Nicotine]] exposure during pregnancy may be an environmental risk.<ref>{{cite journal |vauthors=Tiesler CM, Heinrich J |title=Prenatal nicotine exposure and child behavioural problems |journal=[[European Child & Adolescent Psychiatry]] |volume=23 |issue=10 |pages=913–929 |date=October 2014 |pmid=25241028 |pmc=4186967 |doi=10.1007/s00787-014-0615-y}}</ref>

Extreme [[premature birth]], very [[low birth weight]], and extreme neglect, abuse, or social deprivation also increase the risk<ref>{{cite journal |vauthors=Botting N, Powls A, Cooke RW, Marlow N |title=Attention deficit hyperactivity disorders and other psychiatric outcomes in very low birthweight children at 12 years |journal=[[Journal of Child Psychology and Psychiatry|Journal of Child Psychology and Psychiatry, and Allied Disciplines]] |volume=38 |issue=8 |pages=931–941 |date=November 1997 |pmid=9413793 |doi=10.1111/j.1469-7610.1997.tb01612.x |url=https://onlinelibrary.wiley.com/doi/10.1111/j.1469-7610.1997.tb01612.x |access-date=22 March 2022 |url-status=live |archive-url=https://web.archive.org/web/20220517212252/https://onlinelibrary.wiley.com/doi/10.1111/j.1469-7610.1997.tb01612.x |archive-date=17 May 2022}}</ref><ref name="nimh" /><ref name="Thapar-2012">{{cite journal |vauthors=Thapar A, Cooper M, Jefferies R, Stergiakouli E |title=What causes attention deficit hyperactivity disorder? |journal=[[Archives of Disease in Childhood]] |volume=97 |issue=3 |pages=260–265 |date=March 2012 |pmid=21903599 |pmc=3927422 |doi=10.1136/archdischild-2011-300482 |type=Review. Research Support, Non-U.S. Gov't }}</ref> as do certain infections during pregnancy, at birth, and in early childhood. These infections include, among others, various viruses ([[measles]], [[Varicella zoster virus|varicella zoster]] [[encephalitis]], [[rubella]], [[enterovirus 71]]).<ref name="Millichap_2008">{{cite journal |vauthors=Millichap JG |title=Etiologic classification of attention-deficit/hyperactivity disorder |journal=[[Pediatrics (journal)|Pediatrics]] |volume=121 |issue=2 |pages=e358–e365 |date=February 2008 |pmid=18245408 |doi=10.1542/peds.2007-1332 |type=Review |s2cid=24339363}}</ref> At least 30% of children with a [[traumatic brain injury]] later develop ADHD<ref name="Eme-2012" /> and about 5% of cases are due to brain damage.<ref name="Erk_2009" />

Some studies suggest that in a small number of children, artificial [[food dye]]s or [[preservatives]] may be associated with an increased prevalence of ADHD or ADHD-like symptoms,<ref name="nimh" /><ref name="pmid22232312">{{cite journal |vauthors=Millichap JG, Yee MM |title=The diet factor in attention-deficit/hyperactivity disorder |journal=[[Pediatrics (journal)|Pediatrics]] |volume=129 |issue=2 |pages=330–337 |date=February 2012 |pmid=22232312 |doi=10.1542/peds.2011-2199 |url=http://pediatrics.aappublications.org/content/129/2/330.long |url-status=live |s2cid=14925322 |archive-url=https://web.archive.org/web/20150911071727/http://pediatrics.aappublications.org/content/129/2/330.long |archive-date=11 September 2015}}</ref> but the evidence is weak and may apply to only children with [[food sensitivities]].<ref name="Sonu_2013" /><ref name="pmid22232312" /><ref name="EncycFoodSafety">{{cite encyclopedia |vauthors=Tomaska LD, Brooke-Taylor S |title=Food Additives&nbsp;– General |pages=[{{google books|mX1XAQAAQBAJ |page=449|plainurl=yes}} 449]–54 |encyclopedia=Encyclopedia of Food Safety |volume=3 |veditors=Motarjemi Y, Moy GG, Todd EC |publisher=Elsevier/Academic Press |location=Amsterdam |edition=1st |date=2014 |isbn=978-0-12-378613-5 |oclc=865335120}}</ref> The [[European Union]] has put in place regulatory measures based on these concerns.<ref name="FDAdyecomm">{{cite web |date=March 2011 |url=https://www.fda.gov/downloads/AdvisoryCommittees/CommitteesMeetingMaterials/FoodAdvisoryCommittee/UCM248549.pdf |title=Background Document for the Food Advisory Committee: Certified Color Additives in Food and Possible Association with Attention Deficit Hyperactivity Disorder in Children |publisher=U.S. Food and Drug Administration |url-status=live |archive-date=6 November 2015 |archive-url=https://web.archive.org/web/20151106080629/https://www.fda.gov/downloads/AdvisoryCommittees/CommitteesMeetingMaterials/FoodAdvisoryCommittee/UCM248549.pdf}}</ref> In a minority of children, [[food intolerance|intolerances]] or [[food allergy|allergies]] to certain foods may worsen ADHD symptoms.<ref name="Nigg_2014" />

Individuals with [[hypokalemic sensory overstimulation]] are sometimes diagnosed as having 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]].<ref>{{Cite journal |last1=Segal |first1=Michael M. |last2=Rogers |first2=Gary F. |last3=Needleman |first3=Howard L. |last4=Chapman |first4=Catherine A. |date=2007–2012 |title=Hypokalemic Sensory Overstimulation |url=https://journals.sagepub.com/doi/10.1177/0883073807307095 |journal=[[Journal of Child Neurology]] |language=en |volume=22 |issue=12 |pages=1408–1410 |doi=10.1177/0883073807307095 |pmid=18174562 |issn=0883-0738}}</ref>

{{Anchor|ADH and Sugar}}<!-- Do not delete this code as it is used to link to this location regarding sugar and ADHD from other articles.-->
Research does not support popular beliefs that ADHD is caused by eating too much refined sugar, watching too much television, bad parenting, poverty or family chaos; however, they might worsen ADHD symptoms in certain people.<ref name="cdc2016facts">{{cite web |title=Facts About ADHD |publisher=Centers for Disease Control and Prevention |url=https://www.cdc.gov/ncbddd/adhd/facts.html |date=6 January 2016 |access-date=20 March 2016 |url-status=live |archive-date=22 March 2016 |archive-url=https://web.archive.org/web/20160322103310/http://www.cdc.gov/ncbddd/adhd/facts.html}}</ref>

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.<ref>{{cite web |url=http://www.euro.who.int/document/MNH/ebrief14.pdf |title=Mental health of children and adolescents |date=15 January 2005 |access-date=13 October 2011 |archive-url=https://web.archive.org/web/20091024102724/http://www.euro.who.int/document/MNH/ebrief14.pdf |archive-date=24 October 2009 |website=WHO Europe}}</ref>{{Better source needed|date=May 2022|reason=The current source is a briefing for a conference, with unclear provenance.}} In other cases, it may be explained by increasing academic expectations, with a diagnosis being a method for parents in some countries to obtain extra financial and educational support for their child.<ref name="Erk_2009" /> Additionally, children who enter school earlier and are of a younger age than their classmates are more likely to have educational and behavioral problems than their peers, which can make them more likely to be diagnosed with ADHD.<ref>{{Cite journal |last1=Evans |first1=William N. |last2=Morrill |first2=Melinda S. |last3=Parente |first3=Stephen T. |date=1 September 2010 |title=Measuring inappropriate medical diagnosis and treatment in survey data: The case of ADHD among school-age children |url=https://linkinghub.elsevier.com/retrieve/pii/S0167629610000962 |journal=[[Journal of Health Economics]] |volume=29 |issue=5 |pages=657–673 |doi=10.1016/j.jhealeco.2010.07.005 |pmid=20739076 |issn=0167-6296 |quote=As Elder and Lubotsky (2009) demonstrate, younger children in classes are more likely to have educational and behavioral problems compared to their peers, and therefore, some children who are relatively young compared to their classroom peers are more likely to be diagnosed with ADHD. These results suggest that the comparison sample for diagnosis should not be other children in class but rather, other children of a similar age within a class.}}</ref> Behaviours typical of ADHD occur more commonly in children who have experienced violence and emotional abuse.<ref name="NICE 2009">{{cite book |title=Attention Deficit Hyperactivity Disorder: Diagnosis and Management of ADHD in Children, Young People and Adults |author=National Collaborating Centre for Mental Health |series=NICE Clinical Guidelines |volume=72 |publisher=[[British Psychological Society]] |location=Leicester |isbn=978-1-85433-471-8 |date=2009 |url=https://www.ncbi.nlm.nih.gov/books/NBK53652/ |via=NCBI Bookshelf |url-status=live |archive-url=https://web.archive.org/web/20160113133612/http://www.ncbi.nlm.nih.gov/books/NBK53652/ |archive-date=13 January 2016}}</ref>