ADHD: I told you so, it’s genetics, not bad parenting!

The world’s largest and most comprehensive study on the origins of ADHD concludes, that 12 different and distinct loci are directly linked to ADHD, making it undeniable … It’s genetics, not bad parenting!


Even though Dr. Barkley specifically explained how ADHD is a neurobiological, genetic and highly heritable, specific neurodevelopmental disorder, all the way back in his 1997 book “ADHD and the Nature of Self-control”, which is where the first unifying theory of ADHD was put together and which has since gone done in history as the prevailing unifying scientific theory of ADHD, even today, that ‘bad parenting’ do not and cannot make a child develop ADHD, the broad public still thinks to believe that it must be due to ‘bad parenting’, anyways.

A COMPLETE explanation for what ADHD really is, really does and how to treat it – 30 videos that explains every aspect of ADHD, in detail. Dr. Russell A. Barkley, Ph.D., is the world’s foremost scientist on ADHD and have been so for more than 40 years. He is also a dear friend of mine, who took time away from his busy schedule to help me understand what ADHD is, when I was lost and trying to regain control of my life, when diagnosed at age 40. He has since become my (unofficial) mentor and still to this day, help me – help you – understand everything about ADHD. And besides that, he is a a very nice, caring and giving human being – which we all owe a great gratitude, for him helping us make our lives with ADHD more manageable. Thank You, Russ!

Fast forward 20 years and we got the proof that ADHD caused a delay in the physical growth of the brain at around 30% lag in maturation of the Inhibitory Control function, that is developed AFTER the Motor Control have already gone online, which is what really causes the hyperactive, impulsive and inattentive behavior characteristic of childhood ADHD, not ‘sensory overload’, ‘artificial food-coloring’ or ‘too much sugar, iPad or gaming’.

Since around 2013, the movement toward attributing ADHD to diets, OMEGA-3 fatty acids, cesarian birth, ‘Insecure Attachment’ and lastly, microbiota have all muddied that waters, and yet again, the general public sided with the notion that ADHD was probably due to parents giving their children way to much Western Style Diet (fast-food, sugary substances, food-coloring etc.) instead of more Kale and fish oil supplements. For a full rundown on this subject (balanced) read this systemic review.

Now, 10 years after that, scientists from all over the world (more than 140 scientist collaborated on this study) have proven that ADHD can be related to 12 distinct loci in the human genome. (A locus (plural loci) in genetics is a fixed position on a chromosome, like the position of a gene or a marker (genetic marker).

This was (or has to be) the straw that broke the Yoga-stretching, Quinoa-eating, Prius-driving, Instagram-posting, Camel-toe-showing, Millennial’s back, and now we can get back from wasting our time on countless mediocre ‘scientific’ studies, trying to manipulate scientific evidence, to fit one’s own agenda of promoting ‘psychobiotics’, ‘neurofeedback’, ‘Scientology’, ‘Big Pharma Conspiracies’, ‘Pedagogical Psychology before Medication’ or any of the claims made by a few and daily repeated mind-numbingly by people who are trying to desperately fit in with the ‘in crowd’.

Finally, We The People, who actually suffer from this disorder, may even get some recognition, especially the parents of those who suffers from ADHD, as to the fact that all their malevolent rhetoric about US may now subside … for ever …

READ’EM’N’WEEP – You’re done, game over, goodbye …

The Proof has landed …

The ‘Holy Grail’ of ADHD genetics …

Demontis and Walters et al. Discovery of the first genome-wide significant risk loci for attention deficit/hyperactivity disorder. Nature Genetics, 2018., DOI: https://doi.org/10.1038/s41588-018-0269-7, Article in Nature: https://www.nature.com/articles/s41588-018-0269-7 Or read the news article published by the study lead author, Ditte Demontis on December 10, 2018: https://mind-the-gap.live/2018/12/10/the-first-risk-genes-for-adhd-has-been-identified/

If you still cling on to your little straw, then here’s a few other articles that might help you ‘undo’ your false beliefs and emotionally based ‘Alternative Facts’ …


ADDITIONAL INFORMATION

See how Scientology ‘explains’ ADHD … WARNING – ‘ADDspeaker is not reliable for any harm that might result in getting into their manipulative world – enter at your own peril!’
Excellent video that describes what ADHD really is …
Explains how Dopamine works in the Brain and what the difference is between medical use and substance abuse … ADHD causes a chronic Dopamine insufficiency in the brain, which is why we need medicine. Since our natural level of Dopamine is so low from birth, medication is needed to raise our Dopamine levels to near normal, so that neuroplasticity can help us overcome our deficits and impairments.
Explains how neuroplasticity works (and why ADHD medication can help alleviate symptoms of ADHD, if taking early in life and up until age 30.
Dr. Barkley explains what ADHD does to our Executive Functions
Dr. Barkley explains the neuroanatomy and neuropsychology of ADHD
Video from ‘ADHD Awareness Month 2018’
http://addspeaker.net/adhd-social-cognition-is-almost-as-bad-as-in-asd
Article that explains how Social Cognition is both the same, and very different between ADHD and ASD.

Scientific References

  1. Faraone, S. V. et al. Attention-deficit/hyperactivity disorder.  Nat. Rev. Dis. Primers, 15020,  https://doi.org/10.1038/nrdp.2015.20  (2015). 
  2. Dalsgaard, S., Leckman, J. F., Mortensen, P. B., Nielsen, H. S. & Simonsen, M.  Effect of drugs on the risk of injuries in children with attention deficit hyperactivity disorder: a prospective cohort study.  Lancet  Psychiatry  2, 702–709 (2015). Chang, Z., 
  3. Lichtenstein, P., D’Onofrio, B. M., Sjolander, A. & Larsson, H. Serious transport accidents in adults with attention-deficit/hyperactivity disorder and the effect of medication: a population-based study.  JAMA Psychiatry  71, 319–325 (2014).
  4. Biederman, J. & Faraone, S. V. Attention-deficit hyperactivity disorder. Lancet  366, 237–248 (2005). 
  5. Dalsgaard, S., Nielsen, H. S. & Simonsen, M. Consequences of ADHD medication use for children’s outcomes.  J. Health Econ.  37, 137–151 (2014). 
  6. Dalsgaard, S., Mortensen, P. B., Frydenberg, M. & Thomsen, P. H. ADHD, stimulant treatment in childhood and subsequent substance abuse in adulthood – a naturalistic long-term follow-up study.  Addict.  Behav.  39, 325–328 (2014). 
  7. Lichtenstein, P. & Larsson, H. Medication for attention deficit-hyperactivity disorder and criminality.  N. Engl. J. Med.  368, 776 (2013). 
  8. Barkley, R. A., Murphy, K. R. & Fischer, M.  ADHD in Adults: What the Science Says. (Guilford Press, New York, 2007). 
  9. Furczyk, K. & Thome, J. Adult ADHD and suicide.  Atten. Defic. Hyperact. Disord.  6, 153–158 (2014).
  10. Dalsgaard, S., Ostergaard, S. D., Leckman, J. F., Mortensen, P. B. & Pedersen, M. G. Mortality in children, adolescents, and adults with attention deficit hyperactivity disorder: a nationwide cohort study.  Lancet 385, 2190–2196 (2015).
  11. Franke, B. et al. The genetics of attention deficit/hyperactivity disorder in adults, a review.  Mol.  Psychiatry  17, 960–987 (2012). 
  12. Faraone, S. V. et al. Molecular genetics of attention-deficit/hyperactivity disorder.  Biol.  Psychiatry  57, 1313–1323 (2005).
  13. Burt, S. A. Rethinking environmental contributions to child and adolescent psychopathology: a meta-analysis of shared environmental influences. Psychol. Bull.  135, 608–637 (2009).
  14. Larsson, H., Anckarsater, H., Rastam, M., Chang, Z. & Lichtenstein, P. Childhood attention-deficit hyperactivity disorder as an extreme of a continuous trait: a quantitative genetic study of 8,500 twin pairs.  J. Child Psychol.  Psychiatry  53, 73–80 (2012).
  15. Christiansen, H. et al. Co-transmission of conduct problems with attention-deficit/hyperactivity disorder: familial evidence for a distinct disorder.  J. Neural Transm. (Vienna)  115, 163–175 (2008).
  16. Kuntsi, J. et al. The separation of ADHD inattention and hyperactivity- impulsivity symptoms: pathways from genetic effects to cognitive impairments and symptoms. J. Abnorm. Child Psychol. 42,127–136 (2014).
  17. Rommelse, N. N., Franke, B., Geurts, H. M., Hartman, C. A. & Buitelaar, J. K. Shared heritability of attention-deficit/hyperactivity disorder and autism spectrum disorder. Eur. Child Adolesc. Psychiatry 19, 281–295 (2010).
  18. Ghirardi, L. et al. The familial co-aggregation of ASD and ADHD: a register-based cohort study. Mol. Psychiatry. 23, 257–262 (2018).
  19. Larsson, H. et al. Risk of bipolar disorder and schizophrenia in relatives of people with attention-deficit hyperactivity disorder. British J. Psychiatry 203, 103–106 (2013).
  20. Faraone, S. V., Biederman, J. & Wozniak, J. Examining the comorbidity between attention deficit hyperactivity disorder and bipolar I disorder: a meta-analysis of family genetic studies. Am. J. Psychiatry 169, 1256–1266 (2012).
  21. Faraone, S. V. & Biederman, J. Do attention deficit hyperactivity disorder and major depression share familial risk factors? J. Nerv. Ment. Dis. 185, 533–541 (1997).
  22. Neale, B. M. et al. Meta-analysis of genome-wide association studies of attention-deficit/hyperactivity disorder. J. Am. Acad. Child Adolesc. Psychiatry 49, 884–897 (2010).
  23. The Brainstorm Consortium. Analysis of shared heritability in common disorders of the brain. Science 360, eaap8757 (2018).
  24. Cross-Disorder Group of the Psychiatric Genomics Consortium. Genetic relationship between five psychiatric disorders estimated from genome-wide SNPs. Nat. Genet. 45, 984–994 (2013).
  25. Cross-Disorder Group of the Psychiatric Genomics Consortium. Identification of risk loci with shared effects on five major psychiatric disorders: a genome-wide analysis. Lancet 381, 1371–1379 (2013).
  26. Hamshere, M. L. et al. High loading of polygenic risk for ADHD in children with comorbid aggression. Am. J. Psychiatry 170, 909–916 (2013).
  27. Hamshere, M. L. et al. Shared polygenic contribution between childhood attention-deficit hyperactivity disorder and adult schizophrenia. British J. Psychiatry 203, 107–111 (2013).
  28. Groen-Blokhuis, M. M. et al. Attention-deficit/hyperactivity disorder polygenic risk scores predict attention problems in a population-based sample of children. J. Am. Acad. Child Adolesc. Psychiatry 53, 1123–1129. e1126 (2014).
  29. Martin, J., Hamshere, M. L., Stergiakouli, E., O’Donovan, M. C. & Thapar, A. Genetic risk for attention-deficit/hyperactivity disorder contributes to neurodevelopmental traits in the general population. Biol. Psychiatry 76, 664–671 (2014).
  30. Middeldorp, C. M. et al. A genome-wide association meta-analysis of attention-deficit/hyperactivity disorder symptoms in population-based pediatric cohorts. J. Am. Acad. Child Adolesc. Psychiatry 55, 896–905.e896 (2016).
  31. Yang, L. et al. Polygenic transmission and complex neuro developmental network for attention deficit hyperactivity disorder: genome-wide association study of both common and rare variants. Am. J. Med. Genet. B Neuropsychiatr Genet. 162B, 419–430 (2013).
  32. Zayats, T. et al. Genome-wide analysis of attention deficit hyperactivity disorder in Norway. PLoS One 10, e0122501 (2015).
  33. Schizophrenia Working Group of the Psychiatric Genomics Consortium. Biological insights from 108 schizophrenia-associated genetic loci. Nature 511, 421–427 (2014).
  34. The 1000 Genomes Project Consortium. A global reference for human genetic variation. Nature 526, 68–74 (2015).
  35. Price, A. L. et al. Principal components analysis corrects for stratification in genome-wide association studies. Nat. Genet. 38, 904–909 (2006).
  36. Willer, C. J., Li, Y. & Abecasis, G. R. METAL: fast and efficient meta- analysis of genomewide association scans. Bioinformatics 26, 2190–2191 (2010).
  37. Bulik-Sullivan, B. K. et al. LD Score regression distinguishes confounding from polygenicity in genome-wide association studies. Nat. Genet. 47, 291–295 (2015).
  38. Purcell, S. M. et al. Common polygenic variation contributes to risk of schizophrenia and bipolar disorder. Nature 460, 748–752 (2009).
  39. Polanczyk, G., de Lima, M. S., Horta, B. L., Biederman, J. & Rohde, L. A. The worldwide prevalence of ADHD: a systematic review and metaregression analysis. Am. J. Psychiatry 164, 942–948 (2007).
  40. Finucane, H. K. et al. Partitioning heritability by functional annotation using genome-wide association summary statistics. Nat. Genet. 47, 1228–1235 (2015).
  41. Zheng, J.  et al. LD Hub: a centralized database and web interface to  perform LD score regression that maximizes the potential of summary level GWAS data for SNP heritability and genetic correlation analysis. Bioinformatics 33, 272–279 (2017).
  42. Bulik-Sullivan, B. et al. An atlas of genetic correlations across human diseases and traits. Nat. Genet. 47, 1236–1241 (2015).
  43. Wray, N. R. & Sullivan, P. F. et al. Genome-wide association analyses identify 44 risk variants and refine the genetic architecture of major depression. Nat. Genet. 50, 668–681 (2018).
  44. Duncan, L. et al. Significant locus and metabolic genetic correlations revealed in genome-wide association study of anorexia nervosa. Am. J. Psychiatry 174, 850–858 (2017).
  45. Benyamin, B. et al. Childhood intelligence is heritable, highly polygenic and associated with FNBP1L. Mol. Psychiatry 19, 253–258 (2014).
  46. Okbay, A. et al. Genetic variants associated with subjective well-being, depressive symptoms, and neuroticism identified through genome-wide analyses. Nat. Genet. 48, 624–633 (2016).
  47. Rietveld, C. A. et al. GWAS of 126,559 individuals identifies genetic variants associated with educational attainment. Science 340, 1467–1471 (2013).
  48. Rietveld, C. A. et al. Common genetic variants associated with cognitive performance identified using the proxy-phenotype method. Proc. Natl Acad. Sci. USA 111, 13790–13794 (2014).
  49. Davies, G. et al. Genome-wide association study of cognitive functions and educational attainment in UK Biobank (N = 112 151). Mol. Psychiatry 21, 758–767 (2016).
  50. Teslovich, T. M. et al. Biological, clinical and population relevance of 95 loci for blood lipids. Nature 466, 707–713 (2010).
  51. Morris, A. P. et al. Large-scale association analysis provides insights into the genetic architecture and pathophysiology of type 2 diabetes. Nat. Genet. 44, 981–990 (2012).
  52. Bradfield, J. P. et al. A genome-wide association meta-analysis identifies new childhood obesity loci. Nat. Genet. 44, 526–531 (2012).
  53. Berndt, S. I. et al. Genome-wide meta-analysis identifies 11 new loci for anthropometric traits and provides insights into genetic architecture. Nat. Genet. 45, 501–512 (2013).
  54. Speliotes, E. K. et al. Association analyses of 249,796 individuals reveal 18 new loci associated with body mass index. Nat. Genet. 42, 937–948 (2010).
  55. Shungin, D. et al. New genetic loci link adipose and insulin biology to body fat distribution. Nature 518, 187–196 (2015).
  56. Tobacco and Genetics Consortium. Genome-wide meta-analyses identify multiple loci associated with smoking behavior. Nat. Genet. 42, 441–447 (2010).
  57. Patel, Y. M. et al. Novel Association of genetic markers affecting CYP2A6 activity and lung cancer risk. Cancer Res. 76, 5768–5776 (2016).
  58. Wang, Y. et al. Rare variants of large effect in BRCA2 and CHEK2 affect risk of lung cancer. Nat. Genet. 46, 736–741 (2014).
  59. Barban, N. et al. Genome-wide analysis identifies 12 loci influencing human reproductive behavior. Nat. Genet. 48, 1462–1472 (2016).
  60. Hammerschlag, A. R. et al. Genome-wide association analysis of insomnia complaints identifies risk genes and genetic overlap with psychiatric and metabolic traits. Nat. Genet. 49, 1584–1592 (2017).
  61. Pilling, L. C. et al. Human longevity is influenced by many genetic variants: evidence from 75,000 UK Biobank participants. Aging 8, 547–560 (2016).
  62. Hawi, Z. et al. The molecular genetic architecture of attention deficit hyperactivity disorder. Mol. Psychiatry 20, 289–297 (2015).
  63. Sia, G. M., Clem, R. L. & Huganir, R. L. The human language-associated gene SRPX2 regulates synapse formation and vocalization in mice. Science 342, 987–991 (2013).
  64. Tsui, D., Vessey, J. P., Tomita, H., Kaplan, D. R. & Miller, F. D. FoxP2 regulates neurogenesis during embryonic cortical development. J. Neurosci. 33, 244–258 (2013).
  65. Schreiweis, C. et al. Humanized Foxp2 accelerates learning by enhancing transitions from declarative to procedural performance. Proc. Natl. Acad. Sci. USA 111, 14253–14258 (2014).
  66. Jensen, C. M. & Steinhausen, H. C. Comorbid mental disorders in children and adolescents with attention-deficit/hyperactivity disorder in a large nationwide study. Atten. Defic. Hyperact. Disord 7, 27–38 (2015).
  67. Larson, K., Russ, S. A., Kahn, R. S. & Halfon, N. Patterns of comorbidity, functioning, and service use for US children with ADHD, 2007. Pediatrics 127, 462–470 (2011).
  68. Peyre, H. et al. Relationship between early language skills and the development of inattention/hyperactivity symptoms during the preschool period: Results of the EDEN mother-child cohort. BMC Psychiatry 16, 380 (2016).
  69. Breiderhoff, T. et al. Sortilin-related receptor SORCS3 is a postsynaptic modulator of synaptic depression and fear extinction. PLoS One 8, e75006 (2013).
  70. Hyde, C. L. et al. Identification of 15 genetic loci associated with risk of major depression in individuals of European descent. Nat. Genet. 48, 1031–1036 (2016).
  71. Caunt, C. J. & Keyse, S. M. Dual-specificity MAP kinase phosphatases (MKPs): shaping the outcome of MAP kinase signalling. FEBS. J. 280, 489–504 (2013).
  72. Mortensen, O. V. MKP3 eliminates depolarization-dependent neurotransmitter release through downregulation of L-type calcium channel Cav1.2 expression. Cell Calcium 53, 224–230 (2013).
  73. Mortensen, O. V., Larsen, M. B., Prasad, B. M. & Amara, S. G. Genetic complementation screen identifies a mitogen-activated protein kinase phosphatase, MKP3, as a regulator of dopamine transporter trafficking. Mol. Biol. Cell. 19, 2818–2829 (2008).
  74. Volkow, N. D., Fowler, J. S., Wang, G., Ding, Y. & Gatley, S. J. Mechanism of action of methylphenidate: insights from PET imaging studies. J. Atten. Disord 6(Suppl 1), S31–S43 (2002).
  75. Volkow, N. D. et al. Therapeutic doses of oral methylphenidate significantly increase extracellular dopamine in the human brain. J. Neurosci. 21, RC121 (2001).
  76. GTEx Consortium. The Genotype-Tissue Expression (GTEx) project. Nat. Genet. 45, 580–585 (2013).
  77. Qu, X. et al. Identification, characterization, and functional study of the two novel human members of the semaphorin gene family. J. Biol. Chem. 277, 35574–35585 (2002).
  78. Okbay, A. et al. Genome-wide association study identifies 74 loci associated with educational attainment. Nature 533, 539–542 (2016).
  79. Zhernakova, D. V. et al. Identification of context-dependent expression quantitative trait loci in whole blood. Nat. Genet. 49, 139–145 (2017).
  80. Hu, H. et al. ST3GAL3 mutations impair the development of higher cognitive functions. Am. J. Hum. Genet. 89, 407–414 (2011).
  81. Oliver, P. L. et al. Disruption of Visc-2, a brain-expressed conserved long noncoding rna, does not elicit an overt anatomical or behavioral phenotype. Cereb. Cortex 25, 3572–3585 (2015).
  82. Sobreira, N., Walsh, M. F., Batista, D. & Wang, T. Interstitial deletion 5q14.3-q21 associated with iris coloboma, hearing loss, dental anomaly, moderate intellectual disability, and attention deficit and hyperactivity disorder. Am. J. Med. Genet. A. 149A, 2581–2583 (2009).
  83. Le Meur, N. et al. MEF2C haploinsufficiency caused by either microdeletion of the 5q14.3 region or mutation is responsible for severe mental retardation with stereotypic movements, epilepsy and/or cerebral malformations. J. Med. Genet. 47, 22–29 (2010).
  84. Novara, F. et al. Refining the phenotype associated with MEF2C haploinsufficiency. Clin. Genet. 78, 471–477 (2010).
  85. Lambert, J. C. et al. Meta-analysis of 74,046 individuals identifies 11 new susceptibility loci for Alzheimer’s disease. Nat. Genet. 45, 1452–1458 (2013).
  86. Gene Ontology Consortium. Gene Ontology Consortium: going forward. Nucleic Acids Res. 43, D1049–D1056 (2015).
  87. Subramanian, A. et al. Gene set enrichment analysis: a knowledge-based approach for interpreting genome-wide expression profiles. Proc. Natl. Acad. Sci. USA 102, 15545–15550 (2005).
  88. de Leeuw, C. A., Mooij, J. M., Heskes, T. & Posthuma, D. MAGMA: generalized gene-set analysis of GWAS data. PLoS Comput. Biol. 11, e1004219 (2015).
  89. Vernes, S. C. et al. Foxp2 regulates gene networks implicated in neurite outgrowth in the developing brain. PLoS. Genet. 7, e1002145 (2011).
  90. Spiteri, E. et al. Identification of the transcriptional targets of FOXP2, a gene linked to speech and language, in developing human brain. Am. J. Hum. Genet. 81, 1144–1157 (2007).
  91. Lek, M. et al. Analysis of protein-coding genetic variation in 60,706 humans. Nature 536, 285–291 (2016).
  92. Ebejer, J. L. et al. Genome-wide association study of inattention and hyperactivity-impulsivity measured as quantitative traits. Twin. Res. Hum. Genet. 16, 560–574 (2013).
  93. Grove, J. et al. Common risk variants identified in autism spectrum disorder. bioRxiv. https://doi.org/10.1101/224774 (2017).
  94. Lindblad-Toh, K. et al. A high-resolution map of human evolutionary constraint using 29 mammals. Nature 478, 476–482 (2011).
  95. Flory, K. et al. Childhood ADHD predicts risky sexual behavior in young adulthood. J Clin Child Adolesc. Psychol. 35, 571–577 (2006).
  96. Marsh, L. E., Norvilitis, J. M., Ingersoll, T. S. & Li, B. ADHD symptomatology, fear of intimacy, and sexual anxiety and behavior among college students in China and the United States. J. Atten. Disord. 19, 211–221 (2015).
  97. Hosain, G. M., Berenson, A. B., Tennen, H., Bauer, L. O. & Wu, Z. H. Attention deficit hyperactivity symptoms and risky sexual behavior in young adult women. J.  Womens  Health  (Larchmt) 21, 463–468 (2012).
  98. Chudal, R. et al. Parental age and the risk of attention-deficit/hyperactivity disorder: a nationwide, population-based cohort study. J. Am. Acad. Child Adolesc. Psychiatry 54, 487–494.e481 (2015).
  99. Chang, Z. et al. Maternal age at childbirth and risk for ADHD in offspring: a population-based cohort study. Int. J. Epidemiol. 43, 1815–1824 (2014).
  100. Ostergaard, S. D., Dalsgaard, S., Faraone, S. V., Munk-Olsen, T. & Laursen, T. M. Teenage parenthood and birth rates for individuals with and without attention-deficit/hyperactivity disorder: a nationwide cohort study. J. Am. Acad. Child Adolesc. Psychiatry 56, 578–584.e573 (2017).
  101. Barbaresi, W. J., Katusic, S. K., Colligan, R. C., Weaver, A. L. & Jacobsen, S. J. Long-term school outcomes for children with attention-deficit/hyperactivity disorder: a population-based perspective. J. Dev. Behav. Pediatr. 28, 265–273 (2007).
  102. Faraone, S. V. et al. Intellectual performance and school failure in children with attention deficit hyperactivity disorder and in their siblings. J. Abnorm. Psychol. 102, 616–623 (1993).
  103. Sniekers, S. et al. Genome-wide association meta-analysis of 78,308 individuals identifies new loci and genes influencing human intelligence. Nat. Genet. 49, 1107–1112 (2017).
  104. Kong, A. et al. Selection against variants in the genome associated with educational attainment. Proc. Natl. Acad. Sci. USA 114, E727–E732 (2017).
  105. Lee, S. S., Humphreys, K. L., Flory, K., Liu, R. & Glass, K. Prospective association of childhood attention-deficit/hyperactivity disorder (ADHD) and substance use and abuse/dependence: a meta-analytic review. Clin. Psychol. Rev. 31, 328–341 (2011).
  106. Halfon, N., Larson, K. & Slusser, W. Associations between obesity and comorbid mental health, developmental, and physical health conditions in a nationally representative sample of US children aged 10 to 17. Acad. Pediatr. 13, 6–13 (2013).
  107. Chen, A. Y., Kim, S. E., Houtrow, A. J. & Newacheck, P. W. Prevalence of obesity among children with chronic conditions. Obesity (Silver Spring) 18, 210–213 (2010).
  108. Cortese, S. et al. Association between ADHD and obesity: A systematic review and meta-analysis. Am. J. Psychiatry 173, 34–43 (2016).
  109. Owens, J. A. A clinical overview of sleep and attention-deficit/hyperactivity disorder in children and adolescents. J. Can. Acad. Child Adolesc. Psychiatry 18, 92–102 (2009).
  110. Lubke, G. H., Hudziak, J. J., Derks, E. M., van Bijsterveldt, T.  C. &  Boomsma, D. I. Maternal ratings of attention problems in ADHD: evidence for the existence of a continuum. J. Am. Acad. Child Adolesc. Psychiatry 48, 1085–1093 (2009).
  111. Cortese, S., Comencini, E., Vincenzi, B., Speranza, M. & Angriman, M. Attention-deficit/hyperactivity disorder and impairment in executive functions: a barrier to weight loss in individuals with obesity? BMC Psychiatry 13, 286 (2013).
  112. Ortal, S. et al. The role of different aspects of impulsivity as independent risk factors for substance use disorders in patients with ADHD: a review. Curr. Drug Abuse Rev. 8, 119–133 (2015).