TY - JOUR
T1 - Attention-deficit-hyperactivity disorder and reward deficiency syndrome
AU - Blum, Kenneth
AU - Chen, Amanda Lih Chuan
AU - Braverman, Eric R.
AU - Comings, David E.
AU - Chen, Thomas J.H.
AU - Arcuri, Vanessa
AU - Blum, Seth H.
AU - Downs, Bernard W.
AU - Waite, Roger L.
AU - Notaro, Alison
AU - Lubar, Joel
AU - Williams, Lonna
AU - Prihoda, Thomas J.
AU - Palomo, Tomas
AU - Oscar-Berman, Marlene
N1 - Copyright:
Copyright 2009 Elsevier B.V., All rights reserved.
PY - 2008
Y1 - 2008
N2 - Molecular genetic studies have identified several genes that may mediate susceptibility to attention deficit hyperactivity disorder (ADHD). A consensus of the literature suggests that when there is a dysfunction in the "brain reward cascade," especially in the dopamine system, causing a low or hypo-dopaminergic trait, the brain may require dopamine for individuals to avoid unpleasant feelings. This high-risk genetic trait leads to multiple drug-seeking behaviors, because the drugs activate release of dopamine, which can diminish abnormal cravings. Moreover, this genetic trait is due in part to a form of a gene (DRD2 A1 allele) that prevents the expression of the normal laying down of dopamine receptors in brain reward sites. This gene, and others involved in neurophysiological processing of specific neurotransmitters, have been associated with deficient functions and predispose individuals to have a high risk for addictive, impulsive, and compulsive behavioral propensities. It has been proposed that genetic variants of dopaminergic genes and other "reward genes" are important common determinants of reward deficiency syndrome (RDS), which we hypothesize includes ADHD as a behavioral subtype. We further hypothesize that early diagnosis through genetic polymorphic identification in combination with DNA-based customized nutraceutical administration to young children may attenuate behavioral symptoms associated with ADHD. Moreover, it is concluded that dopamine and serotonin releasers might be useful therapeutic adjuncts for the treatment of other RDS behavioral subtypes, including addictions.
AB - Molecular genetic studies have identified several genes that may mediate susceptibility to attention deficit hyperactivity disorder (ADHD). A consensus of the literature suggests that when there is a dysfunction in the "brain reward cascade," especially in the dopamine system, causing a low or hypo-dopaminergic trait, the brain may require dopamine for individuals to avoid unpleasant feelings. This high-risk genetic trait leads to multiple drug-seeking behaviors, because the drugs activate release of dopamine, which can diminish abnormal cravings. Moreover, this genetic trait is due in part to a form of a gene (DRD2 A1 allele) that prevents the expression of the normal laying down of dopamine receptors in brain reward sites. This gene, and others involved in neurophysiological processing of specific neurotransmitters, have been associated with deficient functions and predispose individuals to have a high risk for addictive, impulsive, and compulsive behavioral propensities. It has been proposed that genetic variants of dopaminergic genes and other "reward genes" are important common determinants of reward deficiency syndrome (RDS), which we hypothesize includes ADHD as a behavioral subtype. We further hypothesize that early diagnosis through genetic polymorphic identification in combination with DNA-based customized nutraceutical administration to young children may attenuate behavioral symptoms associated with ADHD. Moreover, it is concluded that dopamine and serotonin releasers might be useful therapeutic adjuncts for the treatment of other RDS behavioral subtypes, including addictions.
KW - Attention deficit hyperactivity disorder (ADHD)
KW - Genes
KW - Neurophysiology deficits
KW - Reward deficiency syndrome
KW - Reward dependence
KW - Treatment
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M3 - Review article
C2 - 19183781
AN - SCOPUS:56849084636
VL - 4
SP - 893
EP - 917
JO - Neuropsychiatric Disease and Treatment
JF - Neuropsychiatric Disease and Treatment
SN - 1176-6328
IS - 5
ER -