A Controlled Study of Siblings of Hyperactive Children

Welner, Zila; Welner, Amos; Stewart, Mark; Palkes, Helen; Wish, Eric D.

doi:10.1097/00005053-197708000-00004

Cited by 107 publications

(45 citation statements)

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“…Similarly elevated incidence rates are evident in studies of families including a member with ADHD. In families that include a child with ADHD, over 30% of the siblings also have ADHD (Biederman et al, 1992;Biederman, Keenan & Faraone, 1990;Welner, Welner, Stewart, Palkes, & Wish, 1977). In those families that include an adult with ADHD, the likelihood that at least one child will have this disorder is 57% (Biederman et al, 1995).…”

Section: Genetics Neuroanatomy and Adhdmentioning

confidence: 99%

Electroencephalographic Biofeedback in the Treatment of Attention-Deficit/Hyperactivity Disorder

Monastra

Lynn

Linden

et al. 2005

Appl Psychophysiol Biofeedback

214

166

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Section: Genetics Neuroanatomy and Adhdmentioning

confidence: 99%

Electroencephalographic Biofeedback in the Treatment of Attention-Deficit/Hyperactivity Disorder

Monastra

Lynn

Linden

et al. 2005

Appl Psychophysiol Biofeedback

214

166

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“…This is 2-7 times the frequency found in non-ADHD children. These siblings also were 5 times more likely to have major depression than control children (Welner et al 1977;August and Stewart 1983). Other studies showed that 22% of brothers and 8% of sisters of hyperactive children were hyperactive themselves.…”

Section: Science Of Adhd Neuropsychogenetics Of Adhdmentioning

confidence: 91%

Attention-deficit-hyperactivity disorder and reward deficiency syndrome

Blum

Chen

Braverman³

et al. 2008

NDT

102

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Molecular genetic studies have identified several genes that may mediate susceptibility to attention defi cit 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 drugseeking 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 (DRD 2 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 specifi c neurotransmitters, have been associated with defi cient 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 defi ciency syndrome (RDS), which we hypothesize includes ADHD as a behavioral subtype. We further hypothesize that early diagnosis through genetic polymorphic identifi cation 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.

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“…The controls were not a consecutive series but the first 50 for whom charts were found. Their diag noses were neurotic disorders (17), undiagnosed (15), enuresis or encopresis (10), and miscellaneous (8).…”

Section: Methodsmentioning

confidence: 99%