Evidence map›Paper›PMID 19183781›Full record

ArticleNeuropsychiatric disease and treatment2008

Attention-deficit-hyperactivity disorder and reward deficiency syndrome.

Kenneth Blum, Amanda Lih-Chuan Chen, Eric R Braverman, David E Comings, Thomas J H Chen, Vanessa Arcuri, Seth H Blum, Bernard W Downs, Roger L Waite, Alison Notaro and 5 more

Open access · goldAbstract read
In one paragraph

Article in Neuropsychiatric disease and treatment, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 106 papers, 9 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
106citing papers in PubMed, 9 pooled it
3.5field-weighted citation impact, top 8% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

106 citing papers in PubMed, 9 syntheses or guidelines pooled it, 238 citations in OpenAlex.

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46 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

15 authors at 6 institutions in 4 countries.

Kenneth BlumDepartment of Physiology and Pharmacology, Wake Forest University School of Medicine, Winston-Salem, NC, USA. drd2gene@aol.com
Amanda Lih-Chuan Chen
Eric R Braverman
David E Comings
Thomas J H Chen
Vanessa Arcuri
Seth H Blum
Bernard W Downs
Roger L Waite
Alison Notaro
Joel Lubar
Lonna Williams
Thomas J Prihoda
Tomas Palomo
Marlene Oscar-Berman
Chang Jung Christian University · TWMedical Research Foundation · GBWake Forest University · USCity Of Hope National Medical Center · USHospital Universitario 12 De Octubre · ESSynapse Biomedical (United States) · US

Funding

AFFECTIVE AND CONATIVE CHANGES IN ALCOHOLISMR01AA007112 · NIAAA · BOSTON UNIVERSITY MEDICAL CAMPUS · PI BERMAN, MARLENE OSCAR · 1987 to 2019
$8.3M
AFFECTIVE AND CONATIVE CHANGES IN ALCOHOLISMK05AA000219 · NIAAA · BOSTON UNIVERSITY MEDICAL CAMPUS · PI BERMAN, MARLENE OSCAR · 1997 to 2011
$1.8M
NIAAA NIH HHS K05 AA000219NIAAA NIH HHS R01 AA007112
6 · The paper itself

Abstract

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 (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 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.

Indexed as

attention deficit hyperactivity disorder (ADHD)genesneuropsychological deficitsreward deficiency syndromereward dependencetreatment

Identifiers

PMID19183781
PMCPMC2626918
OpenAlexW2027531652

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.