PubMed Health⌕ Search
Home/Archive/PubMed

PubMed · 10695586

Pathologic gambling.

B K Unwin·M K Davis·J B De Leeuw
View original source ↗Export metadata ↓

Abstract

Pathologic gambling and problem gambling affect approximately 5 to 15 million Americans and are common in young people. The community-minded family physician is in a good position to identify and assist patients who have gambling-related problems and thereby prevent or treat the resultant personal, family and social disruptions. Provider and community education about the depth and breadth of this condition is crucial for the identification and treatment of a growing problem. As with many psychologic conditions, identification of the disorder and treatment of the patient by the family physician comprise the primary treatment. Screening tools, treatment programs and self-help groups provide additional resources for the family physician. An illustrative case report demonstrates the importance of heightened awareness of and screening for this common condition.

Explore related subjects

AlcoholismComorbidityCultureDepressionDiagnosis, DifferentialGamblingHumansMaleMiddle AgedPatient Education as TopicTeaching MaterialsUnited StatesCase ReportsJournal ArticleReview

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

B K Unwin, M K Davis, J B De Leeuw. 2000-02-01. Pathologic gambling.. https://pubmed.ncbi.nlm.nih.gov/10695586/

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

PubMed2000

Kinetics and control of oxidative phosphorylation in rat liver mitochondria after chronic ethanol feeding.

Changes in the kinetics and regulation of oxidative phosphorylation were characterized in isolated rat liver mitochondria after 2 months of ethanol consumption. Mitochondrial energy metabolism was conceptually divided into three groups of reactions, either producing protonmotive force (Deltap) (the respiratory subsystem) or consuming it (the phosphorylation subsystem and the proton leak). Manifestation of ethanol-induced mitochondrial malfunctioning of the respiratory subsystem was observed with various substrates; the respiration rate in State 3 was inhibited by 27+/-4% with succinate plus amytal, by 20+/-4% with glutamate plus malate, and by 17+/-2% with N,N,N',N'-tetramethyl-p-phenylenediamine/ascorbate. The inhibition of the respiratory activity correlated with the lower activities of cytochrome c oxidase, the bc(1) complex, and the ATP synthase in mitochondria of ethanol-fed rats. The block of reactions consuming the Deltap to produce ATP (the phosphorylating subsystem) was suppressed after 2 months of ethanol feeding, whereas the mitochondrial proton leak was not affected. The contributions of Deltap supply (the respiratory subsystem) and Deltap demand (the phosphorylation and the proton leak) to the control of the respiratory flux were quantified as the control coefficients of these subsystems. In State 3, the distribution of control exerted by different reaction blocks over respiratory flux was not significantly affected by ethanol diet, despite the marked changes in the kinetics of individual functional units of mitochondrial oxidative phosphorylation. This suggests the operation of compensatory mechanisms, when control redistributes among the different components within the same subsystem.

Alcoholism↗