Context: Self-medication of anxiety symptoms with alcohol, other drugs, or both has been a plausible mechanism for the co-occurrence of anxiety disorders and substance use disorders. However, owing to the cross-sectional nature of previous studies, it has remained unknown whether self-medication of anxiety symptoms is a risk factor for the development of incident substance use disorder or is a correlate of substance use.
Objective: To examine whether self-medication confers risk of comorbidity.
Design: A longitudinal, nationally representative survey was conducted by the National Institute on Alcohol Abuse and Alcoholism. The National Epidemiologic Survey on Alcohol and Related Conditions assessed DSM-IV psychiatric disorders, self-medication, and sociodemographic variables at 2 time points.
Setting: The United States.
Participants: A total of 34 653 US adults completed both waves of the survey. Wave 1 was conducted in 2001-2002, and wave 2 interviews occurred 3 years later (2004-2005).
Main Outcome Measures: Incident substance use disorders in participants with baseline anxiety disorders and incident anxiety disorders in those with baseline substance use disorders.
Results: Logistic regression analyses revealed that self-medication conferred a heightened risk of new-onset substance use disorders in those with baseline anxiety disorders (adjusted odds ratios [AORs], 2.50-4.99 [P < .01]). Self-medication was associated with an increased risk of social phobia (AOR in baseline alcohol use disorders, 2.13 [P = .004]; AOR in baseline drug use disorders, 3.17 [P = .001]).
Conclusions: Self-medication in anxiety disorders confers substantial risk of incident substance use disorders. Conversely, self-medication in substance use disorders is associated with incident social phobia. These results not only clarify several pathways that may lead to the development of comorbidity but also indicate at-risk populations and suggest potential points of intervention in the treatment of comorbidity.
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http://dx.doi.org/10.1001/archgenpsychiatry.2011.75 | DOI Listing |
J Adolesc Health
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Division of Adolescent and School Health, National Center for HIV, Viral Hepatitis, STD, and TB Prevention, Centers for Disease Control and Prevention, Atlanta, Georgia.
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Department of Chemistry, University of North Carolina at Chapel Hill, Chapel Hill, NC, USA.
As the occurrence of human diseases and conditions increase, questions continue to arise about their linkages to chemical exposure, especially for per-and polyfluoroalkyl substances (PFAS). Currently, many chemicals of concern have limited experimental information available for their use in analytical assessments. Here, we aim to increase this knowledge by providing the scientific community with multidimensional characteristics for 175 PFAS and their resulting 281 ion types.
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The foremost cause of dementia is Alzheimer's disease (AD). The vital pathological hallmarks of AD are amyloid beta (Aβ) peptide and hyperphosphorylated tau (p-tau) protein. The current animal models used in AD research do not precisely replicate disease pathophysiology, making it difficult for researchers to quickly and effectively gather data or screen potential therapy possibilities.
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KG Jebsen Centre for Brain Fluid Research, University of Oslo, Oslo, Norway.
A potential two-way passage of cells and substances between the brain and skull bone marrow may open for new insights into neurological disease. The arachnoid membrane was traditionally considered to restrict cells and larger molecules in CSF from entering the dura and bone marrow directly. However, new data on exchange between brain and skull bone marrow have recently emerged.
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