We found that only about 1 of 5 patients with an anxiety disorder reports ever having used alcohol explicitly for anxiety relief.5 Indeed, patients with anxiety disorders who self-medicate were at increased risk for SUD; however, patients who did not self-medicate were still at greater risk for SUD than those with no anxiety disorder. The amount of alcohol consumed accounted for only about half of the increased risk of alcohol dependence for patients with anxiety disorders who self-medicate. For patients with anxiety disorders who do not self-medicate, the amount of alcohol use did not account for any of their increased alcohol use disorder risk. Calling into question the centrality of self-medication in maintaining the anxiety disorder–SUD association, Thomas and colleagues14 presented data that show that successfully treating anxiety disorders, even among a subgroup who report drinking to self-medicate, does not eliminate (or even significantly reduce) pathological drinking.
Substance-induced anxiety disorders. DSM-IV establishes an anxiety disorder as independent of a co-occurring SUD only if it began before the onset of any SUD and persisted during periods of abstinence from drug and alcohol use that lasted at least 4 weeks. The second of these criteria indicates that substance-induced anxiety disorders remit in the absence of ongoing drug or alcohol use and, therefore, do not require specific treatment.15
Grant and colleagues1 used DSM-IV criteria to evaluate the extent of independent versus dependent anxiety disorders and mood disorders in individuals with SUDs from the NESARC dataset. They reported that “only a few individuals were classified as having only substance induced-disorders.”1(p807) Furthermore, because anxiety disorders begin after SUDs for up to half of those with both disorders, it is the second criterion (the resolution of anxiety disorder symptoms with abstinence) that was extremely rare in the NESARC sample.16 On the basis of these findings, Grant and colleagues1 concluded that clinicians should rarely withhold treatment for anxiety disorders simply because an individual has a comorbid SUD, even if the SUD began before the anxiety disorder.
However, the conclusion that anxiety disorders are not likely to resolve when SUDs are treated should not be taken to mean that pathological use might not contribute to the maintenance of anxiety disorder symptoms. In fact, there is evidence to suggest that pathological substance use does exacerbate anxiety symptoms, and it renders anxiety disorders more persistent and less responsive to treatment.17,18 Thus, as with the self-medication view, the idea of substance-induced anxiety disorders as an explanation for the anxiety disorder–SUD correlation is only partially supported; ie, while SUDs worsen anxiety disorders and anxiety disorder outcomes, simply eliminating problematic drug and alcohol use does not routinely resolve established anxiety disorders.
Dependence susceptibility and the “telescoping” of SUD risk. Telescoping refers to an accelerated transition from a nonpathological to a pathological state.19 Basic neuroscience has long linked disruptions in neurosystems, such as the hypothalamic-pituitary-adrenal axis and the basolateral amygdala, to the development of both anxiety disorders and physical substance dependence.20-22 On the basis of this etiological overlap, we hypothesized that individuals with anxiety disorders should be especially susceptible to developing physical dependence on alcohol, manifested in a telescoping of the time from early drinking landmarks (eg, first regular drinking) to alcohol dependence landmarks (eg, first withdrawal symptoms). This telescoping effect has been found in alcohol-dependent patients who have an anxiety disorder compared with those who do not have an anxiety disorder.23 Furthermore, the telescoping effect was observed whether the anxiety disorder preceded or followed the SUD.
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