Abstract
<h3>To the Editor. —</h3> The results of two studies<sup>1,2</sup>in theArchiveshave been interpreted as being suggestive of reduced benzodiazepine receptor sensitivity (or, more specifically, a shift in benzodiazepine receptor "setpoint"<sup>2</sup>) resulting in reduced ɣ-aminobutyric acid (GABA) function in panic disorder, with these abnormalities possibly being pathogenic. We suggest two possible alternative or additional explanations. <i>These Results Could Be Secondary to Chronic Alcohol Use</i>.—In both studies,<sup>1,2</sup>drinking history was either not assessed or not reported. Yet there is a strong relationship between alcohol abuse and the panic-related disorders.<sup>3-5</sup>Data<sup>6-9</sup>attest to the fact that rates of panic disorder in alcoholics and rates of alcohol abuse in patients with panic disorder are unusually high compared with the rates in the general population.<sup>10</sup> There is increasing evidence that alcohol mediates many of its pharmacologic effects through the GABA-ergic receptor system, from behavioral, electrophysiological, and
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