{'fraction_non_alphanumeric': 0.026921406860616587, 'fraction_numerical': 0.029526704298740773, 'mean_word_length': 5.260869565217392, 'pattern_counts': {'":': 0, '<': 0, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
Stress, the hypothalamic-pituitary-adrenal axis, and vulnerability to drug abuse.

In nonlaboratory settings, social users of cocaine are sometimes able to control their drug intake so their patterns of use do not escalate to levels that would increase their risk of dependency and toxicity (Siegel 1984). This suggests that there may be factors in addition to the primary reinforcing properties of cocaine that determine why some individuals can remain casual recreational users while others progress to compulsive drug use. Individual reactivity to anxiety or stress, either mitigated or induced by cocaine, may represent one such factor that could influence the awareness or perception of the reinforcing efficacy of the drug. Clinical evidence supports the concept that anxiety may be involved in the etiology of cocaine use and/or withdrawal. For example, initial cocaine use produces profound subjective feelings of well-being and a decrease in anxiety in humans (Gawin and Ellinwood 1988, 1989). Interestingly, some of the major symptoms observed during withdrawal from chronic cocaine intoxication can also include severe anxiety as well as restlessness, agitation, and depression (Gawin and Ellinwood 1989). In fact, a subpopulation of chronic cocaine users may actually be self-medicating to regulate painful feelings and psychiatric symptoms via their drug use (Gawin 1986; Khantzian 1985; Kleber and Gawin 1984), especially since increased rates of affective disorders and anxiety are observed in these individuals (Brady and Lydiard 1992; Kilbey et al. 1992; Rounsaville et al. 1991). Cocaine has even been reported to precipitate episodes of panic attack in some individuals (Anthony et al. 1989; Aronson and Craig 1986; Washton and Gold 1984). Since panic disorder only became apparent following chronic cocaine use in many of these cases, the drug may have functioned as a precipitating as well as a causative factor in a neurobiologically vulnerable individual (Aronson and Craig 1986). Since environmental events can also influence the onset and/or duration of anxiety and depression (Brown et al. 1973; Leff et al. 1970; Lloyd 1980), changes in the amount, severity, or perception of environmental stress may actually predispose sensitive individuals to engage in compulsive drug use.