Then, the RR using PA and PP are identical (2.0); however, the DIFF is 5% using PA but is 15% using PP. Moderators of the relationship of PA versus PP Given www.selleckchem.com/products/nutlin-3a.html that PA almost always decreases over time and PP usually increases over time (Hughes et al., 2003), we anticipated that the relationship of PA and PP would change with different follow-up durations; however, we did not find that whether follow-ups were at 6 months versus longer influenced our results. This may be because relapse and recycling of new quit attempts are rare after 6 months (Hughes, Peters, & Naud, 2008). We believe that the relationship of PA and PP for follow-ups of less than 6 months may differ from those reported herein, but this hypothesis requires testing.

Another likely influence on the relationship of PA to PP is how soon after a quit date successful abstinence begins (Hughes et al., 2003). For example, most PA measures require abstinence to begin within the first month after a quit date. Almost no PP measures do so. Thus, if long-term abstinence is due to a ��late quit,�� this would not be a PA-defined success but would be a PP-defined success. Although late quits have thought to be unusual, recent experience with nicotine blocking agents such as varenicline suggest that they can induce late quit successes (Fagerstrom & Hughes, 2008). However, in our analyses, we did not find that the relationship of PP to PA differed between varenicline and other medication conditions. One possible explanation for this is that other study medications (in our case this was NRT and bupropion) also induce later quits or prevent a lapse from becoming relapse.

For example, clinical studies have found that NRT (Shiffman et al., 2006) and bupropion (West, Baker, Cappelleri, & Bushmakin, 2008) also are nicotine blockers and thus can also result in delayed quitting. Assets and limitations The major assets of our analyses include our use of (a) within-study rather than between-study comparisons of PA versus PP, (b) a larger more comprehensive sample of studies, (c) meta-analytic techniques that allowed derivation of equations for estimating PA from PP and vice versa, and (d) direct tests whether PA and PP produce similar effect sizes for treatment outcomes. One important liability of our analyses is that we only examined studies testing a pharmacological treatment.

It is reasonable to hypothesize that the therapeutic effects of psychosocial treatments take longer to take effect than do pharmacological treatments. If this is the case (and we cannot find empirical verification Drug_discovery of this assumption), then psychosocial treatments might especially produce late quitters, and thus, the relationship of PA to PP might differ for psychosocial versus medication trials. A second liability is that many of the articles were not clear on the exact sample sizes used for PA and PP measures nor on whether biochemical verification was required for both PA and PP or for only one of the two.