The present study provides the first longitudinal evidence for processes linking depression symptoms in emerging adulthood to smoking uptake in young adulthood. Higher depression symptoms in emerging adulthood (age 18–19 years old) predicted declines in non-smoking alternative reinforcers across time, which in turn, predicted increases in smoking uptake/rate in young adulthood (age 18–19 years old). These findings highlight that depression in emerging adulthood is a risk factor for subsequent smoking because of its negative influence on alternative reinforcers and suggest that promoting greater alternative reinforcers or mitigating declines may prevent smoking uptake and increases in smoking rate in young adults.
These findings bridge the research showing that reductions in reinforcing activities are a consequence of depression and research showing that substance use is acquired and maintained within the context of fewer alternative reinforcers (12
). Here, we show that declining alternative reinforcers link depression symptoms to the establishment of young adult smoking. Behavioral theory posits that the probability of substance use increases as a function of decreases in alternative sources of reinforcement as well as the availability of substances. As elevated depression symptoms precipitate declines in substitute alternative reinforcers, young adults may be more likely to choose to smoke and to find smoking more rewarding (20
). A consistently lower level of substitute alternative reinforcers may promote smoking persistence and continued elevations in depression symptoms. Recent research indicates that young adult smokers have fewer substitute reinforcers than ex-smokers (15
) and almost half of smokers seeking smoking cessation treatment have elevated depression symptoms (24
Depression, even at subclinical levels is often accompanied by withdrawal and less involvement in rewarding activities (12
). In addition to being an easily available reinforcer, nicotine may mitigate these losses by increasing the salience of rewarding stimuli in the environment and by enhancing reward from the non-smoking reinforcers that are present in the environment (23
). The role of nicotine in reward processing may explain why depressed smokers are more likely to choose smoking as their preferred activity and why they report needing significantly more alternative reinforcers to quit smoking compared to smokers without a depression diagnosis (22
). Our findings suggest that similar relationships exist for subclinical levels of depression and the establishment of smoking as a habit.
From a clinical standpoint these findings emphasize the importance of young adulthood as an opportune time to prevent smoking uptake and promote smoking cessation. About 50% of the sample had elevated depression symptoms, which increased the likelihood of smoking via diminished substitute alternative reinforcers. Interventions directed toward emerging adults with elevated depression symptoms and focused on increasing alternative reinforcers or preventing declines in alternative reinforcers may have a significant impact on preventing young adult smoking. These interventions may involve facilitating the identification and daily involvement in pleasurable activities not linked to smoking or drug use and/or preventing declines in these the pleasurable activities through self-monitoring and time allocation. These interventions also could be informed, in part, by successful depression prevention programs, which target young people with elevated depression symptoms and have an impact on a range of behaviors that commonly co-occur with cigarette smoking (55
In addition, a context of elevated depression symptoms and reduced reinforcers may promote increases in smoking rate, less interest in quitting and a decreased likelihood of successful smoking cessation (15
). Incentive-based approaches may increase motivation to enroll and achieve initial abstinence, while behavioral therapy can facilitate smoking cessation skills and a repertoire of substitute alternative reinforcers to smoking. Recent research suggests that these approaches hold promise in promoting smoking cessation and abstinence from other substance of abuse (15
It is important to point out that only a portion of those with elevated depression symptoms smoked cigarettes. A feature of depression, not present in all young people with elevated depression symptoms, may be responsible for the observed relationships. Anhedonia, or loss of interest in usual rewarding activities, may help explain the heterogeneity (57
). A temporary loss of interest or a dispositional diminished capacity to derive pleasure from activities that others typically find rewarding warrant further investigation (58
). Identification of the distinct aspect(s) of depression that impact smoking behavior may help to better define young adults who are at risk for smoking and highlight valuable treatment targets.
As our model accounted for about 30% of the variance in smoking, other mechanisms explaining the relationship between depression and young adult smoking should be evaluated in future research. The enhancement of positive affect and the management of negative affect are potential mechanisms to consider. Depression is associated with lower levels of positive affect and higher levels of negative affect (61
). Lower levels of positive affect predict smoking progression among adolescents (64
) and an inability to achieve smoking abstinence (65
) and shorter time to relapse in adults (66
). Less involvement in reinforcing activities and diminished reward from usual activities (decreased hedonia) are associated with a reduction in positive affect (61
). Likewise, young adults with elevated depression symptoms may smoke because it either relieves negative affect or it decreases the variability in negative affect (68
It is important to note that we did not find evidence for a direct effect of depression symptoms on smoking uptake, only an indirect effect. Evaluation of more complex relationships between depression and smoking, such as indirect effects, may provide a better understanding of the comorbidity and highlight targets for smoking prevention and cessation interventions (69
). We also considered the possibility that smoking contributed to depression symptoms directly and indirectly through a decline in substitute reinforcers. However, we did not find support for a direct or indirect effect of smoking on depression symptoms in young adulthood. Although evidence exists for reductions in depression among adolescents who progressed along the smoking uptake continuum (70
), these mood modulation effects may diminish with greater smoking experience (71
To our knowledge, this is the first longitudinal investigation of how depression can influence smoking progression and the establishment of regular smoking practices during emerging and young adulthood. Along with the several study strengths (e.g., large sample, repeated measures of key variables, control for many confounding influences), the limitations must be noted. One potential limitation is that we are not able to measure the extent of depression as diagnostic assessments were not completed. Higher levels of depression as measured by the CES-D may have been reflective of clinical episodes rather than subclinical depression symptoms. In addition, we are not able to clearly discern smoking uptake from an increase in smoking rate among more regular smokers in the mediation model. We are not aware of a two-piece model that can accommodate multiple associated processes and indirect effects. Finally, our annual assessment intervals may not have allowed us to capture finer-grained changes in our variables of interest. However, the model does highlight a general and novel connection between subclinical depression, alternative reinforcers, and smoking behavior among young adults. A better understanding of how elevated depression symptoms foster regular smoking in some young adults, but not others may help inform smoking prevention and smoking cessation interventions specifically designed for this age group. A reduction in smoking in this age group could have a significant impact on smoking attributable morbidity and mortality.