Previous investigations have found that the relationship between MD and obesity are moderated by a variety of individual difference characteristics (Anderson et al., 2006
; Barry et al., 2008
; Carpenter et al., 2000
; Faith et al., 2002
; Fuemmeler et al., 2009
; Heo et al., 2006
; Herva et al., 2006
; Onyike et al., 2003
; Richardson et al., 2003
; Simon et al., 2006
). The present study extended this literature by examining tobacco use as a novel, theory-based candidate moderator of the MD-obesity relationship in a sample of nationally representative adults participating in the NESARC.
Univariate analyses showed that MD was associated with higher rates of obesity and higher BMI values. Based on maladaptive coping explanations of the MD-obesity relation, we hypothesized that tobacco use would moderate this association, such that tobacco use would diminish the strength of the relationship between MD and obesity. In support of this hypothesis, results indicated that both tobacco use indicators (i.e., past year smoking status and TD) significantly moderated the predictive influence of past-year MD on current obesity and BMI value. MD was significantly and robustly associated with obesity among nonsmokers and TD-respondents (ORs ≥ 1.65, ps < .0001), whereas the corresponding relationships among smokers and TD+ participants were substantially weaker and nonsignificant (ORs ≤ 1.10, ps ≥ .10). The same pattern was found when BMI value was the outcome. MD+ participants had higher BMIs then MD- participants only among nonsmokers and TD- respondents. Each of these findings remained consistent when adjusting for relevant sociodemographic variables and psychiatric and substance use disorders. Furthermore, supplemental analyses indicated that these associations were not entirely accounted for by extraneous confounding or explanatory factors (e.g., psychiatric medication use, smoking heaviness, underweight status). Additional analyses found that recent desire to quit did not moderate MD-obesity associations among current smokers. Given these analyses and results showing that smoking heaviness did not account for the findings, it appears that these results are specific to tobacco use indicators that differentiate smokers versus nonsmokers or people with versus without TD, and do not generalize to variables that explain individual differences among current smokers.
The moderational effect of past year MD and tobacco use indicators on obesity was unique from corresponding lifetime MD and tobacco use characteristics. There was additional evidence of a less robust, but statistically significant, lifetime MD × smoking status interaction that was unique from corresponding past-year characteristics. These findings are generally consistent with previous cross-sectional reports that other moderators impact the relationship between past-year MD and current obesity (Carpenter et al., 2000
; Onyike et al., 2003
Given extant data that gender moderates the relationship between MD and obesity (Carpenter et al., 2000
) as well as the link between smoking and MD (Husky et al., 2008
) with stronger associations among women, we explored whether the interaction between MD and tobacco use was moderated by gender. Supplemental analyses indicated that the moderating influence of MD on obesity did not significantly differ by gender (i.e., a three way MD× Tobacco Use × Gender interaction; p
s > .72). Thus, the extent to which tobacco use offset MD-obesity relationships was similar for both genders. There are several potential explanations for this finding. It is possible that while women may be more likely to engage in unhealthy behaviors to cope with MD, they may not be more prone than men to substitute one maladaptive coping mechanism for another. Relatedly, a prior study found little evidence of any gender differences in addiction substitution patterns, such that both men and women receiving treatment for opiate addiction exhibited similar patterns of substituting alcohol for heroin use (Almog, Anglin, & Fisher, 1993
). An alternative explanation of the lack of gender differences is that both men and women may both use tobacco to counteract the depressogenic effects of obesity (i.e., using tobacco to manage the mood-dysregulating effects of stigma, social isolation, and immobility associated with obesity).
There are several plausible accounts of the primary finding that tobacco use moderated MD-obesity associations in the overall sample. Previous investigations suggest that depression is associated with higher caloric intake (Rohde et al., 2008
; Simon et al., 2008
), more frequent binge eating (Linde et al., 2004
), and less physical activity (Rohde et al., 2008
) in an effort to cope with depressive disturbance, and that some of these relationships mediate the association between depression and obesity (Rohde et al., 2008
). Thus, it is possible that individuals who do not use tobacco may be especially vulnerable to the effects of MD on these intermediate processes that increase obesity risk. Alternatively, tobacco use, which has been reported as a means to manage depressed mood and counter fatigue and inactivity (Gilbert et al., 2000
; Ikard et al., 1969
; Leventhal & Avis, 1976
; Piper et al., 2004
; Tate et al., 1991
), may potentially offset MD-related obesity risk.
Other research indicates that individuals with underlying dysregulation of brain reward systems may substitute drug use and unhealthy eating for one another because both food and drugs share mood-altering properties, and therefore help individuals overcome reward deficits (Sussman & Black, 2008
). Accordingly, tobacco may compete with food for brain reward sites, especially among individuals with MD, who have been demonstrated to exhibit brain reward system dysregulation (Tremblay, Naranjo, Cardenas, Herrmann, & Busto, 2002
). Therefore, substitute addiction processes (Sussman & Black, 2008
) may potentially explain why tobacco may reduce the association between MD and obesity. However, both tobacco dependence and any past-year tobacco use both had moderational effects. Thus, any substitution that may have been operating was not limited to addictive patterns of tobacco use.
Although the impetus for this analysis was based on the notion that tobacco use may offset the effect of MD on obesity, the cross-sectional nature of the study allows for alternative causal explanations of the present findings. Previous evidence also suggests a prospective effect of obesity on depression, which may be due to difficulty coping with stigma, negative self-image, social isolation, and other factors (Roberts et al., 2003
). Perhaps tobacco use can buffer against the negative psychological effects of being obese. Alternatively, tobacco use may inversely associate with shared factors that underlie the covariation of depression and obesity, such as neural catecholamine abnormalities, genetic factors, and personality traits associated with a propensity to experience negative emotions (Fuemmeler et al., 2009
; Hainer, Kabrnova, Aldhoon, Kunesova, & Wagenknecht, 2006
One can also interpret the present findings as indicative that MD acts as a moderator of the association between tobacco use and obesity, such that MD amplifies the inverse relation between tobacco use and obesity (see ). Indeed univariate analyses showed that tobacco use tended to be associated with lower rates of obesity and lower BMIs. Consistent with this finding, previous reports have found that tobacco use is associated with lower rates of obesity (Bakhshi et al., 2008
; Molarius, Seidell, Kuulasmaa, Dobson, & Sans, 1997
). It is possible that the extent to which nicotine has appetite suppressant and metabolic-enhancing effects that reduces obesity risk is greater in people with MD. However, while research suggests that depressed smokers exhibit greater sensitivity to the effects of nicotine on mood (Faith, Flint, Fairburn, Goodwin, & Allison, 2001
; Farmer et al., 2002
; Pomerleau et al., 2005
; Spring et al., 2008
), they do not appear to differentially sensitive to nicotine’s appetite-suppressant effects (Spring et al., 2008
). Another related explanation is that the type of depression that leads people to smoke involves depressive episodes that include reduced appetite, which could impact BMI. Supplemental analyses eliminating respondents with reduced appetite demonstrated that endorsing this symptom may have accounted for some of the moderational effects on categorical obesity outcomes, but did not entirely account for moderational effects on BMIs. This pattern suggests that loss of appetite may explain some of the moderating effect of tobacco use on of MD’s association with extreme BMI levels, but not gradual BMI differences.
Finally, it should be noted that although our results indicate that tobacco use reduces the MD-smoking association, smoking elevates the risk of cardiovascular disease and various cancers and smoking cessation reduces these risks (Ockene, Kuller, Svendsen, & Meilahn, 1990
). Therefore, we are not advocating for increased tobacco use as a strategy to prevent or treat obesity in depressed individuals. Instead, it is important to consider the health impacts of these behavioral mechanisms in terms of the complex and interacting systems in which they function.
This study had several limitations, including a cross-sectional correlational design, self-report of height and weight for BMI calculation, no biochemical verification of tobacco use, lack of data on underlying mechanisms (e.g., physical activity patterns, diet, and coping responses to depressed mood), and absence of additional measures of adiposity other than BMI. Despite limitations, this study had several offsetting strengths, such as the use of a nationally representative sample, exploration across multiple moderators (i.e., smoking status and TD) and multiple outcomes (i.e., obesity status and BMI), use of valid clinical interview assessments to generate DSM-IV MD and TD diagnoses, and rigorous examination of extraneous confounding and explanatory variables.
To our knowledge, this is the first study to examine whether tobacco use moderates the association between MD and obesity. The unique moderational relationship demonstrated herein warrants future investigation as it points to putative etiological mechanisms that could account for the relationship between MD and obesity. Additional clarification of the temporal and causal nature of this moderational relationship using longitudinal and experimental research designs would be informative. In addition, future investigations directly measuring unhealthy eating and physical inactivity in addition to affective coping patterns as potential mechanisms explaining our findings would be useful for understanding the etiological processes linking MD and obesity. Such research could also have implications for matching obesity interventions to patients with individual difference factors that predict favorable treatment response. For example, the present findings may suggest that obesity interventions which target depressive symptoms may be more effective among nonsmokers. However, further research is required to evaluate the clinical validity of this prediction.