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University of Nebraska–Lincoln

Health and Addiction Vulnerability Laboratory

Health Research

Obesity and Cigarette Smoking

Major health risks associated with obesity and cigarette smoking (Mokdad et al., 2004; Office of the U.S. Surgeon General, 2004; USDHHS, 2007) appear to be multiplicative among a subpopulation (20%) of smokers who are also obese. Specifically, obese smokers are at a 3.5 to 11 fold elevate risk of circulatory disease mortality compared with lean never smokers, lean smokers and overweight smokers (Freedman et al. 2006; Healton et al., 2006; Wee et al., 2001). Despite the greater than expected mortality risk associated with obese smokers, very little is known about mechanisms that contribute to comorbid obesity and cigarette smoking. For example, initial human self-administration and animal conditioned place preference evidence suggests that obesity diminishes nicotinic reward (Blendy et al., 2005). However, these findings left many unanswered questions about whether there are common underlying mechanisms that differentially influence food and nicotine reinforcement pathways in obese smokers.

Pilot work and secondary analyses from Dr. McChargue’s lab has attempted to untangle the interplay among affective vulnerability, smoking behavior and eating behavior of obese smokers. The primary assumptions were that obese smokers would be more emotionally labile to individualized stressor cues compared with non-obese smokers. They further examined whether urges mapped onto their emotional responses and whether smoking a cigarette selectively alleviated such responses. Results showed that obese smokers compared with non-obese smokers had greater reductions in positive affect, but not negative affect following a stressor (Salvi & McChargue, November 2007). They also show that rumination tendencies differentiated cardiovascular stress responses with obese smokers high in rumination showing the greatest cardiovascular response (Herrera, Highland & McChargue, November 2008). In addition, obese smokers report greater stress-induced urges to smoke compared with non-obese smokers and compared with their own urges to binge eat (Herrera & McChargue, April 2009). Analogous to prior research (Blendy et al., 2005); smoking a nicotine-containing cigarette did not produce the selective alleviation of negative affect following a stressor among obese smokers. Results showed that non-obese females had greater affective alleviation from a nicotine-containing cigarette compared with a cigarette without nicotine; where obese females showed greater affect alleviation from the cigarette without nicotine (McChargue et al., under review).

The aforementioned data continued to leave questions about the role of stress in reward seeking behavior among obese smokers. Specifically, it is unclear whether stress elicits cigarette seeking behavior over food seeking behavior. Dr. McChargue’s data are conflicting. He shows that stress-induced urges are selective to smoking and not food among obese smokers, but obese smokers do not experience greater affect alleviation from smoking. Furthermore, it was unclear whether neurobiological stress parameters would differentiate obese smokers from non-obese smokers. His self-report data show a diminished reward response with stress-induced decreased positive affect responses being selective to obese smokers, yet his stress-induced cardiovascular data is selectively elevated among obese smokers who ruminate. These data may implicate that obese smokers’ stress mechanisms are more associated with physiological parameters versus self-reported negative affective experiences.

Grants targeted to further elucidate his data include a NIH/NCI R03 grant submission that proposes to explore a) whether neuroendocrine and sympathetic indices differentiate psychological stress responses between obese smokers and non-obese smoker and b) whether psychological stress produces a selective bias in attention to reward cues (cigarette and/or food). He is also writing an NIH/NIDA R01 application to examine differences in nicotine reinforcement compared with food reinforcement among obese smokers. Obese and non-obese smokers will undergo two separate psychological stress inductions followed by a behavioral task where smokers have a choice to earn tokens for a targeted reward (food or cigarettes) compared with a constant reward (money). Specific aims are partially justified by published data showing that nicotine deprived female smokers will work harder for sweet foods compared with a constant reward as the demands of food proportionally increase (Spring, Pingitore & McChargue, 2003). He is also currently analyzing data that may show that obese smokers will work harder for nicotine vs. money following a stressor as compared with a neutral condition. The targeted grants will help to further disentangle stress-induced reward seeking behavior among obese smokers. Ultimately, his research plans include the eventual treatment trial targeting either smoking cessation, weight control and/or affect regulation skills among obese smokers.