Weight gain frequently follows smoking cessation(2). Fear of weight gain is cited as a key reason not to quit(3) and actual weight gain is a primary reason for relapse, especially among women(6). Although the causes of weight gain following smoking cessation are complex(2), increased caloric intake is recognized as one of the primary sources(2,7,8). Just as exposure to smoking cues can induce smoking, exposure to food cues can induce feeding, even in sated animals(9). One explanation for increased caloric intake is that there are common neural mechanisms for food and cigarette reward and that nicotine addiction, which results in changes in brain encoding of smoking cues, also results in changes in brain encoding of food cues. The goal of this application is to test this prediction. We propose to use fMRI to test the prediction that nicotine addiction is associated with a decrease in the limbic response to food cues whereas cessation results in an increase in the limbic response to food cues. In accordance with the incentive-sensitization theory of drug addiction(13,14) we also predict that differences in neural encoding of food reward is specific to incentive salience encoding of food cues and is not characterized by differences in perceptual or neural response to food receipt. To evaluate these predictions we will examine brain response to food odors, equally pleasant and intense floral odors, food receipt, and receipt of a tasteless solution in smokers, non-smokers, and acutely abstinent smokers. To compliment the neuroimaging data we also plan to gather perceptual and behavioral measures of food reward including 1) assessment of hedonic ratings of food and floral odors, and food receipt; 2) assessment of the amount a subject will work for a food reward; and 3) ad lib consumption of chocolate chip cookies. Responses on these measures will then be used as covariates to predict neural response to food aromas in smokers, nonsmokers and acutely deprived smokers. If the data support our predictions then we will use it to support an R01 application to test whether brain and behavioral response to food can be used to predict weight gain during smoking cessation. If brain response does predict weight gain then we will have developed a method to identify individuals at risk for relapse so that they can be targeted for further therapeutic intervention. ? ? ?
| Geha, Paul; Cecchi, Guillermo; Todd Constable, R et al. (2017) Reorganization of brain connectivity in obesity. Hum Brain Mapp 38:1403-1420 |
| Rudenga, K J; Sinha, R; Small, D M (2013) Acute stress potentiates brain response to milkshake as a function of body weight and chronic stress. Int J Obes (Lond) 37:309-16 |
| Geha, Paul Y; Aschenbrenner, Katja; Felsted, Jennifer et al. (2013) Altered hypothalamic response to food in smokers. Am J Clin Nutr 97:15-22 |
| Felsted, Jennifer A; Ren, Xueying; Chouinard-Decorte, Francois et al. (2010) Genetically determined differences in brain response to a primary food reward. J Neurosci 30:2428-32 |
| Small, D M (2009) Individual differences in the neurophysiology of reward and the obesity epidemic. Int J Obes (Lond) 33 Suppl 2:S44-8 |
| Small, Dana M; Veldhuizen, Maria G; Felsted, Jennifer et al. (2008) Separable substrates for anticipatory and consummatory food chemosensation. Neuron 57:786-97 |
