Stress, appetite and smoking relapse

Converging evidence indicates that concern about weight gain after abstinence increases reluctance to attempt smoking cessation, and that post-cessation weight gain is associated with smoking relapse. Chronic smoking causes numerous neurobiological changes, and smoking abstinence is associated with changes in appetite. Elucidating biobehavioral mechanisms associated with these effects of abstinence is critical in identifying those at high risk for weight gain and for planning appropriate treatment contingencies. The long-term goal of our research is to delineate the interactions of neurobiological mechanisms responsible for appetite regulation and tobacco addiction. The specific goal of this project is to determine the extent to which levels of appetite-regulating peptides (i.e., leptin, ghrelin, GLP-1, neuropeptide Y, and orexin) measured during smoking and during the early phase of abstinence predict subsequent changes in appetite, dietary intake, weight, and relapse during smoking cessation. We will also examine the extent to which abstinence-induced blunted adrenocortical and cardiovascular responses to stress predict changes in appetite, dietary intake, weight, and relapse over the first three months of a cessation attempt. This application is a continuation of our focused program investigating the role of stress in smoking relapse while taking into account that the effects of stress do not operate in vacuum, and that there is a need to clearly identify interactions of stress effects with other motivational and mood states. We have completed studies identifying specific psychobiological patterns of the stress response sensitive to individual and situational factors in smokers and non-smokers. We recently completed a series of studies that examined changes in hypothalamic-pituitary- adrenocortical responses to stress following short-term smoking abstinence and evaluated the extent to which these changes predict early relapse. The composite work and literature have provided relevant directions to guide the development of the proposed program. PUBLIC HEALTH RELEVANCE: Tobacco addiction/dependence is the leading preventable cause of cancer and cardiovascular diseases. Evidence indicates that weight gain occurring after smoking abstinence increases reluctance to attempt smoking cessation, especially among women. There is also evidence that post-cessation weight gain is associated with smoking relapse. We plan to determine the extent to which changes in appetite-related peptides and stress response during early abstinence predict subsequent weight gain and smoking relapse. Gaining a better understanding of these factors will be essential in designing interventions to address weight gain and stress effects during cessation, and to subsequently reduce smoking relapse rates. Reducing smoking relapse will have a direct public health impact in reducing the burden of smoking-related diseases.

This study is funded by the National Institutes of Health (NIH)/ National Institute for Drug Abuse (NIDA)

Stress, taste, and appetite regulation

Many individuals change their eating habits under stress. There are many explanations for the variation in eating behavior. First, eating may act as a distraction from the stressor, and could therefore be a reward. Secondly, dieting behavior may collapse under stressful conditions, therefore leading the individual to consume more calories when stressed. Finally, some individuals may use eating as a coping strategy to extinguish stress and negative emotions. Although these explanations are plausible, they do not encompass the entire picture of an individual under stress. By gathering information about individual differences, such as psychological factors (i.e., restraint, mood, anxiety), behavioral factors (i.e., smoking), biological factors (i.e., cardiovascular reactivity, cortisol reactivity), and environmental factors (i.e., stress), we may be able to better understand what characteristics predispose individuals to these behaviors.

Although the majority of people report changing their eating habits under stress, the direction in which consumption goes is not as clear. Some people report overeating while stressed, while others report undereating. Many theories have developed to explain the differences between overeaters and undereaters. The proposed study will include a laboratory stress protocol to examine the extent to which exposure to acute stress influences appetite. The study will include the assessment of physiological and mood response to acute challenges and examines tastes perception, food consumption, and food preference after a period of stress or rest.

This study is funded by the University of Minnesota.

Sweet Taste and Pain

It is well documented that sweet taste (sucrose ingestion) is associated with an increase in pain threshold and this phenomenon occurs across ages, cultures and geographic regions (Lewkowski, Ditto, Roussos, & Young, 2003; Lewkowski, Young, Ghosh, & Ditto, 2008). The mechanisms for why this occurs are not well known, although a combination of factors are likely involved. There is little research examining the interaction of those potentially predisposed to later development of hypertension and the effect of sweet taste on pain perception and nociception compared to those who have no family history of hypertension. We are currently examining this relationship in hopes of serving as a building block to discover mechanisms associated with pain sensation regulation that are intertwined with blood pressure regulation and the development of hypertension. The study includes include a laboratory stress protocol to examine the extent to which exposure to sweet taste and acute stress influences cardiovascular responses and pain. The study includes the assessment of physiological and mood response to acute challenges and examines cardiovascular, hormonal and pain responses after a period of stress or rest. Results from this study may provide insight that can spawn future studies that lead to early diagnosis for those at risk and prevention of myocardial infarctions.