Weight gain following smoking cessation.

Smoking generally suppresses body weight below "normal," and smoking cessation allows weight to return to normal. This weight gain following cessation appears to be due to a transient increase in eating coupled with the removal of acute metabolic effects of each cigarette, with no change in physical activity. Nevertheless, tobacco smoke (and specifically nicotine) does not appear to be simply either an anorectic or a thermogenic agent. Although there may be no easy explanation for the effects of smoking on energy balance, the most parsimonious explanation may be that smoking lowers body weight "set point" and cessation raises set point. The transient changes in eating are therefore secondary to the changes in body weight set point. This notion is supported by animal research with nicotine as well as with other drugs, and it is also supported less directly by the pattern of changes observed with changes in smoking status among humans. A set-point explanation for weight gain after smoking cessation may also help explain the lack of success of interventions designed to prevent this weight gain. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Is weight gain after smoking cessation inevitable?

Weight gain after smoking cessation was studied in a naturalistic setting where (1) all smokers quit and (2) risk factors for postcessation weight gain were modified. Participants were 332 military recruits (227 men, 105 women), 86 of whom were smokers who quit during 6 weeks of basic training. Results showed no significant weight changes for smokers who quit. Pretest smoking rates and feat of weight gain were unrelated to changes in weight. Results suggest that an intensive program that limits access to alcohol and foods that are high in fat and that increases physical activity can attenuate weight gain after smoking cessation. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Predictors of weight change following smoking cessation

Smoking behavior and weight change over a 5-year period were studied in 1,749 adult males of the Normative Aging Study. While men who quit smoking generally gained more weight than those in other smoking categories, 36% either lost weight or maintained the same weight after quitting. The major research focus was to predict the direction of weight change after smoking cessation. Among the characteristics most related to weight gain after quitting were heavier tar consumption, younger age, and leanness of body build. Conversely, traits related to weight loss were lighter smoking, older age, and stoutness of build.     

Nicotine gum dose and weight gain after smoking cessation.

The authors examined weight gain in 79 abstinent cigarette smokers during treatment with placebo or with 2 mg or 4 mg of nicotine gum. Results indicated that nicotine gum suppressed weight gain in a linear fashion with increasing nicotine dose. At 90 days postcessation, placebo gum users gained 3.7 kg, 2-mg gum users gained 2.1 kg, and 4-mg gum users gained 1.7 kg. Assessment of nicotine replacement by means of pre- and postcessation salivary cotinine levels revealed that smokers who replaced a greater percentage of their baseline cotinine levels during treatment gained less weight. Percentage of baseline cotinine replaced remained related to weight gain after the number of pieces of gum used was controlled. Implications for smokers hoping to minimize postcessation weight gain are discussed. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

How much weight gain occurs following smoking cessation: A comparison of weight gain using both continuous and point prevalence abstinence.

Estimates of postcessation weight vary widely. This study determined the magnitude of weight gain in a cohort using point prevalence and continuous abstinence criteria for cessation. Participants were 196 volunteers who participated in a smoking cessation program and who either continuously smoked (n?=?118), were continuously abstinent (n?=?51), or who were point prevalence abstinent (n?=?27) (i.e., quit at the 1-year follow-up visit but not at others). Continuously abstinent participants gained over 13 lbs. (5.90 kg) at 1 year, significantly more than continuously smoking (M?=?2.4 lb.) and point prevalence abstinent participants (M?=?6.7 lbs., or 3.04 kg). Individual growth curve analysis confirmed that weight gain and the rate of weight gain (pounds per month) were greater among continuously smoking participants and that these effects were independent of gender, baseline weight, smoking and dieting history, age, and education. Results suggest that studies using point prevalence abstinence to estimate postcessation weight gain may be understanding postcessation weight gain. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Is leptin sensitivity the link between smoking cessation and weight gain?

We performed a case-control study to investigate the association of the poor metaboliser genotype of the cytochrome P450 2D6 gene with Parkinson's disease (PD). Genotyping was determined by the polymerase chain reaction followed by digestion with restriction enzymes. The poor metaboliser genotype was more frequent in 112 patients with PD than in 206 matched controls (odds ratio 1.7, 95% CI: 0.94-2.45). A meta-analysis of these results together with ten other published studies gave a pooled odds ratio for the poor metaboliser genotype of 1.47 (95% CI: 1.18-1.96, P=0.01). Thus, the poor metaboliser genotype has a small but highly significant association with PD which would be easily missed in small studies. Research now should focus on the mechanism of this association.     

Smoking-specific weight gain concerns and smoking cessation in a working population.

Smoking cessation rates, progression in stage of change for smoking cessation, and serious quit attempts were examined over 2 years in a cohort of 242 men and women smokers (mean age 39.7 years, mean body mass index [BMI] 26.3) as a function of expressing concern about gaining weight because of quitting smoking. Participants were employees of 25 companies who were in a worksite health promotion program aimed at reducing risk factors for cardiovascular disease. Multivariate odds ratios (controlled for age, education, job class, sex, and BMI) for quitting smoking, attempting to quit smoking, and progressing in stage of change for smoking cessation as a function of weight concern were not significant. Interactions between sex and weight concern, and BMI and weight concern were also not significant. These findings, in a working, predominantly blue-collar population, and those of other studies, suggest that concern about gaining weight is, at best, a weak predictor of change in smoking behavior among most smokers. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

The role of weight concern and self-efficacy in smoking cessation and weight gain among smokers in a clinic-based cessation program

We have previously reported that Vicia graminea lectin (VGA)- and Vicia unijuga lectin (VUA)-binding glycoproteins (Vgu glycoproteins), malignant tumor-associated antigens, exist in human meconium and amniotic fluid. To examine the origin of Vgu glycoprotein, their presence, some of their chemical and serological properties and their biosynthesis in the human fetal membrane, amnion and chorion laeve and accompanying membrane cells were examined. Perchloric acid-soluble fractions were prepared from human amnion and chorion laeve, after which VUA-binding components (Vgu glycoproteins) were separated by HPLC and affinity chromatography using immobilized VUA. Biosynthesis of the antigens in primary cultured cells prepared from the amnion and chorion laeve were examined by pulse-labeling and immunoprecipitation using immobilized VUA and compared with those in cultured human cancer cells. The results indicated that the serological properties of VUA-binding components in fetal membranes were similar to those of meconium and amniotic fluid, that many molecular species of VUA-binding components were synthesized in amnion and chorion laeve cells and that about 40-50% of antigens synthesized are secreted from cells while antigens synthesized in cultured cancer cells human were hardly secreted with more than 95% of the antigens remaining in the cells. From these results, we concluded that a large part of Vgu glycoproteins found in amniotic fluid is synthesized in cells of the amnion and chorion laeve and secreted into the fluid, and that Vgu glycoproteins synthesized in cancer cells were not secreted, rather they were retained in the cells.     

Smoking cessation and weight gain

Recent studies have led to new insights into the pathogenesis of multiple myeloma, including appreciation of the potential role of human herpesvirus-8 infection and further characterization of some of the cytogenetic abnormalities present in this disease. New strategies to optimize the use of allogeneic and autologous stem cell transplantation include the development of various immunotherapeutic techniques to enhance the antitumor effect, and, in the case of allogeneic transplantation, to reduce toxicity. In addition, increasing evidence supports the role of biphosphonates in preventing the bone destruction typical of this disease, and possibly in improving the survival of certain groups of patients.     

Smoking cessation and weight gain.

Investigated determinants of weight gain after quitting smoking in 2 smoking treatment outcome studies in which 255 Ss (mean age 37 yrs) participated. It was hypothesized that (a) abstinence would result in weight gain; (b) postquitting weight gain would be predicted by pretreatment tobacco use, a history of weight problems, and eating patterns; and (c) relapse to smoking would follow weight gain. The 1st 2 hypotheses were confirmed. Year-long abstainers gained more weight than relapsers. Most of the weight gain occurred during the 1st 6 mo following quitting. Number of cigarettes smoked at pretreatment and past maximum body weight correlated positively with weight gain. Scores on a measure of eating control in specific situations, especially emotional ones, explained 27% of the variance in weight gain among abstinent Ss at a 1-yr follow-up. A measure of persistent hunger also predicted weight gain at a 1-yr follow-up. Eating disinhibition scores, number of cigarettes smoked at pretreatment, and maximum body weight were not correlated among Ss abstinent for the year. Disinhibition score and maximum body weight, however, correlated positively in the entire sample of Ss. Contrary to the 3rd hypothesis, greater weight gain during the 1st mo predicted continued abstinence, not relapse. (19 ref) (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Influences of gender and weight gain on short-term relapse to smoking in a cessation trial.

Few researchers have studied whether weight gain has an impact on short-term relapse to smoking. The authors of this study investigated predictors of relapse among 989 participants (60% women) in a randomized, double-blind, 10-week multicenter trial to determine the effect of fluoxetine (30 or 60 mg) versus placebo in combination with behavioral counseling for smoking cessation. Medication compliance and smoking status were biochemically verified. At Visit 2, participants were asked to set a quit date within the subsequent 2 visits. A proportional hazards regression model was used to predict risk of relapse within the first 3 months of quitting. Weight gain predicted relapse, but for men only. Female gender also predicted relapse. The results led the authors to question whether postcessation weight gain interventions should be restricted to women smokers. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Predictors of initial smoking cessation and relapse through the first 2 years of the Lung Health Study.

Analyses were made separately for men and women of the predictors of end-of-treatment (4 months) smoking cessation and subsequent relapse at 12 and 24 months among 3,923 participants enrolled in the Lung Health Study's 12-week cognitive–behavioral group smoking cessation program. Nicotine gum (2 mg) was available to all participants. Men were more likely than women to quit smoking initially, but relapse rates were similar for both genders. Baseline variables associated with initial quitting for both genders included greater education, lower nicotine dependence, and fewer respiratory symptoms. The best predictor of relapse between 4 and 12 months was smoking at least 1 cigarette between quit day and 4 months. Nicotine gum use at 12 months predicted relapse by 24 months for both genders. Greater social and environmental support for quitting smoking were the only factors that predicted both initial quitting and relapse for both genders. Clinical implications are discussed. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Weight gain as a function of smoking cessation and 2-mg nicotine gum use among middle-aged smokers with mild lung impairment in the first 2 years of the Lung Health Study.

Assessed the extent and predictors of weight change among sustained nonsmoking special intervention participants in the Lung Health Study. The intervention included a 12-session group program and 2-mg nicotine gum. At 12 mo, female sustained quitters (SQs; n?=?248) had gained a mean of 8.4% (5.3 kg) of their baseline weight, whereas male SQs (n?=?443) had gained 6.7% (5.5 kg). By 24 mo, female SQs had gained 9.8% of their baseline weight compared with 6.9% for men. Nicotine gum usage delayed a portion of the weight gain. Multiple regression analysis showed that weight gain at 12 mo was associated with a higher baseline salivary cotinine level, a lower baseline body mass index, drinking less alcohol per week, and a lower cotinine level at 12 mo (indicating less or no nicotine gum use). Moderate weight gain may be a long-term consequence of smoking cessation, a portion of which can be delayed with 2-mg nicotine gum. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Changes in energy balance following smoking cessation and resumption of smoking in women.

Caloric intake, resting metabolic rate (RMR), leisure-time physical activity, and sensitivity and preference for sweet taste were prospectively examined in 7 female smokers across 3 weeks during periods of normal smoking (Week 1), complete cessation (Week 2), and resumption of smoking (Week 3). Energy balance changed significantly across weeks, as caloric intake increased (largely as a result of alcohol consumption) and RMR decreased during cessation, followed by decreased caloric intake and increased RMR with resumption of smoking. Activity and taste sensitivity and preference remained unchanged. Smoking cessation may thus cause rapid change in energy balance, which is quickly reversed on resumption of smoking. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Eating orientation, postcessation weight gain, and continued abstinence among female smokers receiving an unsolicited smoking cessation intervention.

Predictors of weight gain following smoking cessation were assessed among 1,219 female smokers enrolled in a health maintenance organization. Women randomized to the treatment group received a cessation intervention without regard to their interest in quitting smoking. It was hypothesized that cessation would result in subsequent weight gain and postcessation weight gain would be associated with scores on a modified Restraint Scale, the Disinhibition Scale, and a scale assessing tendency to eat during periods of negative affect. Persons who abstained from smoking over the 18-month study gained more weight than did intermittent smokers and continuous smokers, and among 762 women who reported at least 1 on-study attempt to quit smoking, 36% gained weight. Weight gain was associated with disinhibited eating and negative affect eating but not with restrained eating. Weight gain also was associated with continued abstinence from smoking. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Effects of smoking cessation on maternal airway function and birth weight

Recombinant human neutrophil leukotriene B4 (LTB4) omega-hydroxylase (cytochrome P450 4F3) has been purified to a specific content of 14. 8 nmol of P450/mg of protein from yeast cells. The purified enzyme was homogenous as judged from the SDS-PAGE, with an apparent molecular weight of 55 kDa. The enzyme catalyzed the omega-hydroxylation of LTB4 with a Km of 0.64 microM and Vmax of 34 nmol/min/nmol of P450 in the presence of rabbit hepatic NADPH-P450 reductase and cytochrome b5. Furthermore, various eicosanoids such as 20-hydroxy-LTB4, 6-trans-LTB4, lipoxin A4, lipoxin B4, 5-HETE and 12-HETE, and 12-hydroxy-stearate and 12-hydroxy-oleate were efficiently omega-hydroxylated, although their Km values were much higher than that of LTB4. In contrast, no activity was detected toward laurate, palmitate, arachidonate, 15-HETE, prostaglandin A1, and prostaglandin E1, all of which are excellent substrates for the CYP4A fatty acid omega-hydroxylases. This is the first time human neutrophil LTB4 omega-hydroxylase has been isolated in a highly purified state and characterized especially with respect to its substrate specificity.     

Relapse following smoking cessation: A situational analysis.

Data on the antecedents of relapse crises (actual or near lapses in abstinence) were collected from 183 former smokers who called a relapse-counseling hotline. Most relapse crises were associated with anxiety, anger, and depression. One-third of relapse crises were associated with positive feeling states and were frequently precipitated by other smokers, eating, and alcohol consumption. Withdrawal symptoms played a part in only half of the episodes. Ss' coping responses rather than situational antecedents distinguished relapse crises resulting in smoking from those in which abstinence was maintained. A combination of cognitive and behavioral responses was most successful. Behavioral coping was subject to situational influences; Ss who had been drinking alcohol were less likely to engage in behavioral coping, and depression diminished its effectiveness. Cognitive coping responses, which were less affected by these variables, may be critical components of former smokers' coping repertoires. (31 ref) (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Correspondence programs for smoking cessation and weight control: A comparison of two strategies in the Minnesota Heart Health Program.

Evaluated the popularity and effectiveness of 2 correspondence programs for weight loss (WL) and smoking cessation (SMC) by canvassing 31,400 households in a suburban community for participants. The programs included a 6-mo correspondence program costing $5 (PRG 1) and the same program for free but requiring a $60 deposit to be refunded based on success in WL or SMC (PRG 2). Sign-up included 1,304 people for WL and 142 for SMC. PRG 1 was about 5 times as popular as PRG 2. Validated weight change after 6 mo averaged about 4 lbs for PRG 1 and 8 lbs for PRG 2. Corresponding rates of SMC were about 9% and 20%, respectively. Correspondence programs may be cost-effective methods for reaching individuals who might not otherwise participate in behavior change programs. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Reconciling conflicting findings regarding postcessation weight concerns and success in smoking cessation.

Correlates of concern about weight gain following smoking cessation and self-efficacy about controlling weight gain were examined in 940 men and 1,166 women who were surveyed on 2 occasions as part of a randomized trial of work-site interventions for smoking cessation. Weight concerns were positively associated with female sex, body weight, dieting for weight control, nicotine addiction, and social encouragement to quit. Bivariate analyses replicated prior findings that elevated weight concerns are associated with a reduced likelihood of quitting smoking, at least in women. Analyses controlling for demographics, nicotine dependence, and social factors replicated prior findings that weight concerns are not negatively related to smoking cessation and that some measures of concern are positively related to cessation. These analyses suggest that conflicting findings found in this literature are due primarily to how weight concerns are defined and whether covariates like nicotine addiction are used in data analyses. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Cigarette smoking, weight gain, and coronary mortality: results from the Chicago Western Electric Study

BACKGROUND: Prospective studies of overweight and coronary heart disease (CHD) have presented inconsistent findings. Previous inconsistencies may be explained by the modifying effect of cigarette smoking on the association between weight gain and coronary mortality. METHODS AND RESULTS: We prospectively studied 1531 men 40 to 59 years of age who were employed at the Hawthorne Works of the Western Electric Company in Chicago, Ill. Information collected at the initial examination in 1958 included recalled weight at age 20, present weight, height, smoking status, and other CHD risk factors. Vital status was known for all men on the 25th anniversary: 257 CHD deaths occurred over 31,644 person-years of experience. Cox regression analysis was used to investigate risk of coronary mortality associated with change in body mass index (deltaBMI) and its modification by smoking status after adjustment for age, major organ system disease, family history of CHD, and BMI at age 20. Adjustment was not performed for blood pressure or serum total cholesterol because these are intervening variables. DeltaBMI was positively associated with risk of coronary mortality in never-smokers but not in current-smokers (P for interaction =.088). For never-smokers with deltaBMI classified as stable, low gain, moderate gain, or high gain, adjusted relative risks of coronary mortality were 1.00, 1.75, 1.75, and 3.07, respectively (P for trend=.010). For current-smokers, the respective adjusted relative risks were 1.00, 0.78, 1.05, and 1.03 (P for trend=.344). CONCLUSIONS: These results support the hypothesis that cigarette smoking modifies the association between weight gain and coronary mortality. Future investigations of weight gain and coronary mortality should account for the modifying effect of cigarette smoking.