Weight gain, related concerns, and treatment outcomes among adolescent smokers enrolled in cessation treatment.

We examined associations of weight concerns and weight gain with adolescent tobacco cessation treatment and whether these effects differed by gender or ethnoracial group. Participants were 115 urban adolescents recruited for a randomized clinical trial of nicotine replacement therapy. Baseline weight gain concerns were assessed using the Eating Disorders module from the Diagnostic Interview for the Child and Adolescent (DICA-IV). The average weight gain during the trial was 0.59 +/- 2.85 kg among the 43.5% of participants who completed the treatment study. As indicated by the DICA, baseline weight gain concerns were not associated with weight gain during treatment, study completion, or abstinence from smoking at 3-month posttreatment follow-up; these results did not vary by gender or ethnoracial group. Adolescents who quit smoking gained no more weight during the trial than those who smoked.

A link between adolescent nicotine metabolism and smoking topography.

Adult slow nicotine metabolizers have lower smoke exposure, carbon monoxide levels, and plasma nicotine levels than normal and fast metabolizers. Emerging evidence suggests nicotine metabolism influences smoking topography. This study investigated the association of nicotine metabolism (the ratio of plasma 3-hydroxycotinine to cotinine; 3OHCOT/COT) with smoking topography in adolescent smokers (n = 85; 65% female, 68% European American; mean age, 15.3 +/- 1.2 years; mean cigarettes per day, 18.5 +/- 8.5; mean Fagerström Test for Nicotine Dependence, 7.0 +/- 1.2) presenting for a nicotine replacement therapy trial. Measures obtained included puff volume, interpuff interval, number of puffs, puff duration, and puff velocity. Linear regression analysis controlling for hormonal contraception use showed that 3OHCOT/COT ratios predicted mean puff volume in the overall sample (t = 2.126; P = 0.037; adjusted R(2) = 0.067). After gender stratification, faster metabolism predicted higher mean puff volume (t = 2.81; P = 0.009; adjusted R(2) = 0.192) but fewer puffs (t = -3.160; P = 0.004; adjusted R(2) = 0.237) and lower mean puff duration (t = -2.06; P = 0.048; adjusted R(2) = 0.101) among boys only, suggesting that as nicotine metabolism increases, puff volume increases but puffing frequency decreases. No significant relationships were found between nicotine metabolism and total puff volume, mean puff duration, interpuff interval, or puff velocity. If confirmed in a broader sample of adolescent smokers, these findings suggest that as among dependent adult smokers, rate of metabolism among adolescent boys is linked to select parameters of puffing behavior that may affect cessation ability.

Age at menarche and weight concerns in relation to smoking trajectory and dependence among adolescent girls enrolled in a smoking cessation trial.

Many girls adopt dieting and other practices (i.e. cigarette smoking) to control weight during puberty. This analysis explored the relationship between age at menarche and onset of daily smoking, and whether this relationship was influenced by weight concerns among treatment seeking female adolescents. The sample consisted of 71 participants enrolled in a smoking cessation trial (age 15.2+/-1.3 years; 74.7% European American, baseline BMI 24.7+/-5.4, age at menarche 11.7+/-1.3 years, Fagerström Test for Nicotine Dependence score 7.0+/-1.2). Over 60% of participants reported weight concerns at baseline, based on responses to the Eating Disorders module from the Diagnostic Interview for Children and Adolescents. Linear regression analyses revealed a significant association between age at menarche and age of onset of daily smoking (beta=0.18+/-0.09, p=0.038). Having weight concerns did not modify the relationships between age at menarche and smoking trajectory/severity or abstinence. Findings support previous research showing that early maturation represents a risk factor for substance use. Further study in larger samples that include non-treatment-seeking adolescent female smokers is warranted.

Does allowing adolescents to smoke at home affect their consumption and dependence?

Negative parental attitudes towards smoking decrease adolescent smoking initiation but limited research explores the relationship between parental attitudes and degree of adolescent smoking among established smokers. The aim of this study was to examine the relationship between parental allowance of smoking in the home and adolescent smoking behavior and level of dependence. Interviews from 408 youths seeking assistance to quit smoking showed that adolescents who were allowed to smoke at home smoked more cigarettes per day and had higher scores on the Fagerström Test of Nicotine Dependence than those not allowed to smoke at home. Studies that additionally evaluate parental smoking status and the temporal relationship of parental allowance of smoking with changes in adolescent smoking behavior are warranted to clarify public health implications of parental smoking interdictions.

Measuring nicotine intake among highly-dependent adolescent smokers: comparability of saliva and plasma cotinine concentrations.

Cotinine is the most common biomarker used to assess nicotine exposure and abstinence. It can be measured in various matrices including saliva, plasma, and urine. Previous research with adults has shown high correlations between saliva and plasma cotinine concentrations. However, the research has not examined this relationship in adolescents. Additionally, variability in saliva flow and metabolism across gender, ethnicity, and age may impact the relationship between saliva and plasma cotinine concentration. Our aim was to examine the relationship between saliva and plasma cotinine concentration in a group of nicotine-dependent adolescent smokers. Additionally, we examined these correlations across gender, ethnicity and age. The sample consisted of 66 adolescent smokers (age 15.1+/-1.3, 63.6% girls, 66.7% European American, CPD 18.3+/-8.5, FTND 7.1+/-1.3). Saliva and plasma specimens were collected before the treatment phase of a nicotine replacement therapy trial and analyzed. The relationship between saliva and plasma cotinine concentration was analyzed using Pearson's correlation coefficients. We performed a secondary analysis using multiple regressions to compare correlations across race, gender and age. Results indicated a positive correlation between saliva cotinine and plasma cotinine concentration (r=0.84, p<0.001). Differences in correlations across age were significant (t=3.03, p<0.01). Differences across ethnicity approached significance (t=-1.93, p=0.058). Future research should seek to further validate saliva-to-plasma cotinine concentration ratios in adolescents as well as characterize saliva-to-plasma concentration differences and their underlying mechanisms.

Progression to daily smoking: is there a gender difference among cessation treatment seekers?

The goal of this study was to develop an understanding the developmental trajectory of smoking behaviors in adolescents who seek smoking cessation treatment to inform tailored prevention and treatment efforts; this includes identifying gender differences in smoking behaviors. Smoking trajectory was examined retrospectively in 639 treatment-seeking adolescents (59% female; 44% African American, 50% European American, mean +/- SD daily cigarettes per day [CPD] 19.16 +/- 7.2 for both girls and boys). Smoking trajectory variables examined included age at first cigarette, age at daily smoking (a proxy measure for onset of dependence), and age at treatment request. The time interval from first cigarette to daily smoking was shorter for girls than for boys (mean +/- SD 0.9 +/- 1.1 years for girls, 1.3 +/- 1.5 years for boys, p < 0.01). From this clinical sample of adolescent smokers, findings suggest only a brief window of opportunity for secondary preventive interventions before the development of tobacco dependence. Additional research is needed to explore the specific factors that differentially affect smoking trajectory in girls compared to boys.

Alcohol use and tobacco abstinence among adolescents in cessation treatment: preliminary findings.

Although adult alcohol use is negatively associated with tobacco cessation, this relationship has not been reported for adolescents. We assessed the relationship between alcohol use and point prevalence abstinence from smoking in a sample of tobacco-dependent adolescents undergoing cessation treatment. Alcohol use both at baseline and) during tobacco cessation treatment was examined as predicting smoking abstinence in 101 adolescents (age=15.1years, S.D.=1.31years; age at first cigarette=11.3years, S.D.=1.93years; age at first drink=12.01years, S.D.=2.87years) attending a total of 642 treatment visits. Mixed regression analysis showed that participants who reported alcohol use during tobacco cessation treatment were significantly less likely to abstain from tobacco smoking (OR=0.42, 95% CI=0.23-0.78, t=-2.78, df=540, p=0.0057). However, pre-enrollment alcohol use was not significantly associated with either short- or long-term tobacco abstinence. If confirmed in a larger group of adolescents, our findings suggest that youths attempting to quit smoking should abstain from alcohol.

Adolescent nicotine metabolism: ethnoracial differences among dependent smokers.

Variations in nicotine metabolism are thought to contribute to differences in cigarette consumption between African Americans and Caucasian adult smokers. To investigate the potential mechanism of previously documented lower smoking rates among African-American adolescent smokers seeking cessation treatment, we measured nicotine metabolite ratios as markers of the metabolic disposition of nicotine, which is generally considered to be under the influence of cytochrome P450 (CYP) 2A6. Plasma ratios of trans-3'-hydroxycotinine (3HC) to cotinine (COT) were examined in 92 cessation treatment-seeking adolescents (mean age 15.2 years, standard deviation [SD] 1.3, 69% female, 31% African American, mean Fagerström Test for Nicotine Dependence [FTND] 6.5, SD 1.6, mean years smoked 2.6, SD 1.6). Groups were similar in age, gender distribution, and mean FTND score. Analysis with independent t tests revealed significantly lower number of cigarettes per day (CPD) (15.1, SD 7.6 vs 19.6, SD 8.0, P=.013) and nicotine metabolite ratios (0.27, SD 0.15 vs 0.35, SD 0.16, P=.026) in African-American compared to Caucasian adolescent smokers. Consistent with metabolic variation, mean COT/CPD ratio was significantly higher in African-American compared to Caucasian adolescents. Results remained statistically significant when comparing menthol smokers by ethnicity. These findings are consistent with those found among adult smokers and provide a putative mechanism for reported ethnoracial differences in adolescent cigarette consumption. Our results underscore the need for measures independent of consumption for determining degree of nicotine dependence and treatment selection across ethnicities, even among youths.

Effects of the mixed mu/kappa opioid nalbuphine on cocaine-induced changes in subjective and cardiovascular responses in men.

Kappa opioid agonists functionally antagonize some abuse-related and locomotor effects of cocaine, and reduce cocaine self-administration by rhesus monkeys. We compared the cardiovascular and subjective effects of acute doses of the mu/kappa opioid nalbuphine alone (5 mg/70 kg, intravenous (i.v.)), with cocaine alone (0.2 mg/kg, i.v.), and with nalbuphine+cocaine in combination, under placebo-controlled, double-blind conditions. Subjects met American Psychiatric Association Diagnostic and Statistical Manual (DSM-IV) criteria for current cocaine abuse. Nalbuphine serum levels exceeded 50 ng/ml within 10 min after injection, and cocaine plasma levels exceeded 130 ng/ml within 4 min. Cocaine's pharmacokinetic profile did not change after concurrent nalbuphine administration. The nalbuphine+cocaine combination was safe and without synergistic effects on heart rate and systolic or diastolic blood pressure. Moreover, the addition of cocaine did not increase the subjective effects of nalbuphine. Visual Analog Scale (VAS) ratings of High, Euphoria, Stimulated, and Good Effect were equivalent after nalbuphine+cocaine and nalbuphine alone, and both were significantly higher than after cocaine alone (area under the curve analysis) (p<0.05-0.01). Peak VAS ratings of High, Stimulated, Good Effect, and Drug Effect were also significantly higher after nalbuphine+cocaine than after cocaine alone (p<0.01). Addiction Research Center Inventory (ARCI) scores were equivalent for nalbuphine+cocaine and nalbuphine alone, but the PCAG, MBG, and amphetamine scores were significantly higher after both nalbuphine+cocaine and nalbuphine alone than after cocaine alone (p<0.01-0.003). Thus, there were no additive interactions between nalbuphine and cocaine on cardiovascular, subjective, or drug level measures after acute administration.

Effects of intravenous cocaine and cigarette smoking on luteinizing hormone, testosterone, and prolactin in men.

Cocaine and nicotine have a number of similar behavioral and neurobiological effects. This study compared the acute effects of cocaine and cigarette smoking on luteinizing hormone (LH), testosterone (T), and prolactin. Twenty-four men who met American Psychiatric Association Diagnostic and Statistical Manual criteria for cocaine abuse or nicotine dependence were given intravenous cocaine (0.4 mg/kg) or placebo-cocaine, or smoked a low or high nicotine cigarette under controlled conditions. Placebo-cocaine or low nicotine cigarette smoking did not change LH, T, or prolactin. Peak plasma levels of 254 +/- 18 ng cocaine/ml and 22.6 +/- 3.4 ng nicotine/ml were measured at 8 and 14 min, respectively. LH increased significantly after both i.v. cocaine and high nicotine cigarette smoking (P < 0.01). These LH increases were significantly correlated with increases in cocaine and nicotine plasma levels (P < 0.001-0.003), and high nicotine cigarette smoking stimulated significantly greater increases in LH release than i.v. cocaine (P < 0.05). Testosterone levels did not change significantly after either cocaine or after high nicotine cigarette smoking. After i.v. cocaine, prolactin decreased significantly and remained below baseline levels throughout the sampling period (P < 0.05-0.01). After high nicotine cigarette smoking, prolactin increased to hyperpro-lactinemic levels within 6 min and remained significantly above baseline levels for 42 min (P < 0.05-0.03). The rapid increases in LH and reports of subjective "high" after both i.v. cocaine and high nicotine cigarette smoking illustrate the similarities between these drugs and suggest a possible contribution of LH to their abuse-related effects.