Добірка наукової літератури з теми "Adult Nicotine Treatment (ANT)"

It is now acknowledged that Attention-deficit Disorder with Hyperactivity (ADHD) is not limited to children or adolescents. Regardless of culture, up to 4% of the adults in the general population might be diagnosed with ADHD, a disorder often accompanied by comorbid psychiatric disorders. Among those is Substance Abuse including cigarette smoking. Indeed, ADHD patients tend to start with drugs earlier than normal controls. Pharmacological treatments of ADHD chiefly encompass amphetamine salts, methylphenidate and atomoxetine with a good tolerance and effectiveness. These treatments are even better tolerated now that long-acting, extended-release formulations and transdermal delivery systems become available. But it is likely that some patients will still not respond, especially when comorbid disorders are associated. Other agents are being tested as future pharmacotherapies of ADHD. Here we propose a review of the literature concerned with the relationships between cigarette smoking and ADHD in adolescent and adult patients, and an overview of the future pharmacotherapies of ADHD related with nicotine receptor agonists.

Abstract Introduction Existing treatments can aid tobacco smoking cessation, but they have low efficacy. Because there is a network of neural systems involved in tobacco addiction, combination treatments may provide greater efficacy. Chronic nicotine and amitifadine have each been shown to significantly reduce nicotine self-administration in rats. This study was conducted to determine if the combination of chronic nicotine with amitifadine, a triple monoamine reuptake inhibitor with CYP2B inhibitory effects, would reduce nicotine self-administration to a greater extent than either alone or placebo. Methods This study tested the combination of nicotine plus amitifadine in young adult female Sprague-Dawley rats self-administering nicotine (0.03 mg/kg/infusion). This combination was compared with each treatment alone and the vehicle during continuing nicotine self-administration as well as during resumption of self-administration after a week of enforced abstinence, modeling a quit attempt. Finally, we studied the residual effects of these therapies after discontinuation of treatment. Results Treatment with either chronic nicotine or amitifadine alone significantly reduced nicotine self-administration relative to controls. The combination of the treatments significantly enhanced this effect. After treatment withdrawal, all of the groups showed increases in nicotine self-administration, but only the combined treatment group remained significantly below control rates of nicotine self-administration. Conclusions This study showed the promise of amitifadine as a possible new treatment for smoking cessation and suggested that amitifadine is more effective when given with chronic nicotine. The improved efficacy of the amitifadine and nicotine combination may be potentiated by amitifadine’s inhibitory effects on CYP2B, which slows nicotine metabolism. Implications This study replicated the effects that chronic nicotine or chronic amitifadine, a triple reuptake inhibitor, significantly reduces nicotine self-administration in rats. It extends those findings by showing that the combination of chronic nicotine plus amitifadine causes significantly greater reduction in nicotine self-administration than either drug treatment alone. The combination of chronic amitifadine and chronic nicotine also causes a persistent significant reduction in nicotine self-administration after the end of treatment. The amitifadine and nicotine treatment should be assessed in humans to determine whether this combination provides greater efficacy in smoking cessation than transdermal nicotine treatment alone.

AbstractWe examined the variation and heritability of DSM-IV nicotine withdrawal (NW) in adult and adolescent male and female twin cigarette smokers (who reported smoking 100 or more cigarettes lifetime). Telephone diagnostic interviews were completed with 3,112 Australian adult male and female smokers (53% women; age: 24–36) and 702 Missouri adolescent male and female smokers (59% girls; age: 15–21). No gender or cohort differences emerged in rates of meeting criteria for NW (44%). Latent class analyses found that NW symptoms were best conceptualized as a severity continuum (three levels in adults and two levels in adolescents). Across all groups, increasing NW severity was associated with difficulty quitting, impairment following cessation, heavy smoking, depression, anxiety, conduct disorder and problems with alcohol use. NW was also associated with seeking smoking cessation treatment and with smoking persistence in adults. The latent class structure of NW was equally heritable across adult and adolescent smokers with additive genetic influences accounting for 49% of the variance and the remaining 51% of variance accounted for by unique environmental influences. Overall, findings suggest remarkable similarity in the pattern and heritability of NW across adult and adolescent smokers, and highlight the important role of NW in psychiatric comorbidity and the process of smoking cessation across both age groups.

Abstract Introduction During adolescence, exposure to nicotine or cannabis independently induces effects on neuromaturation and later cognitive function. However, the potential effect of both drugs under co-use conditions has become of increasing concern given the prevalence of e-cigarettes, legalization of cannabis, and availability of synthetic “spice” cannabinoid agonists. Aims and Methods The current studies investigated the effects of exposure to a cannabinoid receptor agonist (WIN55,212-2) and/or nicotine over a discrete time period in mid-adolescence on later intravenous nicotine self-administration in adult male and female mice. We further examined whether cannabinoid agonist administration in adulthood would alter nicotine reinforcement, with either acute or chronic pairing across 7 days. Results We found that adult males exhibited increased nicotine self-administration at a lower, rewarding nicotine dose following adolescent cannabinoid exposure, either alone or with nicotine coadministration. In contrast, adult females demonstrated an opposing effect in which adolescent cannabinoid and nicotine coexposure resulted in decreased nicotine intake compared with the nicotine only and control groups. Furthermore, after maintaining nicotine self-administration across sessions, pretreatment with a low dose of the cannabinoid agonist decreased nicotine intake in both male and female control mice, and this lowering effect was evidenced after both acute and chronic treatment. However, the cannabinoid agonist was ineffective in altering nicotine intake in mice previously exposed to nicotine, cannabinoid agonist, or both during adolescence. Conclusions These data provide evidence that adolescent drug exposure can alter later nicotine reinforcement in a sex-specific manner and can further modulate the effectiveness of interventions in reducing nicotine intake during adulthood. Implications These studies demonstrate a significant impact of nicotine, cannabinoids, or coexposure on developmental processes during adolescence. Differential effects were observed within each sex, with opposing results found for cannabinoid exposure on nicotine intake in males and females. Intriguingly, we also evidenced resistance to the lowering effects of a cannabinoid agonist on nicotine intake in adulthood based on adolescent drug exposure. Thus, these findings have important implications for our understanding of the impact of nicotine and cannabinoids (eg, Δ9-tetrahydrocannabinol (THC) and synthetic “spice” cannabinoids) during development, with further implications for the effectiveness of therapeutic interventions based on prior drug exposure in youth.

The acaricidal activity of the petroleum ether extract of leaves ofTetrastigma leucostaphylum(Dennst.) Alston (family: Vitaceae) againstRhipicephalus (Boophilus) annulatuswas assessed using adult immersion test (AIT). The per cent of adult mortality, inhibition of fecundity, and blocking of hatching of eggs were studied at different concentrations. The extract at 10% concentration showed 88.96% inhibition of fecundity, 58.32% of adult tick mortality, and 50% inhibition of hatching. Peak mortality rate was observed after day 5 of treatment. Mortality of engorged female ticks, inhibition of fecundity, and hatching of eggs were concentration dependent. The LC50value of the extract againstR. (B.) annulatuswas 10.46%. The HPTLC profiling of the petroleum ether extract revealed the presence of at least seven polyvalent components. In the petroleum ether extract, nicotine was identified as one of the components up to a concentration of 5.4%. However, nicotine did not reveal any acaricidal activity up to 20000 ppm (2%). Coconut oil, used as diluent for dissolving the extract, did not reveal any acaricidal effects. The results are indicative of the involvement of synergistic or additive action of the bioactive components in the tick mortality and inhibition of the oviposition.

Abstract Introduction Nonadherence to pharmacotherapies complicates studies of comparative pharmacotherapy effectiveness. Modeling adherence and abstinence simultaneously may facilitate analysis of both treatment acceptability and effectiveness. Methods Secondary analyses of a three-arm randomized comparative trial of nicotine patch, varenicline, and combination nicotine patch and lozenge among adult daily smokers (N = 1086) were conducted. Adherence rates collected via interactive voice response systems during the first 27 days of quitting were compared across treatment conditions. Repeated measures latent class analyses of adherence and abstinence in 3-day parcels through 27 days of a quit attempt were conducted with treatment, demographic, and smoking history covariates. Results Adherence varied across treatments and was lowest for nicotine lozenge use in combination nicotine replacement therapy (NRT). Five latent classes that differed significantly in 6-month abstinence rates were retained, including three subgroups of adherent participants varying in treatment response and two nonadherent groups varying in abstinence probabilities. Nonadherence was more likely among those receiving varenicline and combination NRT, relative to patch monotherapy. Varenicline and combination NRT did not promote abstinence among adherent latent classes but did promote abstinence among those partially adherent, relative to patch alone. Combination therapy attenuated increased risk of treatment disengagement with more years smoking. Minority smokers, those high in dependence, and those with shorter past abstinence were at increased risk for low-adherence and low-abstinence latent classes. Conclusions Varenicline and combination nicotine patch and lozenge are less likely to be used as directed and may not increase first-month abstinence better than patch alone when taken adherently. Implications This secondary analysis of adherence and abstinence in a comparative effectiveness trial shows that adherence is highest for the nicotine patch, next highest for varenicline, and lowest for combination nicotine patch and lozenge therapy due to low lozenge use. Distinct latent classes were found that varied in both first-month abstinence and adherence. Varenicline and combination NRT may not enhance abstinence over patch alone among smokers who take medication adherently. Adherent use of medication especially benefits those who are low in dependence and have positive quitting histories; it is less beneficial to at-risk smokers and members of racial minorities.

Abstract Introduction The main objective of this study was to explore the mechanism of nicotine improving cognitive impairments in ischemic rats. Methods Twenty adult male Sprague–Dawley (SD) rats underwent ischemic model surgery by injecting endothelin-1 into the left thalamus, which were classified into four different groups with different intervention: nicotine (1.5 mg/kg/d), dihydro-β-erythroidine (DHβE; 3 mg/kg/d), nicotine (1.5 mg/kg/d) + DHβE (3 mg/kg/d), or saline, after ischemic model surgery. Another five male SD rats also underwent same surgery, while not injecting endothelin-1 but saline, as the control group. Morris water maze (MWM) test was adopted to assess the cognition. All the rats underwent the MWM test, micro positron emission tomography imaging with 2-[18F]-A-85380, and messenger RNA (mRNA) test of α 4 nicotinic acetylcholine receptor (nAChR), β 2 nAChR, tumor necrosis factor-alpha (TNF-α), IL-1β, and IL-6. Results The MWM test showed the rats given nicotine showing better memory than ischemic rats (p < .05), whereas the rats given DHβE or both nicotine and DHβE did not show any statistical difference from the ischemic rats (p > .05). Micro positron emission tomography imaging showed higher uptake of tracer in the left thalamus and whole brain in rats given nicotine than in ischemic rats, but the rats given DHβE or both nicotine and DHβE did not. By real-time PCR test, the mRNA of α 4 nAChR and β 2 nAChR in rats given nicotine increased significantly compared with ischemic rats and decreased TNF-α, IL-1β, and IL-6 mRNA (all ps < .05). Conclusions By activating α 4β 2 nAChRs, nicotine plays a role in inhibiting the inflammatory factors, which contributes to improving cognitive impairment in ischemic rats. Implications It is well acknowledged that vascular cognitive impairment (VCI) is the second most common cause of dementia after Alzheimer’s disease. Cholinergic agents have potential for the symptomatic treatment of the cognitive symptoms of dementia, but the exact mechanism still remains unclear. There are potential complex associations and interactions between VCI and inflammation. This study showed that nicotine had anti-inflammatory potency, which is most likely because of the activation of the nAChRs. By activating α4β2 nAChRs, nicotine played a role in inhibiting the inflammatory factors, which contribute to improving cognitive impairment in ischemic rats.

Abstract Introduction Individuals with psychiatric conditions smoke at higher rates than the general population and may need more intensive treatment to quit. We examined whether or not extended treatment with nicotine patch, combined with behavior counseling, would disproportionally benefit smokers with versus without a lifetime psychiatric condition. Methods We conducted a secondary analysis of data from an effectiveness trial of treatment with 12 counseling sessions (48 weeks) and 21-mg nicotine patch (8, 24, or 52 weeks) among 525 adult daily smokers. A structured clinical interview assessed past and current psychiatric disorders (major depression, generalized anxiety disorder, alcohol abuse and/or dependence, and substance abuse and/or dependence), as described in the Diagnostic and Statistical Manual of Mental Disorders (Fourth Edition). Abstinence was bioverified at week 52. Logistic regression evaluated the effect of the psychiatric status × treatment duration interaction on abstinence at week 52, covarying for sociodemographics, baseline psychological symptoms, and treatment adherence. Results At baseline, 115 (21.9%) participants were diagnosed with one or more psychiatric conditions. The psychiatric status × treatment duration interaction was significant for week 52 abstinence (p = .027). Abstinence rates between smokers with versus without a psychiatric condition in the 24-week treatment arm (9.3% vs. 31.5% abstinent) significantly differed from the 8-week treatment arm (18.8% vs. 22.3%), p = .017. Abstinence rates for smokers with (22.5%) versus without a psychiatric condition (19.7%) in the 52-week treatment arm did not differ from those in the 8-week arm. Conclusions Targeted smoking cessation treatment, rather than extending treatment duration, may be especially warranted to optimize treatment for smokers with comorbid mood, anxiety, and substance use disorders. Implications Individuals with psychiatric conditions smoke at higher rates and have greater difficulty quitting compared to those in the general population, but little is known about how to best optimize treatment for this high tobacco burden population. The present study found that cessation response to extended duration treatment with the transdermal nicotine patch did not differ for smokers with versus without comorbid anxiety, mood, and substance use disorders in a large-scale clinical effectiveness trial. Development of targeted behavioral treatments may be required to optimize abstinence outcomes for this high-risk population, rather than simply extending the duration of pharmacotherapy treatments.

Abstract Introduction This study explored the efficacy of combination lorcaserin and nicotine patch for smoking cessation treatment and prevention of postsmoking cessation weight gain. Methods We conducted a trial in which 61 adult daily smokers were asked to quit smoking using a combination of lorcaserin and nicotine patch. During the first 2 weeks of treatment prior to the quit day, participants were randomized to receive either lorcaserin (10 mg twice daily) plus nicotine patch (21 mg) or placebo plus nicotine patch (21 mg). Following this 2-week period, participants received both medications for 12 weeks. Outcomes included 4-week continuous smoking abstinence at the end of treatment (weeks 7–10 postquit attempt), weight change, ad libitum smoking, withdrawal symptoms, and ratings of cigarette reward. Results Biochemically confirmed continuous smoking abstinence from 7 to 10 weeks postquit attempt was 31.1% (90% confidence interval, 21.4%–40.8%). Participants who quit smoking showed no weight gain; in fact, mean weight change was minus 0.16 kg (SD = 3.27) over the study period. There was an unexpected but strong association (p = .006) between a decrease in sensory enjoyment of smoking and successful quit outcome on this regimen. During the prequit randomization period, lorcaserin versus placebo reduced the impact of smoking to relieve craving for cigarettes as well as the sensory enjoyment of smoking (p = .005). Adherence and tolerability to lorcaserin and nicotine patch was good. Conclusions The combination of lorcaserin and nicotine patch was well tolerated, associated with a relatively high smoking abstinence rate, and effectively prevented weight gain associated with quitting smoking. Implications This report provides an important contribution to the literature because it details evidence of a medication combination—lorcaserin and nicotine—that is effective for smoking cessation and for ameliorating weight gain associated with smoking cessation. For many smokers, postcessation weight gain is a major obstacle to quitting, and this medication combination provides a suitable treatment option for these smokers. Clinical Trial Registration NCT02906644

Group-based tobacco dependence treatment has been known to help smokers to quit in general adult populations, but the feasibility and efficacy of this type of smoking cessation treatment in correctional settings remain uncertain. A 6-week group-based smoking cessation treatment with nicotine replacement therapy (NRT) in the form of nicotine patches was implemented in seven male prison facilities, in the Northeast, among smokers who were born biologically as male. Exhaled breath carbon monoxide (CO) levels were collected from participants at each session to confirm smoking status. Participants were evaluated at the 1-month post-group treatment follow-up to determine abstinence. Those who were lost to follow-up were recorded as continued smoking and not using NRT nicotine patches. The goal of the study was to explore the feasibility and preliminary efficacy of conducting a smoking cessation treatment program for incarcerated smokers. A total of 350 inmates were screened, 177 inmates were enrolled across the prison sites for the 6-week program, and 102 inmates completed the program. A majority of those enrolled reported that they began smoking when they were between 15 and 19 years of age (44.9%) and were smoking on average for 26 years. Less than half (21.3%) reported ever using electronic cigarettes at baseline and in Session 1,116 individuals who attended reported a median CO level of 18.0 parts per million (ppm). At a 1-month follow-up, 43 individuals reported a median CO level of 5.00 ppm. The study demonstrated preliminary efficacy and feasibility of group-based smoking cessation treatment with NRT nicotine patches in incarcerated smokers.

Masters of Science
It is well documented that cigarette smoking and nicotine exposure create widespread physiological disorders in humans and animals. The primary tobacco constituent that is responsible for the toxicological consequences associated with the effects of tobacco smoke is nicotine (Van Lancker 1977). After maternal nicotine exposure, the fetal gonads and lungs are the principle sites of nicotine damage (Szuts et al. 1978, Mosier & Jansons 1972). Whilst the fetal lung has received widespread attention in this regard (Maritz 1988), the testis has never been studied. Therefore, I have chosen to explore the effects of maternal nicotine exposure on the testis of male offspring by evaluating various aspects of the male reproductive tract. It is believed that, in adult male smokers (Rosenberg 1987, Handelsman et al. 1984) and sexually mature animals (Mattison 1982) that are exposed to nicotine, male fertility may be compromised. However, these studies provide conflicting data on single parameters. It was therefore my objective to identify the effect of nicotine exposure on the male reproductive tract and to establish possible sites through which these effects may be mediated in adult male rats. The influence of nicotine was then investigated in male offspring after maternal nicotine treatment (MNT), and in sexually mature adult males after direct adult nicotine treatment (ANT). In the former experiment (MNT), 7 day pregnant rats were exposed to Img nicotine/kg body weight/day. Therefore, these offspring were indirectly exposed to nicotine during fetal development and early neonatal development. After weaning the animals were divided into two groups. One group did not receive further treatment (withdrawn group), whilst the other group was continually treated till adulthood (nicotine group), after which both groups were sampled together with the control. In the latter experiment (ANT), the animals were treated daily for 3 weeks and were sampled as above (MNT animals). The fundamental parameter investigated in both experiments to assess reproductive status was sperm quality (motility and morphology). Thereafter, it was necessary to establish a possible site where the effects of nicotine would occur. Testicular growth, epididymal structure, and plasma testosterone content were measured as probable localities of nicotine's effect. The results signify that maternal nicotine exposure poses a greater threat to the male reproductive system than adult nicotine exposure. In the MNT experiment, progressive sperm motility of the nicotine and withdrawn groups were 1.7% and 3.4% respectively. The proportion of abnormal sperm was 72% in each of the above groups. The lower quality sperm that is evident after nicotine exposure implies that the fertilizing ability of the animals may be impaired during adulthood. The data on testicular growth indicates that nicotine exposure during early development results in slower testicular development until maturity. The epididymal lining of these animals also increased after nicotine exposure, indicating increased cellular activity. However, these results from testicular and epididymal studies are inconclusive and need further work. In the ANT experiment, progressive sperm motility of the nicotine group was 1.2%, whilst the proportion of abnormal sperm was 58%. No other parameter was affected after nicotine exposure to adult animals. From the above data it is evident that nicotine exposed animals were subject to greater nicotine damage after maternal nicotine exposure during early development. Moreover, within the maternal nicotine treated experiment, the withdrawal of nicotine after weaning did not appear to reverse the injurious effects of nicotine that were established during early development. These effects were evident since the nicotine and withdrawn groups showed similar levels of damage in all instances. The most profound effects after adult nicotine exposure and maternal nicotine exposure were on sperm quality. The probable site of sperm impairment appears to be via retarded testicular growth and possibly, structural status of the epididymis after maternal nicotine exposure. The results from adult nicotine exposure however, suggest that sperm cells may be directly affected by nicotine exposure. An epidemiological survey was included to validate the basic conclusions established in animal research when compared to clinical data from human patients. No statistically significant changes were observed in this study between the patient's spermiogram results versus his smoking habits, and, that of his mother. From the level of significance it was concluded that cigarette smoking does not appear to be a cause of impaired fertility in already infertile patients. However, the data does suggest that cigarette smoking may well be a precipitating agent in male infertility. Experimentally, nicotine exposure impairs the male reproductive system to some extent. The effects of which are irreversible after indirect exposure (MNT) during development and may begin with poor testicular development. The effects of adult nicotine exposure implies that nicotine exposure in mature animals (ANT) acts directly on sperm cells to incapacitate them. It is well advised that cigarette smoking should be curbed in pregnant women and in adult males to alleviate contributing effects to male infertility.

Thesis (Honors paper)--Florida State University, 2008.
Advisor: Carlos A. Bolaños, Florida State University, College of Arts and Sciences, Dept. of Psychology. Includes bibliographical references.

The chapter on treatments for substance use disorders discusses and reviews the use of medication-assisted treatments with (a) methadone, buprenorphine/naloxone, and naltrexone for opioid use disorders; (b) disulfiram, acamprosate, naltrexone, and several off-label medications for alcohol use disorders; and (c) nicotine replacement therapies, bupropion, and varenicline for tobacco use disorders. The chapter reviews the mechanisms of action, clinical characteristics, potential medication interactions, and adverse effects of these medications, followed by an in-depth discussion of their clinical use in these disorders. The chapter also briefly reviews several non-Food and Drug Administration (FDA)-approved medicines studied for cocaine, cannabis, and amphetamine use disorders. It also briefly discusses complementary and alternative pharmacotherapies, such as the use of cannabinoids. It also discusses the use of these medicines in women of childbearing age, notably for pregnancy and breastfeeding considerations. Finally, the chapter includes a table of approved substance use disorder medicines that includes each medicine’s generic and brand names, usual adult doses, pertinent clinical comments, black box warnings, and FDA indications.

Objective. Marijuana is the most widely used illicit substance in the United States and in 2018 alone, an estimated 40.3 million adults reported using marijuana in the past year. This is concerning since growing research suggests that marijuana use is associated with adverse health and life outcomes, such as mental health issues, and cognitive impairment. Thus, determining factors that influence marijuana use-related problems is critical for understanding how to effectively implement prevention, intervention, and treatment efforts. Because research has proposed that emotion dysregulation is a transdiagnostic risk factor for substance use and addiction, the investigation of emotion regulation capabilities in marijuana users is warranted. Furthermore, since prior studies suggest that stress may lead to greater marijuana use-related problems, additional research into how emotion dysregulation may affect these relationships is needed. Thus, the current study examines how emotion dysregulation moderates the association between stress and problematic marijuana use in adults through an online survey. Methods. 852 adults reporting any lifetime marijuana use completed an online survey through Qualtrics. Participants completed a brief demographic questionnaire and were asked to report their past 30-day use of marijuana, alcohol, nicotine, and illicit substances. To assess past month problematic marijuana use, participants completed the Marijuana Problem Scale (MPS). To assess emotion dysregulation, participants completed the Difficulties in Emotion Regulation Scale (DERS). Participants completed the Perceived Stress Scale (PSS) and the Holmes-Rahe Life Stress Inventory (H-RLSI) to assess past month perceived stress and past year stressful life events, respectively. We investigated the association between scores on the DERS, PSS, and H-RLSI with scores on the MPS. Additionally, we conducted hierarchical multiple linear regression models to test whether emotion dysregulation, stress, and their interaction predicted problematic marijuana use. Results. Scores on the DERS (r = .53, p < .001), PSS (r = .13, p < .001), and H-RLSI (r = .32, p < .001) were significantly correlated with scores on the MPS. Additionally, emotion dysregulation (B = .32, p < .001), stressful life events (B = .21, p < .001), and their interaction (B = .07, p = .003) were significant predictors of problematic marijuana use. Finally, emotion dysregulation (B = .44, p < .001), perceived stress (B = -.18, p < .001), and their interaction (B = -.06, p = .04) were significant predictors of problematic marijuana use. Conclusion. These findings indicate that when examined separately, greater emotion dysregulation, experiencing more stressful life events in the past year, and experiencing more perceived stress in the past month were associated with greater problematic marijuana use in the past month. However, when examining the moderating role of emotion dysregulation, more stressful life events and less perceived stress predicted greater problematic marijuana use, and these associations were stronger at higher levels of emotion dysregulation. Overall, these results suggest that emotion dysregulation and greater stress may be risk factors for developing problematic marijuana use, and could be possible targets for prevention, intervention, and treatment efforts.