Psychiatry related information on Tobacco Use Disorder

• Cerebrospinal fluid and plasma testosterone levels in post-traumatic stress disorder and tobacco dependence [1].
• The 2004 National Action Plan for Tobacco Cessation recommended that the US Department of Health and Human Services convene a diverse group of experts to ensure that competency in tobacco dependence interventions be a core graduation requirement for all new physicians and other key health care professionals [2].
• Publications in English were sought through a Medline search using the following key words: food habits, eating, feeding behavior, diet, food, nutrition, nutritional status or assessment, tobacco use disorder, tobacco, nicotine and smoking [3].
• CONCLUSION: Residential treatment for tobacco dependence is superior to outpatient treatment in some smokers who are moderately to severely nicotine dependent [4].
• Clinical effectiveness of sustained-release bupropion and behavior therapy for tobacco dependence in a clinical setting [5].

High impact information on Tobacco Use Disorder

• OBJECTIVE--To estimate the overall efficacy and optimal use of the nicotine patch for treating tobacco dependence [6].
• In these families, ADHD is highly comorbid with conduct and oppositional defiant disorders, as well as with alcohol and tobacco dependence [7].
• Because the mesolimbic dopaminergic system is implicated in the reinforcing effects of many drugs, including nicotine, the DDC gene is considered a plausible candidate for involvement in the development of vulnerability to nicotine dependence (ND) [8].
• The usefulness of cotinine as a marker of tobacco dependence is discussed [9].
• Role of functional genetic variation in the dopamine D2 receptor (DRD2) in response to bupropion and nicotine replacement therapy for tobacco dependence: results of two randomized clinical trials [10].

Chemical compound and disease context of Tobacco Use Disorder

• Tobacco dependence and the nicotine patch. Clinical guidelines for effective use [11].
• Although bupropion and nicotine replacement therapy (NRT) are efficacious tobacco dependence treatments, there is substantial interindividual variability in therapeutic response and most smokers relapse [10].
• CONCLUSION: These results suggest that nornicotine may be an effective treatment for tobacco dependence [12].
• This suggests that caffeine consumption may be a contributing factor in the onset, maintenance of and relapse to tobacco dependence [13].
• OBJECTIVE: We investigated whether tobacco smokers and non-smokers differed in platelet tritiated paroxetine binding, a measure of 5HTT sites, and whether severity of nicotine dependence (ND) was related to 5HTT measures [14].

Biological context of Tobacco Use Disorder

• Consequently, monitoring of nicotine binding sites could constitute an interesting approach to understanding the pharmacologic mechanisms involved in tobacco dependence [15].
• Neuroplasticity within the mesoaccumbens dopamine system and its role in tobacco dependence [16].
• The BDNF gene is located in a genomic region on chromosome 11p where we and others have found 'significant' linkage to nicotine dependence (ND) [17].

Anatomical context of Tobacco Use Disorder

• The rational basis for pharmacologic treatment approaches is that tobacco dependence is partially, and critically, mediated by the actions of tobacco-delivered nicotine to the central nervous system [18].

Gene context of Tobacco Use Disorder

• The clinical implications of CYP2A6 polymorphisms have been linked to a decreased risk of tobacco dependence, a decrease in number of cigarettes smoked and reduced risk of tobacco-related cancers [19].
• Allelic variants within the COMT gene are therefore potential candidates for examining interindividual differences in vulnerability to nicotine dependence (ND) [20].
• The aim of the present study was to determine which characteristics of smoking, particularly the Fagerström Test for Nicotine Dependence (FTND) score, were associated with the risk of developing COPD [21].
• These data provide support to the notion that the blockade of CB1 receptors can oppose tobacco dependence, withdrawal and even relapse, though the time window of efficacy and/or the schedule of administration remain to be established [22].
• It is concluded that nicotinic receptors containing the beta2 subunit play a major role in the discriminative stimulus and taste aversion effects of nicotine that may reflect psychological aspects of tobacco dependence [23].

Analytical, diagnostic and therapeutic context of Tobacco Use Disorder

• CONCLUSION: Since bPiDDB decreased nicotine self-administration specifically, this novel nicotinic receptor antagonist may constitute a lead for the development of a clinically useful treatment for tobacco dependence [24].
• While only 23% of California HMOs covered the nicotine patch or gum, 69% covered at least one form of the pharmacotherapy and one type of counseling to treat tobacco dependence [25].
• ND symptoms were measured in five indicators, including a measure based on the criteria for tobacco dependence in the International Classification of Diseases-10th Revision (ICD-10), the Hooked on Nicotine Checklist, and three symptom clusters (withdrawal, self-medication, and ND/cravings symptoms) [26].
• Through June 2001, there were approximately 32 million patient exposures to bupropion (9 million for smoking cessation) in clinical practice, and more than 8000 patients have been studied in clinical trials for tobacco dependence [27].
• All smokers completed a baseline questionnaire, which assessed smoking history, nicotine dependence [Fagerstrom Test for Nicotine Dependence (FTND)], nicotine withdrawal [Hughes-Hatsukami Withdrawal Scale (HHWS)], and depression [Center for Epidemiological Studies on Depression (CES-D)] [28].

References