Online Encyclopedia for Genetic Epidemiology Studies

Ø A Genetic Association for Cigarette Smoking Behaviour: Dopaminergic genes are likely candidates for heritable influences on cigarette smoking. In an accompanying article, Lerman et al. (1999) report associations between allele 9 of a dopamine transporter gene polymorphism (SLC6A3-9) and lack of smoking, late initiation of smoking, and length of quitting attempts. The present investigation extended their study by examining both smoking behaviour and personality traits in a diverse population of non-smokers, current smokers, and former smokers (N = 1,107). A significant association between SLC6A3-9 and smoking status was confirmed and was due to an effect on cessation rather than initiation. The SLC6A3-9 polymorphism was also associated with low scores for novelty seeking, which was the most significant personality correlate of smoking cessation. It is hypothesized that individuals carrying the SLC6A3-9 polymorphism have altered dopamine transmission, which reduces their need for novelty and reward by external stimuli, including cigarettes - http://www.apa.org/journals/features/hea1817.pdf

Ø NIDA (National Institute of Drug Abuse) Research on Smoking Behaviour - Research Monograph, Number 17: In this monograph, after giving an overview of the general problems associated with smoking, a detailed account is given on the epidemiological patterns of smoking behaviour; biological, psychological and sociocultural factors in the aetiology of the smoking behaviour; the economical and medical consequences of smoking; and at the end the behavioural changes that are required to prevent the onset of smoking plus the curative ways to stop this unhealthy habit - http://www.drugabuse.gov/pdf/monographs/download17.html

Ø Effect of smoke-free workplaces on smoking behaviour: systematic review: Smoke-free workplaces not only protectnon-smokers from the dangers of passive smoking, they also encouragesmokers to quit or to reduceconsumption. The combined effects of people stopping smoking and reducing consumption reduces total cigarette consumption by 29%. To achieve similar results through taxation would require cigarette taxes per pack to increase from $0.76 to $3.05 in the United States and from £3.44 to £6.59 in the United Kingdom - http://bmj.bmjjournals.com/cgi/content/full/325/7357/188

Ø The Behavioural Pharmacology Program: Report on the behavioural pharmacology program, the main objectives of which are to understand reinforcing actions of nicotine and nicotine analogues, gain insight into the neurobehavioral actions of nicotine, and develop animal behaviour techniques to screen nicotine analogues for their nicotine eliciting properties. Used controlled experiments with self-administration of nicotine by rats to establish reinforcer function of nicotine. Found response of 2-methylnicotine equivalent to that of nicotine (i.e. behaviourally active) - http://tobaccodocuments.org/product_design/1000128587-8596.html

Ø Selected Cigarette Smoking Initiation and Quitting Behaviours Among High School Students - United States 1997: As with other drug addictions, nicotine dependence is a progressive, chronic, and relapsing disorder (1). The optimal public health strategy is to prevent tobacco use completely or to intervene as early in the smoking behaviour continuum as possible. Once adolescents have established a pattern of regular use, their behaviour is usually compelled by nicotine dependence as well as social factors. Efforts are needed to help youth break the cycle of addiction and prevent the disability and death associated with tobacco use - http://www.cdc.gov/mmwr/preview/mmwrhtml/00052816.htm

Ø Nicotine and Smoking Behaviour: Most studies of cigarette smoking and smoking cessation have focused on the psychopharmacological effects of nicotine; relatively few have explored the role of sensory aspects of cigarette smoke. A major finding of this analysis is that ratings of smoking derived from de-nicotinized, but not nicotine-containing, cigarettes appear to vary with level of tobacco dependence, suggesting that sensory factors may be more important to highly dependent, as compared to less-dependent, smokers. The implications of these findings for smoking cessation treatment and for future research are discussed - http://www.duke.edu/~jdlane/SMOKWWW.HTM

Ø Interdependence - smoking behaviour & mood in natural setting: Although the health risks of smoking are well-known, many people choose to begin or to continue to smoke. Many smokers indicate that they smoke because it helps control their mood (for example, smoking to relax, smoking to be alert). It is also known that nicotine, the primary addictive substance in tobacco, can affect mood. It may also be that, once the person smokes regularly for some time, temporary withdrawal from nicotine generates mood disturbances which are then eliminated by smoking, an apparent but false benefit - http://www.trdrp.org/research/PageGrant.asp?grant_id=387

Ø Tobacco-Related Disease Research Program (TRDRP) - Mission: The mission of TRDRP is to support research that focuses on the prevention, causes, and treatment of tobacco-related disease and the reduction of the human and economic costs of tobacco use in California. Our program goals are to fund excellent research addressing all aspects of tobacco use; to widely disseminate the research findings through a variety of media; to encourage and support new scientific infrastructures and networks critical for a comprehensive approach to tobacco control; and to serve as an information resource for those interested in issues of tobacco control - http://www.trdrp.org/Mission.asp

Smoking and Genetics:

Ø Genetic analysis of maximum cigarette-use phenotypes: The Framingham Heart Study data set provided for Genetic Analysis Workshop 13 (GAW13) includes longitudinal data on daily cigarette use. In the past the Framingham data have been used to study important cigarette smoking patterns such as cessation and resumption. Our focus here was to define cigarette-use phenotypes that have potential to be useful in genetic analyses. While the results reported here do not indicate definitive evidence for linkage to specific chromosomal regions, future studies may find it useful to include direct assessments of maximum and quantitative cigarette use. In defining and analyzing quantitative or "maximum use" phenotypes, the choice of how to handle individuals with MAXCIG = 0, or alternatively, individuals who are substance-naive, is a crucial one for genetic studies of nicotine and other substance use. In this study, the linkage results vary greatly depending on whether or not these "unexposed" individuals are included in the analyses - http://www.biomedcentral.com/1471-2156/4/S1/S105

Ø A genome-wide scan to identify loci for smoking rate in the Framingham Heart Study population: Although many years of genetic epidemiological studies have demonstrated that genetics plays a significant role in determining smoking behaviour, little information is available on genomic loci or genes affecting nicotine dependence. Several susceptibility chromosomal regions for nicotine dependence have been reported, but few have received independent confirmation. Our genome-wide scan results on the Framingham Heart Study data provide evidence for significant linkage of smoking rate to chromosome 11 and suggestive linkage to chromosomes 4, 7, 9, 14, and 17. These findings suggest that some of these regions may harbor susceptibility loci for nicotine dependence, and warrant further investigation in this and other populations -http://www.biomedcentral.com/1471-2156/4/S1/S103

Ø A genome-wide search for loci contributing to smoking and alcoholism: Using the Collaborative Study on the Genetics of Alcoholism (COGA) data, we performed a sib-pair linkage analysis of two smoking-related traits and one alcoholism phenotype. Some of the regions studied in this study may represent loci increasing vulnerability to both smoking and alcoholism - http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10597412&dopt=Citation

Ø Association of smoking and personality with a polymorphism of the dopamine transporter gene: Results from a community survey: In studies that used mixed volunteer samples, Lerman et al. [[1999]: Health Psychol 18:14-20] and Sabol et al. [[1999]: Health Psychol 18:7-13] reported on an association of smoking with a polymorphism of the dopamine transporter gene. We attempted to replicate this association in a nonvolunteer community sample of 861 Caucasians. No associations were found with either smoking initiation or smoking cessation -http://www3.interscience.wiley.com/cgi-bin/abstract/72511297/ABSTRACT?CRETRY=1&SRETRY=0

Ø A meta-analysis of estimated genetic and environmental effects on smoking behaviour in male and female adult twins: Numerous twin studies on smoking behaviour have shown that genetic and environmental factors play significant and approximately equal roles in the determination of smoking initiation (SI) and smoking persistence (SP). This study finds that genetic and environmental factors may contribute differently to the determination of smoking initiation and persistence in male and female smokers - http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12492752&dopt=Abstract

Ø Multiple genome-wide analyses of smoking behaviour in the Framingham Heart Study: Cigarette smoking behaviour may have a genetic basis. We assessed evidence for quantitative trait loci (QTLs) affecting the maximum number of cigarettes smoked per day, a trait meant to quantify this behaviour, using data collected over 40 years as part of the Framingham Heart Study's original and offspring cohorts. This study concluded that familial aggregation of the maximum number of cigarettes smoked per day was consistent with a genetic component to this behaviour, and oligogenic segregation analyses using MCMC suggested two important QTLs. Linkage signals on chromosome 20 between 65 and 84 cM were seen using multiple analytical methods. No linkage result, however, met genome-wide statistical significance criteria, and the true relationship between these regions and smoking behaviour remains unclear - http://www.biomedcentral.com/1471-2156/4/S1/S102

Ø GATOR Study (Georgetown Adolescence Tobacco Research study): Data show that cigarette smoking among high school students in the United States has increased from 27.5% in 1991 to 36.4% in 1997 (CDC, 1998). Previous research has focused primarily on either social factors or psychological factors in youth smoking adoption, yet these data fail to explain fully why some youth can experiment with smoking yet not become established smokers, while others transition rapidly to a pattern of established smoking. Research on the genetic basis of smoking may shed some light on this question. The primary aim of the proposed study is to evaluate prospectively the contributions of specific genetic factors (i.e., genotypes for genes important in dopamine regulation) to the adoption of smoking. We will also evaluate whether these genetic effects are mediated by the rewarding effects of the initial smoking experience and/or by novelty-seeking personality - http://www.med.upenn.edu/tturc/adolescence.shtml

Ø The genetic basis for smoking behaviour: a systematic review and meta-analysis: A systematic review of candidate gene studies of smoking behaviour and, where sufficient studies existed, combined reported data using meta-analytic techniques. This study concluded that the evidence for an effect of specific genes was modest, however, and evidence indicated substantial between-study heterogeneity in most cases, with the exception of the effects of the 5HTT and CYP2A6 genes on smoking cessation - http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=15370155&dopt=Citation

Ø The genetic epidemiology of smoking: The data from family, adoption, and twin studies strongly support a substantial genetic influence on the initiation and maintenance of smoking. Liability to initiating smoking results from genetic influences (60%) and from environmental influences shared by members of a twin pair (∼20%) and that are specific to an individual (∼20%). The substantial impact of genetic factors on smoking behaviour has engendered molecular genetic studies of this complex trait - http://taylorandfrancis.metapress.com/media/h8jpnnqqrrg9ceq7ta2w/contributions/k/t/3/7/kt3785n277pw7865.pdf

Measures:

· The Tridimensional Personality Questionnaire: U.S. normative data -The Tridimensional Personality Questionnaire is a self-report personality inventory measuring three major personality dimensions: Novelty Seeking, Harm Avoidance, and Reward Dependence -

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&list_uids=1784653&dopt=Citation

· Relationship of Tridimensional Personality Questionnaire scores and smoking variables in female and male smokers: The likelihood of becoming a smoker may be a function of novelty seeking and reward dependence, whereas degree of dependence or addiction once the habit is entrained may be linked to harm avoidance. Our observations establish the potential utility of the TPQ as a tool for examining environmental and heritable variation in smoking behaviour and may contribute to improved strategies for prevention and treatment of smoking - http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=1504639&dopt=Citation

· Conducting a smoking prevalence survey: How much tobacco people use and the way in which they use it---whether they smoke manufactured cigarettes, chew snuff or spit tobacco, smoke pipes, or roll their own cigarettes---varies widely both across countries and between groups within a country. There is tremendous variation even in patterns and levels of the smoking of manufactured cigarettes, the most common form of tobacco use. Differences in smoking patterns translate eventually into differences in population morbidity and mortality. The main aim of a smoking prevalence survey is to characterize the current smoking behaviour of a given population, and of subpopulations of interest. Such surveys may also monitor exposure to variables that are known to influence smoking, such as the price of tobacco, any restrictions on smoking, and receptivity to tobacco industry messages - http://www.tobacco-control.org/tcrc_Web_Site/Pages_tcrc/Resources/Factsheets/conductingasurvey.pdf

· Statistics Canada - Questionnaire(s) and reporting guide(s) – Youth Smoking Survey (YSS): The main objective of the Youth Smoking Survey (YSS) - http://www.statcan.ca/cgi-bin/imdb/p2SV.pl?Function=getSurvey&SDDS=4401&lang=en&db=IMDB&dbg=f&adm=8&dis=2 is to collects information on the following topics: the prevalence of smoking among students in grades 5 to 9 (in Quebec primary school grades 5 and 6 and secondary school grades 1 to 3); the types of smoking behaviour among children (e.g. experimental smoking, occasional smoking, daily smoking); the social and demographic factors associated with smoking behaviour (e.g. what motivates children to smoke, the influence of family and friends); where and how children obtain cigarettes; attitudes and beliefs about smoking, including awareness of health risks; recollection and opinions on health warning messages on cigarette packages; experience with alcohol, drugs and medications used for non-medical purposes.

o Youth Smoking Survey, 2002 - Grade 5 and 6 (in PDF format) - http://www.statcan.ca/english/sdds/instrument/4401_Q1_V1_E.pdf

o Youth Smoking Survey, 2002 - Grade 7 to 9 (in PDF format) - http://www.statcan.ca/english/sdds/instrument/4401_Q2_V1_E.pdf

o Youth Smoking Survey, 2002 - Parent's Questionnaire (in PDF format) - http://www.statcan.ca/english/sdds/instrument/4401_Q3_V2_E.pdf

· American Academy of Family Physicians - Smoking: 'Why Do I Smoke?' Quiz: Most people smoke for different reasons at different times. Reasons for smoking include psychological issues, habits, social pressures and physical dependence on nicotine. The questionnaire that follows will help you decide which reasons are important in your smoking. If you know the answer to the question - why do I smoke, it will be easier to stop smoking because you can find ways to make up for the things you may miss when you stop - http://familydoctor.org/296.xml

· American Academy of Family Physicians - Assessing Nicotine Dependence: Family physicians can assess the smoking behaviour of their patients in a few minutes, using carefully chosen questions. The CAGE questionnaire for smoking (modified from the familiar CAGE questionnaire for alcoholism), the "four Cs" test and the Fagerström Test for Nicotine Dependence help make the diagnosis of nicotine dependence based on standard criteria. Additional questions can be used to determine the patient's readiness to change and the nature of the reinforcement the patient receives from smoking. These tools can assist family physicians in guiding patients to quit smoking--the single most important thing smokers can do to improve their health - http://www.aafp.org/afp/20000801/579.html

· Nicotine Addiction Test - Find out how much you depend on nicotine: Knowing how addicted you are to nicotine can help you quit. It can help you decide if you need extra help, such as medicine or support from a program. Take this test to find out how hooked you are - http://www.smokefree.gov/guide/nicotine_addiction.asp

· GeneWatch UK Press Release: Gene-Watch v. Oxford University over anti-smoking: GeneWatch UK called for Oxford University to withdraw its funding and support for a genetic test claimed to be related to nicotine addiction. GeneWatch reveals that the claimed link between the gene and nicotine addiction does not meet the usual standards of scientific evidence (it is not statistically significant). And also that the NicoTest website ignores scientific evidence that the test is unlikely to be useful for men - http://www.countrydoctor.co.uk/precis/precis%20-%20Anti-smoking%20complaint.htm

· Technical Note: Automated Homogeneous Immunoassay Analysis of Cotinine in Urine: A study was conducted to evaluate the performance comparison of a homogeneous enzyme immunoassay (EIA) designed to detect cotinine in urine and carbon monoxide (CO) breath measurements to determine smoking status. The study concluded that the EIA test is a rapid, lab-based test that can reliably determine cotinine levels and their relation to smoking status - http://www.ingentaconnect.com/content/pres/jat/2002/00000026/00000003/art00006

Assessment of Smoking Status among Workers Using an Improved Colorimetric Method: We modified a simple colorimetric determination method for urinary nicotine metabolites. The sensitivity and specificity of this method was 96.1% and 96.7%, respectively. This method could be applicable to quantitative identification of smoking status among healthy workers - http://www.niih.go.jp/en/indu_hel/2004/pdf/42-3-6.pdf

Smoking Cessation:

· London Ideas - How could genetics help smokers quit? Despite the wealth of information available about the health benefits of quitting smoking, and the advice and support available for people trying to quit, it is still a very tough challenge for most smokers. The aim of this programme is to look at whether using genetic information might be one way to do this - http://www.londonideas.org/internet/public/quit_smoking/

· Nicotine: Nicotine, in an inhaler, is used to help you stop smoking. It is used for up to 6 months as part of a stop-smoking program. This program may include counselling, education, specific behaviour change techniques, or support groups. With the inhaler, nicotine is inhaled through the mouth and is absorbed in the mouth and throat, but not in the lungs. Eight to ten puffs on the inhaler provide about the same amount of nicotine as one puff on an average cigarette. This nicotine takes the place of the nicotine that you would otherwise get from smoking. In this way, the withdrawal effects of not smoking are less severe. Then, as your body adjusts to not smoking, the use of the nicotine inhaler is decreased gradually over several weeks. Finally, use is stopped altogether - http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/203567.html

· American Cancer Society - Guide to Quitting Smoking: Quitting smoking is not easy, but it can be done. To have the best chance of quitting successfully, you need to know what you’re up against, what your options are, and where to go for help. This document is intended to provide you with this information - http://www.cancer.org/docroot/PED/content/PED_10_13X_Guide_for_Quitting_Smoking.asp

· Mayo clinic guidelines - Products to help you stop smoking: Nicotine replacement products and other medications can help you stop smoking. They can't do all the work, but they'll help you feel more comfortable and in control while you adjust to life without cigarettes. Although you can buy some nicotine replacement products without a prescription, it's best to consult your doctor to decide which product — or combination of products — may be best for you -

http://www.mayoclinic.com/health/stop-smoking-products/HA00065

· Clinician's Packet: Treating Tobacco Use and Dependence: This Clinician's Packet is a how-to guide for implementing the clinical practice guideline. It contains evidence-based information on first-line pharmacologic therapies and counselling that help patients quit. It also contains information about developing a system, advising patients, special populations, and reimbursement; and products for clinicians and consumers - http://www.surgeongeneral.gov/tobacco/clinpack.html

National Centre For Chronic Disease Prevention and Health Promotion: Tobacco Control Program Guidelines & Data - http://www.cdc.gov/tobacco/stat-nat-data.htm

Smoking hazards and pathobiology of smoke-related diseases:

Smoking hazards: http://www.nlm.nih.gov/medlineplus/ency/article/001994.htm

Cigarette Smoking, Metabolic Activation and Carcinogenesis: Epidemiologically, it has been suggested that cigarette smoking is closely associated with an increased risk of cancers in various organs such as the lung, oropharynx, stomach, pancreas, liver and colon. Nevertheless, influences of cigarette smoking on experimental tumorigenesis in organs other than the respiratory tract remain to be elucidated. In our experimental studies, it has been shown that cigarette smoke exposure induces hepatic CYP enzymes, especially CYP1A2, in both rats and hamsters. Keeping these data, the aim of this review is to discuss any relevancy of modulated metabolic activation by cigarette smoking to cancer risk in human - http://www.ingentaconnect.com/content/ben/cdm/2004/00000005/00000005/art00001
Depression and self-medication with nicotine: the modifying influence of the dopamine D4 receptor gene: This study evaluated whether there are genetic subgroups of depressed individuals who are more or less predisposed to engage in self-medication smoking practices. The results of this study suggest that the rewarding effects of smoking and the beneficial effects of nicotine replacement therapy for depressed smokers may depend, in part, on genetic factors involved in dopamine transmission - http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9459071&dopt=Citation

Document Provenance and History