scholarly journals Risk Factors Influencing Smoking Behavior: A Turkish Twin Study

2014 ◽  
Vol 17 (6) ◽  
pp. 563-573 ◽  
Author(s):  
Sevgi Yurt Öncel ◽  
Danielle M. Dick ◽  
Hermine H. Maes ◽  
Fazil Alıev

Aim: In this study, we introduce the first twin study in Turkey, focusing on smoking behavior, and laying the foundation to register all twins born in Turkey for research purposes. Using Turkish twins will contribute to our understanding of health problems in the context of cultural differences. Materials and methods: We assessed 309 twin pairs (339 males and 279 females) aged between 15 and 45 years living in the Kırıkkale and Ankara regions of Turkey, and administered a health and lifestyle interview that included questions about smoking status and smoking history. We analyzed the data using descriptive statistics, t-tests, chi-square tests, and bivariate and multivariate clustered logistic regression. In addition, we fit bivariate Structural Equation Models (SEM) to determine contributions of latent genetic and environmental factors to smoking outcomes in this sample. Results: One hundred seventy-eight participants (28.8%) were identified as smokers, smoking every day for a month or longer, of whom 79.2% were males and 20.8% were females. Mean values for number of cigarettes per day and the Fagerstrom Test of Nicotine Dependence (FTND; Fagerstrom, 1978) score were higher in males than in females, and age of onset was earlier in males. There was a significant positive correlation between the FTND score and number of cigarettes smoked per day, and a significant negative correlation between both variables and age at onset of smoking. Our study showed that gender, presence of a smoking twin in the family, age, alcohol use, marital status, daily sports activities, and feeling moody all played a significant role in smoking behavior among twins. The twin analysis suggested that 79.5% of the liability to FTND was influenced by genetic factors and 20.5% by unique environment, while familial resemblance for smoking initiation was best explained by common environmental factors. Conclusions: Marked differences in the prevalence of smoking behavior in men versus women were observed for the Turkish population. Genetic analyses showed that common environmental factors primarily contributed to smoking initiation, while genetic factors explained a greater proportion of variance in liability to nicotine dependence. Our study shows higher heritability estimate of the FTND scores and higher shared environmental influence on smoking initiation for both males and females than reported in previous studies.

2015 ◽  
Vol 18 (1) ◽  
pp. 43-51 ◽  
Author(s):  
Elizabeth K. Do ◽  
Elizabeth C. Prom-Wormley ◽  
Lindon J. Eaves ◽  
Judy L. Silberg ◽  
Donna R. Miles ◽  
...  

Little is known regarding the underlying relationship between smoking initiation and current quantity smoked during adolescence into young adulthood. It is possible that the influences of genetic and environmental factors on this relationship vary across sex and age. To investigate this further, the current study applied a common causal contingency model to data from a Virginia-based twin study to determine: (1) if the same genetic and environmental factors are contributing to smoking initiation and current quantity smoked; (2) whether the magnitude of genetic and environmental factor contributions are the same across adolescence and young adulthood; and (3) if qualitative and quantitative differences in the sources of variance between males and females exist. Study results found no qualitative or quantitative sex differences in the relationship between smoking initiation and current quantity smoked, though relative contributions of genetic and environmental factors changed across adolescence and young adulthood. More specifically, smoking initiation and current quantity smoked remain separate constructs until young adulthood, when liabilities are correlated. Smoking initiation is explained by genetic, shared, and unique environmental factors in early adolescence and by genetic and unique environmental factors in young adulthood; while current quantity smoked is explained by shared environmental and unique environmental factors until young adulthood, when genetic and unique environmental factors play a larger role.


Author(s):  
Ruzilawati Abu Bakar

Objective: The aim of this study was to assess smoking behavior among Malay male smokers in Kelantan, Malaysia.Methods: Volunteers (n=496) were recruited in the study by randomly selected manner. The participants were categorized as smokers (n=248) and non-smoking controls (n=248). All participants were given data collection sheets to record their information. The participants who were selected in smokers group (n=248) were given a form containing questionnaires regarding their smoking behavior. The participants were asked about their smoking history such as smoking initiation age, factors that influence smoking behavior, number of cigarettes daily, number of quitting attempts, and methods of quitting attempts. The validated Malay version of Fagerstrom test for nicotine dependence (FTND-M) was used to measure physical dependence on nicotine among smokers.Results: The study revealed that smokers in this study group were mainly light smokers. More than half of the participants, i.e., 51.6% (n=128), in this study had an FTND-M score lower than 2 (very low nicotine dependence). The minimum smoking initiation age of the participants in this study was 10 years whereas the maximum age was 40 years. Most of the participants start smoking at the age of <20 years with the higher frequency being18 years. More than half of the participants (58.5%) claimed that peer influence is the main factor initiating their smoking behavior. From the study, about 50.4% (n=125) of participants used <10 sticks of cigarettes per day, 39.1% (n=97) used 11-20 sticks, 9.39% (n=23) used 21-30 sticks, while1.2% of the participants used more than 31 sticks of cigarettes per day. Our data indicate that only 10.9% (n=27) of participants had tried more than5 times to quit smoking. Even though new effective treatments are now available, almost half of the participants, i.e., 51.6% (n=128), had tried to quit smoking without any intervention.Conclusion: Data obtained from this study later may help the public health policy makers and practitioners, especially in Kelantan, Malaysia, to make smoking prevention strategies more effective.Keywords: Smoking behavior, Male smoker, Malay male and smoking assessment. 


2006 ◽  
Vol 9 (1) ◽  
pp. 64-72 ◽  
Author(s):  
Ulla Broms ◽  
Karri Silventoinen ◽  
Pamela A. F. Madden ◽  
Andrew C. Heath ◽  
Jaakko Kaprio

AbstractBoth genetic and environmental factors affect smoking initiation and maintenance, but less is known about the genetic architecture of various other smoking-related behaviors. The aim of this study is to examine the genetic architecture of smoking behavior in a large twin cohort. Questionnaires with an extensive smoking history section were mailed to same-sex adult twins of the Finnish twin cohort. The final study population included 2923 monozygotic and 6018 dizygotic twin pairs aged 24 to 88 years. Two-stage bivariate genetic modeling of age at initiation with amount smoked (less than 20 cigarettes per day vs. 20 or more) and age at initiation with smoking cessation was done by using the Mx statistical package. For men the heritability estimate for age at initiation was .59 (95% confidence interval [CI] .49–.69), for amount smoked .54 (95% CI .45–.62) and for smoking cessation .58 (95% CI .50–.65). For women the heritability estimates were .36 (95% CI .28–.43), .61 (95% CI .46–.70) and .50 (95% CI .39–.60), respectively. The genetic correlations between age at initiation and amount smoked or smoking cessation were at most .22 in magnitude, indicating that genetic influences in age at initiation accounted for at most about 4% of the genetic factors in amount smoked or in cessation. Genetic factors are important in amount smoked and smoking cessation and they are largely independent of genetic influences on age at initiation. This has implications for defining phenotypes in searches for genes underlying smoking behaviors.


1979 ◽  
Vol 134 (4) ◽  
pp. 343-351 ◽  
Author(s):  
Svenn Torgersen

SummaryBy means of a twin study an attempt was made to throw light upon the aetiology and nosology of phobic fears. Factor analyses revealed five factors, namely separation fears, animal fears, mutilation fears, social fears and nature fears. The study demonstrated that, apart from separation fears, genetic factors play a part in the strength as well as content of phobic fears. Environmental factors, affecting the development of dependence, reserve and neurotic traits generally, seemed also to be of some importance. It was further demonstrated that phobic fears were related to emotional and social adjustment and this was true to an even greater extent for separation fears.


2006 ◽  
Vol 9 (3) ◽  
pp. 431-437 ◽  
Author(s):  
Anu Raevuori ◽  
Anna Keski-Rahkonen ◽  
Richard J. Rose ◽  
Aila Rissanen ◽  
Jaakko Kaprio

AbstractIn the population-based FinnTwin16 study, proportions of genetic and environmental factors contributing to muscle dissatisfaction and muscle-enhancing substance use were assessed in 319 pairs of twin brothers: 141 monozygotic (MZ) and 178 dizygotic (DZ) pairs. In addition there were 86 twin individuals from pairs in which only one co-twin responded. Of all respondents, 30% experienced high muscle dissatisfaction. The corresponding proportion of muscle-enhancing substance use was 10%. The subjects were similar in age (23.8 years, 95% confidence interval [CI] 23.76–23.84), body mass index (23.7, 95% CI 23.5–23.9), and waist circumference (84.5 cm, 95% CI 83.7–85.2), independent of their muscle dissatisfaction or muscle-enhancing substance use status and independent of their zygosity. The MZ polychoric correlation for muscle dissatisfaction was .39 (95% CI .17–.58) and .27 for DZ pairs (95% CI .07–.46). The MZ tetrachoric correlation for muscle-enhancing substance use was .65 (95% CI .28–.87) and .56 for DZ pairs (95% CI .26–.78). The AE model, where additive genetic factors (A) accounted for 42% (95% CI .23–.59) and unique environmental factors (E) 58% (95% CI .41–.77) of the liability, provided the best fit for muscle dissatisfaction. The CE model, where common environmental factors (C) accounted for 60% (95% CI .37–.77) and unique environmental factors (E) 40% (95% CI .23–.63) of the liability, provided the best fit for muscle-enhancing substance use. Both genetic and unique (nonfamilial) environmental factors are involved in muscle dissatisfaction in the population. Nongenetic factors (both familial and non-familial) appear to best explain the use of muscle-enhancing substances.


2017 ◽  
Vol 20 (7) ◽  
pp. 836-842 ◽  
Author(s):  
Jorien L Treur ◽  
Karin J H Verweij ◽  
Abdel Abdellaoui ◽  
Iryna O Fedko ◽  
Eveline L de Zeeuw ◽  
...  

Abstract Introduction Classical twin studies show that smoking is heritable. To determine if shared family environment plays a role in addition to genetic factors, and if they interact (G×E), we use a children-of-twins design. In a second sample, we measure genetic influence with polygenic risk scores (PRS) and environmental influence with a question on exposure to smoking during childhood. Methods Data on smoking initiation were available for 723 children of 712 twins from the Netherlands Twin Register (64.9% female, median birth year 1985). Children were grouped in ascending order of risk, based on smoking status and zygosity of their twin-parent and his/her co-twin: never smoking twin-parent with a never smoking co-twin; never smoking twin-parent with a smoking dizygotic co-twin; never smoking twin-parent with a smoking monozygotic co-twin; and smoking twin-parent with a smoking or never smoking co-twin. For 4072 participants from the Netherlands Twin Register (67.3% female, median birth year 1973), PRS for smoking were computed and smoking initiation, smoking heaviness, and exposure to smoking during childhood were available. Results Patterns of smoking initiation in the four group children-of-twins design suggested shared familial influences in addition to genetic factors. PRS for ever smoking were associated with smoking initiation in all individuals. PRS for smoking heaviness were associated with smoking heaviness in individuals exposed to smoking during childhood, but not in non-exposed individuals. Conclusions Shared family environment influences smoking, over and above genetic factors. Genetic risk of smoking heaviness was only important for individuals exposed to smoking during childhood, versus those not exposed (G×E). Implications This study adds to the very few existing children-of-twins (CoT) studies on smoking and combines a CoT design with a second research design that utilizes polygenic risk scores and data on exposure to smoking during childhood. The results show that shared family environment affects smoking behavior over and above genetic factors. There was also evidence for gene–environment interaction (G×E) such that genetic risk of heavy versus light smoking was only important for individuals who were also exposed to (second-hand) smoking during childhood. Together, these findings give additional incentive to recommending parents not to expose their children to cigarette smoking.


2004 ◽  
Vol 34 (7) ◽  
pp. 1251-1261 ◽  
Author(s):  
HERMINE H. MAES ◽  
PATRICK F. SULLIVAN ◽  
CYNTHIA M. BULIK ◽  
MICHAEL C. NEALE ◽  
CAROL A. PRESCOTT ◽  
...  

Background. Numerous twin studies have reported significant genetic contributions to the variability of tobacco initiation (TI), while fewer studies have shown similar results for the persistence of smoking behavior, or nicotine dependence (ND). As the development of ND requires regular tobacco use (RTU) which in turn requires TI, a conditional approach is necessary.Method. We used structural equation modeling of multi-step conditional processes to examine the relationship between genetic and environmental risk factors for TI, RTU and ND. The tobacco variables were assessed by personal interview in female, male and opposite-sex twin pairs from the population-based Virginia Twin Registry.Results. The results suggested that the liabilities to TI, RTU and ND were correlated. Over 80% of the variance in liability to TI and RTU were shared, and a smaller proportion was shared between RTU and ND. The heritabilities were estimated at 75%, 80% and 60% respectively for TI, RTU and ND. The variance specific to liability to RTU was entirely accounted for by additive genetic factors. Only a modest part of the heritability in liability of ND was due to genetic factors specific to ND. Shared environmental factors were not significant. No sex differences were found for the sources of variation or causal paths, but prevalences were significantly greater in males versus females.Conclusions. This study showed significant overlap in the contribution of genetic factors to individual differences in TI, RTU and ND. Furthermore, there was evidence for significant additional genetic factors specific to RTU and ND.


1990 ◽  
Vol 39 (4) ◽  
pp. 447-458 ◽  
Author(s):  
A.C. Heath

AbstractWe consider three alternative parametric models to describe genetic and environmental influences on smoking initiation and smoking persistence. Under the single liability dimension model, the same genetic and environmental influences which determine smoking initiation also influence smoking persistence. Under the independent liability dimensions model, independent initiation and persistence dimensions determine onset of smoking, and persistence in those who become smokers. The combined model also postulates separate initiation and persistence dimensions, but allows for the possibility that some smokers are so low on liability to smoke on the initiation dimension that they become ex-smokers for this reason. Reanalyses of London twin data published by Eaves and Eysenck support the single liability dimension model. We discuss the difficulty of reconciling this finding with the hypothesis that nicotine dependence is a major determinant of smoking persistence, but caution that sample sizes in the London twin study were small.


2018 ◽  
Vol 21 (3) ◽  
pp. 179-190 ◽  
Author(s):  
Hermine H. Maes ◽  
Kate Morley ◽  
Michael C. Neale ◽  
Kenneth S. Kendler ◽  
Andrew C. Heath ◽  
...  

Background: Considerable evidence from twin and adoption studies indicates that genetic and shared environmental factors play a role in the initiation of smoking behavior. Although twin and adoption designs are powerful to detect genetic and environmental influences, they do not provide information on the processes of assortative mating and parent–offspring transmission and their contribution to the variability explained by genetic and/or environmental factors. Methods: We examined the role of genetic and environmental factors in individual differences for smoking initiation (SI) using an extended kinship design. This design allows the simultaneous testing of additive and non-additive genetic, shared and individual-specific environmental factors, as well as sex differences in the expression of genes and environment in the presence of assortative mating and combined genetic and cultural transmission, while also estimating the regression of the prevalence of SI on age. A dichotomous lifetime ‘ever’ smoking measure was obtained from twins and relatives in the ‘Virginia 30,000’ sample and the ‘Australian 25,000’. Results: Results demonstrate that both genetic and environmental factors play a significant role in the liability to SI. Major influences on individual differences appeared to be additive genetic and unique environmental effects, with smaller contributions from assortative mating, shared sibling environment, twin environment, cultural transmission, and resulting genotype-environment covariance. Age regression of the prevalence of SI was significant. The finding of negative cultural transmission without dominance led us to investigate more closely two possible mechanisms for the lower parent–offspring correlations compared to the sibling and DZ twin correlations in subsets of the data: (1) age × gene interaction, and (2) social homogamy. Neither of the mechanism provided a significantly better explanation of the data. Conclusions: This study showed significant heritability, partly due to assortment, and significant effects of primarily non-parental shared environment on liability to SI.


Imaging ◽  
2020 ◽  
Vol 12 (1) ◽  
pp. 15-20
Author(s):  
György Jermendy ◽  
Márton Kolossváry ◽  
Ibolya Dudás ◽  
Ádám L. Jermendy ◽  
Alexisz Panajotu ◽  
...  

AbstractBackground and aimsNon-alcoholic fatty liver disease (NAFLD) increases cardiovascular morbidity and mortality, and carries poor long-term hepatic prognosis. Data about the role of genetic and environmental factors in the hepatic lipid accumulation are limited. The aim of the study was to evaluate the genetic and environmental impact on the hepatic lipid accumulation within a cohort of adult twin pairs.Patients and methodsWe investigated 182 twin subjects [monozygotic (MZ, n = 114) and dizygotic (DZ, n = 68) same-gender twins (age 56.0 ± 9.6 years; BMI 27.5 ± 5.0 kg/m2; females 65.9%)] who underwent computed tomography (CT) with a 256-slice scanner. Using non-enhanced CT-images, we calculated the average value of hepatic attenuation [expressed in Hounsfield unit (HU)] suggesting hepatic lipid content. Crude data were adjusted to age, sex, BMI and HbA1c values. Intra-pair correlations were established, and structural equation models were used for quantifying the contribution of additive genetic (A), common environmental (C) and unique environmental (E) components to the investigated phenotype.ResultsThe study cohort represented a moderately overweight, middle-aged Caucasian population. There was no significant difference between MZ and DZ twin subjects regarding hepatic CT-attenuation (57.9 ± 12.6 HU and 59.3 ± 11.7 HU, respectively; p = 0.747). Age, sex, BMI and HbA1c adjusted co-twin correlations between the siblings showed that MZ twins have stronger correlations of HU values than DZ twins (rMZ = 0.592, p < 0.001; rDZ = 0.047, p = 0.690, respectively). Using the structural equation model, a moderate additive genetic dependence (A: 38%, 95% CI 15–58%) and a greater unique environmental influence (E: 62%, 95% CI 42–85%) was found. Common environmental influence was not identified (C: 0%).ConclusionThe results of our classical CT-based twin study revealed moderate genetic and greater environmental influences on the phenotypic appearance of hepatic steatosis, commonly referred to as NAFLD. Favorable changes of modifiable environmental factors are of great importance in preventing or treating NAFLD.


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