青年時期由于壓力而染上煙癮的人,，成年后很難戒除，這種現(xiàn)象很可能是基因在作怪,。最新研究發(fā)現(xiàn)一種基因的變異會導致煙癮難以戒除。先前的研究表明年輕時染上吸煙習慣的人成年后很可能變成煙鬼,，研究結(jié)果也表明越早接觸煙草越難戒除,。
基因的差異或許可以解釋這個現(xiàn)象。在最新研究中科學家發(fā)現(xiàn)編碼細胞尼古丁受體的基因中一個核苷酸的改變可導致肺癌發(fā)生率的增高,，因為這個基因可以協(xié)助尼古丁擴散,。
研究小組比較了2827個煙齡30年以上,，少年時每天抽至少一包煙的人。其中有1051位16歲以前開始抽煙的人染上煙癮的概率是其他人的1.5倍,，這部分人的基因中有6個位點核苷酸序列改變,。
研究人員推測上癮的原因可能是癮君子大腦對尼古丁的反應發(fā)生改變。（生物谷Bioon.com）
生物谷推薦原始出處：
PLoS Genet. 2008 July; 4(7): e1000125. doi: 10.1371/journal.pgen.1000125.
A Candidate Gene Approach Identifies the CHRNA5-A3-B4 Region as a Risk Factor for Age-Dependent Nicotine Addiction
Robert B. Weiss,1* Timothy B. Baker,2 Dale S. Cannon,3 Andrew von Niederhausern,1 Diane M. Dunn,1 Nori Matsunami,1 Nanda A. Singh,1 Lisa Baird,1 Hilary Coon,3 William M. McMahon,3 Megan E. Piper,2 Michael C. Fiore,2 Mary Beth Scholand,1 John E. Connett,4 Richard E. Kanner,5 Lorise C. Gahring,5,6 Scott W. Rogers,6,7 John R. Hoidal,5 and Mark F. Leppert1*
1Department of Human Genetics, Eccles Institute of Human Genetics, University of Utah School of Medicine, Salt Lake City, Utah, United States of America
2Department of Medicine, Center for Tobacco Research and Intervention, University of Wisconsin School of Medicine, Madison, Wisconsin, United States of America
3Department of Psychiatry, University of Utah School of Medicine, Salt Lake City, Utah, United States of America
4Division of Biostatistics, School of Public Health, University of Minnesota, Minneapolis, Minnesota, United States of America
5Department of Internal Medicine, Division of Respiratory, Critical Care and Occupational Pulmonary Medicine, University of Utah School of Medicine, Salt Lake City, Utah, United States of America
6Geriatric Research Education and Clinical Center, Salt Lake City VA Medical Center, Salt Lake City, Utah, United States of America
7Department of Neurobiology and Anatomy, University of Utah School of Medicine, Salt Lake City, Utah, United States of America
Abstract
People who begin daily smoking at an early age are at greater risk of long-term nicotine addiction. We tested the hypothesis that associations between nicotinic acetylcholine receptor (nAChR) genetic variants and nicotine dependence assessed in adulthood will be stronger among smokers who began daily nicotine exposure during adolescence. We compared nicotine addiction—measured by the Fagerstrom Test of Nicotine Dependence—in three cohorts of long-term smokers recruited in Utah, Wisconsin, and by the NHLBI Lung Health Study, using a candidate-gene approach with the neuronal nAChR subunit genes. This SNP panel included common coding variants and haplotypes detected in eight α and three β nAChR subunit genes found in European American populations. In the 2,827 long-term smokers examined, common susceptibility and protective haplotypes at the CHRNA5-A3-B4 locus were associated with nicotine dependence severity (p=2.0×10−5; odds ratio=1.82; 95% confidence interval 1.39–2.39) in subjects who began daily smoking at or before the age of 16, an exposure period that results in a more severe form of adult nicotine dependence. A substantial shift in susceptibility versus protective diplotype frequency (AA versus BC=17%, AA versus CC=27%) was observed in the group that began smoking by age 16. This genetic effect was not observed in subjects who began daily nicotine use after the age of 16. These results establish a strong mechanistic link among early nicotine exposure, common CHRNA5-A3-B4 haplotypes, and adult nicotine addiction in three independent populations of European origins. The identification of an age-dependent susceptibility haplotype reinforces the importance of preventing early exposure to tobacco through public health policies.
