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עמוד בית
Mon, 26.02.24

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January 2017
Gabriel Munter MD, Yehuda Brivik MD, Yossi Freier-Dror MA and Shoshana Zevin MD

Background: Cigarette smoking is a widespread problem around the world. In Israel, the prevalence of smoking is 23%. Smokers who are Orthodox abstain from smoking during the Sabbath, i.e., from sundown Friday to sundown Saturday, due to a religious prohibition. The prevalence of smoking among Orthodox men is 13%. However, there are no data on patterns of smoking or on the addiction profiles in this population.

Objectives: To explore the smoking patterns, motivation for smoking and nicotine addiction among Orthodox Jewish men, compared to non-Orthodox men, as well as the differences in the urge to smoke and withdrawal symptoms on Saturday versus weekdays in the Orthodox group. 

Methods: The participants completed the Fagerstrom test for nicotine dependence, questionnaires on reasons for smoking and smoking patterns, as well as two brief questionnaires on the urge to smoke and withdrawal symptoms after overnight abstinence on a weekday and after the end of the Sabbath. 

Results: Both groups were strongly addicted to nicotine and there were no differences in the reasons for smoking, withdrawal symptoms and nicotine craving after an overnight abstinence on weekdays. However, religious smokers had low levels of craving for nicotine and few withdrawal symptoms during Sabbath abstinence when compared to weekdays. 

Conclusions: Although we found no difference in the baseline characteristics with regard to nicotine addiction, smoking motivation, urge to smoke and withdrawal symptoms between religious and non-religious groups, the former are able to abstain from smoking during 25 hours of the Sabbath every week with significantly fewer withdrawal symptoms compared to week days.

 

February 2011
G. Altarescu, D. Rachmilewitz and S. Zevin

Background: Ulcerative colitis (UC) is a common and difficult-to-treat disease. In non-smokers the relative risk of developing UC[1] is 2.9 compared with smokers, who tend to have a later onset and a milder disease. Nicotine is the component of cigarette smoke responsible for the favorable effects in UC. Nicotine is metabolized by the enzyme CYP2A6. Subjects who are homozygotes for CYP2A6*4 gene polymorphism are poor nicotine metabolizers, while homozygotes for CYP2A6*1A polymorphism are extensive metabolizers.

Objectives: To compare the frequency of CYP2A6 and CHRNA3 polymorphisms among smokers and non-smokers with UC, and their effect on disease severity.

Methods: Data on the age at onset of disease, disease activity, and treatment were obtained from questionnaires completed by the 69 subjects in our study group. CYP2A6

*1A,*4A and CHRNA3 polymorphisms were determined by polymerase chain reaction and restriction enzyme analysis.

Results: Nine percent of the patients were current smokers, 30% were former smokers and 61% non-smokers. Among smokers and former smokers 63% were homozygotes for CYP2A6*1A and 4% were homozygotes for CYP2A6*4A, whereas among non-smokers 66% were homozygotes for CYP2A6*4A (P < 0.0001). There was no significant effect of CYP2A6 or CHRNA3 genotype on UC activity.

Conclusions: We found a very high proportion of poor nicotine metabolizers among non-smoking patients with UC and a very low proportion among current and former smokers, making it difficult to determine the effect of poor metabolizer genotype on disease activity in smokers with UC. However, it may be possible to identify UC patients who are poor metabolizers of nicotine and who may benefit from nicotine or nicotine-like pharmacological treatment.






[1] UC = ulcerative colitis



 
March 2003
R. Eliakim and F. Karmeli

Background: Chronic nicotine administration has a dual effect on inflammatory bowel disease: augmentation of jejunitis and amelioration of colitis. We previously showed that chronic nicotine administration has divergent regional effects on small bowel and colonic mucosal mediators and blood flow.

Objective: To examine the effects of nicotine administration on cytokine levels in normal rat small bowel mucosa, colonic mucosa, and blood.

Methods: Male Sprague-Dawley rats weighing 200–250 g were given nicotine (12.5 μg/ml) that was dissolved in tap water. Rats were sacrificed on days 1, 2, 7 and 14 after nicotine initiation; blood was withdrawn, and small bowel and colon were resected, washed and weighed. Mucosal scrapings were extracted in 2 ml Krebs-Hemselest buffer for determination of interleukins-2, 6 and 10 using the Biosource International Immunoassay Kit.

Results: Nicotine decreased IL-10[1] and increased IL-6 levels in small bowel mucosa (from 3.5 ±  0.5 to 0.4 ± 0.1 pg/ml and from 1.9±0.4 to 13.6±0.4 pg/ml respectively; P < 0.05). Nicotine decreased IL-2 levels in the colon (from 15.8±3.0 to 7.9±1.0 pg/ml; P < 0.05), having no effect on IL-10 or IL-6 levels. Rats treated with nicotine had lower IL-6 and IL-2 blood levels compared to control rats.

Conclusions: Nicotine has different regional effects on small bowel and colonic cytokine mucosal levels, which might explain some of its opposite effects on small bowel and colonic inflammation.






[1] IL = interleukin


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