Selective attention to smoking cues in former smokers

Repeated drug use modifies the emotional and cognitive processing of drug-associated cues. These changes are supposed to persist even after prolonged abstinence. Several studies demonstrated that smoking cues selectively attract the attention of smokers, but empirical evidence for such an attentional bias among successful quitters is inconclusive. Here, we investigated whether attentional biases persist after smoking cessation. Thirty-eight former smokers, 34 current smokers, and 29 non-smokers participated in a single experimental session. We used three measures of attentional bias for smoking stimuli: A visual probe task with short (500 ms) and long (2000 ms) picture stimulus durations, and a modified Stroop task with smoking-related and neutral words. Former smokers and current smokers, as compared to non-smokers, showed an attentional bias in visual orienting to smoking pictures in the 500 ms condition of the visual probe task. The Stroop interference index of smoking words was negatively related to nicotine dependence in current smokers. Former smokers and mildly dependent smokers, as compared to non-smokers, showed increased interference by smoking words in the Stroop task. Neither current nor former smokers showed an attentional bias in maintained attention (2000 ms visual probe task). In conclusion, even after prolonged abstinence smoking cues retain incentive salience in former smokers, who differed from non-smokers on two attentional bias indices. Attentional biases in former smokers operate mainly in early involuntary rather than in controlled processing, and may represent a vulnerability factor for relapse. Therefore, smoking cessation programs should strengthen self-control abilities to prevent relapses.     

Review article: smoking cessation as primary therapy to modify the course of Crohn's disease

This article aims to offer an updated review of the effects of smoking on inflammatory bowel disease, and provide a review of the methods of achieving smoking cessation. A systematic review of Embase and Medline databases was conducted. Smoking causes opposing effects on ulcerative colitis and Crohn's disease. The odds ratio of developing ulcerative colitis for smokers compared with lifetime non-smokers is 0.41. Conversely, smokers with Crohn's disease have a more aggressive disease requiring more therapeutic intervention. Smoking cessation is associated with a 65% reduction in the risk of a relapse as compared with continued smokers, a similar magnitude to that obtained with immunosuppressive therapy. Although difficult to achieve smoking cessation can best be encouraged by accessing appropriate counselling services, nicotine replacement therapy and bupropion. Using a combination of these treatments there is an improved chance of success of up to 20% compared with an unassisted quit attempt. Smoking cessation unequivocally improves the course of Crohn's disease and should be a primary therapeutic aim in smokers with Crohn's disease.     

An analysis of factors influencing short-term and sustained response to infliximab treatment for Crohn's disease

BACKGROUND: 59-81% of patients given infliximab for Crohn's disease will respond. Although now in widespread use, little consensus exists regarding the optimal place in patient care. Recently developed guidelines have identified need for markers that predict response. AIMS: We aimed to identify markers of response to infliximab given for Crohn's disease. METHODS: Markers of response (defined at 4 weeks) were prospectively assessed in 74 infliximab-treated patients with Crohn's disease. Patients were followed-up to 1 year. RESULTS: Fifty-four of 74 (73%) patients responded. Univariate analysis identified that smokers were less likely to respond than non-smokers [P = 0.005, odds ratio (OR) 0.22]. Patients established on immunosuppression (P = 0.034, OR 7.31) and with isolated colonic disease (P = 0.042, OR 3.83) were more likely to respond. Multiple logistic regression confirmed smoking (P = 0.035, OR 0.24) and colonic disease (P = 0.035, OR 4.87) as independent markers of response. One-year relapse rates differed significantly between smokers and non-smokers (100% vs. 39.6%, P = 0.0026, relative risk 3.2) and between patients established on immunomodulators or not (58.0% vs. 92.8%, P = 0.0054, relative risk 2.6). CONCLUSIONS: Smoking has a strong adverse effect on the response rates and maintenance of response to infliximab. Patients on immunomodulators have a more favourable short- and long-term response. These results have important implications for clinical practice.     

吸烟对2型糖尿病男性患者血糖控制的影响

目的：探讨吸烟对2型糖尿病男性患者空腹血糖（FBG）,餐后2 h 血糖（2hPBG）,糖化血红蛋白（HbA1 C）的影响。方法选取2型糖尿病男性患者142例,按吸烟情况分为不吸烟组（从不吸烟,n ＝44）,戒烟组（戒烟半年以上,n ＝33）,少量吸烟组（每天≤20支,n ＝33）,大量吸烟组（每天＞20支,n ＝32）,采用现场调查结合病例对照研究的方法,询问患者年龄、糖尿病病程、工作活动强度、吸烟、降糖药的应用等情况,测量血压、身高、体重、腰围、臀围,计算体重指数（BMI）、腰臀比（WHR）等指标,实验室检测葡萄糖（GLU）、2hPBG、HbA1 C,比较各组间血糖、糖化血红蛋白的差异;逐步回归及偏相关分析,了解吸烟对血糖控制影响的显著性及影响程度。结果（1）不吸烟组与大量吸烟组相比 FBG、2hPBG 明显降低（P ＜0．01）,HbA1 C 有所降低但差异无统计学意义（P ＞0．05）;不吸烟组与戒烟组比较2hPBG 有所升高（P ＜0．05或 P ＜0．01）;（2）少量吸烟组与大量吸烟组比较 FBG、2hPBG所降低但差异无统计学意义（P ＞0．05）;吸烟组与戒烟组相比 FBG、2hPBG、HbA1 C 均增高（P ＜0．05或P ＜0．01）;（3）吸烟是 HbA1 C 的独立危险因素（P ＜0．05,β＝－0．216）,FBG、2hPBG、HbA1 C 与日吸烟量、吸烟年限等无明显相关性（P ＞0．05）。结论吸烟是与年龄、BMI、工作活动强度、DM病程、用药情况等影响无关,为2型糖尿病男性患者血糖控制水平差的独立危险因素;吸烟组与戒烟组,戒烟组与不吸烟组之间血糖控制指标（FBG、2hPBG、HbA1 C）等的差异,表明大量吸烟不利于2型糖尿病男性患者血糖的控制,戒烟对2型糖尿病男性患者血糖控制有明显的积极的作用,在餐后血糖的控制上甚至优于从不吸烟患者。     

A longitudinal study of developmental trajectories to young adult cigarette smoking

This study examined smoking trajectories between adolescence and adulthood in an African American cohort followed prospectively from first grade to age 32. We classified non-smokers, former smokers, current smokers/late adopters (initiated after age 18), and current smokers/early adopters (initiated before age 17). Results show that almost half of the population were currently smoking. Multiple logistic regression analyses showed that non-smokers differed most from the three smoking groups on social integration. Non-smokers were less likely to have left home before the age of 18, to have had more drug use parental supervision as an adolescent, to have moved less, and to attend church more frequently as an adult. Those current smokers who initiated early differed from the non-smokers and also from the former smokers and the current smokers who adopted smoking after the age of 18; they were more likely to be rated as aggressive or both shy and aggressive by their first grade teachers and to have drug problems as adults. Current smokers were less likely to attend church as adults than the non-smokers and former smokers. Neither mother's smoking or lifetime depression was related to smoking. The findings elucidate the contribution of factors over the life course that have an impact on smoking initiation, continuation, and cessation. They highlight the importance of targeting African American children and adolescents for prevention despite the fact that African American youth have the lowest rates of smoking across all ethnic groups. Possible interventions could be aimed at early aggressive behavior, parental supervision and monitoring, and other social integration efforts.     

Retrospective analysis in smoking cessation research

The use of retrospective data in smoking research represents possible sources of bias resulting from: (1) baseline incomparability of current, former, and non-smokers, (2) instability of parameters under investigation, and (3) difficulties in recall. A self-report measure of smoking motives was employed in a longitudinal design to examine bias associated with retrospective data analysis. Thirty-six pairs of former smokers and recidivists (smokers who had tried to quit) were matched on age and amount smoked. Although initial responses for both groups were comparable, former smokers were significantly higher on smoking motive factors after quitting compared to recidivists who stayed essentially the same. The findings suggest that mean differences in smoking motives between recidivists and former smokers assessed cross-sectionally may not accurately reflect the magnitude of the differences that existed when both groups were smoking.     

Cigarette smoking substantially alters plasma microRNA profiles in healthy subjects

Circulating microRNAs (miRNAs) are receiving attention as potential biomarkers of various diseases, including cancers, chronic obstructive pulmonary disease, and cardiovascular disease. However, it is unknown whether the levels of circulating miRNAs in a healthy subject might vary with external factors in daily life. In this study, we investigated whether cigarette smoking, a habit that has spread throughout the world and is a risk factor for various diseases, affects plasma miRNA profiles. We determined the profiles of 11 smokers and 7 non-smokers by TaqMan MicroRNA array analysis. A larger number of miRNAs were detected in smokers than in non-smokers, and the plasma levels of two-thirds of the detected miRNAs (43 miRNAs) were significantly higher in smokers than in non-smokers. A principal component analysis of the plasma miRNA profiles clearly separated smokers and non-smokers. Twenty-four of the miRNAs were previously reported to be potential biomarkers of disease, suggesting the possibility that smoking status might interfere with the diagnosis of disease. Interestingly, we found that quitting smoking altered the plasma miRNA profiles to resemble those of non-smokers. These results suggested that the differences in the plasma miRNA profiles between smokers and non-smokers could be attributed to cigarette smoking. In addition, we found that an acute exposure of ex-smokers to cigarette smoke (smoking one cigarette) did not cause a dramatic change in the plasma miRNA profile. In conclusion, we found that repeated cigarette smoking substantially alters the plasma miRNA profile, interfering with the diagnosis of disease or signaling potential smoking-related diseases.     

Neurocognitive consequences of cigarette smoking in young adults--a comparison with pre-drug performance

The present study examined effects of current and past regular cigarette smoking in young adult subjects. One hundred and twelve 17-21-year-old subjects, assessed since infancy, were evaluated using a battery of neurocognitive tests for which commensurate measures were obtained at 9-12 years of age, prior to the initiation of regular smoking. Smokers, determined by urinalysis and self-report, were categorized as heavy (>9 cigarettes per day) and light (<9 cigarettes per day) current smokers and former smokers, the latter having smoked cigarettes regularly in the past but not for at least 6 months. A third of the subjects were currently smoking cigarettes regularly with half of these being heavy smokers. Among former smokers, the average duration of smoking was slightly less than 2 years. Overall IQ, memory, processing speed, vocabulary, attention and abstract reasoning were the primary outcomes with comparisons being made between each of the three user groups and a control group who never smoked regularly. After accounting for potentially confounding factors including clinical assessment, marihuana use and pre-drug performance in the relevant cognitive domain, current regular smokers did significantly worse than non-smokers in a variety of cognitive areas predicated upon verbal/auditory competence including receptive and expressive vocabulary, oral arithmetic, and auditory memory. This impact of current smoking appears to behave in a dose-response and duration-related fashion. In contrast, former smokers differed from the non-smokers only in the arithmetic task. These results suggest that regular smoking during early adulthood is associated with cognitive impairments in selected domains and that these deficits may be reversed upon cessation. Together, the findings add to the body of evidence to be used in persuading adolescents and young adults against the initiation of smoking and, if currently smoking, the advantages of stopping.     

Lack of startle modulation by smoking cues in smokers

Rationale The startle reflex methodology has been used to study the effects of nicotine in humans and the motivational effects of smoking cues in smokers. However, no other studies investigate startle modulation by smoking cues in smokers compared to non-smokers. In the other studies, smoking deprivation was manipulated in smokers or smokers were not compared directly to non-smokers.Objective The goal of this study was to examine the temporal course of information processing following the presentation of a smoking-related cue using the startle probe methodology in smokers compared to non-smokers.Methods Thirty-four smokers were selected on the basis of nicotinic dependence according to the DSM-IV, and compared to 34 non-smokers. During testing, subjects viewed neutral pictures and smoking related pictures displayed on a computer screen. Acoustic startle stimuli were delivered at various times after picture onset (60, 120 or 5000 ms) to examine inhibition by lead stimulus and the affective modulation of startle.Results The magnitude of startle reflex inhibition increased in smokers compared to non-smokers, at 60 and 120 ms. In all, there was no Picture×Group interaction effect.Conclusion We showed that smoking cues have no impact on the startle reflex of either group, even if, in line with previous results, prepulse inhibition was higher in smokers than non-smokers. These results suggest that smoking cues have no effect on the positive reinforcement of nicotine consumption, and that cognitive factors play a primary role in the development and maintenance of tobacco dependence.     

Effects of cigarette smoking status on delay discounting in schizophrenia and healthy controls

Background

Delay discounting is a measure of future-oriented decision-making and impulsivity. Cigarette smoking is associated with rapid discounting of the value of delayed outcomes. In schizophrenia, however, cigarette smoking improves certain neurocognitive impairments associated with the disorder which may explain the high smoking rates in this population. This study examined the relationship between cigarette smoking and delay discounting in schizophrenia and control participants.

Methods

A total of N = 130 participants, including those with schizophrenia (n = 68) and healthy controls (n = 62) were assessed on the Kirby Delay Discounting Task and compared across smoking status (smokers; non-smokers) and smoking history (current, former; never smokers).

Results

Smokers exhibited higher discounting rates (i.e., were more impulsive) than non-smokers of the same diagnostic group. Current and former smokers with schizophrenia exhibited similar and significantly higher discounting rates than never smokers, suggesting that in schizophrenia delay discounting is a trait-dependent phenomenon independent of current cigarette smoking. Consistent with previous studies, there was a trend for higher discounting rates in control current smokers compared to control former and never smokers.

Conclusions

Smokers with and without schizophrenia have higher rates of delay discounting than non-smokers. However, in schizophrenia, rapid delay discounting appears to be a trait associated with having ever been a smoker (i.e., current and former smoking).     

Tobacco smoking in relation to analgesic drug use in a national adult population sample

BACKGROUND: Nicotine is known to produce pain-inhibitory effects. Here, we examine whether there is a relation between tobacco smoking and analgesic drug use (ADU). METHODS: A probability sample of the German national population aged 18-79 with 7124 participants (participation rate: 61.4%) was used. All individuals underwent a health examination and ADU was assessed as part of an interview conducted by a study physician. RESULTS: Current and former smokers had higher odds for ADU than never smokers. Current heavy smokers (>20 cigarettes per day) had an odds ratio (OR) of 1.8 (95% confidence interval, CI, 1.4-2.3) for ADU three times per month or less and an OR of 3.1 (CI 2.0-4.8) for ADU once a week to daily, with never smokers as the reference group. Former heavy smokers had an OR of 2.0 (CI 1.3-3.2) for ADU once a week to daily compared to never smokers. CONCLUSION: The findings suggest that current and former smokers, particularly current and former heavy smokers, are more likely to use analgesic drugs than never smokers.     

Differential use of other tobacco products among current and former cigarette smokers by income level

With the declining sales of cigarettes, the tobacco industry has been promoting other forms of combustible and smokeless tobacco to current and former cigarette smokers. Exposure to the promotion of tobacco products has been shown to vary by income level. We combined the 2006 through 2011 National Surveys on Drug Use and Health to compare the prevalence and patterns of other tobacco use (cigar, snuff, and chewing tobacco) between current and former cigarette smokers by income level. Other tobacco use was minimal among females and among male non-smokers. Approximately a third of both current and former male cigarette smokers reported past-year other tobacco use. Overall, current smokers were more likely than former smokers to have used cigars (adjusted odds ratio (AOR) 1.69, 95% CI 1.50–1.92) or snuff (AOR 1.14, 95% CI 1.01–1.28) in the past year. The association of smoking status with other tobacco use differed by income level (interaction term p-value < 0.001). Among lower income groups, current smokers were more likely to use cigars and snuff compared to former smokers. Among the highest income group, former smokers were just as likely to use smokeless tobacco as current smokers. The differing patterns of use of other tobacco between current and former smokers by income level highlight a need for studies to understand the motivations for the use of these products and their role in smoking cessation.     

The effects of smoking and indomethacin on small intestinal permeability

BACKGROUND: Smoking modulates inflammatory bowel disease, protecting from ulcerative colitis on the one hand and worsening the course of Crohn's disease on the other. This influence might occur through changes in intestinal permeability, because permeability is increased in most patients with Crohn's disease. AIM: To study the influence of smoking on small intestinal permeability and its increase induced by indomethacin. METHODS: 50 smokers and 50 nonsmokers underwent a 51Cr-EDTA basal permeability test and the same test after challenge with indomethacin 125 mg p.o. RESULTS: Small intestinal permeability was the same in smokers (median 1.22%; IQR 1.00-1.58) and nonsmokers (1.24%; 0.94-1.66). Basal small intestinal permeability was lower in females (1.09%; 0.87-1.33) than in males (1.48%; 1.18-1.88). Indomethacin challenge increased permeability by 110% (71-141) in smokers, vs. 156% (78-220) in the nonsmokers (P=0.04). CONCLUSION: Smoking reduces the effect of NSAID on small intestinal permeability. It is therefore unlikely that the adverse effect of smoking on Crohn's disease is related to its influence on intestinal permeability.     

Smoking history and the incidence of age-related macular degeneration—Results from the Muenster Aging and Retina Study (MARS) cohort and systematic review and meta-analysis of observational longitudinal studies

To compare the association of smoking with age-related macular degeneration (AMD) in the Muenster Aging and Retina Study (MARS) cohort with current evidence. Adjusted risk ratios for incident AMD in MARS were compared with findings of a systematic review and meta-analysis of observational prospective studies. 9.6% of MARS participants progressed to AMD over a median of 30.9 months. In MARS the adjusted risk ratio in current versus never smokers was 3.25 (95% confidence interval [1.50–7.06]), and 1.28 [0.70–2.33] in former smokers versus never smokers. The meta-analysis of previous studies showed a pooled adjusted risk ratio of 2.51 [1.09–5.76] in current versus never smokers. Inclusion of the MARS findings removed between-study heterogeneity and accentuated the pooled adjusted risk ratio for current smokers to 2.75 [1.52–4.98]. Specific analyses in MARS revealed a protective effect for time since smoking cessation in former smokers with an adjusted risk ratio = 0.50 [0.29–0.89] per log(year). Current smoking nearly triples AMD incidence, while smoking cessation lowers AMD incidence in a non-linear fashion even in the elderly.     

Phenotypic and genetic relationship between BMI and cigarette smoking in a sample of UK adults

In addition to the health hazards posed individually by cigarette smoking and obesity, the combination of these conditions poses a particular impairment to health. Genetic factors have been shown to influence both traits and, to understand the connection between these conditions, we examined both the observed and genetic relationship between adiposity (an electrical impedance measure of body mass index (BMI)) and cigarettes smoked per day (CPD) in a large sample of current, former, and never smokers in the United Kingdom. In former smokers, BMI was positively associated with cigarettes formerly smoked; further, the genetic factors related to a greater number of cigarettes smoked were also responsible for a higher BMI. In current smokers, there was a positive association between BMI and number of cigarettes smoked, though this relationship did not appear to be influenced by similar genetic factors. We found a positive genetic relationship between smoking in current/former smokers and BMI in never smokers (who would be unmarred by the effects of nicotine). In addition to CPD, in current smokers, we looked at two variables, time from waking to first cigarette and difficulty not smoking for a day, that may align better with cigarette and food ‘craving.’ However, these smoking measures provided mixed findings with respect to their relationship with BMI. Overall, the positive relationships between the genetic factors that influence CPD in smokers and the genetic factors that influence BMI in former and never smokers point to common biological influences behind smoking and obesity.     

The influence of cigarette smoking on circulating concentrations of antioxidant micronutrients

Cigarette smoke is a significant source of oxidative stress, one potential mechanism for its untoward health effects. The antioxidant defense system is partly comprised of antioxidant micronutrients, making it important to understand the relationship between cigarette smoking and circulating concentrations of antioxidant micronutrients. A synthesis of the literature shows that compared with nonsmokers, on average, active smokers have greater than 25% lower circulating concentrations of ascorbic acid, alpha-carotene, beta-carotene, and cryptoxanthin. The differences in blood concentrations of these micronutrients in former smokers is intermediate between never and current smokers, but average circulating concentrations of alpha-carotene, beta-carotene, and cryptoxanthin were 16-22% lower in former smokers compared with never smokers. Differences in dietary habits between smokers and nonsmokers could potentially account for these associations. Dietary micronutrient intake is associated with blood micronutrient concentrations. Furthermore, patterns of micronutrient consumption by smoking status mimic the pattern of associations observed for blood concentrations. For example, when pooled across studies intake of vitamin C was 16% lower in current smokers and 2% lower in former smokers than in never smokers; the corresponding figures for beta-carotene were 17 and 4%, respectively. Despite the strong potential for confounding, the differences observed between current smokers and nonsmokers seem to be due to an acute effect of smoking based on results of studies of smoking and antioxidant micronutrient concentrations that have either adjusted for dietary antioxidant micronutrient intake and other potential confounding factors or documented short term changes in circulating antioxidant micronutrient concentrations in smokers before and after smoking cigarettes. The associations observed with active smoking also appear to hold true for passive smoking, implying that even low-dose exposures to tobacco smoke can result in lowered circulating antioxidant micronutrient concentrations. Smoking was more weakly associated with circulating concentrations of vitamin E and the nonprovitamin A carotenoids lutein/zeaxanthin and lycopene. The combined evidence supports the conclusion that cigarette smoking is independently associated with lowered circulating concentrations of ascorbic acid and provitamin A carotenoids. These associations have implications for the design and interpretation of epidemiologic studies of antioxidant micronutrients in relation to health and disease. To the extent that these micronutrients are associated with health and longevity, this evidence documents yet another deleterious consequence of cigarette smoking on human health.     

Irritable bowel, smoking and oesophageal acid exposure: an insight into the nature of symptoms of gastro-oesophageal reflux

BACKGROUND: In gastro-oesophageal reflux disease, oesophageal acid exposure correlates with symptoms but explains only a small fraction of their variance. AIMS: To elucidate the effects of irritable bowel syndrome and smoking on gastro-oesophageal reflux disease symptoms and to clarify whether they modulate the relationship between oesophageal acid exposure and symptoms. METHODS: The relationship between oesophageal acid exposure, irritable bowel syndrome (Rome I criteria), smoking status and symptoms was investigated in patients with a normal gastroscopy who underwent a 24-h oesophageal pH monitoring. RESULTS: Of 256 patients with gastro-oesophageal reflux disease, 16% were smokers and 50% met the criteria for irritable bowel syndrome (irritable bowel syndrome+). The extent of oesophageal acid exposure was unrelated to smoking or irritable bowel syndrome status. Oesophageal acid exposure, irritable bowel syndrome status and current smoking independently predicted symptoms. Irritable bowel syndrome and smoking modulated the effect of oesophageal acid exposure on symptoms: oesophageal acid exposure was predictive of symptoms only in non-smokers. However, irritable bowel syndrome was a significant predictor of symptoms both in smokers and in non-smokers. Smoking was associated with symptoms only in irritable bowel syndrome+, while oesophageal acid exposure was associated with symptoms irrespective of irritable bowel syndrome status. CONCLUSIONS: In patients with non-erosive gastro-oesophageal reflux disease, smoking and irritable bowel syndrome independently predicted symptoms, without affecting the extent of oesophageal acid exposure. The relationship between oesophageal acid exposure and symptoms was affected significantly, and in opposite directions, by smoking and irritable bowel syndrome.     

The relation between alcohol consumption and smoking abstinence: results from the Working Well Trial

The current study examined the relation between drinking and smoking abstinence in a community-based sample from the Working Well Trial (WWT). At baseline, drinking level was related to smoking history (never, former, or current smoker; P < .0001) and abstinence history. Mean monthly alcohol consumption increased linearly with decreases in duration of recent abstinence (i.e., longest period quit in the past year among current smokers; P < .05) and current abstinence (i.e., time since quitting among former smokers; P < .0001), even controlling for relevant demographic factors. Among baseline smokers, lower beer consumption predicted smoking abstinence at 4-year follow-up (P< .01). A trend towards significance was found for total alcohol consumption (P = .06). The results suggest (a) a dose-response relation between baseline drinking and duration of smoking abstinence, and (b) that heavier drinkers are less likely to quit smoking over a 4-year period.     

Enhanced drug metabolism in cigarette smokers.

The effect of cigarette smoking on salivary antipyrine disappearance rate, and as an index of hepatic drug metabolism, was studied in 42 healthy subjects. Antipyrine half life was significantly shorter in smokers compared with non-smokers. To determine whether this difference was due solely to tobacco consumption eight subjects were restudied two months after they stopped smoking. The mean antipyrine disappearance rate in this group increased by 23% in contrast to that of a control group, which did not alter. Cigarette smoking contributes to the considerable variation in interindividual rates of drug metabolism.     

长期吸烟者血浆皮质醇及β-内啡肽的变化

目的·· :探讨长期吸烟者在戒烟前后血浆皮质醇和 β-内啡肽水平的变化及形成机制。方法·· :于戒烟前后采集长期吸烟者静脉血 ,用放射免疫方法检测血浆皮质醇及血浆 β-内啡肽的含量。结果·· :长期吸烟者的血浆皮质醇(227.82ng·ml-1±s40.03ng·ml-1)及血浆 β-内啡肽(14.68ng·ml-1±s4.48ng·ml-1)明显高于正常组 ;戒断后长期吸烟组的血浆皮质醇(271.92ng·ml-1±s32.19ng·ml-1)明显升高 ,而血浆 β-内啡肽(8.16ng·ml-1±s4.97ng·ml-1)明显降低。结论·· :血浆皮质醇及 β-内啡肽可作为判断戒烟治疗效果的指标之一 ,而改善内源性阿片肽系统及下丘脑 -垂体 -肾上腺轴的功能可能对戒烟有助。