Farley Amanda C, Hajek Peter, Lycett Deborah, Aveyard Paul
Primary Care Clinical Sciences, University of Birmingham, Birmingham, UK.
Cochrane Database Syst Rev. 2012 Jan 18;1:CD006219. doi: 10.1002/14651858.CD006219.pub3.
Most people who stop smoking gain weight. There are some interventions that have been designed to reduce weight gain when stopping smoking. Some smoking cessation interventions may also limit weight gain although their effect on weight has not been reviewed.
To systematically review the effect of: (1) Interventions targeting post-cessation weight gain on weight change and smoking cessation.(2) Interventions designed to aid smoking cessation that may also plausibly affect weight on post-cessation weight change.
Part 1 - We searched the Cochrane Tobacco Addiction Group's Specialized Register and CENTRAL in September 2011.Part 2 - In addition we searched the included studies in the following "parent" Cochrane reviews: nicotine replacement therapy (NRT), antidepressants, nicotine receptor partial agonists, cannabinoid type 1 receptor antagonists and exercise interventions for smoking cessation published in Issue 9, 2011 of the Cochrane Library.
Part 1 - We included trials of interventions that were targeted at post-cessation weight gain and had measured weight at any follow up point and/or smoking cessation six or more months after quit day.Part 2 - We included trials that had been included in the selected parent Cochrane reviews if they had reported weight gain at any time point.
We extracted data on baseline characteristics of the study population, intervention, outcome and study quality. Change in weight was expressed as difference in weight change from baseline to follow up between trial arms and was reported in abstinent smokers only. Abstinence from smoking was expressed as a risk ratio (RR). We used the most rigorous definition of abstinence available in each trial. Where appropriate, we performed meta-analysis using the inverse variance method for weight and Mantel-Haenszel method for smoking using a fixed-effect model.
Part 1: Some pharmacological interventions tested for limiting post cessation weight gain (PCWG) resulted in a significant reduction in WG at the end of treatment (dexfenfluramine (Mean difference (MD) -2.50 kg, 95% confidence interval (CI) -2.98 to -2.02, 1 study), phenylpropanolamine (MD -0.50 kg, 95% CI -0.80 to -0.20, N=3), naltrexone (MD -0.78 kg, 95% CI -1.52 to -0.05, N=2). There was no evidence that treatment reduced weight at 6 or 12 months (m). No pharmacological intervention significantly affected smoking cessation rates.Weight management education only was associated with no reduction in PCWG at end of treatment (6 or 12m). However these interventions significantly reduced abstinence at 12m (Risk ratio (RR) 0.66, 95% CI 0.48 to 0.90, N=2). Personalised weight management support reduced PCWG at 12m (MD -2.58 kg, 95% CI -5.11 to -0.05, N=2) and was not associated with a significant reduction of abstinence at 12m (RR 0.74, 95% CI 0.39 to 1.43, N=2). A very low calorie diet (VLCD) significantly reduced PCWG at end of treatment (MD -3.70 kg, 95% CI -4.82 to -2.58, N=1), but not significantly so at 12m (MD -1.30 kg, 95% CI -3.49 to 0.89, N=1). The VLCD increased chances of abstinence at 12m (RR 1.73, 95% CI 1.10 to 2.73, N=1). There was no evidence that cognitive behavioural therapy to allay concern about weight gain (CBT) reduced PCWG, but there was some evidence of increased PCWG at 6m (MD 0.74, 95% CI 0.24 to 1.24). It was associated with improved abstinence at 6m (RR 1.83, 95% CI 1.07 to 3.13, N=2) but not at 12m (RR 1.25, 95% CI 0.83 to 1.86, N=2). However, there was significant statistical heterogeneity.Part 2: We found no evidence that exercise interventions significantly reduced PCWG at end of treatment (MD -0.25 kg, 95% CI -0.78 to 0.29, N=4) however a significant reduction was found at 12m (MD -2.07 kg, 95% CI -3.78 to -0.36, N=3).Both bupropion and fluoxetine limited PCWG at the end of treatment (bupropion MD -1.12 kg, 95% CI -1.47 to -0.77, N=7) (fluoxetine MD -0.99 kg, 95% CI -1.36 to -0.61, N=2). There was no evidence that the effect persisted at 6m (bupropion MD -0.58 kg, 95% CI -2.16 to 1.00, N=4), (fluoxetine MD -0.01 kg, 95% CI -1.11 to 1.10, N=2) or 12m (bupropion MD -0.38 kg, 95% CI -2.00 to 1.24, N=4). There were no data on WG at 12m for fluoxetine.Overall, treatment with NRT attenuated PCWG at the end of treatment (MD -0.69 kg, 95% CI -0.88 to -0.51, N=19), with no strong evidence that the effect differed for the different forms of NRT. There was evidence of significant statistical heterogeneity caused by one study which reported a 4.3 kg reduction in PCWG due to NRT. With this study removed, the difference in weight change at end of treatment was -0.45 kg (95% CI -0.66 to -0.27, N=18). There was no evidence of an effect on PCWG at 12m (MD -0.42 kg, 95% CI -0.92 to 0.08, N=15).We found evidence that varenicline significantly reduced PCWG at end of treatment (MD -0.41 kg, 95% CI -0.63 to -0.19, N=11), but this effect was not maintained at 6 or 12m. Three studies compared the effect of bupropion to varenicline. Participants taking bupropion gained significantly less weight at the end of treatment (-0.51 kg (95% CI -0.93 to -0.09 kg), N=3). Direct comparison showed no significant difference in PCWG between varenicline and NRT.
AUTHORS' CONCLUSIONS: Although some pharmacotherapies tested to limit PCWG show evidence of short-term success, other problems with them and the lack of data on long-term efficacy limits their use. Weight management education only, is not effective and may reduce abstinence. Personalised weight management support may be effective and not reduce abstinence, but there are too few data to be sure. One study showed a VLCD increased abstinence but did not prevent WG in the longer term. CBT to accept WG did not limit PCWG and may not promote abstinence in the long term. Exercise interventions significantly reduced weight in the long term, but not the short term. More studies are needed to clarify whether this is an effect of treatment or a chance finding. Bupropion, fluoxetine, NRT and varenicline reduce PCWG while using the medication. Although this effect was not maintained one year after stopping smoking, the evidence is insufficient to exclude a modest long-term effect. The data are not sufficient to make strong clinical recommendations for effective programmes to prevent weight gain after cessation.
大多数戒烟者会体重增加。已经设计了一些干预措施来减少戒烟时的体重增加。一些戒烟干预措施也可能限制体重增加,尽管它们对体重的影响尚未得到综述。
系统评价:(1)针对戒烟后体重增加的干预措施对体重变化和戒烟的影响。(2)旨在帮助戒烟且可能合理影响体重的干预措施对戒烟后体重变化的影响。
第一部分 - 我们于2011年9月检索了Cochrane烟草成瘾小组的专业注册库和CENTRAL。第二部分 - 此外,我们检索了以下“母本”Cochrane综述中纳入的研究:尼古丁替代疗法(NRT)、抗抑郁药、尼古丁受体部分激动剂、大麻素1型受体拮抗剂以及发表在2011年第9期《Cochrane图书馆》上的戒烟运动干预措施。
第一部分 - 我们纳入了针对戒烟后体重增加的干预措施的试验,这些试验在任何随访点测量了体重和/或在戒烟日六个月或更长时间后测量了戒烟情况。第二部分 - 如果选定的母本Cochrane综述中纳入的试验报告了任何时间点的体重增加情况,我们就将其纳入。
我们提取了关于研究人群、干预措施、结局和研究质量的基线特征数据。体重变化以试验组从基线到随访的体重变化差异表示,仅在戒烟者中报告。戒烟以风险比(RR)表示。我们使用了每个试验中可用的最严格的戒烟定义。在适当的情况下,我们使用固定效应模型,采用体重的逆方差法和吸烟的Mantel-Haenszel法进行荟萃分析。
第一部分:一些测试用于限制戒烟后体重增加(PCWG)的药物干预措施在治疗结束时导致体重显著减轻(右芬氟拉明(平均差异(MD)-2.50 kg,95%置信区间(CI)-2.98至-2.02,1项研究)、苯丙醇胺(MD -0.50 kg,95% CI -0.80至-0.20,N = 3)、纳曲酮(MD -0.78 kg,95% CI -1.52至-0.05,N = 2))。没有证据表明治疗在6个月或12个月时减轻了体重。仅体重管理教育在治疗结束时(6个月或12个月)与PCWG的减轻无关。然而,这些干预措施在12个月时显著降低了戒烟率(风险比(RR)0.66,95% CI 0.48至0.90,N = 2)。个性化体重管理支持在12个月时降低了PCWG(MD -2.58 kg,95% CI -5.11至-0.05,N = 2),并且在12个月时与戒烟率的显著降低无关(RR 0.74,95% CI 0.39至1.43,N = 2)。极低热量饮食(VLCD)在治疗结束时显著降低了PCWG(MD -3.70 kg,95% CI -4.82至-2.58,N = 1),但在12个月时不显著(MD -1.30 kg,95% CI -3.49至0.89,N = 1)。VLCD增加了12个月时的戒烟机会(RR 1.73,95% CI 1.10至2.73,N = 1)。没有证据表明减轻对体重增加的担忧的认知行为疗法(CBT)降低了PCWG,但有一些证据表明在6个月时PCWG增加(MD 0.74,95% CI 0.24至1.24)。它与6个月时戒烟率的提高相关(RR 1.83,95% CI 1.07至3.13,N = 2),但在12个月时不相关(RR 1.25,95% CI 0.83至1.86,N = 2)。然而,存在显著的统计学异质性。第二部分:我们没有发现运动干预措施在治疗结束时显著降低PCWG的证据(MD -0.25 kg,95% CI -0.78至0.29,N = 4),但在12个月时发现显著降低(MD -2.07 kg,95% CI -3.78至-0.36,N = 3)。安非他酮和氟西汀在治疗结束时限制了PCWG(安非他酮MD -1.12 kg,95% CI -1.47至-0.77,N = 7)(氟西汀MD -0.99 kg,95% CI -1.36至-0.61,N = 2)。没有证据表明这种效果在6个月时持续存在(安非他酮MD -0.58 kg,95% CI -2.16至1.00,N = 4),(氟西汀MD -0.01 kg,95% CI -1.11至1.10,N = 2)或12个月时(安非他酮MD -0.38 kg,95% CI -2.00至1.24,N = 4)。没有关于氟西汀12个月时体重增加的数据。总体而言,NRT治疗在治疗结束时减轻了PCWG(MD -0.69 kg,95% CI -0.88至-0.51,N = 19),没有有力证据表明不同形式的NRT效果不同。有证据表明由一项研究引起了显著的统计学异质性,该研究报告NRT使PCWG降低了4.3 kg。排除该研究后,治疗结束时体重变化的差异为-0.45 kg(95% CI -0.66至-0.27,N = 18)。没有证据表明对12个月时的PCWG有影响(MD -0.42 kg,95% CI -0.92至0.08,N = 15)。我们发现证据表明伐尼克兰在治疗结束时显著降低了PCWG(MD -0.41 kg,95% CI -0.63至-0.19,N = 11),但这种效果在6个月或12个月时未维持。三项研究比较了安非他酮与伐尼克兰的效果。服用安非他酮的参与者在治疗结束时体重增加显著较少(-0.51 kg(95% CI -0.93至-0.09 kg),N = 3)。直接比较显示伐尼克兰与NRT之间的PCWG没有显著差异。
尽管一些测试用于限制PCWG的药物疗法显示出短期成功的证据,但它们的其他问题以及缺乏长期疗效数据限制了它们的使用。仅体重管理教育无效,且可能降低戒烟率。个性化体重管理支持可能有效且不降低戒烟率,但数据太少无法确定。一项研究表明VLCD增加了戒烟率,但从长远来看并不能防止体重增加。接受体重增加的CBT并不能限制PCWG,且从长远来看可能不会促进戒烟。运动干预措施从长远来看显著减轻了体重,但短期内没有。需要更多研究来阐明这是治疗效果还是偶然发现。安非他酮、氟西汀、NRT和伐尼克兰在使用药物期间降低了PCWG。尽管戒烟一年后这种效果未维持,但证据不足以排除适度的长期效果。数据不足以对预防戒烟后体重增加的有效方案提出强有力的临床建议。