Neurology：吸烟会增加罹患痴呆症风险

佚名

     生物谷报道：荷兰科学家最近发表研究论文说，与已经成功戒烟和从不吸烟的人比起来，吸烟者日后罹患早老性痴呆症及其他种类痴呆症的风险要高出不少。

    据路透社9月3日报道，荷兰鹿特丹伊拉斯默斯医学中心的莫尼克·布莱特勒博士及其同事通过研究发现，年龄超过55岁的吸烟者出现痴呆症状的可能性，较之年龄相仿的不吸烟者高出50％。
    布莱特勒和同事在其发表于Neurology杂志上的论文中表示，他们曾经对将近7000名年龄不小于55岁的人进行了平均为期7年的追踪研究。在此期间，总共有706名被研究者患上了各种不同类型的痴呆症。

    目前人们已经确知有一种名叫APOE4（也叫做阿朴脂蛋白E4）的基因能够增加一个人罹患痴呆的风险。研究发现，对于那些体内已经存在着此种基因的人来说，吸烟并不会对他们今后是否患上早老性痴呆症产生任何影响。但如果那些体内没有该基因的人持续吸烟的话，他们未来患上早老性痴呆症的危险会提高70％。

    吸烟可能会导致人体出现中风症状，而此种情况反过来也会对大脑造成损伤并最终发展到痴呆这一步，布莱特勒说。布莱特勒说，“吸烟会增加患脑血管疾病（中风）的风险，而这与痴呆同样有着密不可分的联系。”

    他还说：“所谓氧化应激(Oxidative  Stress)是导致痴呆症状出现的另外一项作用机制，它会对人体血管内的细胞造成伤害，并导致动脉硬化。与不吸烟者相比，吸烟者体内的氧化应激现象往往会表现得更为激烈，而在早老性痴呆症患者身上，人们同样发现了这种氧化应激水平有所升高。”

    所谓氧化应激的过程其实与生锈十分类似，就是通过化学反应对人体DNA造成损伤。

英文原文：http://www.consumeraffairs.com/news04/2007/09/dementia_smoking.html

原始出处:

NEUROLOGY 2007;69:998-1005

Relation between smoking and risk of dementia and Alzheimer disease

The Rotterdam Study

C. Reitz, MD, PhD, T. den Heijer, MD, PhD, C. van Duijn, PhD, A. Hofman, MD, PhD and M.M.B. Breteler, MD, PhD

From the Departments of Epidemiology & Biostatistics (C.R., T.d.H., C.v.D., A.H., M.M.B.B.) and Neurology (T.d.H.), Erasmus Medical Center, Rotterdam, The Netherlands.

Address correspondence and reprint requests to DrB. Breteler, Department of Epidemiology & Biostatistics, Erasmus Medical Center, PO Box 1738, 3000DR Rotterdam, The Netherlands m.breteler@erasmusmc.nl

Background and Objective: Previous studies relating smoking with the risk of dementia have been inconsistent and limited in their validity by short follow-up times, large intervals between baseline and follow-up assessments, and unspecific determination of dementia diagnosis. We re-assessed after longer follow-up time in the large population-based cohort of the Rotterdam Study whether smoking habits and pack-years of smoking are associated with the risk of dementia, Alzheimer disease (AD), and vascular dementia (VaD).

Methods: Prospective population-based cohort study in 6,868 participants, 55 years or older and free of dementia at baseline. First, Cox proportional hazard models were used to relate smoking status at baseline with the risks of incident dementia, VaD, and AD, using never smokers as the reference category in all analyses. Then Cox proportional hazard models were used to relate pack-years of smoking with the risks of incident dementia, VaD, and AD. To explore the impact of the APOE ${varepsilon}$ 4 allele, sex, and age on the association between smoking status and dementia, we repeated all analyses stratifying, in separate models, by APOE ${varepsilon}$ 4 genotype, sex, and median of age.

Results: After a mean follow-up time of 7.1 years, current smoking at baseline was associated with an increased risk of dementia (HR 1.47, 95% CI 1.18 to 1.86) and AD (HR 1.56, 95% CI 1.21 to 2.02). This increase in disease risk was restricted to persons without the APOE ${varepsilon}$ 4 allele. There was no association between current smoking and risk of VaD, and there was no association between past smoking and risk of dementia, AD, or VaD.

Conclusion: Current smoking increases the risk of dementia. This effect is more pronounced in persons without the APOE ${varepsilon}$ 4 allele than APOE ${varepsilon}$ 4 carriers.

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