Department of Psychiatry, University of California San Diego, La Jolla, San Diego, CA, USA.
Center for Behavior Genetics of Aging, University of California, La Jolla, San Diego, CA, USA.
Addiction. 2022 Apr;117(4):1049-1059. doi: 10.1111/add.15710. Epub 2021 Oct 28.
Smoking is associated with increased risk for brain aging/atrophy and dementia. Few studies have examined early associations with brain aging. This study aimed to measure whether adult men with a history of heavier smoking in early mid-life would have older than predicted brain age 16-28 years later.
Prospective cohort observational study, utilizing smoking pack years data from average age 40 (early mid-life) predicting predicted brain age difference scores (PBAD) at average ages 56, 62 (later mid-life) and 68 years (early old age). Early mid-life alcohol use was also evaluated.
Population-based United States sample.
PARTICIPANTS/CASES: Participants were male twins of predominantly European ancestry who served in the United States military between 1965 and 1975. Structural magnetic resonance imaging (MRI) began at average age 56. Subsequent study waves included most baseline participants; attrition replacement subjects were added at later waves.
Self-reported smoking information was used to calculate pack years smoked at ages 40, 56, 62, and 68. MRIs were processed with the Brain-Age Regression Analysis and Computation Utility software (BARACUS) program to create PBAD scores (chronological age-predicted brain age) acquired at average ages 56 (n = 493; 2002-08), 62 (n = 408; 2009-14) and 68 (n = 499; 2016-19).
In structural equation modeling, age 40 pack years predicted more advanced age 56 PBAD [β = -0.144, P = 0.012, 95% confidence interval (CI) = -0.257, -0.032]. Age 40 pack years did not additionally predict PBAD at later ages. Age 40 alcohol consumption, but not a smoking × alcohol interaction, predicted more advanced PBAD at age 56 (β = -0.166, P = 0.001, 95% CI = -0.261, -0.070) with additional influences at age 62 (β = -0.115, P = 0.005, 95% CI = -0.195, -0.036). Age 40 alcohol did not predict age 68 PBAD. Within-twin-pair analyses suggested some genetic mechanism partially underlying effects of alcohol, but not smoking, on PBAD.
Heavier smoking and alcohol consumption by age 40 appears to predict advanced brain aging by age 56 in men.
吸烟与大脑老化/萎缩和痴呆的风险增加有关。很少有研究探讨与大脑老化的早期关联。本研究旨在测量中年早期吸烟量较大的成年男性，其大脑年龄是否会比预测的年龄大 16-28 岁。
前瞻性队列观察研究，利用平均年龄为 40 岁（中年早期）的吸烟包年数据来预测平均年龄为 56 岁、62 岁（中年后期）和 68 岁（老年早期）时的预测脑龄差异评分（PBAD）。还评估了中年早期的饮酒情况。
美国人群基础样本。
参与者/病例：参与者为欧洲裔为主的男性双胞胎，他们曾于 1965 年至 1975 年在美国军队服役。结构磁共振成像（MRI）在平均年龄为 56 岁时开始进行。随后的研究波次包括了大多数基线参与者；在后续波次中增加了替换的参与者。
使用自我报告的吸烟信息来计算 40 岁、56 岁、62 岁和 68 岁时的吸烟包年数。使用 Brain-Age Regression Analysis and Computation Utility 软件（BARACUS）程序对 MRI 进行处理，以创建 PBAD 评分（实际年龄-预测脑龄），这些评分在平均年龄为 56 岁（n=493；2002-08 年）、62 岁（n=408；2009-14 年）和 68 岁（n=499；2016-19 年）时获得。
在结构方程模型中，40 岁时的吸烟包年数预测了更先进的 56 岁 PBAD [β=-0.144，P=0.012，95%置信区间（CI）=-0.257，-0.032]。40 岁时的吸烟包年数并不能预测以后年龄的 PBAD。40 岁时的饮酒量，但不是吸烟与饮酒的交互作用，预测了 56 岁时更先进的 PBAD（β=-0.166，P=0.001，95%CI=-0.261，-0.070），并且在 62 岁时还有其他影响（β=-0.115，P=0.005，95%CI=-0.195，-0.036）。40 岁时的饮酒量并不能预测 68 岁时的 PBAD。双胞胎内的配对分析表明，酒精对 PBAD 的影响部分受到遗传机制的影响，但吸烟则不然。
中年早期吸烟量和饮酒量较大的男性，其大脑老化速度似乎会在 56 岁时比同龄人更快。
Zotero 插件