Nutritional influences on lung function

描述(由申请人提供)： 这项建议调查营养因素与肺的关系。 功能与慢性阻塞性肺疾病(COPD)。该项目将 使用三个数据源来研究以下假设。首先，做 抗氧化剂保护肺免受内源性和外源性损伤 氧化剂？这一研究问题将通过纵向数据来解决 来自标准化老龄化研究(NAS)，这是一项针对2280名男性的前瞻性研究。 食物频率中维生素C、维生素E和β胡萝卜素的膳食摄入量数据 调查问卷(1987年首次发放)将根据以下内容进行审查 随后13年期间的肺结果，包括强迫 第一秒呼气量(FEV1)，乙酰甲胆碱 响应性和COPD事件。需要纵向证据来评估 因果关系。第二，较低的血脂水平是否会增加呼吸道疾病的风险 结果呢？将使用三个数据来源来解决这一研究问题。 使用《第三次全国健康与营养报告》的横断面数据 检查调查，我们将调查血脂谱(总， 低密度脂蛋白和高密度脂蛋白胆固醇；载脂蛋白AI和B)对肺功能和 普遍存在的慢性阻塞性肺病风险。血脂与肺功能的关系也将是 在NAS队列中进行了调查。预期数据允许考虑 有时间维度的问题，例如，血脂水平是否发生变化 预测肺部结局的变化。最后，横截面数据来自 中国，一个天生低胆固醇的人群，将被研究到 考虑一下在不同暴露范围的人群中的假设。 我们还将考虑脂类和抗氧化剂可能产生的联合作用。 暴露在肺结果上，考虑到一些候选抗氧化剂， 例如维生素E和β-胡萝卜素是脂溶的。总体目标 是了解营养如何影响肺功能，包括绝对的 衡量指标和下降速度，以及营养如何影响患病风险 肺部疾病。研究营养因素和营养的综合方法 提出了它们对肺转归的潜在影响。

DESCRIPTION (provided by applicant): This proposal investigates the relation of nutritional factors to lung function and chronic obstructive pulmonary disease (COPD). The project will use three data sources to investigate the following hypotheses. First, do antioxidants protect the lung from damage caused by endogenous and exogenous oxidants? This research question will be addressed with longitudinal data from the Normative Aging Study (NAS), a prospective study of 2,280 men. Dietary intake data on vitamins C and E and betacarotene from food frequency questionnaires (first administered 1987) will be examined in relation to pulmonary outcomes over the subsequent 13-year period, including forced expiratory volume in the first second (FEV1), methacholine airways responsiveness, and incident COPD. Longitudinal evidence is needed to assess causality. Second, do lower lipid levels increase the risk of respiratory outcomes? Three data sources will be used to address this research question. Using cross-sectional data from the Third National Health and Nutrition Examination Survey, we will investigate the relation of lipid profile (total, LDL and HDL cholesterol; apolipoproteins AI and B) to lung function and to prevalent COPD risk. The relation of lipids to lung function also will be investigated in the NAS cohort. The prospective data allow consideration of questions with a time dimension, for example whether changes in lipid profile predict changes in pulmonary outcomes. Finally, cross-sectional data from China, a population with naturally low cholesterol, will be studied to consider the hypothesis in a population with a different range of exposure. We will also consider the possible joint effects of lipids and antioxidant exposures on lung outcomes, given that some of the candidate antioxidants, for example vitamin E and betacarotene, are lipid-soluble. The overall objectives are to understand how nutrition affects lung function, including absolute measures as well as rate of decline, and how nutrition affects the risk of lung disease. An integrated approach to the study of nutritional factors and their potential influences on lung outcomes is proposed.