Using sibling models to unpack the relationship between education and cognitive functioning in later life.
Using sibling models to unpack the relationship between education and cognitive functioning in later life.
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DOI：
10.1016/j.ssmph.2021.100960
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发表时间：
2022-03
期刊：
影响因子：
--
通讯作者：
Sicinski K
中科院分区：
文献类型：
--
作者：
Herd P;Sicinski K
随着人口老龄化和痴呆症患病率的增加，解开教育程度和晚年认知功能之间强大而持久的联系越来越重要。我们确实知道，从具有强大因果设计的研究中，增加受教育年限的政策可以改善晚年的认知功能。然而，这些研究并没有说明为什么受教育程度较高的老年人相对保留了认知功能。然而，由于方法上的限制和对这种关系的一些关键解释的忽视，研究的重点是为什么受到阻碍。因此，我们测试的解释包括前因因素，特别是家庭环境，青少年智商和遗传因素，以及成人中介机制，特别是健康行为和健康。我们采用了威斯康星州纵向研究，其中包括80年的前瞻性收集的数据，样本的每3个高中毕业生，和一个选定的兄弟姐妹，从类1957年。兄弟姐妹模型，并纳入前瞻性收集的早期和中年协变量，使我们能够解决先前文献的解释和方法的局限性，以更好地解开教育和以后的生活认知功能之间的关系。我们发现很少有证据表明，早期生活的遗传禀赋和环境，或中年健康和健康行为，解释这种关系。然而，青少年的认知确实很重要;较高的教育程度与青少年的认知功能有关，有助于防止青少年在以后的生活中认知功能水平低下。然而，青少年的认知和教育，独立地与以后的生活认知功能在相对相似的幅度。教育程度与以后生活认知功能的关系不仅仅是青少年认知功能的功能。教育与晚年认知的关系还不太清楚。影响教育的遗传因素不影响晚年认知。青少年的认知影响晚年的认知，部分是通过教育。教育的影响与青少年的认知无关。中年健康和健康行为并不能调解这些关系。
As the population ages and the prevalence of dementia increases, unpacking robust and persistent associations between educational attainment and later life cognitive functioning is increasingly important. We do know, from studies with robust causal designs, that policies that increase years of schooling improve later life cognitive functioning. Yet these studies don't illuminate why older adults with greater educational attainment have relatively preserved cognitive functioning. Studies focused on why, however, have been hampered by methodological limitations and inattention to some key explanations for this relationship. Consequently, we test explanations encompassing antecedent factors, specifically family environments, adolescent IQ, and genetic factors, as well as adult mediating mechanisms, specifically health behaviors and health. We employ the Wisconsin Longitudinal Study, which includes 80 years of prospectively collected data on a sample of 1 in every 3 high school graduates, and a selected sibling, from the class of 1957. Sibling models, and the inclusion of prospectively collected early and midlife covariates, allows us to address the explanatory and methodological limitations of the prior literature to better unpack the relationship between education and later life cognitive functioning. We find little evidence that early life genetic endowments and environments, or midlife health and health behaviors, explain the relationship. Adolescent cognition, however, does matter; higher educational attainment, linked to antecedent adolescent cognitive functioning, helps protect against lower levels of cognitive functioning in later life. Both adolescent cognition and education, however, independently associate with later life cognitive functioning at relatively similar magnitudes. Educational attainment's relationship to later life cognitive functioning is not simply a function of adolescent cognitive functioning. The education and late life cognition relationship is not well understood. Genetic factors influencing education do not influence late life cognition. Adolescent cognition influences late life cognition, in part, via education. Education's influence is independent of adolescent cognition. Midlife health and health behaviors do not mediate these relationships.
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