Glycosylated hemoglobin level, race/ethnicity, and cognition in midlife and early old age.

Glycosylated hemoglobin level, race/ethnicity, and cognition in midlife and early old age.
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DOI:
10.1080/15427609.2020.1743810
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发表时间:
2020
影响因子:
2.4
通讯作者:
Tarraf W
Tarraf W
中科院分区:
心理学3区
文献类型:
--
作者:
Ortiz K;Garcia MA;Briceño E;Diminich ED;Arévalo SP;Vega IE;Tarraf W

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将种族/民族中糖化血红蛋白水平(HbA1c)差异与中年和老年早期认知功能联系起来的经验证据有限。我们使用来自健康与退休研究(HRS, 2006-2014)的生物标志物数据,研究对象是50-64岁的成年人(到2014年为57-73岁),并拟合多项logistic回归模型,评估基线HbA1c、认知功能(使用Langa-Weir分类)和8年间死亡率之间的关系。此外,我们测试了种族/民族的修改效应。在年龄和性别调整的模型中,高HbA1c水平与认知障碍(无痴呆)(CIND; RRR= 2.3; 95%CI=[1.38;3.84]; p<0.01)和痴呆(RRR= 4.00; 95%CI=[1.76;9.10]; p<0.01)较低的基线认知和较高的相对风险比(RRR; vs.正常认知)相关。调整社会人口统计学、行为风险因素和其他健康状况解释了CIND较高的RRR,并将痴呆症的RRR降低了约30%。HbA1c水平与认知能力下降的斜率无关,我们没有发现HbA1c因种族/民族而改变的证据。在中年关键时期进行针对性的血糖控制干预可以保护基线认知,缓冲认知功能障碍的下游发展。这可以产生重要的公共卫生效益,并减少与认知障碍有关的负担,特别是在患代谢疾病风险较高的种族/少数民族中。
Empirical evidence linking racial/ethnic differences in glycosylated hemoglobin levels (HbA1c) to cognitive function in midlife and early old age is limited. We use biomarker data from the Health and Retirement Study (HRS, 2006–2014), on adults 50–64 years at baseline (57–73 years by 2014), and fit multinomial logistic regression models to assess the association between baseline HbA1c, cognitive function (using Langa-Weir classifications) and mortality across 8-years. Additionally, we test for modification effects by race/ethnicity. In age- and sex-adjusted models high HbA1c level was associated with lower baseline cognition and higher relative risk ratios (RRR; vs. normal cognition) for cognitive impairment no dementia (CIND; RRR= 2.3; 95%CI=[1.38;3.84]; p<0.01), and dementia (RRR= 4.00; 95%CI=[1.76;9.10]; p<0.01). Adjusting for sociodemographic, behavioral risk factors, and other health conditions explained the higher RRR for CIND and attenuated the RRR for dementia by approximately 30%. HbA1c levels were not linked to the slope of cognitive decline, and we found no evidence of modification effects for HbA1c by race/ethnicity. Targeting interventions for glycemic control in the critical midlife period can protect baseline cognition and buffer against downstream development of cognitive impairment. This can yield important public health benefits and reductions in burdens associated with cognitive impairment, particularly among race/ethnic minorities who are at higher risk for metabolic diseases.
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