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血糖稍高亦增加心脏病风险
研究人员说,如果个体血糖水平轻微增高(包括非糖尿病者),那么他发生缺血性心血管疾病的可能性将增加69%。
该项由来自哥本哈根大学的研究人员领衔实施的研究纳入了80,000人的研究结果发表在美国心脏病学会杂志。直至目前,威胁心脏健康的首要因素一直是胆固醇。
哥本哈根大学医院主任医师、哥本哈根大学助理教授Marianne Benn,解释道:
“我们知道糖尿病患者和胆固醇水平高的人更易患缺血性心脏病,但我们的研究也使独立考察血糖水平的影响变为可能。令我们吃惊的是,即使轻微的血糖增高,长期下去也似乎是危险的,也就是说,单单就糖这一独立因素来说,也一样可以导致负面差异。
研究人员发现,即使无糖尿病的健康个体血糖正常、空腹血糖值在6mmol(=108mg)/L以下,几年之后,仅仅血糖的稍微升高(1mmol[18mg])就使心脏病发作的风险增加69%。
研究人员调查了哥本哈根总体人口学研究、哥本哈根城市心脏研究以及哥本哈根缺血性心脏病研究中共计80522名丹麦人的数据
他们发现轻微增高的血糖水平本身已足够导致心血管损害。
然而这些研究并不足以证明心血管疾病和增高的血糖水平之间的关联。根据研究人员说法,这些研究的参与者可能都有健康问题或者有影响他们体重和心脏的一些问题。目前研究中的遗传分析去除了三个大型研究中所分析的干扰因素,使研究的焦点充分集中于糖的影响上。
虽然研究人员相信缺血性心血管疾病的风险是由糖直接导致,但他们不明所以然。他们说道,为使全球健康获益,应该限制糖的摄入。
哥本哈根大学医院主任医师、哥本哈根大学卫生和医学科学系临床教授Borge Nordestgaard说道:
“世界卫生组织估计所有死亡中的6%是由于血糖增高引起的。因此,我们得出的结果可能有在设计全球范围内心脏疾病以及早逝的预防方案中发挥重大作用的潜力。”
根据世界卫生组织的说法,每年有1700万名患者死于心脏相关疾病,并且在未来几年中这一数字将有所增加。
Nonfasting glucose, ischemic heart disease, and myocardial infarction: a mendelian randomization study.
J Am Coll Cardiol 2012;5925:2356-65
Benn M Tybjærg-Hansen A McCarthy MI Jensen GB Grande P Nordestgaard BG
Department of Clinical Biochemistry, Herlev Hospital, Herlev, Denmark; Copenhagen General Population Study, Herlev Hospital, Herlev, Denmark; Copenhagen University Hospitals, Faculty of Health Sciences, University of Copenhagen, Copenhagen, Denmark.
Abstract
The purpose of this study was to test whether elevated nonfasting glucose levels associate with and cause ischemic heart disease (IHD) and myocardial infarction (MI). Elevated fasting plasma glucose levels associate with increased risk of IHD, but whether this is also true for nonfasting levels and whether this is a causal relationship is unknown. Using a Mendelian randomization approach, we studied 80,522 persons from Copenhagen, Denmark. Of those, IHD developed in 14,155, and MI developed in 6,257. Subjects were genotyped for variants in GCK (rs4607517), G6PC2 (rs560887), ADCY5 (rs11708067), DGKB (rs2191349), and ADRA2A (rs10885122) associated with elevated fasting glucose levels in genome-wide association studies. Risk of IHD and MI increased stepwise with increasing nonfasting glucose levels. The hazard ratio for IHD in subjects with nonfasting glucose levels ≥11 mmol/l (≥198 mg/dl) versus <5 mmol/l (<90 mg/dl) was 6.9 (95% confidence interval [CI]: 4.2 to 11.2) adjusted for age and sex, and 2.3 (95% CI: 1.3 to 4.2) adjusted multifactorially; corresponding values for MI were 9.2 (95% CI: 4.6 to 18.2) and 4.8 (95% CI: 2.1 to 11.2). Increasing number of glucose-increasing alleles was associated with increasing nonfasting glucose levels and with increased risk of IHD and MI. The estimated causal odds ratio for IHD and MI by instrumental variable analysis for a 1-mmol/l (18-mg/dl) increase in nonfasting glucose levels due to genotypes combined were 1.25 (95% CI: 1.03 to 1.52) and 1.69 (95% CI: 1.28 to 2.23), and the corresponding observed hazard ratio for IHD and MI by Cox regression was 1.18 (95% CI: 1.15 to 1.22) and 1.09 (95% CI: 1.07 to 1.11), respectively. Like common nonfasting glucose elevation, plasma glucose-increasing polymorphisms associate with increased risk of IHD and MI. These data are compatible with a causal
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