黑人青壮年摄入高果糖玉米糖浆甜饮料导致心血管疾病风险和发病率过高--CARDIA 研究。

IF 4.4 2区 医学 Q1 NUTRITION & DIETETICS
Luanne Robalo DeChristopher, Katherine L Tucker
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引用次数: 0

摘要

背景:20 世纪 80 年代初,美国食品供应从蔗糖转向高果糖玉米糖浆/(HFCS),黑人/白人心脏病死亡率的差距开始扩大。HFCS 中的果糖含量超过了公认的安全标准/GRAS,导致食品/饮料中的游离果糖/(未配对果糖)空前超标。从 20 世纪 80 年代初开始,来自 HFCS 的人均过量游离果糖开始超过引发果糖吸收不良的剂量/(5-10 克)。果糖吸收不良会导致肠道菌群失调和膳食肽/促泌素/(GLP-1/GIP)的肠道原位果糖化,从而形成动脉粥样硬化的高级糖化终产物。这两者都会导致肠道内分泌功能失调,是心血管疾病/(CVD)的风险因素。有限的研究表明,非裔美国人的果糖吸收不良率高于其他人。心血管疾病风险始于生命早期:方法:利用 1985-86 年开始的冠状动脉-成人发病风险/(CARDIA)研究数据(2186 名黑人和 2277 名白人参与者,年龄在 18-30 岁之间)来验证以下假设:摄入 HFCS 甜饮料会增加心血管疾病的风险/发病率,黑人比白人更容易增加心血管疾病的风险/发病率,而且摄入量更低;而橙汁--一种低过量游离果糖的果汁,其总糖和总果糖含量相当,但果糖与葡萄糖的比例为 1:1,即:低过量游离果糖、低过量游离果糖、低过量游离果糖和低过量游离果糖、而低过量游离果糖果汁则不然。采用 Cox 比例危险模型计算危险比:结果:与吸烟(HR = 1.6)相比,摄入 HFCS 甜饮料与更高的心血管疾病风险(HR = 1.7)相关。黑人比白人摄入较少的 HFCS 甜饮料时心血管疾病风险更高。仅在黑人参与者中,摄入量低至每周 3 次与较少摄入/从不摄入相比,心血管疾病风险高出一倍(HR 2.1,95% CI 1.2-3.7;P = 0.013)。有序关系的概率接近显著性。在黑人参与者中,心血管疾病发病率从每周≤2次的59.8/1000猛增62%至每周3-6次的96.9/1000。在白人参与者中,心血管疾病发病率从≤1.5次/周的37.6/1000上升到2次/周-1次/日的41.1/1000--增加了9%。高血压在每日饮用含氢氟碳化合物甜味饮料的黑人中发病率最高:结论:在过去的 40 年中,HFCS 无处不在,其果糖与葡萄糖的比率高于公认的安全比率,这可能是导致心血管疾病种族差异的原因之一,因为黑人的果糖吸收率较高、未配对/过量的游离果糖诱发肠道菌群失调以及膳食肽/蛋白(GLP-1/GIP)的肠道果糖基化。这些紊乱会导致动脉粥样硬化斑块;促进胰岛素不足/失调/饱腹感改变/血糖异常;减少保护性微生物群代谢物;增加高血压、心血管疾病的发病率和死亡率。
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Disproportionately higher cardiovascular disease risk and incidence with high fructose corn syrup sweetened beverage intake among black young adults-the CARDIA study.

Background: The black/white heart disease mortality disparity began increasing in the early 1980's, coincident with the switch from sucrose to high-fructose-corn-syrup/(HFCS) in the US food supply. There has been more fructose in HFCS than generally-recognized-as-safe/GRAS, which has contributed to unprecedented excess-free-fructose/(unpaired-fructose) in foods/beverages. Average- per-capita excess-free-fructose, from HFCS, began exceeding dosages/(5-10 g) that trigger fructose-malabsorption in the early 1980's. Fructose malabsorption contributes to gut-dysbiosis and gut-in-situ-fructosylation of dietary peptides/incretins/(GLP-1/GIP) which forms atherosclerotic advanced-glycation-end-products. Both dysregulate gut endocrine function and are risk factors for cardiovascular disease/(CVD). Limited research shows that African Americans have higher fructose malabsorption prevalence than others. CVD risk begins early in life.

Methods: Coronary-Artery-Risk-Development-in-Adults/(CARDIA) study data beginning in 1985-86 with 2186 Black and 2277 White participants, aged 18-30 y, were used to test the hypothesis that HFCS sweetened beverage intake increases CVD risk/incidence, more among Black than White young adults, and at lower intakes; while orange juice-a low excess-free-fructose juice with comparable total sugars and total fructose, but a 1:1 fructose-to-glucose-ratio, i.e., low excess-free-fructose, does not. Cox proportional hazards models were used to calculate hazard ratios.

Results: HFCS sweetened beverage intake was associated with higher CVD risk (HR = 1.7) than smoking (HR = 1.6). CVD risk was higher at lower HFCS sweetened beverage intake among Black than White participants. Intake, as low as 3 times/wk, was associated with twice the CVD risk vs. less frequent/never, among Black participants only (HR 2.1, 95% CI 1.2-3.7; P = 0.013). Probability of an ordered relationship approached significance. Among Black participants, CVD incidence jumped 62% from 59.8/1000, among ≤ 2-times/wk, to 96.9/1000 among 3-6 times/wk consumers. Among White participants, CVD incidence increased from 37.6/1000, among ≤ 1.5-times/wk, to 41.1/1000, among 2 times/wk-once/d - a 9% increase. Hypertension was highest among Black daily HFCS sweetened beverage consumers.

Conclusion: The ubiquitous presence of HFCS over-the-past-40 years, at higher fructose-to-glucose ratios than generally-recognized-as-safe, may have contributed to CVD racial disparities, due to higher fructose-malabsorption prevalence among Black individuals, unpaired/excess-free-fructose induced gut dysbiosis and gut fructosylation of dietary peptides/incretins (GLP-1/GIP). These disturbances contribute to atherosclerotic plaque; promote incretin insufficiency/dysregulation/altered satiety/dysglycemia; decrease protective microbiota metabolites; and increase hypertension, CVD morbidity and mortality.

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来源期刊
Nutrition Journal
Nutrition Journal NUTRITION & DIETETICS-
CiteScore
9.80
自引率
0.00%
发文量
68
审稿时长
4-8 weeks
期刊介绍: Nutrition Journal publishes surveillance, epidemiologic, and intervention research that sheds light on i) influences (e.g., familial, environmental) on eating patterns; ii) associations between eating patterns and health, and iii) strategies to improve eating patterns among populations. The journal also welcomes manuscripts reporting on the psychometric properties (e.g., validity, reliability) and feasibility of methods (e.g., for assessing dietary intake) for human nutrition research. In addition, study protocols for controlled trials and cohort studies, with an emphasis on methods for assessing dietary exposures and outcomes as well as intervention components, will be considered. Manuscripts that consider eating patterns holistically, as opposed to solely reductionist approaches that focus on specific dietary components in isolation, are encouraged. Also encouraged are papers that take a holistic or systems perspective in attempting to understand possible compensatory and differential effects of nutrition interventions. The journal does not consider animal studies. In addition to the influence of eating patterns for human health, we also invite research providing insights into the environmental sustainability of dietary practices. Again, a holistic perspective is encouraged, for example, through the consideration of how eating patterns might maximize both human and planetary health.
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