DeChristopher Luanne R, Auerbach Brandon J, Tucker Katherine L
Independent Researcher, M.Sc. Biochemistry, Molecular Biology, P.O. Box 5542, Eugene, OR, 97405, USA.
Department of Primary Care, Virginia Mason Medical Center, Seattle, WA, USA.
BMC Nutr. 2020 Dec 8;6(1):70. doi: 10.1186/s40795-020-00396-x.
Researchers have sought to explain the black-white coronary heart disease (CHD) mortality disparity that increased from near parity to ~ 30% between 1980 and 2010. Contributing factors include cardiovascular disease prevention and treatment disparities attributable to disparities in insurance coverage. Recent research suggests that dietary/environmental factors may be contributors to the disparity. Unabsorbed/luminal fructose alters gut bacterial load, composition and diversity. There is evidence that such microbiome disruptions promote hypertension and atherosclerosis. The heart-gut axis may, in part, explain the black-white CHD disparity, as fructose malabsorption prevalence is higher among African Americans. Between 1980 and 2010, consumption of excess-free-fructose-the fructose type that triggers malabsorption-exceeded dosages associated with fructose malabsorption (~ 5 g-10 g), as extrapolated from food availability data before subjective, retroactively-applied loss adjustments. This occurred due to an industrial preference shift from sucrose to high-fructose-corn-syrup (HFCS) that began ~ 1980. During this period, HFCS became the main sweetener in US soda. Importantly, there has been more fructose in HFCS than thought, as the fructose-to-glucose ratio in popular sodas (1.9-to-1 and 1.5-to-1) has exceeded generally-recognized-as-safe levels (1.2-to-1). Most natural foods contain a ~ 1-to-1 ratio. In one recent study, ≥5 times/wk. consumers of HFCS sweetened soda/fruit drinks/and apple juice-high excess-free-fructose beverages-were more likely to have CHD, than seldom/never consumers.
Jackson-Heart-Study data of African Americans was used to test the hypothesis that regular relative to low/infrequent intake of HFCS sweetened soda/fruit drinks increases CHD risk, but not orange juice-a low excess-free-fructose juice. Cox proportional hazards models were used to calculate hazard ratios using prospective data of 3407-3621 participants, aged 21-93 y (mean 55 y).
African Americans who consumed HFCS sweetend soda 5-6x/wk. or any combination of HFCS sweetened soda and/or fruit drinks ≥3 times/day had ~ 2 (HR 2.08, 95% CI 1.03-4.20, P = 0.041) and 2.5-3 times higher CHD risk (HR 2.98, 95% CI 1.15-7.76; P = 0.025), respectively, than never/seldom consumers, independent of confounders. There were no associations with diet-soda or 100% orange-juice, which has a similar glycemic profile as HFCS sweetened soda, but contains a ~ 1:1 fructose-to-glucose ratio.
The ubiquitous presence of HFCS in the food supply may pre-dispose African Americans to increased CHD risk.
研究人员一直试图解释1980年至2010年间黑人和白人冠心病（CHD）死亡率差距从几乎持平增加到约30%的现象。促成因素包括保险覆盖差异导致的心血管疾病预防和治疗差异。最近的研究表明，饮食/环境因素可能是造成这种差距的原因。未吸收/肠腔中的果糖会改变肠道细菌数量、组成和多样性。有证据表明，这种微生物群紊乱会促进高血压和动脉粥样硬化。心-肠轴可能部分解释了黑人和白人冠心病的差异，因为非裔美国人中果糖吸收不良的患病率更高。1980年至2010年间，从主观的、追溯性应用的损失调整前的食物供应数据推断，过量游离果糖（即引发吸收不良的果糖类型）的摄入量超过了与果糖吸收不良相关的剂量（约5克至10克）。这是由于始于1980年左右的工业偏好从蔗糖转向高果糖玉米糖浆（HFCS）所致。在此期间，HFCS成为美国汽水的主要甜味剂。重要的是，HFCS中的果糖含量比人们认为的要高，因为流行汽水中的果糖与葡萄糖比例（1.9比1和1.5比1）已超过普遍认可的安全水平（1.2比1）。大多数天然食物的比例约为1比1。在最近的一项研究中，每周饮用HFCS甜味汽水/果汁饮料/苹果汁（高过量游离果糖饮料）≥5次的消费者患冠心病的可能性比很少/从不饮用的消费者高。
利用非裔美国人的杰克逊心脏研究数据来检验以下假设：相对于低/不经常摄入HFCS甜味汽水/果汁饮料，经常摄入会增加冠心病风险，但橙汁（低过量游离果糖果汁）不会。使用Cox比例风险模型，根据3407 - 3621名年龄在21 - 93岁（平均55岁）参与者的前瞻性数据计算风险比。
每周饮用5 - 6次HFCS甜味汽水的非裔美国人，或每天饮用HFCS甜味汽水和/或果汁饮料≥3次的任何组合的非裔美国人，患冠心病的风险分别比从不/很少饮用者高约2倍（风险比2.08，95%置信区间1.03 - 4.20，P = 0.041）和2.5 - 3倍（风险比2.98，95%置信区间1.15 - 7.76；P = 0.025），与混杂因素无关。与无糖汽水或100%橙汁没有关联，100%橙汁的血糖特征与HFCS甜味汽水相似，但果糖与葡萄糖比例约为1:1。
食品供应中HFCS的普遍存在可能使非裔美国人患冠心病的风险增加。
