背景:食用水果与降低心血管疾病(CVD)风险相关,但潜在机制尚不清楚。我们调查了水果消费与肥胖标志物的横断面和前瞻性关联,血压,脂质,低度炎症,血糖,和氧化应激。
方法:主要分析包括基线时来自英国生物库的365534名中年人,其中11510人和38988人分别被纳入第一次和第二次随访,基线时无CVD和癌症。使用问卷评估基线时的水果消费频率。我们评估了水果与肥胖的横断面和前瞻性关联(体重指数,腰围和体脂百分比),收缩压和舒张压,脂质(低密度和高密度脂蛋白,甘油三酯和载脂蛋白B),血糖(血红蛋白A1c),低度炎症(C反应蛋白)和氧化应激(γ-谷氨酰转移酶)使用线性回归模型校正社会经济和生活方式因素.在一个子集中重复分析,进行两到五次完整的24小时饮食评估(n=26596),以调整总能量摄入。
结果:基线时的水果消费量通常与基线时的肥胖和生物标志物呈弱负相关。这些关系中的大多数并没有在后续行动中持续存在,除了与舒张压呈负相关,C反应蛋白,γ-谷氨酰转移酶和肥胖。然而,对于大多数机制来说,在进一步调整的模型中,高和低水果消耗(>3vs<1份/天)之间的平均水平变化小于0.1个标准偏差(SD)(而所有这些差异均<0.2SD)。例如,首次随访时,与低水果摄入量相比,高腰围和舒张压分别降低1cm和1mmHg(95%置信区间:分别为-1.8,-0.1和-1.8,-0.3).24小时饮食评估子集的分析显示出整体相似的关联。
结论:我们观察到那些报告高水果消费量与低水果消费量的人之间的肥胖和心脏代谢生物标志物差异很小,其中大多数没有持续随访。未来对其他机制的研究和对混杂因素的详细评估可能会进一步阐明水果与心血管疾病的相关性。
BACKGROUND: Fruit consumption has been associated with a lower cardiovascular disease (CVD) risk but the underlying mechanisms are unclear. We investigated the cross-sectional and prospective associations of fruit consumption with markers of adiposity, blood pressure, lipids, low-grade inflammation, glycaemia, and oxidative stress.
METHODS: The main analyses included 365 534 middle-aged adults from the UK Biobank at baseline, of whom 11 510, and 38 988 were included in the first and second follow-up respectively, free from CVD and cancer at baseline. Fruit consumption frequency at baseline was assessed using a questionnaire. We assessed the cross-sectional and prospective associations of fruit with adiposity (body mass index, waist circumference and %body fat), systolic and diastolic blood pressure, lipids (low-density and high-density lipoproteins, triglycerides and apolipoprotein B), glycaemia (haemoglobin A1c), low-grade inflammation (C-reactive protein) and oxidative stress (gamma-glutamyl-transferase) using linear regression models adjusted for socioeconomic and lifestyle factors. Analyses were repeated in a subset with two to five complete 24-h dietary assessments (n = 26 596) allowing for adjustment for total energy intake.
RESULTS: Fruit consumption at baseline generally showed weak inverse associations with adiposity and biomarkers at baseline. Most of these relationships did not persist through follow-up, except for inverse associations with diastolic blood pressure, C-reactive protein, gamma-glutamyl transferase and adiposity. However, for most mechanisms, mean levels varied by less than 0.1 standard deviations (SD) between high and low fruit consumption (> 3 vs < 1 servings/day) in further adjusted models (while the difference was < 0.2 SD for all of them). For example, waist circumference and diastolic blood pressure were 1 cm and 1 mmHg lower in high compared to low fruit intake at the first follow-up (95% confidence interval: -1.8, -0.1 and -1.8, -0.3, respectively). Analyses in the 24-h dietary assessment subset showed overall similar associations.
CONCLUSIONS: We observed very small differences in adiposity and cardiometabolic biomarkers between those who reported high fruit consumption vs low, most of which did not persist over follow-up. Future studies on other mechanisms and detailed assessment of confounding might further elucidate the relevance of fruit to cardiovascular disease.