Ndanuko Rhoda N, Tapsell Linda C, Charlton Karen E, Neale Elizabeth P, O'Donnell Katrina M, Batterham Marijka J
School of Medicine, University of Wollongong, Northfields Avenue, Wollongong, NSW, Australia.
School of Medicine, University of Wollongong, Northfields Avenue, Wollongong, NSW, Australia.
Nutrition. 2017 Jan;33:285-290. doi: 10.1016/j.nut.2016.07.011. Epub 2016 Jul 27.
The aim of this study was to examine the relationship between sodium and potassium intakes and blood pressure (BP) in a clinical sample.
Secondary analysis of baseline data from 328 participants (mean age: 43.6 ± 8 y, mean body mass index [BMI]: 32.4 ± 4.2 kg/m, mean systolic BP [SBP]/diastolic BP [DBP]: 124.9 ± 14.5/73.3 ± 9.9 mm Hg) of the 12-mo HealthTrack randomized controlled weight loss trial was conducted. Resting BP and 24-h urine sodium and potassium were measured. Dietary intake was evaluated with 4-d food records and self-reported diet histories.
Urinary sodium was positively correlated (Spearman's rho) with SBP (r = 0.176; P = 0.001) and DBP (r = 0.150; P = 0.003). The ratio of sodium to potassium was positively correlated with SBP (r = 0.1; P = 0.035). Urinary sodium (F [4,323] = 20.381; P < 0.0005; adjusted R = 0.231) and sodium-to-potassium ratio (F[4,323] = 25.008; P < 0.0005; adjusted R = 0.227) significantly predicted SBP after controlling for age, sex, BMI, and hypertension medication use. Dietary sodium and potassium significantly predicted urinary sodium (B = 0.33, t = 4.032, P < 0.01) and potassium (B = 0.67, t = 8.537, P < 0.01) excretion, respectively, after adjustment for energy and BMI. Median dietary sodium intake was 3197 mg/d and median dietary potassium intake was 2886 mg/d. Cereal-based products and dishes were the major contributors (22%) to total sodium intake.
In the present study, a high dietary sodium intake and high sodium-to-potassium ratio predicted high SBP. This suggests a need to focus dietary advice on reduction of sources of sodium and increasing sources of potassium in weight loss interventions to improve BP control.
本研究旨在探讨临床样本中钠和钾摄入量与血压（BP）之间的关系。
对12个月的健康追踪随机对照减肥试验中328名参与者（平均年龄：43.6±8岁，平均体重指数[BMI]：32.4±4.2kg/m²，平均收缩压[SBP]/舒张压[DBP]：124.9±14.5/73.3±9.9mmHg）的基线数据进行二次分析。测量静息血压以及24小时尿钠和钾含量。通过4天的食物记录和自我报告的饮食史来评估饮食摄入量。
尿钠与收缩压（Spearman秩相关系数）呈正相关（r = 0.176；P = 0.001），与舒张压呈正相关（r = 0.150；P = 0.003）。钠钾比与收缩压呈正相关（r = 0.1；P = 0.035）。在控制年龄、性别、BMI和高血压用药情况后，尿钠（F[4,323] = 20.381；P < 0.0005；调整后R = 0.231）和钠钾比（F[4,323] = 25.008；P < 0.0005；调整后R = 0.227）能显著预测收缩压。在调整能量和BMI后，饮食中的钠和钾分别能显著预测尿钠（B = 0.33，t = 4.032，P < 0.01）和尿钾（B = 0.67，t = 8.537，P < 0.01）排泄量。饮食钠摄入量中位数为3197mg/d，饮食钾摄入量中位数为2886mg/d。谷类制品和菜肴是总钠摄入量的主要贡献者（22%）。
在本研究中，高饮食钠摄入量和高钠钾比预示着高收缩压。这表明在减肥干预措施中，饮食建议需要聚焦于减少钠的来源并增加钾的来源，以改善血压控制。
