Jain Nishank, Minhajuddin Abu T, Neeland Ian J, Elsayed Essam F, Vega Gloria L, Hedayati S Susan
Division of Nephrology, Department of Internal Medicine, Veterans Affairs North Texas Health Care System, Dallas, TX (NJ, EFE, and SSH); the Division of Nephrology, Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas, TX (NJ, EFE, and SSH); the Division of Biostatistics, Department of Clinical Sciences, University of Texas Southwestern Medical Center, Dallas, TX (ATM); the Division of Cardiology, Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas, TX (IJN); and the Department of Clinical Nutrition and Center for Human Nutrition, University of Texas Southwestern Medical Center, Dallas, TX (GLV).
Am J Clin Nutr. 2014 May;99(5):992-8. doi: 10.3945/ajcn.113.077362. Epub 2014 Feb 19.
Previous studies that reported an association of dietary Na(+) intake with metabolic syndrome were limited by the use of imprecise measures of obesity, Na(+) intake, or exclusion of multiethnic populations. The effect of dietary K(+) intake on obesity is less well described.
We hypothesized that high dietary Na(+) and low K(+), based on the ratio of urinary Na(+) to K(+) (U[Na(+)]/[K(+)]) in a first-void morning urinary sample, is independently associated with total body fat.
In a prospective population-based cohort, 2782 participants in the community-dwelling, probability-sampled, multiethnic Dallas Heart Study were analyzed. The primary outcome established a priori was total-body percentage fat (TBPF) measured by dual-energy X-ray absorptiometry. The main predictor was U[Na(+)]/[K(+)]. Robust linear regression was used to explore an independent association between U[Na(+)]/[K(+)] and TBPF. The analyses were stratified by sex and race after their effect modifications were analyzed.
Of the cohort, 55.4% were female, 49.8% African American, 30.8% white, 17.2% Hispanic, and 2.2% other races. The mean (±SD) age was 44 ± 10 y, BMI (in kg/m(2)) was 30 ± 7, TBPF was 32 ± 10%, and U[Na(+)]/[K(+)] was 4.2 ± 2.6; 12% had diabetes. In the unadjusted and adjusted models, TBPF increased by 0.75 (95% CI: 0.25, 1.25) and 0.43 (0.15, 0.72), respectively (P = 0.003 for both), for every 3-unit increase in U[Na(+)]/[K(+)]. A statistically significant interaction was found between race and U[Na(+)] /[K(+)], so that the non-African American races had a higher TBPF than did the African Americans per unit increase in U[Na(+)]/[K(+)] (P-interaction < 0.0001 for both). No interaction was found between sex and U[Na(+)]/[K(+)].
The ratio of dietary Na(+) to K(+) intake may be independently associated with TBPF, and this association may be more pronounced in non-African Americans. Future studies should explore whether easily measured spot U[Na(+)]/[K(+)] can be used to monitor dietary patterns and guide strategies for obesity management.
以往报告膳食钠(Na⁺)摄入量与代谢综合征之间存在关联的研究,因肥胖测量方法不精确、钠摄入量测量不准确或排除多民族人群而受到限制。膳食钾(K⁺)摄入量对肥胖的影响描述较少。
我们假设,根据晨尿样本中尿钠(Na⁺)与钾(K⁺)的比值(U[Na⁺]/[K⁺]),高膳食Na⁺和低K⁺与全身脂肪独立相关。
在一项基于人群的前瞻性队列研究中,对达拉斯心脏研究中2782名社区居住、概率抽样、多民族参与者进行了分析。预先设定的主要结局是通过双能X线吸收法测量的全身脂肪百分比(TBPF)。主要预测指标是U[Na⁺]/[K⁺]。采用稳健线性回归探讨U[Na⁺]/[K⁺]与TBPF之间的独立关联。在分析性别和种族的效应修饰后,对分析进行分层。
该队列中,55.4%为女性,49.8%为非裔美国人,30.8%为白人,17.2%为西班牙裔,2.2%为其他种族。平均(±标准差)年龄为44±10岁,体重指数(kg/m²)为30±7,TBPF为32±10%,U[Na⁺]/[K⁺]为4.2±2.6;12%患有糖尿病。在未调整和调整模型中,U[Na⁺]/[K⁺]每增加3个单位,TBPF分别增加0.75(95%置信区间:0.25,1.25)和0.43(0.15,0.72)(两者P = 0.003)。在种族与U[Na⁺]/[K⁺]之间发现了具有统计学意义的交互作用,因此,U[Na⁺]/[K⁺]每增加一个单位,非非裔美国人的TBPF高于非裔美国人(两者P交互<0.0001)。在性别与U[Na⁺]/[K⁺]之间未发现交互作用。
膳食Na⁺与K⁺摄入量之比可能与TBPF独立相关,且这种关联在非非裔美国人中可能更为明显。未来的研究应探讨易于测量的即时U[Na⁺]/[K⁺]是否可用于监测饮食模式并指导肥胖管理策略。