1.
Effect of dietary sodium restriction on blood pressure in type 2 diabetes: A meta-analysis of randomized controlled trials.
Ren, J, Qin, L, Li, X, Zhao, R, Wu, Z, Ma, Y
Nutrition, metabolism, and cardiovascular diseases : NMCD. 2021;(6):1653-1661
Abstract
AIMS: Although current guidelines recommend reduction of salt intake in patients with diabetes, the benefits of reducing salt intake in people with type 2 diabetes mellitus (T2DM) lack clear evidence. Therefore, we performed a meta-analysis of available randomized controlled trials (RCTs) of sodium restriction and blood pressure (BP) in patients with T2DM. DATA SYNTHESIS We performed a systematic search of the online databases that evaluated the effect of dietary sodium restriction on BP in patients with T2DM. Sodium intake was expressed by 24 h urinary sodium excretion (UNaV). Q statistics and I2 were used to explore between-study heterogeneity. A random-effects model was used in the presence of significant heterogeneity; otherwise, a fixed-effects model was applied. Eight RCTs with 10 trials (7 cross-over and 3 parallel designs) were included in the meta-analysis. Compared with ordinary sodium intake, dietary sodium restriction significantly decreased UNaV (weighted mean difference, WMD: -38.430 mmol/24 h; 95% CI: -41.665 mmol/24 h to -35.194 mmol/24 h). Sodium restriction significantly lowered systolic BP (WMD: -5.574 mm Hg; 95% CI: -8.314 to -2.834 mm Hg; I2 = 0.0%) and diastolic BP (WMD: -1.675 mm Hg; 95% CI: -3.199 to -0.150 mm Hg; I2 = 0.0%) with low heterogeneity among the studies. No publication bias was found from Begg's and Egger's tests. CONCLUSIONS Sodium restriction significantly reduces SBP and DBP in patients with T2DM.
2.
Formulas to Estimate Dietary Sodium Intake From Spot Urine Alter Sodium-Mortality Relationship.
He, FJ, Ma, Y, Campbell, NRC, MacGregor, GA, Cogswell, ME, Cook, NR
Hypertension (Dallas, Tex. : 1979). 2019;(3):572-580
Abstract
To study the effect of formulas on the estimation of dietary sodium intake (sodium intake) and its association with mortality, we analyzed the TOHP (Trials of Hypertension Prevention) follow-up data. Sodium intake was assessed by measured 24-hour urinary sodium excretion and estimations from sodium concentration using the Kawasaki, Tanaka, and INTERSALT (International Cooperative Study on Salt, Other Factors, and Blood Pressure) formulas. We used both the average of 3 to 7 urinary measurements during the trial period and the first measurement at the beginning of each trial. Additionally, we kept sodium concentration constant to test whether the formulas were independently associated with mortality. We included 2974 individuals aged 30 to 54 years with prehypertension, not assigned to sodium intervention. During a median 24-year follow-up, 272 deaths occurred. The average measured sodium intake was 3766±1290 mg/d. All estimated values, including those with constant sodium concentration, were systematically biased with overestimation at lower levels and underestimation at higher levels. There was a significant linear association between the average measured sodium intake (ie, gold standard method) and mortality. This relationship was altered by using the estimated sodium intakes. There appeared to be a J- or U-shaped relationship for the average estimated sodium by all formulas. Despite variations in the sodium-mortality relationship among various formulas, a common pattern was that all estimated values including those with constant sodium appeared to be inversely related to mortality at lower levels of sodium intake. These results demonstrate that inaccurate estimates of sodium cannot be used in association studies, particularly as the formulas per se seem to be related to mortality independent of sodium.
3.
Errors in estimating usual sodium intake by the Kawasaki formula alter its relationship with mortality: implications for public health.
He, FJ, Campbell, NRC, Ma, Y, MacGregor, GA, Cogswell, ME, Cook, NR
International journal of epidemiology. 2018;(6):1784-1795
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Abstract
BACKGROUND Several cohort studies with inaccurate estimates of sodium reported a J-shaped relationship with mortality. We compared various estimated sodium intakes with that measured by the gold-standard method of multiple non-consecutive 24-h urine collections and assessed their relationship with mortality. METHODS We analysed the Trials of Hypertension Prevention follow-up data. Sodium intake was assessed in four ways: (i) average measured (gold standard): mean of three to seven 24-h urinary sodium measurements during the trial periods; (ii) average estimated: mean of three to seven estimated 24-h urinary sodium excretions from sodium concentration of 24-h urine using the Kawasaki formula; (iii) first measured: 24-h urinary sodium measured at the beginning of each trial; (iv) first estimated: 24-h urinary sodium estimated from sodium concentration of the first 24-h urine using the Kawasaki formula. We included 2974 individuals aged 30-54 years with pre-hypertension, not assigned to sodium intervention. RESULTS During a median follow-up of 24 years, 272 deaths occurred. The average sodium intake measured by the gold-standard method was 3769 ± 1282 mg/d. The average estimated sodium over-estimated the intake by 1297 mg/d (95% confidence interval: 1267-1326). The average estimated value was systematically biased with over-estimation at lower levels and under-estimation at higher levels. The average measured sodium showed a linear relationship with mortality. The average estimated sodium appeared to show a J-shaped relationship with mortality. The first measured and the first estimated sodium both flattened the relationship. CONCLUSIONS Accurately measured sodium intake showed a linear relationship with mortality. Inaccurately estimated sodium changed the relationship and could explain much of the paradoxical J-shaped findings reported in some cohort studies.