Development of a Culinary Intervention (Cooking Class) for Salt Reduction in Japanese Home Cooking: Strategies and Assessment.

Introduction: Culinary interventions (cooking classes) are a potential educational tool for salt reduction in the home diet, but their content has never been reported in detail. This study aimed to develop a cooking class for salt reduction, describe its rationale and structure so that other parties could replicate it, and preliminarily assess its impact on salt intake. Methods: A multidisciplinary research team developed a cooking class package to reduce salt content in the Japanese home diet. The package comprised its developmental policy, teaching methodology, a menu and recipes, and an implementation manual and aimed to allow third parties to replicate and modify the content. The team took the following step-by-step developmental approach. First, traditional home meals were modeled to create strategies contributing to a target of 2 g salt/meal. Then, educational topics were developed through these strategies, and finally, a dietitian produced menus and prepared documents for the class. The impact of the cooking class was assessed in a nonrandomized study of community residents. The outcome was differences in urinary salt excretion before and after the intervention. General linear models were used to account for the possible confounders. Results: The authors assumed 4-7 g salt/meal from analyzing typical Japanese home diets and developed 3 strategies: (1) restricting salt content in the main dish, (2) maintaining good tastes without salty dishes, and (3) balancing nutrition with low-salt dishes. On the basis of these strategies, the authors selected a total of 5 educational topics that participants could learn and apply at home: 1a, a simple and reliable technique to limit salt in a serving; 2a, excluding salty dishes; 2b, staple foods with notable flavor and aroma; 3a, flavoring without salt in side dishes; and 3b, ingredients that should be used intentionally. The team dietitian translated these educational topics into a menu and recipes for hands-on training and prepared a manual for conducting the class. The class developed using this approach was successfully overseen by a dietitian outside the research team. In the validation study, the intervention group (n=52) showed a greater decrease in urinary salt excretion than the control group (n=46), with an adjusted difference of -1.38 g (p=0.001). Conclusions: The authors developed a cooking class package for salt reduction so that third parties could replicate and modify the class. The significant salt reduction noted in this study warrants further studies to apply this cooking class to other populations.

Screening tool for identifying adults with excessive salt intake among community-dwelling adults: a population-based cohort study.

BACKGROUND: Excessive salt intake is widely known to be a cause of hypertension, cardiovascular events, and so on. However, simple tools for screening excessive salt intake are lacking. OBJECTIVE: We aimed to develop a simple screening tool to identify community-dwelling adults with excessive salt intake. METHODS: The present study involved participants who received health check-ups in Fukushima, Japan, in 2016 and 2017. We defined data from the 2016 check-up as the derivation set, and data from those who received check-ups in 2017 but not 2016 as the validation set. The outcome measure was excessive salt intake, defined as the estimated daily salt intake of 1 SD or more. Candidate predictors associated with the outcome were extracted using the Delphi method by an expert panel and narrowed down with clinical expertise and stepwise backward selection. The screening tool was developed using a coefficient-based multivariable scoring method and externally validated. RESULTS: A total of 1101 participants were included in the derivation set and 249 in the validation set. At the conclusion of the deviation process, 8 predictors were selected and scored. The areas under the receiver operating characteristic curve for derivation and external validation were 0.70 (95% CI: 0.67, 0.74) and 0.71 (95% CI: 0.62, 0.80), respectively. The calibration slope and intercept for external validation were 1.16 and -0.03, respectively. CONCLUSION: We developed a screening tool to identify adults with excessive salt intake. By extracting groups with excessive salt intake, target populations needing intervention for salt reduction can be highlighted efficiently.

Effects of self-monitoring of daily salt intake estimated by a simple electrical device for salt reduction: a cluster randomized trial.

Recently, a simple device for self-monitoring of daily salt intake was developed, and it is recommended by The Japanese Society of Hypertension. This study aimed to investigate the effects of this device on salt reduction and on lowering blood pressure. In this single blinded, cluster randomized controlled trial, families were randomly assigned to either an intervention or a control group. Participants in both groups attended lectures about salt reduction, but only the intervention group used the self-monitoring device to estimate their daily salt intake. The main outcome measure was the difference in the estimated daily salt intake by spot urine between the two groups after 4 weeks. The secondary outcome was the difference in blood pressure. A total of 105 families (158 participants) were randomized. The mean daily salt intake was 9.04 (SD 1.77) g/day in the control group and 9.37 (SD 2.13) g/day in the intervention group at baseline. After 4 weeks, the mean daily salt intake was 8.97 (SD 1.97) g/day in the control group and 8.60 (SD 2.25) g/day in the intervention group; the mean difference between the two groups was -0.50 g/day (95% confidence interval (CI) -0.95, -0.05; P = 0.030). The mean difference in systolic blood pressure was -4.4 mm Hg (95% CI -8.7, -0.1; P = 0.044). This is the first randomized controlled trial to demonstrate the effectiveness of a device for self-monitoring of salt intake with a significant reduction in daily salt intake and systolic blood pressure.

Effects of atorvastatin on renal function in patients with dyslipidemia and chronic kidney disease: assessment of clinical usefulness in CKD patients with atorvastatin (ASUCA) trial.

BACKGROUND: Dyslipidemia is a risk factor for the progression of chronic kidney disease (CKD). While conventional lipid lowering therapy provides a benefit to CKD management, the effect of statins on eGFR remains unclear. METHODS: A prospective, multi-center, open-labeled, randomized trial. Total of 349 CKD patients with hyperlipidemia were randomized into 2 groups, and followed for 2 years. Group A included patients who were treated with atorvastatin. Group C were treated with conventional lipid lowering drugs other than statin. Primary endpoint was changes in eGFR. Secondary endpoints included changes in urinary albumin excretion, serum LDL-C, serum triglyceride, cardio-vascular events and all-cause mortality. RESULTS: As the primary endpoint, eGFR decreased by 2.3 ml/min/1.73 m2 in Group A and by 2.6 ml/min/1.73 m2 in Group C, indicating that there was no difference in change of eGFR between the two groups. As secondary endpoints, atorvastatin succeeded to reduce serum LDL-C level significantly and rapidly, but conventional therapy did not. In fact, mean LDL-C level did not reach the target level of 100 mg/dl in Group C. Serum triglyceride was lowered only by atorvastatin, but not conventional drugs. The number of cardiovascular events and all-cause mortality did not differ between in two groups. CONCLUSION: The ASUCA (Assessment of Clinical Usefulness in CKD Patients with Atorvastatin) trial demonstrated that atorvastatin failed to exhibit reno-protections compared to conventional therapy in Japanese patients with dyslipidemia and CKD. It would be due in part to the ability of atorvastatin to more potently reduce serum LDL and triglycerides compared to conventional therapy.

Vitamin D3/VDR resists diet-induced obesity by modulating UCP3 expression in muscles.

BACKGROUND: The impact of vitamin D3 (VD3) on obesity has been reported in the past. Our study was aimed at investigating the possible mechanisms by which VD3 affects obesity induced by a high fat diet. METHODS: Eight-week-old C57BL/6 J male mice were fed a normal- or high-fat diet for 9 weeks and were treated with a gavage of vehicle (corn oil) or cholecalciferol (50 µg/kg, daily). Body weight, white adipose tissue weight, blood lipid and glucose levels were measured. In addition, we investigated the expression of 1,25(OH)2D3 (calcitriol)/VDR-regulated genes involved in energy and lipid metabolism, such as of uncoupling protein 3 (UCP3), by using qRT-PCR in the liver, adipose tissue, skeletal muscle and C2C12, L6, and H-EMC-SS cells. We also measured UCP3 promoter transcription in the same cell lines using a Dual Luciferase Assay. Furthermore, we analyzed the binding site consensus sequences of VDR on the UCP3 promoter. RESULTS: Mice consuming a high-fat diet treated with cholecalciferol had lower body weight and adipose tissue weight and higher expression of UCP3 compared to the other treatment groups. Changes in the expression of genes correlated with calcitriol/VDR. Luciferase activity was dose-dependently associated with calcitriol/VDR levels. We confirmed the functional VDR binding site consensus sequences at -2200, -1561, -634, and +314 bp in the UCP3 promoter region. CONCLUSION: We suggest that VD3/VDR inhibits weight gain by activating UCP3 in the muscles.

Transcriptional activation of the wild-type and mutant vitamin D receptors by vitamin D3 analogs.

The active form of vitamin D3 (1α,25(OH)2D3, also known as calcitriol) controls the expression of target genes via the vitamin D receptor (VDR). Vitamin D-dependent rickets type II (VDDRII) is a congenital disease caused by inactivating mutations in the VDR The condition is treated with high doses of calcitriol, but the therapeutic effects of other synthetic VD3 analogs have not yet been investigated. In the present study, we analyzed the transcriptional activity of seven different VD3 analogs with VDRs carrying ligand-binding domain mutations identified in VDDRII patients. Wild-type VDR (WT-VDR) and seven mutant VDRs were expressed in TSA201 human embryonic kidney cells, HepG2 human liver cancer cells, and MC3T3-E1 mouse calvaria cells, and their transcriptional activation with VD3 analogs were analyzed by performing transient expression assays, western blotting, and quantitative real-time PCR. The results demonstrated that falecalcitriol stimulated significantly higher transcriptional activation of the WT-VDR and some mutant VDRs than did calcitriol. Calcitriol showed almost no transcriptional activation of the VDR with the I268T mutation identified in a severe case of VDDRII, whereas falecalcitriol caused a dose-dependent increase in the activation of this mutant VDR. Our findings demonstrate that falecalcitriol has a VDR activation profile distinct from that of calcitriol and may exhibit therapeutic effects even on difficult-to-treat VDDRII cases resistant to calcitriol. It is also possible that VDDRII patients responding to high doses of calcitriol could be appropriately treated with low doses of falecalcitriol.

Growth hormone regulates the expression of UCP2 in myocytes.

OBJECTIVE: To determine if and how growth hormone (GH) signaling is involved in energy metabolism. DESIGN: We used human embryonic kidney TSA201 cells, human H-EMC-SS chondrosarcoma cells, rat L6 skeletal muscle cells, and murine C2C12 skeletal muscle myoblasts to investigate GH-induced expression of uncoupling protein2 (UCP2) to the GHR/JAK/STAT5 pathway by a combination of a reporter assay, electrophoretic mobility shift assay (EMSA), real-time quantitative PCR, Western blotting. RESULTS: We demonstrated that the regulation energy metabolism, which was hypothesized to be directly acted on by GH, involves UCP2 via activated STAT5B, a signal transducer downstream of GH. We also showed that the sequence at the -586 'TTCnGA' may function as a novel putative consensus sequence of STAT5s. CONCLUSION: The results suggest that GH regulates energy metabolism directly in myocytes and that UCP2 participates in the signal transduction pathway that functions downstream of the GHR/JAK/STAT.

Effects of atorvastatin on renal function in patients with dyslipidemia and chronic kidney disease: rationale and design of the ASsessment of clinical Usefulness in CKD patients with Atorvastatin (ASUCA) trial.

BACKGROUND: Since dyslipidemia has been shown to be an independent risk factor for the progression of chronic kidney disease (CKD), low-density lipoprotein cholesterol (LDL-C)-lowering therapy can be potentially associated with inhibition of CKD progression. The ASsessment of clinical Usefulness in CKD patients with Atorvastatin (ASUCA) trial was designed to determine whether atorvastatin has protective effects on renal function in patients with dyslipidemia and CKD. METHODS: We decided to carry out a prospective multi-center, open-labeled, randomized trial to compare the reno-protective effects between diet therapy alone and atorvastatin plus diet therapy in patients with dyslipidemia (LDL-C ≥ 140 mg/dL if not treated or LDL-C ≥ 100 mg/dL if treated with lipid-lowering drugs in subjects taking dyslipidemia-treating agents other than statins) and CKD [estimated glomerular filtration rate (eGFR) < 60 mL/min/1.73 m(2)]. The primary endpoint is the change in eGFR (mL/min/1.73 m(2)) as calculated by the modified MDRD equation for Japanese after 2 years of treatment. RESULTS: Enrollment began in April 2009 and was completed in March 2011. A total of 334 patients (213 male and 121 female) were randomly assigned to either diet therapy alone or atorvastatin plus diet therapy and included in an intent-to-treat population. In the atorvastatin and control groups, the mean ages were 63.2 and 63.1 years, mean eGFRs were 55.9 and 54.0 mL/min/1.73 m(2), and median urinary albumin/creatinine ratios were 24.9 and 29.1 mg/g, respectively. CONCLUSIONS: This study distinguishes itself from similar studies by increasing statistical accuracy derived from its significantly larger sample size and longitudinal magnitude. The results of this study will help to determine whether atorvastatin has reno-protective effects in patients with dyslipidemia and CKD.