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Reducing the intake of sodium is an important public health goal for Americans. Since the 1970s, an array of public health interventions and national dietary guidelines has sought to reduce sodium intake. However, the U.S. population still consumes more sodium than is recommended, placing individuals at risk for diseases related to elevated blood pressure. Strategies to Reduce Sodium Intake in the United States evaluates and makes recommendations about strategies that could be implemented to reduce dietary sodium intake to levels recommended by the Dietary Guidelines for Americans . The book reviews past and ongoing efforts to reduce the sodium content of the food supply and to motivate consumers to change behavior. Based on past lessons learned, the book makes recommendations for future initiatives. It is an excellent resource for federal and state public health officials, the processed food and food service industries, health care professionals, consumer advocacy groups, and academic researchers.

Despite efforts over the past several decades to reduce sodium intake in the United States, adults still consume an average of 3,400 mg of sodium every day. A number of scientific bodies and professional health organizations, including the American Heart Association, the American Medical Association, and the American Public Health Association, support reducing dietary sodium intake. These organizations support a common goal to reduce daily sodium intake to less than 2,300 milligrams and further reduce intake to 1,500 mg among persons who are 51 years of age and older and those of any age who are African-American or have hypertension, diabetes, or chronic kidney disease. A substantial body of evidence supports these efforts to reduce sodium intake. This evidence links excessive dietary sodium to high blood pressure, a surrogate marker for cardiovascular disease (CVD), stroke, and cardiac-related mortality. However, concerns have been raised that a low sodium intake may adversely affect certain risk factors, including blood lipids and insulin resistance, and thus potentially increase risk of heart disease and stroke. In fact, several recent reports have challenged sodium reduction in the population as a strategy to reduce this risk. Sodium Intake in Populations recognizes the limitations of the available evidence, and explains that there is no consistent evidence to support an association between sodium intake and either a beneficial or adverse effect on most direct health outcomes other than some CVD outcomes (including stroke and CVD mortality) and all-cause mortality. Some evidence suggested that decreasing sodium intake could possibly reduce the risk of gastric cancer. However, the evidence was too limited to conclude the converse-that higher sodium intake could possibly increase the risk of gastric cancer. Interpreting these findings was particularly challenging because most studies were conducted outside the United States in populations consuming much higher levels of sodium than those consumed in this country. Sodium Intake in Populations is a summary of the findings and conclusions on evidence for associations between sodium intake and risk of CVD-related events and mortality.

The developmental process of the mammalian blastocyst involves the intricate interplay of cellular and molecular mechanisms, including electrolyte dynamics within the trophectoderm (TE). We hypothesized that sodium (Na.sup.+) is actively transported from the TE into the blastocyst cavity, driving water influx and promoting blastocyst expansion. In this study, we investigated the dynamics of Na.sup.+ concentration in the TE of mouse embryos using sodium-binding benzofuran isophthalate (SBFI), a dual-wavelength Na.sup.+ -sensitive fluorescent indicator. Observations revealed three distinct patterns of Na.sup.+ dynamics, each correlating with variations in blastocyst cross-sectional area and developmental outcomes. Embryos exhibiting an initial decrease followed by stabilization of Na.sup.+ concentration (Group A) demonstrated the highest rates of hatching, suggesting a relationship between Na.sup.+ flux and successful embryonic development. In contrast, embryos with transient increases (Group B) displayed reduced hatching rates and developmental progression. Further, the inhibition of Na.sup.+ /K.sup.+ -ATPase activity disrupted Na.sup.+ flux and blastocyst cavity expansion, emphasizing its critical role in blastocyst formation. This study highlights the potential of dual-wavelength imaging for elucidating electrolyte dynamics in preimplantation embryos and its implications for optimizing embryo culture systems in reproductive medicine.

The Dispatched protein, which is related to the NPC1 and PTCH1 cholesterol transporters.sup.1,2 and to H.sup.+-driven transporters of the RND family.sup.3,4, enables tissue-patterning activity of the lipid-modified Hedgehog protein by releasing it from tightly -localized sites of embryonic expression.sup.5-10. Here we determine a cryo-electron microscopy structure of the mouse protein Dispatched homologue 1 (DISP1), revealing three Na.sup.+ ions coordinated within a channel that traverses its transmembrane domain. We find that the rate of Hedgehog export is dependent on the Na.sup.+ gradient across the plasma membrane. The transmembrane channel and Na.sup.+ binding are disrupted in DISP1-NNN, a variant with asparagine substitutions for three intramembrane aspartate residues that each coordinate and neutralize the charge of one of the three Na.sup.+ ions. DISP1-NNN and variants that disrupt single Na.sup.+ sites retain binding to, but are impaired in export of the lipid-modified Hedgehog protein to the SCUBE2 acceptor. Interaction of the amino-terminal signalling domain of the Sonic hedgehog protein (ShhN) with DISP1 occurs via an extensive buried surface area and contacts with an extended furin-cleaved DISP1 arm. Variability analysis reveals that ShhN binding is restricted to one extreme of a continuous series of DISP1 conformations. The bound and unbound DISP1 conformations display distinct Na.sup.+-site occupancies, which suggests a mechanism by which transmembrane Na.sup.+ flux may power extraction of the lipid-linked Hedgehog signal from the membrane. Na.sup.+-coordinating residues in DISP1 are conserved in PTCH1 and other metazoan RND family members, suggesting that Na.sup.+ flux powers their conformationally driven activities.

Background The World Health Organization (WHO) has established recommended daily intakes for sodium and potassium. However, there is currently some controversy regarding the association between sodium intake, potassium intake, the sodium-to-potassium ratio, and overall mortality. To assess the correlations between sodium intake, potassium intake, the sodium-to-potassium ratio, and overall mortality, as well as the potential differences in sodium and potassium intake thresholds among different population groups, we analyzed data from NHANES 2003–2018. Methods NHANES is an observational cohort study that estimates sodium and potassium intake through one or two 24-h dietary recalls. Hazard ratios (HR) for overall mortality were calculated using multivariable adjusted Cox models accounting for sampling design. A total of 13855 out of 26288 participants were included in the final analysis. Restricted cubic spline analyses were used to examine the relationship between sodium intake, potassium intake, and overall mortality. If non-linearity was detected, we employed a recursive algorithm to calculate inflection points. Results Based on one or two 24-h dietary recalls, the sample consisted of 13,855 participants, representing a non-institutionalized population aged 40–80 years, totaling 11,348,771 person-months of mean follow-up 99.395 months. Daily sodium intake and daily potassium intake were inversely associated with all-cause mortality. Restrictive cubic spline analysis showed non-linear relationships between daily sodium intake, potassium intake, sodium–potassium ratio, and total mortality. The inflection point for daily sodium intake was 3133 mg/d, and the inflection point for daily potassium intake was 3501 mg/d, and the inflection point for daily sodium–potassium ratio intake was 1.203 mg/mg/d. In subgroup analyses, a significant interaction was found between age and high sodium intake, which was further confirmed by the smooth curves that showed a U-shaped relationship between sodium intake and all-cause mortality in the elderly population, with a inflection point of 3634 mg/d. Conclusion Nonlinear associations of daily sodium intake, daily potassium intake and daily sodium–potassium ratio intake with all-cause mortality were observed in American individuals. The inflection point for daily sodium intake was 3133 mg/d. And the inflection point for daily sodium intake was 3634 mg/d in elderly population. The inflection point for daily potassium intake was 3501 mg/d. The inflection point for daily sodium–potassium ratio intake was 1.203 mg/mg/d, respectively, A healthy diet should be based on reasonable sodium intake and include an appropriate sodium-to-potassium ratio.

Sodium intake is undoubtedly indispensable for normal body functions but can be detrimental when taken in excess of dietary requirements. The consequences of excessive salt intake are becoming increasingly clear as high salt consumption persists across the globe. Salt has long been suspected to promote the development of hypertension and cardiovascular diseases and is now also recognized as a potential modulator of inflammatory and autoimmune diseases through its direct and indirect effects on immune cells. The finding that, in addition to the kidneys, other organs such as the skin regulate sodium levels in the body prompted new hypotheses, including the concept that skin-resident macrophages might participate in tissue sodium regulation through their interactions with lymphatic vessels. Moreover, immune cells such as macrophages and different T cell subsets are found in sodium-rich interstitial microenvironments, where sodium levels modulate their function. Alterations to the intestinal bacterial community induced by excess dietary salt represent another relevant axis whereby salt indirectly modulates immune cell function. Depending on the inflammatory context, sodium might either contribute to protective immunity (for example, by enhancing host responses against cutaneous pathogens) or it might contribute to immune dysregulation and promote the development of cardiovascular and autoimmune diseases.

Background The current research on the association of sodium excretion with health outcomes is inconclusive, despite its linear relationship with blood pressure. Moreover, there is a lack of evidence regarding sodium intake. This study aims to estimate sodium intake, examine its associations with mortality, and explore potential factors that may mediate these associations. Methods Based on a nationwide community-based population cohort in China that covered 215 counties from 31 provinces, we collected fasting morning urine from 270,991 participants aged 35–75 years during Dec 2015 and Dec 2019. We calculated 24-h urinary sodium excretion using the Kawasaki formula, and estimated daily sodium intake by adjusting for sweat excretion based on a model with ambient temperature. We fitted Cox regression models to examine its independent hazard ratios (HR) and 95% confidence intervals (CI) on mortality, and assessed the causal mediation effects of metabolic factors. Results Among the included participants with an average age of 56 years, the mean of estimated daily sodium intake was 222.9 ± 71.0 mmol. Sodium intake was lower in elderly and women, but higher in participants living in the north or rural areas ( P  < 0.001 for both). In participants without antihypertensive treatment, blood pressure was positively related to sodium intake (4.14/1.58 mmHg per 100 mmol/day, P  < 0.001). Compared with participants in the quintile 3 of sodium intake (i.e., 200.8–235.1 mmol/day), those in the quintile 1 (i.e., < 163.5 mmol/day) had an adjusted HR of 1.17 (95% CI: 1.05–1.30) for cardiovascular mortality, after adjusting for demographic, socioeconomic, behavioural, and clinical characteristics, as well as urinary potassium, with heart rate (29.4%) and blood glucose (18.5%) as major significant mediators. In the meantime, participants in the quintile 5 (i.e., > 278.8 mmol/day) had an adjusted HR of 1.18 (95% CI: 1.05–1.32), with systolic blood pressure (24.6%) and body mass index (2.4%) playing substantial mediating effects. Conclusions Both high and low sodium intake are associated with increased cardiovascular mortality. The lowest risk is observed at an estimated sodium intake of 200.8–235.1 mmol/day (equivalent to 4.6–5.4 g/day). Mediation analysis suggests that blood pressure, heart rate and glycaemic disorders could be plausible explanations for this U-shaped association.

Background The current prospective cohort study aimed to explore the potential associations between dietary sodium (Na), potassium (K), and sodium-to-potassium (Na-to-K) ratio with an incidence risk of cardiovascular disease (CVD) among Iranian adults. Methods The participants of the Tehran Lipid and Glucose Study (men and women aged 30–84 years, n = 2050), free of CVD at baseline (2006–2008) were included. Dietary intakes were assessed using a validated food frequency questionnaire (FFQ), and incident CVD (i.e., coronary heart disease, stroke, and CVD mortality) were documented up to March 2018. Cox proportional hazard models were used to estimate hazard ratios (HRs) and 95% confidence interval (CI) regarding the association between dietary Na, K, and Na-to-K ratio with CVD events. Results During a median follow-up of 10.6 years, 10.14% of participants experienced CVD outcomes. A 41% increased risk of CVD in relation to each increase in 1000 mg/d of Na intake. In the fully-adjusted model, higher Na intake (> 4143 versus < 3049 mg/d) was significantly related to the increased risk of CVD (HR = 1.99, 95% CI = 1.06–3.74). Independent of the well-known risk factors, a 56% reduced risk of CVD was observed in the participants with a higher dietary K intake (HR = 0.44, 95% CI = 0.20–0.94). A Higher Na-to-K ratio was associated with an increased risk of CVD (HR = 1.99, 95% CI = 1.13–3.52). Conclusion Our study showed that the Na-to-K ratio might independently predict future risk of CVD events in adults.

Magnesium plays a vital role in enhancing plant resilience under salt stress. However, its specific function in maintaining ion homeostasis, particularly in regulating sodium uptake, remains unclear. Recognizing that magnesium deficiency leads to increased potassium uptake and accumulation, and given that sodium and potassium possess the same charge, we hypothesize that salt stress disrupts ion homeostasis to a greater extent in magnesium-deficient plants compared to those deficient in potassium. To test this hypothesis, Vicia faba plants were cultivated hydroponically and subjected to moderate salinity stress (50 mM NaCl) for 2 weeks starting from four weeks after transplanting. The plants were grown under varying levels of magnesium (0.5 mM sufficient; 0.02 mM deficient) and potassium (2 mM sufficient; 0.3 mM deficient), with harvesting occurring two weeks after exposure to salinity. The results indicated that under salinity conditions, magnesium deficiency had a more severe adverse effects on plant growth and gas exchange parameters than potassium deficiency. Stomatal movement was notably restricted in magnesium-deficient plants, potentially due to the over accumulation of soluble sugars and chloride. In magnesium-deficient plants the Na.sup.+/Mg.sup.2+ ratio was significantly higher in leaves (17-fold) and in roots (14-fold) relative to Mg.sup.2+ sufficient plants under salinity stress. Furthermore, the higher K.sup.+/Mg.sup.2+ ratio in magnesium-deficient conditions, observed under both saline and non-saline environments, suggests that potassium's antagonistic effect remains unchanged even under stress conditions. Our findings emphasize for the first time that magnesium, rather than potassium, serves a crucial function in regulating the ion homeostasis necessary for normal plant growth and development in saline environments.

Sodium and heavy metals are among the key elements to which humans are exposed due to environmental pollution and food consumption. Investigating the association between heavy metals, urinary sodium excretion, and obesity is of significant importance, given potential implications for public health. Therefore, this study aims to explore the relationship between heavy metals, urinary sodium excretion, and overweight and obesity in the Korean population. Data from 6,609 participants in the Korea National Health and Nutrition Examination Survey (KNHANES) from 2008 to 2012 were analyzed. Associations between heavy metals (cadmium, mercury), urinary arsenic, sodium excretion levels, and overweight/obesity were assessed using polytomous logistic regression models, adjusting for confounders. Higher mercury (OR = 1.57, 95% CI = 1.31-1.88) and urinary sodium (OR = 2.21, 95% CI = 1.84-2.66) levels are associated with an increased risk of overweight and obesity. Notably, participants with elevated levels of both mercury and urinary sodium had the highest odds of being overweight and obesity (OR = 3.61, 95% CI = 2.61-5.00). In contrast, other heavy metals, such as serum cadmium and urinary arsenic, were not statistically significantly associated with the risk of overweight and obesity. This finding highlights the intricate multiplicative effect between mercury and sodium on obesity, necessitating further research to validate and understand the connections. Heavy metals, particularly mercury, exert an influence on obesity, and the possibility of an enhanced impact on obesity, especially when acting in conjunction with salt, is indicated.