The burden of cardiovascular disease attributable to high dietary sodium intake in Australia between 1990 and 2019.

BACKGROUND: Diets high in sodium are associated with adverse cardiovascular outcomes. We aimed to quantify the burden of cardiovascular disease (CVD) attributable to high dietary sodium consumption in the Australian population. METHODS: Using data from the Global Burden of Disease (GBD) 2019, we estimated the age-standardised rates (per 100 000 population) and the total numbers of years lived with a disability (YLDs), years of life lost (YLLs), disability-adjusted life years (DALYs), and deaths for CVD attributable to high sodium (≥1000 mg/day) consumption in the Australian population, by sex and age groups (≥25 years) between 1990 and 2019. The study compared Australian estimates with similar high-income countries (Group of 20 [G20] members). RESULTS: From 1990 to 2019, the age-standardized rates of CVD deaths, DALYs, YLDs, and YLLs per 100 000 population in Australia attributable to high sodium decreased. However, between 2013 and 2019, the total number of CVD deaths increased, and the number of CVD YLDs increased exponentially for both sexes for the whole period between 1990 and 2019. Men had a two-fold higher rate for high sodium CVD burden, compared to females between 1990 to 2019. Individuals aged between 80 and 84 years had the highest rates of CVD burden during the same period; however, older age groups reported the greatest decline in CVD burden compared to young and middle-aged adults in Australia. The age-standardised rates for high sodium attributable CVD consistently contributed more towards DALYs than YLDs in 2019 for both sexes. When compared to G20 countries, Australians displayed the lowest age-standardized rates for CVD deaths, DALYs, YLDs, and YLLs alongside Turkey, France, and the United Kingdom in 2019. CONCLUSION: While age-standardized CVD burden attributable to high sodium consumption decreased for both sexes over the past 30 years, the total number of CVD deaths showed an increase between 2013 and 2019. This study underscores the need for sustained efforts to address the rising absolute number of CVD deaths, especially among men and older people, and emphasizes the importance of continued vigilance in monitoring and implementing strategies to reduce the impact of high sodium consumption on cardiovascular health in Australia.

Cardiovascular Disease Burden Attributable to High Sodium Intake in China: A Longitudinal Study from 1990 to 2019.

BACKGROUND: Overconsumption of sodium has been identified as a key driving factor for diet-related cardiovascular diseases (CVDs). China, being a country bearing a hefty burden of CVD, has a large population with diverse cultural traditions and ethnic beliefs, which complicates the patterns of dietary sodium intake, necessitating a systematic investigation into the profile of the high sodium intake (HSI)-related burden of CVD within its subregions. This study aims to estimate the evolving patterns of HSI-induced CVD burden across China from 1990 to 2019. METHODS: The methodology used in the Global Burden of Disease Study was followed to assess deaths and disability-adjusted life years (DALYs) by age, sex, region, and socio-demographic index (SDI). The estimated annual percentage change (EAPC) was calculated to quantify the secular changes in the age-standardized mortality rate (ASMR) and age-standardized DALY rate (ASDR). RESULTS: In 2019, 0.79 million deaths and 1.93 million DALYs of CVD were attributed to HSI, an increase of 53.91% and 39.39% since 1990, respectively. Nevertheless, a downward trend in ASMR (EAPC: -1.45, 95% CI: -1.55, -1.35) and ASDR (EAPC: -1.61, 95% CI: -1.68, -1.53) was detected over time. ASMR and ASDR were higher for males, individuals aged ≥60 years, and regions with low-middle SDI. A markedly negative association between the EAPC in both ASMR and ASDR and the SDI was found in 2019 (ρ = -0.659, p < 0.001 and ρ = -0.558, p < 0.001, respectively). CONCLUSIONS: The HSI-induced CVD burden is gender-, age-, and socioeconomic-dependent. Integrated and targeted strategies for CVD prevention are anticipated in the future throughout China.

Hypotensive drugs mitigate the high-sodium diet-induced pro-inflammatory activation of mouse macrophages in vivo.

Nowadays, there is an increasing emphasis on the need to alleviate the chronic inflammatory response to effectively treat hypertension. However, there are still gaps in our understanding on how to achieve this. Therefore, research on interaction of antihypertensive drugs with the immune system is extremely interesting, since their therapeutic effect could partly result from amelioration of hypertension-related inflammation, in which macrophages seem to play a pivotal role. Thus, current comprehensive studies have investigated the impact of repeatedly administered hypotensive drugs (captopril, olmesartan, propranolol, carvedilol, amlodipine, verapamil) on macrophage functions in the innate and adaptive immunity, as well as if drug-induced effects are affected by a high-sodium diet (HSD), one of the key environmental risk factors of hypertension. Although the assayed medications increased the generation of reactive oxygen and nitrogen intermediates by macrophages from standard fed donors, they reversed HSD-induced enhancing effects on macrophage oxidative burst and secretion of pro-inflammatory cytokines. On the other hand, some drugs increased macrophage phagocytic activity and the expression of surface markers involved in antigen presentation, which translated into enhanced macrophage ability to activate B cells for antibody production. Moreover, the assayed medications augmented macrophage function and the effector phase of contact hypersensitivity reaction, but suppressed the sensitization phase of cell-mediated hypersensitivity under HSD conditions. Our current findings contribute to the recognition of mechanisms, by which excessive sodium intake affects macrophage immune activity in hypertensive individuals, and provide evidence that the assayed medications mitigate most of the HSD-induced adverse effects, suggesting their additional protective therapeutic activity.

Sex-specific associations between sodium and potassium intake and overall and cause-specific mortality: a large prospective U.S. cohort study, systematic review, and updated meta-analysis of cohort studies.

BACKGROUND: The impact of sodium intake on cardiovascular disease (CVD) health and mortality has been studied for decades, including the well-established association with blood pressure. However, non-linear patterns, dose-response associations, and sex differences in the relationship between sodium and potassium intakes and overall and cause-specific mortality remain to be elucidated and a comprehensive examination is lacking. Our study objective was to determine whether intake of sodium and potassium and the sodium-potassium ratio are associated with overall and cause-specific mortality in men and women. METHODS: We conducted a prospective analysis of 237,036 men and 179,068 women in the National Institutes of Health-AARP Diet and Health Study. Multivariable-adjusted Cox proportional hazard regression models were utilized to calculate hazard ratios. A systematic review and meta-analysis of cohort studies was also conducted. RESULTS: During 6,009,748 person-years of follow-up, there were 77,614 deaths, 49,297 among men and 28,317 among women. Adjusting for other risk factors, we found a significant positive association between higher sodium intake (≥ 2,000 mg/d) and increased overall and CVD mortality (overall mortality, fifth versus lowest quintile, men and women HRs = 1.06 and 1.10, Pnonlinearity < 0.0001; CVD mortality, fifth versus lowest quintile, HRs = 1.07 and 1.21, Pnonlinearity = 0.0002 and 0.01). Higher potassium intake and a lower sodium-potassium ratio were associated with a reduced mortality, with women showing stronger associations (overall mortality, fifth versus lowest quintile, HRs for potassium = 0.96 and 0.82, and HRs for the sodium-potassium ratio = 1.09 and 1.23, for men and women, respectively; Pnonlinearity < 0.05 and both P for interaction ≤ 0.0006). The overall mortality associations with intake of sodium, potassium and the sodium-potassium ratio were generally similar across population risk factor subgroups with the exception that the inverse potassium-mortality association was stronger in men with lower body mass index or fruit consumption (Pinteraction < 0.0004). The updated meta-analysis of cohort studies based on 42 risk estimates, 2,085,904 participants, and 80,085 CVD events yielded very similar results (highest versus lowest sodium categories, pooled relative risk for CVD events = 1.13, 95% CI: 1.06-1.20; Pnonlinearity < 0.001). CONCLUSIONS: Our study demonstrates significant positive associations between daily sodium intake (within the range of sodium intake between 2,000 and 7,500 mg/d), the sodium-potassium ratio, and risk of CVD and overall mortality, with women having stronger sodium-potassium ratio-mortality associations than men, and with the meta-analysis providing compelling support for the CVD associations. These data may suggest decreasing sodium intake and increasing potassium intake as means to improve health and longevity, and our data pointing to a sex difference in the potassium-mortality and sodium-potassium ratio-mortality relationships provide additional evidence relevant to current dietary guidelines for the general adult population. SYSTEMATIC REVIEW REGISTRATION: PROSPERO Identifier: CRD42022331618.

Sodium Intake and Cause-Specific Mortality Among Predominantly Low-Income Black and White US Residents.

IMPORTANCE: Epidemiologic evidence regarding the outcomes of dietary sodium intake on mortality remains limited for low-income individuals, particularly Black people. OBJECTIVE: To investigate the associations of excessive dietary sodium with all-cause and cause-specific mortality among predominantly low-income Black and White Americans. DESIGN, SETTING, AND PARTICIPANTS: This cohort study included participants aged 40 to 79 years from the Southern Community Cohort Study who were recruited at Community Health Centers in 12 southeastern states from 2002 to 2009. Analyses were conducted between March 2022 and June 2023. EXPOSURES: Dietary sodium intake was assessed using a validated food frequency questionnaire at baseline. MAIN OUTCOMES AND MEASURES: Multivariable-adjusted Cox regression was used to estimate hazard ratios (HRs) and 95% CIs for mortality outcomes (all-cause, cardiovascular disease [CVD], coronary heart disease [CHD], stroke, heart failure, cancer, and other) associated with sodium intake. Nonlinear associations and population-attributable risk (PAR) of the mortality burden associated with excess sodium were further assessed. RESULTS: Among the 64 329 participants, 46 185 (71.8%) were Black, 18 144 (28.2%) were White, and 39 155 (60.9%) were female. The mean (SD) age at study enrollment was 51.3 (8.6) years for Black participants and 53.3 (9.3) years for White counterparts. Mean (SD) dietary sodium intake was 4512 (2632) mg/d in Black individuals and 4041 (2227) mg/d in White individuals; 37 482 Black individuals (81.2%) and 14 431 White individuals (79.5%) exceeded the current dietary recommendations of 2300 mg/d. During a median (IQR) follow-up of 13.8 (11.3-15.8) years, 17 811 deaths were documented, including 5701 from CVD. After adjustment for potential confounders, in Black individuals, HRs per 1000-mg increase in daily sodium intake were 1.07 (95% CI, 1.03-1.10) and 1.08 (95% CI, 1.02-1.14) for deaths from total CVD and CHD, respectively; while in White individuals, the corresponding HRs were 1.08 (95% CI, 1.02-1.14) and 1.13 (95% CI, 1.03-1.23). No significant associations were found for cancer mortality. PAR estimates suggest that sodium intake above the recommended threshold may account for 10% of total CVD, 13% of CHD, and 30% of heart failure deaths in this low-income southern population. CONCLUSIONS AND RELEVANCE: In this cohort study of 64 329 low-income Americans, nearly 80% of study participants consumed sodium exceeding the current recommended daily amount, which was associated with 10% to 30% of CVD mortality. Public health programs targeted to reduce sodium intake among this underserved population may be beneficial.

Spatiotemporal trends in the burden of aortic aneurysms caused by high sodium intake from 1990 to 2019: A global, regional, and national analysis.

BACKGROUND AND AIMS: This study, drawing on Global Burden of Disease (GBD) data, examines spatiotemporal trends in mortality and disability-adjusted life years (DALYs) linked to aortic aneurysm (AA) from high sodium intake. The aim is a comprehensive analysis globally, regionally, and nationally spanning 1990 to 2019. METHODS AND RESULTS: Quantifying AA deaths and DALYs due to high sodium intake, incorporating age-standardized mortality rate (ASMR) and age-standardized DALYs rate (ASDR), revealed a global surge. Deaths rose by 86.09 %, DALYs by 74.02 % from 1990 to 2019. EAPC for ASMR and ASDR displayed negative trends (-0.72 and -0.77). High/middle-high Socio-demographic Index (SDI) regions bore higher burdens than lower SDI regions. Males consistently had higher burdens across SDI regions, with both genders showing a slight downward trend. Age-wise, AA deaths and DALYs rose with age, followed by decline. A positive correlation existed between SDI and global burden, inversely related to EAPC for ASMR and ASDR. CONCLUSION: AA burden from high sodium intake is pronounced in high SDI regions, necessitating targeted interventions. The global data highlights a significant increase in AA deaths and DALYs due to high sodium intake, urging prompt and effective control measures.

The contribution of sodium reduction and potassium increase to the blood pressure lowering observed in the Salt Substitute and Stroke Study.

The Salt Substitute and Stroke Study (SSaSS) demonstrated significant reductions in systolic blood pressure (SBP), and the risk of stroke, major cardiovascular events and total mortality with the use of potassium-enriched salt. The contribution of sodium reduction versus potassium increase to these effects is unknown. We identified four different data sources describing the association between sodium reduction, potassium supplementation and change in SBP. We then fitted a series of models to estimate the SBP reductions expected for the differences in sodium and potassium intake in SSaSS, derived from 24-h urine collections. The proportions of the SBP reduction separately attributable to sodium reduction and potassium supplementation were calculated. The observed SBP reduction in SSaSS was -3.3 mmHg with a corresponding mean 15.2 mmol reduction in 24-h sodium excretion and a mean 20.6 mmol increase in 24-h potassium excretion. Assuming 90% of dietary sodium intake and 70% of dietary potassium intake were excreted through urine, the models projected falls in SBP of between -1.67 (95% confidence interval: -4.06 to +0.73) mmHg and -5.33 (95% confidence interval: -8.58 to -2.08) mmHg. The estimated proportional contribution of sodium reduction to the SBP fall ranged between 12 and 39% for the different models fitted. Sensitivity analyses assuming different proportional urinary excretion of dietary sodium and potassium intake showed similar results. In every model, the majority of the SBP lowering effect in SSaSS was estimated to be attributable to the increase in dietary potassium rather than the fall in dietary sodium.

Sex-Specific Association between Sodium Intake Estimated by 24-Hour Urinary Sodium Excretion and Nonalcoholic Fatty Liver Disease: The Community-Based Prospective Cohort Study.

Evidence for the association between high sodium intake and the onset of nonalcoholic fatty liver disease (NAFLD) is insufficient. This study examined the sex-specific association between sodium intake and the risk of NAFLD. This study included 2582 adults (aged 40-69 years; 1011 males and 1571 females). The total sodium excreted over 24 h was estimated from spot urine specimens using Tanaka's equation. Based on these estimates, participants were categorized into three groups according to their 24-h urinary sodium excretion levels: lowest (T1), middle (T2), and highest (T3). In addition, the participants were divided into non-NAFLD (≤36) and NAFLD (>36) groups based on the hepatic steatosis index. During the follow-up period (14 years), NAFLD was observed in 551 participants. The estimated 24-h urinary sodium excretion levels were positively associated with the incidence of NAFLD in all subjects. Upon sex stratification, females in the T2 and T3 groups exhibited adjusted hazard ratios of 1.35 and 1.51, respectively, compared with the T1 group. However, a significant relationship was not observed in males. High intake of sodium, especially among females, may be an important factor contributing to the development of NAFLD. Individuals with high sodium intake should be appropriately counselled and monitored for the risk of NAFLD.

Assessing the effects of tempol on renal fibrosis, inflammation, and oxidative stress in a high-salt diet combined with 5/6 nephrectomy rat model: utilizing oxidized albumin as a biomarker.

BACKGROUND: Oxidative stress has been implicated in the pathogenesis of chronic kidney disease (CKD), prompting the exploration of antioxidants as a potential therapeutic avenue for mitigating disease progression. This study aims to investigate the beneficial impact of Tempol on the progression of CKD in a rat model utilizing oxidized albumin as a biomarker. METHODS: After four weeks of treatment, metabolic parameters, including body weight, left ventricle residual weight, kidney weight, urine volume, and water and food intake, were measured. Systolic blood pressure, urinary protein, oxidized albumin level, serum creatinine (Scr), blood urea nitrogen (BUN), 8-OHdG, TGF-ß1, and micro-albumin were also assessed. Renal fibrosis was evaluated through histological and biochemical assays. P65-NF-κB was quantified using an immunofluorescence test, while Smad3, P65-NF-κB, and Collagen I were measured using western blot. TNF-α, IL-6, MCP-1, TGF-ß1, Smad3, and P65-NF-κB were analyzed by RT-qPCR. RESULTS: Rats in the high-salt diet group exhibited impaired renal function, characterized by elevated levels of blood urea nitrogen, serum creatinine, 8-OHdG, urine albumin, and tubulointerstitial damage, along with reduced body weight. However, these effects were significantly ameliorated by Tempol administration. In the high-salt diet group, blood pressure, urinary protein, and oxidized albumin levels were notably higher compared to the normal diet group, but Tempol administration in the treatment group reversed these effects. Rats in the high-salt diet group also displayed increased levels of proinflammatory factors (TNF-α, IL-6, MCP1) and profibrotic factors (NF-κB activation, Collagen I), elevated expression of NADPH oxidation-related subunits (P65), and activation of the TGF-ß1/Smad3 signaling pathway. Tempol treatment inhibited NF-κB-mediated inflammation and TGF-ß1/Smad3-induced renal fibrosis signaling pathway activation. CONCLUSION: These findings suggest that Tempol may hold therapeutic potential for preventing and treating rats undergoing 5/6 nephrectomy. Further research is warranted to elucidate the mechanisms underlying Tempol's protective effects and its potential clinical applications. Besides, there is a discernible positive relationship between oxidized albumin and other biomarkers, such as 8-OHG, urinary protein levels, mALB, Scr, BUN, and TGF-ß1 in a High-salt diet combined with 5/6 nephrectomy rat model. These findings suggest the potential utility of oxidized albumin as a sensitive indicator for oxidative stress assessment.

The dilemma of sodium intake in preeclampsia: beneficial or detrimental?

Preeclampsia (PE) is a disorder involving de novo development of hypertension plus end organ damage after 20 weeks of gestation. PE is considered to be a heterogeneous disease. There are 2 main types of PE: early-onset (<34 weeks of gestation), which is considered to be a placental disorder and is associated with vasoconstriction, low cardiac output, and placental hypoperfusion and organ damage due to decreased microcirculation to maternal organs; and late-onset PE, which is primarily a disorder of pregnant women with obesity, diabetes, and/or cardiovascular abnormalities. In late-onset PE, there is avid sodium reabsorption by the maternal kidneys, causing hypervolemia and increased cardiac output, along with vasodilatation causing venous congestion of organs. Although PE has been a well-known disease for a long time, it is interesting to note that there is no specific sodium (salt) intake recommendation for these patients. This may be due to the fact that studies since as far back as the 1900s have shown conflicting results, and the reasons for the inconsistent findings have not been fully explained; furthermore, the type of PE in these studies was not specifically defined. Some studies suggest that sodium restriction may be detrimental in early-onset PE, but may be feasible in late-onset PE. To explore this paradox, the current review explains the hemodynamic factors involved in these 2 types of PE, summarizes the findings of the current studies, and highlights the knowledge gaps and the research needed to determine whether increase or restriction of salt or sodium intake is beneficial in different types of PE.

Sex influences blood pressure but not blood pressure variability in response to dietary sodium and potassium in salt-resistant adults.

Dietary sodium and potassium have been shown to affect blood pressure (BP) but their influence on BP variability (BPV) is less studied as is the influence of sex. The aim of this study was to compare 24 h BP and short-term BPV in response to varying dietary levels of sodium and potassium in healthy non-obese normotensive salt-resistant adults. We hypothesized that high sodium would increase short-term BP and BPV while the addition of high potassium would counteract this increase. Furthermore, we hypothesized that women would experience greater increases in BPV under high sodium conditions compared to men while potassium would attenuate this response. Thirty-seven participants (17 M/20 W; 27 ± 5 years old; BMI 24.3 ± 3 kg/m2) completed seven days each of the following randomized diets: moderate potassium/low sodium (MK/LS), moderate potassium/high sodium (MK/HS) and high potassium/high sodium (HK/HS). BP and short-term BPV were assessed using 24 h ambulatory BP monitoring starting on day 6. BPV was calculated using the average real variability (ARV) index. Twenty-four hour, daytime, and nighttime systolic BP (SBP) were lower in women compared to men regardless of diet. However, 24 h and daytime SBP were lowered in women on the HK/HS diet compared to the MK/HS diet. There were no significant effects of diet or sex for 24 h, daytime or nighttime SBP ARV. However, men exhibited a higher 24 hDBP ARV than women regardless of diet. In conclusion, a high potassium diet lowered BP under high sodium conditions in women alone while men exhibited higher short-term BPV that was not influenced by diet.

Using Genetics to Inform Interventions Related to Sodium and Potassium in Hypertension.

BACKGROUND: Hypertension is a key risk factor for major adverse cardiovascular events but remains difficult to treat in many individuals. Dietary interventions are an effective approach to lower blood pressure (BP) but are not equally effective across all individuals. BP is heritable, and genetics may be a useful tool to overcome treatment response heterogeneity. We investigated whether the genetics of BP could be used to identify individuals with hypertension who may receive a particular benefit from lowering sodium intake and boosting potassium levels. METHODS: In this observational genetic study, we leveraged cross-sectional data from up to 296 475 genotyped individuals drawn from the UK Biobank cohort for whom BP and urinary electrolytes (sodium and potassium), biomarkers of sodium and potassium intake, were measured. Biologically directed genetic scores for BP were constructed specifically among pathways related to sodium and potassium biology (pharmagenic enrichment scores), as well as unannotated genome-wide scores (conventional polygenic scores). We then tested whether there was a gene-by-environment interaction between urinary electrolytes and these genetic scores on BP. RESULTS: Genetic risk and urinary electrolytes both independently correlated with BP. However, urinary sodium was associated with a larger BP increase among individuals with higher genetic risk in sodium- and potassium-related pathways than in those with comparatively lower genetic risk. For example, each SD in urinary sodium was associated with a 1.47-mm Hg increase in systolic BP for those in the top 10% of the distribution of genetic risk in sodium and potassium transport pathways versus a 0.97-mm Hg systolic BP increase in the lowest 10% (P=1.95×10-3). This interaction with urinary sodium remained when considering estimated glomerular filtration rate and indexing sodium to urinary creatinine. There was no strong evidence of an interaction between urinary sodium and a standard genome-wide polygenic score of BP. CONCLUSIONS: The data suggest that genetic risk in sodium and potassium pathways could be used in a precision medicine model to direct interventions more specifically in the management of hypertension. Intervention studies are warranted.

Salt restriction for treatment of hypertension - current state and future directions.

PURPOSE OF REVIEW: Given the adverse effects of excess dietary sodium chloride (also known as table salt) on blood pressure (BP) and cardiovascular disease (CVD), restriction of dietary sodium is recommended by numerous guidelines. The strictest of these recommend no more than 1.5 g/day of dietary sodium among hypertensive persons. However, average dietary sodium intake in the population is closer to 5 g/day and there is debate about whether too much sodium restriction may be associated with increased CVD risk. Herein, we aim to provide a balanced update on this topic. RECENT FINDINGS: In 2021, the Salt Substitute and Stroke Study (SSaSS) demonstrated a significant reduction in BP, CVD, and death among Chinese adults randomized to a low sodium salt-substitute supplemented with potassium. This trial largely puts to rest any remaining debate about the benefits of dietary sodium restriction among persons with excess baseline intake (dietary sodium intake fell from approximately 5 down to 4 g/day in the active arm of SSaSS). However, whether achieving and maintaining a dietary sodium of less than1.5 g/day is feasible in real-world settings and whether this low an intake is harmful remain open questions. SUMMARY: Aiming for sodium intakes of 2--3 g/day in the general population and as low as 2 g/day in persons with hypertension or CVD seems most reasonable, but there is some uncertainty around lower targets.

The Burden of Gastric Cancer Attributable to High Sodium Intake: A Longitudinal Study from 1990 to 2019 in China.

BACKGROUNDS: Excessive intake of sodium is a crucial risk factor of gastric cancer. However, it is still unclear whether the profile of gastric cancer burden is attributable to high sodium intake in China. This study aims to evaluate the levels and trends of gastric cancer burden attributable to high sodium intake across China from 1990 to 2019. METHODS: We acquired data from the GBD (Global Burden of Disease Study) 2019 via the Global Health Data Exchange query tool. The details of regions from 1 January 1990 to 31 December 2019 from the China National Center for Food Safety Risk Assessment were also used. We conducted an integrated analysis on the gastric cancer burden attributable to high sodium intake among Chinese residents. The gastric cancer-related deaths, disability-adjusted life years (DALYs), age-standardized mortality rate (ASMR), and age-standardized DALYs rate (ASDR), all being calculated to be attributable to sodium intake, were reckoned as separated by age, sex, SDI, and regions. Then, the estimated annual percentage change (EAPC) was regarded as the secular trends of gastric cancer's ASMR and ASDR due to high sodium intake from 1990 to 2019. We further explored the associations between SDI (Socio-demographic index) and the ASMR and ASDR. The rates were calculated per 100,000 population as age-standardized rates. RESULTS: Briefly, the number of gastric cancer-related deaths and DALYs being attributed to high sodium intake were 37,131.48 (95% UI: 833.14 to 138,478.72) and 873,813.19 (95% UI: 19,283.13 to 3,220,231.82) in 2019; both have increased by a third since 1990. However, the ASMR decreased with an EAPC of -1.72% (95% CI: -2.11% to -1.33%), while ASDR increased with an EAPC of 0.36% (95% CI: 0.08% to 0.68%), respectively. The age-specific numbers and rates of deaths, as well as DALYs of gastric cancer being attributed to high sodium intake, elevated gradually with age. And, they were higher in males than in females. The gastric cancer burden being attributed to high sodium intake in 2019 and its temporal trends from 1990 to 2019 varied greatly by SDI quintile and geographic locations. There was a strong negative association between the EAPC in ASMR and SDI in 2019 (ρ = -0.642, p < 0.001). The EAPC in ASDR and SDI also exhibited a negative connection in 2019 (ρ = -0.538, p = 0.0012). CONCLUSIONS: Overall, using a longitudinal sample from different regions, the study presented that gastric cancer burden attributed to high sodium intake still exists seriously and varies remarkably by regions, sex, and age across China. The disparity of socioeconomic status on disease burden also exists. Integrated and precise approaches for gastric cancer prevention are anticipated in the future.

Potassium intake: the Cinderella electrolyte.

Dietary guidelines recommend intake targets for some essential minerals, based on observational and experimental evidence relating mineral intake levels to health outcomes. For prevention of cardiovascular disease, reducing sodium intake and increasing potassium intake are the principal tools. While reducing sodium intake has received greatest public health priority, emerging evidence suggests that increasing potassium intake may be a more important target for cardiovascular prevention. Increased potassium intake reduces blood pressure and mitigates the hypertensive effects of excess sodium intake, and the recent large Phase III SSaSS trial reported that increasing potassium intake (and reducing sodium intake) in populations with low potassium intake and high sodium intake, through salt substitution (25% KCl, 75%NaCl), reduces the risk of stroke in patients at increased cardiovascular risk. As key sources of potassium intake include fruit, vegetables, nuts, and legumes, higher potassium intake may be associated with healthy dietary patterns. The current review makes the case that increasing potassium intake might represent a more advantageous dietary strategy for prevention of cardiovascular disease. Future research should focus on addressing the independent effect of potassium supplementation in populations with low or moderate potassium intake, and determine effective strategies to increase potassium intake from diet.

Effect of Dietary Sodium on Blood Pressure: A Crossover Trial.

Importance: Dietary sodium recommendations are debated partly due to variable blood pressure (BP) response to sodium intake. Furthermore, the BP effect of dietary sodium among individuals taking antihypertensive medications is understudied. Objectives: To examine the distribution of within-individual BP response to dietary sodium, the difference in BP between individuals allocated to consume a high- or low-sodium diet first, and whether these varied according to baseline BP and antihypertensive medication use. Design, Setting, and Participants: Prospectively allocated diet order with crossover in community-based participants enrolled between April 2021 and February 2023 in 2 US cities. A total of 213 individuals aged 50 to 75 years, including those with normotension (25%), controlled hypertension (20%), uncontrolled hypertension (31%), and untreated hypertension (25%), attended a baseline visit while consuming their usual diet, then completed 1-week high- and low-sodium diets. Intervention: High-sodium (approximately 2200 mg sodium added daily to usual diet) and low-sodium (approximately 500 mg daily total) diets. Main Outcomes and Measures: Average 24-hour ambulatory systolic and diastolic BP, mean arterial pressure, and pulse pressure. Results: Among the 213 participants who completed both high- and low-sodium diet visits, the median age was 61 years, 65% were female and 64% were Black. While consuming usual, high-sodium, and low-sodium diets, participants' median systolic BP measures were 125, 126, and 119 mm Hg, respectively. The median within-individual change in mean arterial pressure between high- and low-sodium diets was 4 mm Hg (IQR, 0-8 mm Hg; P < .001), which did not significantly differ by hypertension status. Compared with the high-sodium diet, the low-sodium diet induced a decline in mean arterial pressure in 73.4% of individuals. The commonly used threshold of a 5 mm Hg or greater decline in mean arterial pressure between a high-sodium and a low-sodium diet classified 46% of individuals as "salt sensitive." At the end of the first dietary intervention week, the mean systolic BP difference between individuals allocated to a high-sodium vs a low-sodium diet was 8 mm Hg (95% CI, 4-11 mm Hg; P < .001), which was mostly similar across subgroups of age, sex, race, hypertension, baseline BP, diabetes, and body mass index. Adverse events were mild, reported by 9.9% and 8.0% of individuals while consuming the high- and low-sodium diets, respectively. Conclusions and Relevance: Dietary sodium reduction significantly lowered BP in the majority of middle-aged to elderly adults. The decline in BP from a high- to low-sodium diet was independent of hypertension status and antihypertensive medication use, was generally consistent across subgroups, and did not result in excess adverse events. Trial Registration: ClinicalTrials.gov Identifier: NCT04258332.